Tokushima University / Educator and Researcher Directory --- Sata, Masataka

Personal Web Page

http://square.umin.ac.jp/TOKUSHIM/

https://researchmap.jp/read0118299 (researchmap)

Field of Study

○	Cardiovascular Medicine

Subject of Study

○	動脈硬化，再生医療，薬物療法，生活習慣病に関する研究

Book / Paper

Book:

1.	田中君枝 and Masataka Sata : 動脈硬化の病態と治療法の開発 - 心外膜脂肪組織の治療標的としての可能性, Jun. 2024.
2.	Zheng Rovert, Yoshihito Saijyo and Masataka Sata : 多発性髄種はなにに気を付ける?, Mar. 2024.
3.	Koji Yamaguchi and Masataka Sata : 3.静脈血栓塞栓症, Dec. 2023.
4.	Shusuke Yagi and Masataka Sata : 循環器疾患の治療標的としての心臓周囲脂肪, 医歯薬出版株式会社, Oct. 2023.
5.	Kenya Kusunose, Zengu Robahto, Hirotsugu Yamada and Masataka Sata : 左室駆出率計測の標準化に向けた展望, Oct. 2023.
6.	MATSUMOTO Rikizo, Susumu Nishio, Yukina Hirata, Sae Morita, Asami Yuasa, 山尾雅美, Takumi Kakimoto, Yu Saitou, Kenya Kusunose, Hirotsugu Yamada, Hisanori Uehara, Mitsuo Shimada and Masataka Sata : 術前の画像検査で肝細胞癌と診断された肝炎症性偽腫瘍の1例, (一社)日本超音波検査学会, Oct. 2023. (Summary) 症例は70代,男性.近医の定期的な血液検査で胆道系酵素の上昇を認めたため,腹部超音波検査を施行したところ,肝左葉内側区に腫瘤を認めた.当院消化器外科に紹介となり,肝内側区切除術が施行され,肝細胞癌と診断された.術後7ヵ月,当院で経過観察目的に施行した造影CT検査で肝左葉外側区に新たに腫瘤を認め,再度精査となった.血液検査では,γ-GTPの軽度上昇を認めるのみで,腫瘍マーカーの上昇は認めなかった.術前の精査目的に施行した腹部超音波検査では,肝左葉外側区(S2)に18×16mm大の腫瘤を認めた.境界明瞭,輪郭は後面が整,前面がやや不整,内部エコーは等輝度で不均質であった.辺縁に比較的厚い低エコー帯を伴っていた.心拍動の影響で血流シグナルの評価は困難であった.腹部造影CT検査では,肝左葉外側区(S2)に2cm大の腫瘤を認め,早期濃染および洗い出しが確認された.本症例は,術前の超音波検査で,肝細胞癌としては非典型的な像を呈していたが,他の画像所見および既往歴から肝細胞癌の再発が否定できず,肝部分切除術が施行され,肝炎症性偽腫瘍と診断された.本症例のように肝細胞癌のリスクが高い症例においても,新規に腫瘤を認めた際には,超音波検査でその特徴を注意深く観察し,典型像と異なる場合には肝炎症性偽腫瘍も鑑別疾患の一つとして考慮した方がよいと考える.(著者抄録) (Keyword) 肝炎(画像診断,外科的療法,病理学) 肝細胞癌肝切除 MRI 腫瘍再発鑑別診断術前評価超音波診断 X線CT 肉芽腫(画像診断,外科的療法,病理学) 肉芽腫-形質細胞(画像診断,外科的療法,病理学) Gadoxetic Acid(診断的利用) Azan染色肝肉芽腫(画像診断,外科的療法,病理学) 腹部CT ヒト高齢者(65∼79) 男 (Link to Publication Site) ● Publication site (DOI): 10.11272/jss.405 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.11272/jss.405 (DOI: 10.11272/jss.405)
7.	Takayuki Ise, 内藤紘一, 佐藤聡見, 小野慎太郎, 石井亜由美, 西川幸治, Muneyuki Kadota, Shusuke Yagi and Masataka Sata : ウェアラブルデバイスとコミュニケーションアプリを用いた遠隔伴走型心リハシステムの開発, Jul. 2023.
8.	田中君枝 and Masataka Sata : 心臓周囲脂肪/内臓脂肪, Apr. 2023.
9.	田中君枝 and Masataka Sata : EPAをめぐるコントロバーシー, Mar. 2023.
10.	Shusuke Yagi, Takayuki Ise, Muneyuki Kadota, Tserensonom Munkhtsetseg, 石井亜由美, 西川幸治 and Masataka Sata : 冠動脈疾患の一次予防に関する身体活動指導, Oct. 2022.
11.	Masataka Sata : 各都道府県における循環器病対策推進協議会の活動報告, Sep. 2022.
12.	Masataka Sata : 選択的心筋ミオシン活性化薬であるomecamtiv mecarbil, Jun. 2022.
13.	Koji Yamaguchi and Masataka Sata : 血管機能不全の診断, Jan. 2022.
14.	Koji Yamaguchi and Masataka Sata : 生活習慣病から起こる心臓病について, Tokushima Medical Association, Dec. 2021. (Summary) Formerly, we used to call the disease caused by hypertension, diabetes, hyperlipidemia, or history of smoking etc ``Adult Disease''. Recently, that is called ``Lifestyle Disease''. Lifestyle disease is associated with ischemic heart disease. Percutaneous coronary intervention using durable polymer(DP)drug-eluting stents(DESs)has been the most common strategy to treat patients with symptomatic coronary artery disease. Use of first-generation DESs reduced in-stent restenosis rates compared with bare metal stents(BMSs); however, their use was associated with late stent thrombosis due to delayed arterial healing. Therefore, the patients with DESs need to continue antiplatelet therapy for more than one month. On the other hand, in several situations where foreign body reaction may occur, stent materials should not be left in the patient. Recently, several clinical trials have supported the efficacy of drugcoated balloons(DCBs)in the treatment of stent restenosis and small vessel de novo lesions. Finally, we propose the following, ① It is possible to prevent the arterioscrelosis and reduce the onset probability of heart disease(ischemic heart disease)by improving lifestyle habit. ② The therapy of ischemic heart disease progresses recently, and we get several new devices for restenosis lesions and severe calcified lesions. ③ It is important for the patients who undergo the catheter therapy to control the status of lifestyle disease. The good relationship between the patient and the doctor is sure to lead the patient to longevity in the future. (Keyword) lifestyle disease / atherosclerotic disease / ischemic heart disease (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050010776440037888 (CiNii: 1050010776440037888)
15.	Masataka Sata : 動脈硬化の成因オイルとの関係, KOKUSEIDO CO., Dec. 2021.
16.	田中君枝 and Masataka Sata : 糖尿病と冠動脈疾患update, 科学評論社, Nov. 2021.
17.	田中君枝 and Masataka Sata : モデル動物の作製と利用-循環器疾患2021 上巻, エル・アイ・シー, Tokyo, Sep. 2021.
18.	田中君枝 and Masataka Sata : 糖尿病における動脈硬化の機序は?, Nankodo, Sep. 2021.
19.	田中君枝 and Masataka Sata : 9.炎症と心腎関連, IGAKU SHUPPAN, May 2021.
20.	Masataka Sata : 編集後記, Dec. 2020.
21.	Masataka Sata and 針谷正祥 : 血管性障害と内科疾患司会者のことば, Sep. 2020.
22.	Koji Yamaguchi and Masataka Sata : 血管治療の進歩と高血圧治療:大動脈瘤・解離,閉塞症動脈硬化症, NIPPONRINSHOSHA Co.,Ltd., Jul. 2020.
23.	伊藤浩, Masataka Sata, 田中敦史, 野出孝一, 室原豊明, 荒木栄一, 稲垣暢也, 植木浩二郎, 石井秀樹, 今井健二郎, 杉山雄太 and 山根俊介 : 糖代謝異常者における循環器病の診断・予防・治療に関するコンセンサスステートメント日本循環器学会・日本糖尿病学会合同委員会編集, Nankodo, Tokyo, Mar. 2020.
24.	Akira Takashima and Masataka Sata : Ⅴ心臓疾患心臓膿瘍(心嚢内膿瘍), Sep. 2019.
25.	田中君枝 and Masataka Sata : 動脈硬化の基礎, Nankodo, Jan. 2018.
26.	Akira Takashima and Masataka Sata : ω系不飽和脂肪酸の心血管イベントリスク低減作用, YODOSHA CO., LTD., 2018.
27.	Masataka Sata : 6., 朝倉書店, Mar. 2017.
28.	Koji Yamaguchi and Masataka Sata : 2. 冠動脈疾患, Iyaku Journal Co., Ltd., Mar. 2017.
29.	Akira Takashima and Masataka Sata : Omega-3 polyunsaturated fatty acids reduce the risk of cardiovascular events in the patients with ischemic heart disease and heart failure, The Vitamin Society of Japan, 2017. (Keyword) atherosclerosis / heart failure / inflammation / ischemic heart disease / omega-3 polyunsaturated fatty acids (Link to Publication Site) ● Publication site (DOI): 10.20632/vso.91.9_542 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390564238026959744 ● Search Scopus @ Elsevier (DOI): 10.20632/vso.91.9_542 (DOI: 10.20632/vso.91.9_542, CiNii: 1390564238026959744)
30.	Koji Yamaguchi and Masataka Sata : 治すLEADER試験の解釈と循環器疾患への応用, MEDICAL VIEW CO., LTD., 2017.
31.	M Shimamura, H Nakagami, Masataka Sata and H Kurinami : A model of stroke and vascular injury in the brain., Springer Japan, Tokyo, Mar. 2016. (Link to Publication Site) ● Publication site (DOI): 10.1007/978-4-431-55813-2_14 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1007/978-4-431-55813-2_14 (DOI: 10.1007/978-4-431-55813-2_14)
32.	Masataka Sata, K Tanaka and Daiju Fukuda : Wire-mediated endovascular injury that induces rapid onset of medial cell apoptosis followed by reproducible neointimal hyperplasia., Springer Japan, Tokyo, Mar. 2016. (Link to Publication Site) ● Publication site (DOI): 10.1007/978-4-431-55813-2_1 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85006760663 (DOI: 10.1007/978-4-431-55813-2_1, Elsevier: Scopus)
33.	Masataka Sata : Mouse Models of Vascular Diseases, Springer Japan, Mar. 2016. (Link to Publication Site) ● Publication site (DOI): 10.1007/978-4-431-55813-2 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85006754106 (DOI: 10.1007/978-4-431-55813-2, Elsevier: Scopus)
34.	Masataka Sata, Tanaka Kimie and Daiju Fukuda : Wire-Mediated Eendovascular Injury That Induces Rapid Onset of Medical Cell Apoptosis Followed by Reproducible Neointimal Hyperplasia., Springer Japan, 2016.
35.	Masataka Sata and しらいしやすこ : 医学監修, 辰巳出版, Tokyo, Dec. 2015.
36.	高島啓, Takayuki Ise and Masataka Sata : 心不全治療に魚油が効く!?-ω-3不飽和脂肪酸慢性心不全治療へ- (第4章慢性心不全の治療 1. 内服治療 ), Medicus SHUPPAN, Osaka, Oct. 2014.
37.	Shusuke Yagi and Masataka Sata : 甲状腺疾患と心臓, Nankodo, Tokyo, Jan. 2014.
38.	Masataka Sata : 第Ⅱ章冠動脈イベントの機序を知る 1 冠動脈イベントのプロセスを理解しよう(TOPICS 心臓周囲脂肪組織とその意義), Nankodo, Tokyo, Oct. 2013.
39.	田中君枝 and Masataka Sata : 第Ⅱ章冠動脈イベントの機序を知る 1 冠動脈イベントのプロセスを理解しよう (1 血管内皮機能とその異常 2 単球とリンパ球 3 動脈硬化プラークの進展 4 動脈硬化プラークの破裂 5 血栓形成を促進させるもの) 冠動脈疾患のパーフェクトマネジメント, Nankodo, Tokyo, Oct. 2013.
40.	Takeshi Soeki and Masataka Sata : 循環器領域における新たな検査法の導入, Nankodo, Tokyo, Jun. 2013.
41.	Michio Shimabukuro, M Dagvasumberel, Masayoshi Ishida, Sachiko Matsumoto, 小塚智沙代, 平良伸一, 屋比久浩市, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Seiichi Oyadomari, 益埼裕章 and Masataka Sata : Ectopic fat deposition, type 2 diabetes mellitus and cardiovascular diseases, Tokushima Medical Association, Tokushima, Apr. 2013. (Summary) There is evidence supporting the notion that excess abdominal fat is predictive of insulin resistance and the presence of related metabolic abnormalities currently referred to as the metabolic syndrome (MetS). Despite the fact that abdominal obesity is a highly prevalent feature of MetS, the mechanisms by which abdominal obesity is causally related to MetS are not fully elucidated. Besides visceral fat accumulation, ectopic lipid deposition, especially in the liver and skeletal muscle, has been implicated in the pathophysiology of diabetes, insulin resistance and obesity-related disorders. In addition, ectopic fat deposition play a critical role in the heart components such as (1) circulatory and locally recruited fat, (2) intra-and extra-myocellular fat, (3) perivascular fat, and (4) pericardial fat. In this review, the contribution of ectopic lipid deposition to global cardiometabolic risk is discussed via possible mechanisms including adipocytokine, insulin resistance and lipotoxicity. (Keyword) Ectopic fat deposition / Diabetes mellitus / Cardiovascular diseases / Obesity / Metabolic syndrome / Lipotoxicity (Tokushima University Institutional Repository) ● Metadata: 109609 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050564287418392064 (Tokushima University Institutional Repository: 109609, CiNii: 1050564287418392064)
42.	沖美環 and Masataka Sata : 動脈硬化を改善する効果があります, 文光堂, Tokyo, Feb. 2013.
43.	原知也 and Masataka Sata : 血管機能を改善する効果があります, 文光堂, Tokyo, Feb. 2013.
44.	田中君枝 and Masataka Sata : 5. 動脈硬化とアレルギー・炎症, 株式会社中外医学社, Tokyo, Jan. 2013.
45.	Yoshio Taketani and Masataka Sata : 4. 治療薬総論硝酸薬, IGAKU-SHOIN Ltd.Tokyo,Japan, Jan. 2013.
46.	Takeshi Soeki and Masataka Sata : 第2章 7. むずかしくてイヤになる動脈硬化のサイエンス, YODOSHA CO., LTD., Tokyo, Nov. 2012.
47.	田中君枝 and Masataka Sata : 第2章糖代謝関連 2．PPARγ, Medical Review Co.,Ltd, Osaka, Jul. 2012.
48.	田中君枝 and Masataka Sata : 第II章 8 トランスレーショナルリサーチに期待する予防医学, NANZANDO Co.,Ltd., Tokyo, Mar. 2012.
49.	Koji Yamaguchi and Masataka Sata : 6. 不安定プラーク破裂に関与する因子は何か?, 株式会社中外医学社, Tokyo, Mar. 2012.
50.	Michio Shimabukuro and Masataka Sata : 心臓病と肥満-メタボリックシンドロームを中心に-, Nankodo, Tokyo, Mar. 2012.
51.	Hirotsugu Kurobe and Masataka Sata : 第6章病態・治療 Tissue Engineering技術による血管の再生, 朝倉書店, Tokyo, Dec. 2011.
52.	田中君枝 and Masataka Sata : 第1章血管構築間葉系細胞, 朝倉書店, Tokyo, Dec. 2011.
53.	Michio Shimabukuro, 山川研, 益崎裕章 and Masataka Sata : 【Ⅰ.基礎・成因】 2. 血管内皮障害の病態, フジメディカル出版, Osaka, May 2011.
54.	Masataka Sata : 2010年の総括, フジメディカル出版, Osaka, May 2011.
55.	Michio Shimabukuro, 山川研, 益崎裕章 and Masataka Sata : 血管内皮機能障害の病態, フジメディカル出版, Osaka, Mar. 2011.
56.	平田陽一郎, 高岡稔, Masataka Sata and 他 : 異所性脂肪-メタボリックシンドロームの新常識, Japan Medkal Journal, Dec. 2010.
57.	田中君枝, Masataka Sata and 他 : 疾患モデルの作製と利用-循環器疾患, LIFE-SCIENCE INFORMATION CENTER, Aug. 2010.
58.	Toshiyuki Niki, Masataka Sata and 他 : Ⅶ.心膜疾患，腫瘍 4.心内血栓, Nankodo, Feb. 2010.
59.	Masataka Sata and K Walsh : Contribution of circulating progenitor cells to vascular repair and lesion formation, Humana Press Inc, Totowa,NJ., Aug. 2007. (Link to Publication Site) ● Publication site (DOI): 10.1007/978-1-59745-001-0_11 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1007/978-1-59745-001-0_11 (DOI: 10.1007/978-1-59745-001-0_11)
60.	Masataka Sata and R Nagai : Vascular regeneration and remodeling by circulating progenitor cells, Springer-Verlag, Tokyo, 2005.
61.	K Walsh and Masataka Sata : Regulation of inflammation by Fas ligand expression on the vascular endothelium, Kluwer Academic Publishers, Boston, 1999.
62.	S Sugiura, H Yamashita, Masataka Sata, H Fujita, S Momomura, T Serizawa and H Sugi : Kinetic property of cardiac myosin in vitro, Kluwer Academic Publishers, Boston, 1995.

Academic Paper (Judged Full Paper):

1.	Kenya Kusunose, T Imai, A Tanaka, M Doi, Y Koide, K Fukumoto, T Kadokami, M Ohishi, H Teragawa, N Ohte, Hirotsugu Yamada, Masataka Sata and K Node : Effects of ipragliflozin on left ventricular diastolic function in patients with type 2 diabetes: A sub-analysis of the PROTECT trial, Journal of Cardiology, Vol.84, No.4, 246-252, 2024. (Summary) We hypothesized that the beneficial effects of sodium-glucose cotransporter-2 (SGLT2) inhibitors on diastolic function might depend on baseline left ventricular (LV) systolic function. To investigate the effects of SGLT2 inhibitors on LV diastolic function in patients with type 2 diabetes mellitus (T2DM), we conducted a post-hoc sub-study of the PROTECT trial, stratifying the data according to LV ejection fraction (LVEF) at baseline. After excluding patients without echocardiographic data at baseline or 24 months into the PROTECT trial, 31 and 38 patients with T2DM from the full analysis dataset of the PROTECT trial who received ipragliflozin or no SGLT2 inhibitor (control), respectively, were included. The primary endpoint was a comparison of the changes in echocardiographic parameters and N-terminal pro-brain natriuretic peptide levels from baseline to 24 months between the two groups stratified according to baseline LVEF. Differences in diastolic functional parameters (e' and E/e') were noted between the two groups. Among the subgroups defined according to median LVEF values, those with higher LVEF (≥60 %) who received ipragliflozin appeared to have a higher e' and lower E/e' than did those who received the standard of care with no SGLT2 inhibitor, indicating longitudinal improvements between baseline and follow up (p = 0.001 and 0.016, respectively). Ipragliflozin generally improved LV diastolic function in patients with type 2 diabetes, the extent of this improvement might appear to vary with LV systolic function. (Keyword) Humans / Diabetes Mellitus, Type 2 / Male / Female / Thiophenes / Sodium-Glucose Transporter 2 Inhibitors / Middle Aged / Ventricular Function, Left / Aged / Glucosides / Diastole / Natriuretic Peptide, Brain / Stroke Volume / Echocardiography / Peptide Fragments / Ventricular Dysfunction, Left (Tokushima University Institutional Repository) ● Metadata: 119605 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jjcc.2024.02.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38378130 ● Search Scopus @ Elsevier (PMID): 38378130 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jjcc.2024.02.002 (Tokushima University Institutional Repository: 119605, DOI: 10.1016/j.jjcc.2024.02.002, PubMed: 38378130)
2.	Shusuke Yagi, Ryosuke Miyamoto, Masayoshi Tasaki, Hiroyuki Morino, Ryuji Otani, Muneyuki Kadota, Takayuki Ise, Hiroki Yamazaki, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Daiju Fukuda, Mitsuharu Ueda and Masataka Sata : The APOA1 p.Leu202Arg variant potentially causes autosomal recessive cardiac amyloidosis., Human Genome Variation, Vol.11, No.1, 2024. (Summary) ApoA-I amyloidosis is an extremely rare form of systemic amyloidosis that commonly involves the heart, kidneys, and liver. ApoA-I amyloidosis is caused by amyloidogenic variants of APOA1 that are inherited in an autosomal dominant manner. Here, we report a 69-year-old man with sporadic cardiac amyloidosis who was born to consanguineous parents and carried a homozygous variant of p.Leu202Arg in APOA1. (Tokushima University Institutional Repository) ● Metadata: 119580 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41439-024-00288-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39152105 ● CiNii @ National Institute of Informatics (CRID): 1050864324980555392 ● Summary page in Scopus @ Elsevier: 2-s2.0-85201547622 (Tokushima University Institutional Repository: 119580, DOI: 10.1038/s41439-024-00288-7, PubMed: 39152105, CiNii: 1050864324980555392, Elsevier: Scopus)
3.	Bollos Christine Anne Leah Locsin, Ryosuke Kasai, Hideki Otsuka, Youichi Otomi, Koji Yamaguchi, Tomomi Matsuura, Tamaki Otani, Takanori Bandoh, Yuya Ueki, Noritake Matsuda, Satoru Takashi, Shota Azane, Yamato Kunikane, Shoichiro Takao, Shusuke Yagi, Masataka Sata, Hitoshi Ikushima and Masafumi Harada : Ventilation/Perfusion Mismatch in Pulmonary Vein Stenosis Secondary to Atrial Fibrillation Ablation, Asia Oceania Journal of Nuclear Medicine & Biology, 2024. (Summary) We present two patients with a history of paroxysmal atrial fibrillation who developed pulmonary vein stenosis (PVS) following atrial fibrillation (AF) ablation. Case 1 involved a female patient in her 50s who was asymptomatic for pulmonary symptoms but was found to have a high degree of left superior PVS 15 months after AF ablation. This was demonstrated using contrast-enhanced computed tomography (CE-CT) and supported by findings of perfusion defects on ventilation-perfusion (V/Q) scan. Case 2 was a male patient in his 60s who developed progressive left superior PVS nine months after AF ablation, evidenced by serial CE-CT and V/Q scans. PVS is a rare but well-known complication of pulmonary vein ablation for the treatment of AF that can lead to severe complications if left untreated. V/Q scans effectively assess the functional significance of PVS by detecting abnormal blood flow segments. Although a V/Q mismatch characterized by reduced perfusion defects is more commonly used in evaluating pulmonary embolism, PVS should not be disregarded as a differential diagnosis. Few studies emphasize the utility of V/Q scans in managing PVS and highlight V/Q mismatch as a notable finding. This case report aimed to highlight their significance. (Link to Publication Site) ● Publication site (DOI): 10.22038/AOJNMB.2024.79650.1561 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.22038/AOJNMB.2024.79650.1561 (DOI: 10.22038/AOJNMB.2024.79650.1561)
4.	Shusuke Yagi, Muneyuki Kadota, Ryo Bando, Ryosuke Miyamoto, Hiroyuki Morino, Akiyoshi Kakutani, Yoshiaki Kubo, Takayuki Ise, Rie Ueno, Tomoya Hara, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Daiju Fukuda and Masataka Sata : Pulmonary Arterial Hypertension in Neurofibromatosis Type 1: A Case with a Novel NF1 Gene Mutation, Internal Medicine, 2024. (Summary) Neurofibromatosis type 1 (NF1) is an autosomal dominant multi-organ disease. The clinical manifestations include not only skin lesions and malignant tumors but also lung complications, including pulmonary arterial hypertension (PAH). However, the association between gene mutations in NF1 and the occurrence of PAH has not yet been elucidated. We herein report a case of isolated PAH in a 67-year-old woman with NF1, presumably caused by a novel heterozygous mutation, c.4485_4486delinsAT (p.Lys1496Ter), in the NF1 gene. (Tokushima University Institutional Repository) ● Metadata: 119521 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.3856-24 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38987187 ● Search Scopus @ Elsevier (PMID): 38987187 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.3856-24 (Tokushima University Institutional Repository: 119521, DOI: 10.2169/internalmedicine.3856-24, PubMed: 38987187)
5.	TOMONORI Takahashi, Tetsuzo Wakatsuki, Takayuki Ise and Masataka Sata : Spontaneous thrombosis of a giant aneurysm complicated with the coronary-to-pulmonary artery fistula: a case report, European Heart Journal. Case Reports, Vol.8, 2024. (Summary) Background A coronary-to-pulmonary artery fistula (CPAF) with a giant aneurysm is a rare clinical occurrence. The rupture of an aneurysm leads to a fatal outcome, thus prompting the incorporation of prophylactic measures, which have encompassed surgical resections or endovascular embolization procedures. The indications for these treatment strategies are controversial, and little has been elucidated regarding the salient characteristics underpinning the selection of a therapeutic strategy. We report a case of a giant aneurysm associated with CPAFs that was thrombosed before interventional treatment. Case summary A 43-year-old woman, who had previously undergone a right adrenalectomy for primary aldosteronism, was referred for an abnormal heart silhouette on a chest X-ray, which had not been seen three years earlier. Contrast-enhanced computed tomography and coronary angiography (CAG) revealed a giant aneurysm on the anterior aspect of the heart associated with two CPAFs. Because of the risk of rupture of the aneurysm, surgical resection was recommended; however, the patient requested endovascular therapy. On the day of intervention, CAG showed spontaneous occlusion of the feeding vessel to the aneurysm, and the aneurysm showed minimal contrast agent, suggesting spontaneous thrombosis. Because of possible recanalization of the aneurysm, coil embolization was performed, without complications. The patient remained asymptomatic, and the aneurysm was completely embolized at the one-year follow-up. Discussion The case shows that minimally invasive endovascular treatment is feasible instead of surgical resection for giant aneurysms associated with CPAFs, depending on their morphological characteristics. This perspective may offer novel insights into treatment strategies for CPAF. (Keyword) Coronary-to-pulmonary artery fistulas / Coronary anomalies / Coronary anomalies / Case report (Link to Publication Site) ● Publication site (DOI): 10.1093/ehjcr/ytae227 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050581766257304960 ● Summary page in Scopus @ Elsevier: 2-s2.0-85192932221 (DOI: 10.1093/ehjcr/ytae227, CiNii: 1050581766257304960, Elsevier: Scopus)
6.	A Fujiyoshi, S Kohsaka, J Hata, M Hara, H Kai, D Masuda, N Miyamatsu, Y Nishio, M Ogura, Masataka Sata, K Sekiguchi, Y Takeya, K Tamura, A Wakatsuki, H Yoshida, Y Fujioka, R Fukazawa, O Hamada, A Higashiyama, M Kabayama, K Kanaoka, K Kawaguchi, S Kosaka, A Kunimura, A Miyazaki, M Nii, M Sawano, M Terauchi, Shusuke Yagi, T Akasaka, T Minamino, K Miura and K Node : JCS 2023 Guideline on the Primary Prevention of Coronary Artery Disease, Circulation Journal, Vol.88, No.5, 763-842, 2024. (Keyword) Humans / Coronary Artery Disease / Primary Prevention / Japan (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-23-0285 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38479862 ● Search Scopus @ Elsevier (PMID): 38479862 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-23-0285 (DOI: 10.1253/circj.CJ-23-0285, PubMed: 38479862)
7.	Uugantsetseg Munkhjargal, Daiju Fukuda, J Maeda, Tomoya Hara, S Okamoto, O Bavuu, Takayuki Yamamoto and Masataka Sata : LCZ696, an Angiotensin Receptor-Neprilysin Inhibitor, Ameliorates, Journal of Atherosclerosis and Thrombosis, Vol.31, No.9, 1333-1340, 2024. (Tokushima University Institutional Repository) ● Metadata: 119293 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.64468 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38616113 ● Search Scopus @ Elsevier (PMID): 38616113 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.64468 (Tokushima University Institutional Repository: 119293, DOI: 10.5551/jat.64468, PubMed: 38616113)
8.	Motoki Sugasaki, S Nakamura, K Teramoto, M Urushihara, Y Inoue, T Nakao, Yasuhiko Nishioka and Masataka Sata : Lupus anticoagulant hypoprothrombinemia syndrome with multiple and high-titer antiphospholipid antibodies strongly interfered with coagulation assays, Blood Coagulation & Fibrinolysis, Vol.35, No.3, 149-153, 2024. (Keyword) Humans / Antibodies, Antiphospholipid / Lupus Coagulation Inhibitor / Hypoprothrombinemias / Antiphospholipid Syndrome / Blood Coagulation Tests / Blood Coagulation Disorders, Inherited (Link to Publication Site) ● Publication site (DOI): 10.1097/MBC.0000000000001282 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38557935 ● Search Scopus @ Elsevier (PMID): 38557935 ● Search Scopus @ Elsevier (DOI): 10.1097/MBC.0000000000001282 (DOI: 10.1097/MBC.0000000000001282, PubMed: 38557935)
9.	Yoshihito Saijyo, Kenya Kusunose, TOMONORI Takahashi, Hirotsugu Yamada, Masataka Sata, Kimi Sato, Noor Albakaa, Tomoko Ishizu, Yoshihiro Seo and JSE TAVI investigators : Impact of Transcatheter Aortic Valve Replacement on Cardiac Reverse Remodeling and Prognosis in Mixed Aortic Valve Disease, Journal of the American Heart Association, Vol.13, No.4, e033289, 2024. (Summary) The management of mixed aortic valve disease (MAVD), defined as the concomitant presence of aortic stenosis (AS) and aortic regurgitation, remains a clinical challenging. The present study assessed the impact of transcatheter aortic valve replacement (TAVR) on cardiac geometry and prognosis in patients with MAVD. A retrospective multicenter TAVR registry was conducted, including patients who underwent TAVR for severe symptomatic AS between January 2015 and March 2019. Patients were subdivided into 2 groups according to concomitant presence of moderate or more severe aortic regurgitation as the MAVD group, and with mild or less severe aortic regurgitation as the isolated AS group. The primary outcome was a composite of cardiovascular death and rehospitalization due to cardiovascular causes. A total of 1742 patients (isolated AS, 1522 patients; MAVD, 220 patients) were included (84.0±5.2 years). Although MAVD exhibited significantly larger left ventricular volumes and higher left ventricular mass index at the TAVR procedure than isolated AS (respectively, <0.001), MAVD showed a greater improvement of left ventricular volumes and left ventricular mass index after TAVR (respectively, ≤0.001). During a median follow-up of 747 days, 301 patients achieved the primary event. The prognosis post-TAVR was comparable between the 2 groups (log-rank =0.65). Even after adjustment using propensity score matching to reduce the potential bias between the 2 groups, similar results were obtained for the entire cohort. Despite more advanced cardiac remodeling in MAVD at the time of TAVR compared with isolated AS, a greater improvement of cardiac reverse remodeling was found in MAVD, and the prognosis following TAVR was comparable between the 2 groups. (Keyword) Humans / Transcatheter Aortic Valve Replacement / Aortic Valve / Aortic Valve Insufficiency / Treatment Outcome / Risk Factors / Aortic Valve Stenosis / Prognosis / Retrospective Studies / Severity of Illness Index / Ventricular Function, Left (Link to Publication Site) ● Publication site (DOI): 10.1161/JAHA.123.033289 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38362873 ● Search Scopus @ Elsevier (PMID): 38362873 ● Search Scopus @ Elsevier (DOI): 10.1161/JAHA.123.033289 (DOI: 10.1161/JAHA.123.033289, PubMed: 38362873)
10.	Yukina Hirata, Yuka Nomura, Yoshihito Saijyo, Masataka Sata and Kenya Kusunose : Reducing echocardiographic examination time through routine use of fully automated software: a comparative study of measurement and report creation time, Journal of Echocardiography, 2024. (Summary) Manual interpretation of echocardiographic data is time-consuming and operator-dependent. With the advent of artificial intelligence (AI), there is a growing interest in its potential to streamline echocardiographic interpretation and reduce variability. This study aimed to compare the time taken for measurements by AI to that by human experts after converting the acquired dynamic images into DICOM data. Twenty-three consecutive patients were examined by a single operator, with varying image quality and different medical conditions. Echocardiographic parameters were independently evaluated by human expert using the manual method and the fully automated US2.ai software. The automated processes facilitated by the US2.ai software encompass real-time processing of 2D and Doppler data, measurement of clinically important variables (such as LV function and geometry), automated parameter assessment, and report generation with findings and comments aligned with guidelines. We assessed the duration required for echocardiographic measurements and report creation. The AI significantly reduced the measurement time compared to the manual method (159 ± 66 vs. 325 ± 94 s, p < 0.01). In the report creation step, AI was also significantly faster compared to the manual method (71 ± 39 vs. 429 ± 128 s, p < 0.01). The incorporation of AI into echocardiographic analysis led to a 70% reduction in measurement and report creation time compared to manual methods. In cases with fair or poor image quality, AI required more corrections and extended measurement time than in cases of good image quality. Report creation time was longer in cases with increased report complexity due to human confirmation of AI-generated findings. This fully automated software has the potential to serve as an efficient tool for echocardiographic analysis, offering results that enhance clinical workflow by providing rapid, zero-click reports, thereby adding significant value. (Tokushima University Institutional Repository) ● Metadata: 118962 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12574-023-00636-6 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38308797 ● Search Scopus @ Elsevier (PMID): 38308797 ● Search Scopus @ Elsevier (DOI): 10.1007/s12574-023-00636-6 (Tokushima University Institutional Repository: 118962, DOI: 10.1007/s12574-023-00636-6, PubMed: 38308797)
11.	Yukina Hirata, Takumasa Tsuji, Jun'ichi Kotoku, Masataka Sata and Kenya Kusunose : Echocardiographic artificial intelligence for pulmonary hypertension classification, Heart, Vol.110, No.8, 586-593, 2024. (Summary) The classification of pulmonary hypertension (PH) is crucial for determining the appropriate therapeutic strategy. We investigated whether machine learning (ML) algorithms may assist in echocardiographic PH prediction, where current guidelines recommend integrating several different parameters. We obtained physical and echocardiographic data from 885 patients who underwent right heart catheterisation (RHC). Patients were classified into three groups: non-PH, precapillary PH and postcapillary PH, based on values obtained from RHC. Using 24 parameters, we created predictive models employing four different classifiers and selected the one with the highest area under the curve. We then calculated the macro-average classification accuracy for PH on the derivation cohort (n=720) and prospective validation data set (n=165), comparing the results with guideline-based echocardiographic assessment obtained from each cohort. Logistic regression with elastic net regularisation had the highest classification accuracy, with areas under the curves of 0.789, 0.766 and 0.742 for normal, precapillary PH and postcapillary PH, respectively. The ML model demonstrated significantly better predictive accuracy than the guideline-based echocardiographic assessment in the derivation cohort (59.4% vs 51.6%, p<0.01). In the independent validation data set, the ML model's accuracy was comparable to the guideline-based PH classification (59.4% vs 57.8%, p=0.638). This preliminary study suggests promising potential for our ML model in predicting echocardiographic PH. Further research and validation are needed to fully assess its clinical utility in PH diagnosis and treatment decision-making. (Tokushima University Institutional Repository) ● Metadata: 118966 (Link to Publication Site) ● Publication site (DOI): 10.1136/heartjnl-2023-323320 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38296266 ● Search Scopus @ Elsevier (PMID): 38296266 ● Search Scopus @ Elsevier (DOI): 10.1136/heartjnl-2023-323320 (Tokushima University Institutional Repository: 118966, DOI: 10.1136/heartjnl-2023-323320, PubMed: 38296266)
12.	N Yamaguchi, Yukina Hirata, Susumu Nishio, TOMONORI Takahashi, Yoshihito Saijo, Muneyuki Kadota, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata and Kenya Kusunose : Pulmonary Pressure-flow responses to exercise in heart failure treated with angiotensin receptor neprilysin inhibitor., International Journal of Cardiology, Vol.400, 131789, 2024. (Summary) The role of the angiotensin receptor neprilysin inhibitor (ARNI) in cardiac function, particularly its impact on pulmonary circulation, remains underexplored. Recent studies have described abnormal mean pulmonary artery pressure (mPAP)-cardiac output (CO) responses as having the potential to assess the disease state. The aim of this study was to assess the effects of ARNI on pulmonary circulation in heart failure. We measured echocardiographic parameters post 6-min walk (6 MW) and compared the changes with baseline and follow-up. Our hypothesis was that pulmonary pressure-flow relationship of the pulmonary circulation obtained by 6 MW stress echocardiography would be improved with treatment. We prospectively enrolled 39 heart failure patients and conducted the 6 MW test indoors. Post-6 MW echocardiography measured echocardiographic variables, and CO was derived from electric cardiometry. Individualized ARNI doses were optimized, with follow-up echocardiographic evaluations after 1 year. Left ventricular (LV) volume were significantly reduced (160.7 ± 49.6 ml vs 136.0 ± 54.3 ml, P < 0.001), and LV ejection fraction was significantly improved (37.6 ± 11.3% vs 44.9 ± 11.5%, P < 0.001). Among the 31 patients who underwent 6 MW stress echocardiographic study at baseline and 1 year later, 6 MW distance increased after treatment (380 m vs 430 m, P = 0.003). The ΔmPAP/ΔCO by 6 MW stress decreased with treatment (6.9 mmHg/L/min vs 2.8 mmHg/L/min, P = 0.002). The left atrial volume index was associated with the response group receiving ARNI treatment for pulmonary circulation. Initiation of ARNI was associated with improvement of left ventricular size and LVEF. Additionally, the 6 MW distance increased and the ΔmPAP/ΔCO was improved to within normal range with treatment. (Tokushima University Institutional Repository) ● Metadata: 118925 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijcard.2024.131789 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38246422 ● Search Scopus @ Elsevier (PMID): 38246422 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ijcard.2024.131789 (Tokushima University Institutional Repository: 118925, DOI: 10.1016/j.ijcard.2024.131789, PubMed: 38246422)
13.	S Yamaguchi, M Maeda, K Oba, G Maimaituxun, O Arasaki, Shusuke Yagi, Kenya Kusunose, Takeshi Soeki, Hirotsugu Yamada, Daiju Fukuda, H Masuzaki, Masataka Sata and Michio Shimabukuro : Sex differences in the association between epicardial adipose tissue volume and left atrial volume index, BMC Cardiovascular Disorders, Vol.24, No.1, 46, 2024. (Summary) Sex disparities in the association between epicardial adipose tissue volume (EATV) and cardiovascular disease have been reported. The sex-dependent effects of EATV on left atrial (LA) size have not been elucidated. Consecutive 247 subjects (median 65 [interquartile range 57, 75] years; 67% of men) who underwent multi-detector computed tomography without significant coronary artery disease or moderate to severe valvular disease were divided into two groups: patients with sinus rhythm (SR) or atrial fibrillation (AF). Sex differences in the association between the EATV index (EATVI) (mL/m) and LA volume index (LAVI) in 63 SR (28 men and 35 women) and 184 AF (137 men and 47 women) patients were evaluated using univariate and multivariate regression analyses. In overall that includes both men and women, the relationship between EATVI and LAVI was not significantly correlated for patients with SR and AF. The relationship between EATVI and LAVI differed between men and women in both SR and AF groups. In SR patients, there was a positive relationship between EATVI and LAVI in men, but not in women. In contrast, in patients with AF, a negative relationship was found between EATVI and LAVI in women, whereas no association was found in men. We evaluated sex differences in the association between EATVI and LAVI in patients with either SR or AF, and found a positive relationship in men with SR and a negative relationship in women with AF. This is the first report to evaluate sex differences in the relationship between EATVI and LAVI, suggesting that EAT may play a role, at least in part, in sex differences in the etiology of AF. (Keyword) Humans / Female / Male / Epicardial Adipose Tissue / Sex Characteristics / Heart Atria / Atrial Fibrillation / Atrial Appendage / Adipose Tissue (Tokushima University Institutional Repository) ● Metadata: 118911 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12872-023-03569-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38218772 ● Search Scopus @ Elsevier (PMID): 38218772 ● Search Scopus @ Elsevier (DOI): 10.1186/s12872-023-03569-1 (Tokushima University Institutional Repository: 118911, DOI: 10.1186/s12872-023-03569-1, PubMed: 38218772)
14.	Y Higashikuni, W Liu and Masataka Sata : Nocturnal blood pressure and left ventricular hypertrophy in patients with diabetes mellitus, Hypertension Research, Vol.47, No.3, 819-822, 2023. (Tokushima University Institutional Repository) ● Metadata: 118910 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41440-023-01562-x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38148349 ● Search Scopus @ Elsevier (PMID): 38148349 ● Search Scopus @ Elsevier (DOI): 10.1038/s41440-023-01562-x (Tokushima University Institutional Repository: 118910, DOI: 10.1038/s41440-023-01562-x, PubMed: 38148349)
15.	Kenya Kusunose, T Tsuji, Yukina Hirata, TOMONORI Takahashi, Masataka Sata, K Sato, N Albakaa, T Ishizu, J Kotoku and Y Seo : Unsupervised cluster analysis reveals different phenotypes in patients after transcatheter aortic valve replacement, European Heart Journal Open, Vol.4, No.1, oead136, 2023. (Summary) The aim of this study was to identify phenotypes with potential prognostic significance in aortic stenosis (AS) patients after transcatheter aortic valve replacement (TAVR) through a clustering approach. This multi-centre retrospective study included 1365 patients with severe AS who underwent TAVR between January 2015 and March 2019. Among demographics, laboratory, and echocardiography parameters, 20 variables were selected through dimension reduction and used for unsupervised clustering. Phenotypes and outcomes were compared between clusters. Patients were randomly divided into a derivation cohort ( = 1092: 80%) and a validation cohort ( = 273: 20%). Three clusters with markedly different features were identified. Cluster 1 was associated predominantly with elderly age, a high aortic valve gradient, and left ventricular (LV) hypertrophy; Cluster 2 consisted of preserved LV ejection fraction, larger aortic valve area, and high blood pressure; and Cluster 3 demonstrated tachycardia and low flow/low gradient AS. Adverse outcomes differed significantly among clusters during a median of 2.2 years of follow-up ( < 0.001). After adjustment for clinical and echocardiographic data in a Cox proportional hazards model, Cluster 3 (hazard ratio, 4.18; 95% confidence interval, 1.76-9.94; = 0.001) was associated with increased risk of adverse outcomes. In sequential Cox models, a model based on clinical data and echocardiographic variables ( = 18.4) was improved by Cluster 3 ( = 31.5; = 0.001) in the validation cohort. Unsupervised cluster analysis of patients after TAVR revealed three different groups for assessment of prognosis. This provides a new perspective in the categorization of patients after TAVR that considers comorbidities and extravalvular cardiac dysfunction. (Tokushima University Institutional Repository) ● Metadata: 118909 (Link to Publication Site) ● Publication site (DOI): 10.1093/ehjopen/oead136 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38188937 ● Search Scopus @ Elsevier (PMID): 38188937 ● Search Scopus @ Elsevier (DOI): 10.1093/ehjopen/oead136 (Tokushima University Institutional Repository: 118909, DOI: 10.1093/ehjopen/oead136, PubMed: 38188937)
16.	Munkhtsetseg Tserensonom, Shusuke Yagi, Takayuki Ise, Yutaka Kawabata, Muneyuki Kadota, Tomoya Hara, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Lipoprotein (a) is a risk factor of aortic valve calcification in patients with a risk of atherosclerosis, The Journal of Medical Investigation : JMI, Vol.70, No.3.4, 450-456, 2023. (Summary) Aortic valve calcification (AVC), which causes aortic stenosis (AS), is more common in elderly persons. Controlling for conventional risk variables did not, however, reduce the incidence of AS. Thus, residual risk factors of AS should be identified. We enrolled 513 patients who underwent coronary angiography with computed tomography because of suspicion of coronary artery disease (CAD) or ruling out of CAD before aortic valve replacement. Calcium volume was calculated with a commercially available application. Conventional and lipid-related risk factors including serum levels of Lp(a) were evaluated for all patients. Calcium volume and Lp(a) levels were significantly higher in patients who underwent aortic valve replacement than in those who did not. A single regression analysis showed that the calcium volume was positively associated with age and the Lp(a) levels and negatively associated with the estimated glomerular filtration rate. No statistical significance was observed for other risk factors, including oxidized low-density lipoprotein, omega-3 fatty acids levels. The multiple regression analysis revealed that age (P<0.001), female sex (P<0.05), Lp(a) (P<0.01), and hemoglobin A1c (P<0.01) were determinants of the calcium volume. The area under the curve in receiver operating characteristic analysis of Lp(a) for implementation of AVR was 0.65 at an Lp(a) cut-off level of 16 mg/dL. In conclusion, the serum Lp(a) level is a potent risk factor of AVC in patients with high risk of atherosclerosis. J. Med. Invest. 70 : 450-456, August, 2023. (Keyword) Humans / Female / Aged / Aortic Valve / Lipoprotein(a) / Calcium / Aortic Valve Stenosis / Atherosclerosis / Risk Factors / Coronary Artery Disease (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.70.450 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37940531 ● Search Scopus @ Elsevier (PMID): 37940531 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.70.450 (DOI: 10.2152/jmi.70.450, PubMed: 37940531)
17.	PT Pham, Oyunbileg Bavuu, JR Kim-Kaneyama, XF Lei, T Yamamoto, K Otsuka, Kumiko Suto, Kenya Kusunose, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Michio Shimabukuro, GN Barber, Masataka Sata and Daiju Fukuda : Innate Immune System Regulated by Stimulator of Interferon Genes, a Cytosolic DNA Sensor, Regulates Endothelial Function, Journal of the American Heart Association, Vol.12, No.22, e030084, 2023. (Summary) Background Sterile inflammation caused by metabolic disorders impairs endothelial function; however, the underlying mechanism by which hyperglycemia induces inflammation remains obscure. Recent studies have suggested that stimulator of interferon genes (STING), a key cytosolic DNA sensor in the innate immune system, contributes to the pathogenesis of inflammatory diseases. This study examines the role of the STING in endothelial dysfunction in streptozotocin-induced diabetic mice. Methods and Results Injection of streptozotocin promoted the expression of STING and DNA damage markers in the aorta of wild-type mice. Streptozotocin elevated blood glucose and lipid levels in both wild-type and STING-deficient mice, which showed no statistical differences. Genetic deletion of STING ameliorated endothelial dysfunction as determined by the vascular relaxation in response to acetylcholine (<0.001) and increased endothelial nitric oxide synthase phosphorylation in the aorta (<0.05) in STZ-injected mice. Endothelium-independent vascular response to sodium nitroprusside did not differ. Treatment with a direct STING agonist, cyclic GMP-AMP, or mitochondrial DNA increased inflammatory molecule expression (eg, and ) and decreased endothelial nitric oxide synthase phosphorylation in human umbilical vein endothelial cells, partially through the STING pathway. Cyclic GMP-AMP significantly impaired endothelial function of aortic segments obtained from wild-type mice, which was ameliorated in the presence of C-176, a STING inhibitor, or a neutralizing interferon-β antibody. Furthermore, the administration of C-176 ameliorated endothelial dysfunction in STZ-induced diabetic mice (<0.01). Conclusions The DNA damage response regulated by STING impairs endothelial function. STING signaling may be a potential therapeutic target of endothelial dysfunction caused by hyperglycemia. (Tokushima University Institutional Repository) ● Metadata: 119425 (Link to Publication Site) ● Publication site (DOI): 10.1161/JAHA.123.030084 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37947148 ● CiNii @ National Institute of Informatics (CRID): 1360863109951763328 ● Summary page in Scopus @ Elsevier: 2-s2.0-85178405175 (Tokushima University Institutional Repository: 119425, DOI: 10.1161/JAHA.123.030084, PubMed: 37947148, CiNii: 1360863109951763328, Elsevier: Scopus)
18.	T Yamaji, T Harada, M Kajikawa, T Maruhashi, S Kishimoto, FM Yusoff, K Chayama, C Goto, A Nakashima, H Tomiyama, B Takase, T Kohro, T Suzuki, T Ishizu, S Ueda, T Yamazaki, T Furumoto, K Kario, T Inoue, K Watanabe, Y Takemoto, T Hano, Masataka Sata, Y Ishibashi, K Node, K Maemura, Y Ohya, T Furukawa, H Ito, A Yamashina, S Koba and Y Higashi : Role of Small Dense Low-density Lipoprotein Cholesterol in Cardiovascular Events in Patients with Coronary Artery Disease and Type 2 Diabetes Mellitus Receiving Statin Treatment, Journal of Atherosclerosis and Thrombosis, Vol.31, No.4, 478-500, 2023. (Summary) There is little information on the relationships of serum small dense low-density lipoprotein cholesterol (sdLDL-C) levels and serum triglyceride (TG) levels with cardiovascular events in patients with coronary artery disease (CAD) and type 2 diabetes mellitus (DM) who are receiving statins. The aim of this study was to evaluate the relationships of serum TG levels and sdLDL-C levels as residual risks for cardiovascular events in patients with CAD and type 2 DM who were being treated with statins. The subjects were divided into four groups based on TG levels and sdLDL-C levels: sdLDL-C of <40.0 mg/dL and TG of <150 mg/dL, sdLDL-C of 40.0 mg/dL and TG of <150 mg/dL, sdLDL-C of <40.0 mg/dL and TG of 150 mg/dL, and sdLDL-C of 40.0 mg/dL and TG of 150 mg/dL. During a median follow-up period of 1419 days, cardiovascular events occurred in 34 patients. The incidences of cardiovascular events were significantly higher in patients with sdLDL-C of 40.0 mg/dL and TG of <150 mg/dL and in patients with sdLDL-C of 40.0 mg/dL and TG of 150 mg/dL, but not in patients with sdLDL-C of <40.0 mg/dL and TG of 150 mg/dL, than in patients with sdLDL-C of <40.0 mg/dL and TG of <150 mg/dL. Under the condition of treatment with statins, patients with CAD and type 2 DM who had sdLDL-C levels of 40.0 mg/dL had a high risk for cardiovascular events even though serum TG levels were controlled at <150 mg/dL. (Keyword) Small dense low-density lipoprotein cholesterol / Triglycerides / Type 2 diabetes mellitus / Statin / Cardiovascular events (Tokushima University Institutional Repository) ● Metadata: 118732 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.64416 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37926523 ● CiNii @ National Institute of Informatics (CRID): 1390581148794792704 ● Summary page in Scopus @ Elsevier: 2-s2.0-85189720109 (Tokushima University Institutional Repository: 118732, DOI: 10.5551/jat.64416, PubMed: 37926523, CiNii: 1390581148794792704, Elsevier: Scopus)
19.	TOMONORI Takahashi, H Iwano, K Shibayama, T Kitai, H Tanaka, Hirotsugu Yamada, Masataka Sata and Kenya Kusunose : The Clinical Utility of Noninvasive Forrester Classification in Acute Heart Failure from PREDICT Study, The American Journal of Cardiology, Vol.207, 75-81, 2023. (Summary) The Forrester classification plays a crucial role in comprehending the underlying pathophysiology of heart failure (HF) and is employed to categorize the severity and predict the outcomes of patients with acute HF. Our objective was to assess the predictive value of the Forrester classification, based on noninvasive hemodynamic measurements obtained through Doppler echocardiography at admission, in forecasting the short-term prognosis posthospitalization of patients with acute HF. Patients were recruited for the Prospect trial to elucidate the utility of EchocarDIography-based Cardiac ouTput in acute heart failure (PREDICT) study, a multicenter, prospective study conducted in Japan. Participants were stratified into 4 profiles using cardiac index (CI) and early mitral filling velocity (E)/early-diastolic mitral annular velocity (e') ratio obtained from Doppler echocardiography upon admission (profile I: CI >2.2, E/e' ≤15, profile II: CI >2.2, E/e' >15, profile III: CI ≤2.2, E/e' ≤15, profile IV: CI ≤2.2, E/e' >15). The primary composite outcome of the study was all-cause mortality or worsening HF during the 14 days of hospitalization. Cox proportional hazards model analysis was employed to identify prognostic factors during the observation period. A total of 270 subjects, with a mean age of 74 ± 14 years and a male proportion of 60%, were enrolled in the study. During the 14-day period of hospitalization, 58 participants (22%) had a composite outcome. Patients with low CI (i.e., profiles III and IV) demonstrated an elevated risk of composite outcome after adjusting for confounding variables, as evidenced by the adjusted hazard ratios of 5.85 (95% confidence interval 1.17 to 29.09, p <0.01, vs profile III) and 6.50 (95% confidence interval 1.53 to 27.68, p <0.01, vs profile IV) in comparison with profile I, respectively. In conclusion, the Forrester classification, derived from noninvasive Doppler echocardiography at admission, may predict early deterioration in patients hospitalized with acute HF. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.amjcard.2023.08.119 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37734303 ● Search Scopus @ Elsevier (PMID): 37734303 ● Search Scopus @ Elsevier (DOI): 10.1016/j.amjcard.2023.08.119 (DOI: 10.1016/j.amjcard.2023.08.119, PubMed: 37734303)
20.	Sanae Morita, Yukina Hirata, Susumu Nishio, TOMONORI Takahashi, Yoshihito Saijo, Hirotsugu Yamada, Masataka Sata and Kenya Kusunose : Correlation between energy loss index and B-type natriuretic peptide: a vector flow mapping study, Journal of Echocardiography, Vol.22, No.1, 25-33, 2023. (Summary) Vector Flow Mapping (VFM) and Energy Loss (EL) evaluation are emerging echocardiographic techniques that offer detailed insights into cardiac function. This study aimed to explore the relationship between EL parameters and B-type natriuretic peptide (BNP) levels, a well-established marker of heart failure severity. Our study prospectively enrolled 62 patients experiencing shortness of breath and suspected heart failure, who underwent echocardiography and had BNP levels measured between January 2018 and August 2020. Patients were stratified based on BNP levels, and their clinical and echocardiographic characteristics were evaluated. Univariate and multivariate regression analyses were performed to assess the correlation between BNP levels and various echocardiographic variables, including VFM parameters. Patients were stratified into two groups based on their BNP levels: BNP < 200 pg/ml (n = 53) and BNP 200 pg/ml (n = 9). Patients with BNP 200 pg/ml presented significantly different clinical and echocardiographic characteristics, such as older age, larger left ventricular mass and volume indices, higher pulmonary artery systolic pressure, higher E/e' ratio, and larger EL parameters. Multivariate regression analysis demonstrated the E/e' ratio and ELA (EL during Atrial contraction phase/A wave ratio as significant determinants of logBNP. Receiver operating characteristic curve analysis showed ELA/A > 36.0 J/m as a significant predictor of high BNP with 89% sensitivity and 85% specificity. ELA/A demonstrated an incremental diagnostic value over elevated left atrial pressure for predicting high BNP (C statistic = 0.98 vs 0.74, P = 0.006). This study provides novel insights into the potential utility of EL parameters as auxiliary indicators of cardiac load, thereby enhancing our understanding of heart failure. (Link to Publication Site) ● Publication site (DOI): 10.1007/s12574-023-00623-x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37707682 ● Summary page in Scopus @ Elsevier: 2-s2.0-85170841573 (DOI: 10.1007/s12574-023-00623-x, PubMed: 37707682, Elsevier: Scopus)
21.	N Masaki, T Adachi, H Tomiyama, T Kohro, T Suzuki, T Ishizu, S Ueda, T Yamazaki, T Furumoto, K Kario, T Inoue, S Koba, Y Takemoto, T Hano, Masataka Sata, Y Ishibashi, K Node, K Maemura, Y Ohya, T Furukawa, H Ito, Y Higashi, A Yamashina and B Takase : Reduced reactive hyperemia of the brachial artery in diabetic patients assessed by repeated measurements: The FMD-J B study, Physiological Reports, Vol.11, No.16, e15786, 2023. (Summary) Type 2 diabetes mellitus (T2DM) is a major cause of microvascular dysfunction. However, its effect on blood flow patterns during ischemic demand has not been adequately elucidated. In this study, we investigated the hypothesis that microvascular dysfunction in patients with T2DM manifests as brachial reactive hyperemia (BRH), defined as the ratio of peak blood flow velocities in a brachial artery before and after forearm cuff occlusion. The study enrolled 943 subjects (men, n = 152 [T2DM] and n = 371 [non-T2DM]; women, n = 107 [T2DM] and n = 313 [non-T2DM], respectively) with no history of cardiovascular disease. Semiautomatic measurements were obtained three times at 1.5-year intervals to confirm the reproducibility of factors involved in BRH for each sex. An age-adjusted mixed model demonstrated attenuated BRH in the presence of T2DM in both men (p = 0.022) and women (p = 0.031) throughout the study period. Post hoc analysis showed that the estimated BRH was significantly attenuated in patients with T2DM regardless of sex, except at baseline in women. In multivariate regression analysis, T2DM was a negative predictor of BRH at every measurement in men. For women, BRH was more strongly associated with alcohol consumption. Repeated measurements analysis revealed that T2DM was associated with attenuated postocclusion reactive hyperemia. (Keyword) Male / Humans / Female / Brachial Artery / Diabetes Mellitus, Type 2 / Hyperemia / Reproducibility of Results / Forearm (Tokushima University Institutional Repository) ● Metadata: 118556 (Link to Publication Site) ● Publication site (DOI): 10.14814/phy2.15786 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37607768 ● Summary page in Scopus @ Elsevier: 2-s2.0-85168568959 (Tokushima University Institutional Repository: 118556, DOI: 10.14814/phy2.15786, PubMed: 37607768, Elsevier: Scopus)
22.	Yasutomi Higashikuni, Wenhao Liu and Masataka Sata : Not a small frog in a big pond: targeting bradykinin receptor B2 signaling in vascular smooth muscle cells for treatment of hypertension, Hypertension Research, Vol.46, No.10, 2415-2418, 2023. (Link to Publication Site) ● Publication site (DOI): 10.1038/s41440-023-01385-w (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37507534 ● Search Scopus @ Elsevier (PMID): 37507534 ● Search Scopus @ Elsevier (DOI): 10.1038/s41440-023-01385-w (DOI: 10.1038/s41440-023-01385-w, PubMed: 37507534)
23.	Yuichiro Okushi, Yoshihito Saijyo, Hirotsugu Yamada, Hiroaki Toba, Robert Zheng, Hiromitsu Seno, TOMONORI Takahashi, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata and Kenya Kusunose : Effectiveness of surveillance by echocardiography for Cancer therapeutics-related cardiac dysfunction of patients with breast Cancer, Journal of Cardiology, Vol.82, No.6, 467-472, 2023. (Summary) Cancer therapeutics-related cardiac dysfunction (CTRCD) affect the prognosis of patients with breast cancer. Echocardiographic surveillance of patients treated with anti-human epidermal growth factor receptor type 2 (HER2) antibodies has been recommended, but few reports have provided evidence on patients with breast cancer only. We aimed to evaluate the effectiveness of echocardiographic surveillance for breast cancer patients. We identified 250 patients with breast cancer who were treated with anti-HER2 antibodies from July 2007 to September 2021. We divided 48 patients with echocardiographic surveillance every 3 months into the surveillance group and 202 patients without echocardiographic surveillance into the non-surveillance group. In the surveillance group, patients with a considerable reduction in global longitudinal strain of 15 % were considered for the initiation of cardioprotective drugs. The composite outcome of CTRCD and acute heart failure was the study endpoint. The mean age was 59 ± 12 years. During the follow-up period of 15 months (12-17 months), 12 patients reached the endpoint. The surveillance group had significantly lower incidence of the composite outcome (2.1 % vs. 5.5 %, adjusted odds ratio: 0.28, 95 % confidential intervals: 0.09-0.94; p = 0.039) and higher rates of prescriptions of cardioprotective drugs than the non-surveillance group. The incidence of cardiac complications was significantly lower in the surveillance group than the non-surveillance group, which supports the effectiveness of echocardiographic surveillance in patients with breast cancer. (Tokushima University Institutional Repository) ● Metadata: 118455 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jjcc.2023.07.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37481235 ● Summary page in Scopus @ Elsevier: 2-s2.0-85166962366 (Tokushima University Institutional Repository: 118455, DOI: 10.1016/j.jjcc.2023.07.002, PubMed: 37481235, Elsevier: Scopus)
24.	Tomoya Hara, Daiju Fukuda, Byambasuren Ganbaatar, Phuong Tran Pham, Kunduziayi Aini, Arief Rahadian, Kumiko Suto, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Olive mill wastewater and hydroxytyrosol inhibits atherogenesis in apolipoprotein E-deficient mice, Heart and Vessels, Vol.38, No.11, 1386-1394, 2023. (Summary) The Mediterranean diet, which is characterized by high consumption of olive oil, prevents cardiovascular disease. Meanwhile, olive mill wastewater (OMWW), which is obtained as a byproduct during olive oil production, contains various promising bioactive components such as water-soluble polyphenols. Hydroxytyrosol (HT), the major polyphenol in OMWW, has anti-oxidative and anti-inflammatory properties; however, the atheroprotective effects of OMWW and HT remain to be fully understood. Here, we investigated the effect of OMWW and HT on atherogenesis. Male 8-week-old apolipoprotein E-deficient mice were fed a western-type diet supplemented with OMWW (0.30%w/w) or HT (0.02%w/w) for 20 weeks. The control group was fed a non-supplemented diet. OMWW and HT attenuated the development of atherosclerosis in the aortic arch as determined by Sudan IV staining (P < 0.01, respectively) without alteration of body weight, plasma lipid levels, and blood pressure. OMWW and HT also decreased the production of oxidative stress (P < 0.01, respectively) and the expression of NADPH oxidase subunits (e.g., NOX2 and p22phox) and inflammatory molecules (e.g. IL-1β and MCP-1) in the aorta. The results of in vitro experiments demonstrated that HT inhibited the expression of these molecules that were stimulated with LPS in RAW264.7 cells, murine macrophage-like cells. OMWW and HT similarly attenuated atherogenesis. HT is a major component of water-soluble polyphenols in OMWW, and it inhibited inflammatory activation of macrophages. Therefore, our results suggest that the atheroprotective effects of OMWW are at least partially attributable to the anti-inflammatory effects of HT. (Tokushima University Institutional Repository) ● Metadata: 118456 (Link to Publication Site) ● Publication site (DOI): 10.1007/s00380-023-02290-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37462755 ● Search Scopus @ Elsevier (PMID): 37462755 ● Search Scopus @ Elsevier (DOI): 10.1007/s00380-023-02290-5 (Tokushima University Institutional Repository: 118456, DOI: 10.1007/s00380-023-02290-5, PubMed: 37462755)
25.	A Tanaka, I Taguchi, I Hisauchi, H Yoshida, Michio Shimabukuro, H Hongo, T Ishikawa, T Kadokami, Shusuke Yagi, Masataka Sata and K Node : Clinical effects of a selective urate reabsorption inhibitor dotinurad in patients with hyperuricemia and treated hypertension: a multicenter, prospective, exploratory study (DIANA), European Journal of Medical Research, Vol.28, No.1, 238, 2023. (Summary) Dotinurad is a newer urate-lowering agent that selectively inhibits urate transporter 1 in the renal proximal tubule and increases urinary urate excretion. Currently, little is known about the clinical efficacies of dotinurad in patients with hyperuricemia and hypertension. The aim of this study was to assess the clinical effects of a selective urate reabsorption inhibitor dotinurad on serum uric acid (SUA) levels and relevant vascular markers in patients with hyperuricemia and treated hypertension. This investigator-initiated, multicenter, prospective, single-arm, open-label, exploratory clinical trial in Japan enrolled patients with hyperuricemia and treated hypertension who received a 24-week dotinurad therapy (a starting dose at 0.5 mg once daily and up-titrated to 2 mg once daily). The primary endpoint was a percentage change in the SUA level from baseline to week 24. The secondary endpoints were cardiovascular and metabolic measurements, including changes in the cardio-ankle vascular index (CAVI) and derivatives of reactive oxygen metabolites (d-ROMs) concentration at week 24. Fifty patients (mean age 70.5 ± 11.0 years, with 76.0% being men, and mean SUA level 8.5 ± 1.2 mg/dL) were included in the analysis. The percentage change from baseline in the SUA level at week 24 was - 35.8% (95% confidence interval [CI] - 39.7% to - 32.0%, P < 0.001), with approximately three quarters of patients achieving an SUA level of ≤ 6.0 mg/dL at week 24. The proportional changes from baseline in the geometric mean of CAVI and d-ROMs at week 24 were 0.96 (95% CI 0.92 to 1.00, P = 0.044) and 0.96 (95% CI 0.92 to 1.00, P = 0.044), respectively. In addition to meaningful SUA-lowering effects, 24 weeks of dotinurad therapy may favorably affect arterial stiffness and oxidative stress markers, suggesting off-target vascular protection of dotinurad. Further research is expected to verify our findings and elucidate the entire off-target effects of dotinurad. Trial registration jRCTs021210013, registration date June 24, 2021. (Keyword) Male / Humans / Middle Aged / Aged / Aged, 80 and over / Female / Hyperuricemia / Uric Acid / Prospective Studies / Uricosuric Agents / Hypertension (Tokushima University Institutional Repository) ● Metadata: 118457 (Link to Publication Site) ● Publication site (DOI): 10.1186/s40001-023-01208-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37461063 ● Search Scopus @ Elsevier (PMID): 37461063 ● Search Scopus @ Elsevier (DOI): 10.1186/s40001-023-01208-1 (Tokushima University Institutional Repository: 118457, DOI: 10.1186/s40001-023-01208-1, PubMed: 37461063)
26.	Kenya Kusunose, Shuichiro Kashima and Masataka Sata : Evaluation of the Accuracy of ChatGPT in Answering Clinical Questions on the Japanese Society of Hypertension Guidelines, Circulation Journal, Vol.87, No.7, 1030-1033, 2023. (Summary) To assist healthcare providers in interpreting guidelines, clinical questions (CQ) are often included, but not always, which can make interpretation difficult for non-expert clinicians. We evaluated the ability of ChatGPT to accurately answer CQs on the Japanese Society of Hypertension Guidelines for the Management of Hypertension (JSH 2019).Methods and Results: We conducted an observational study using data from JSH 2019. The accuracy rate for CQs and limited evidence-based questions of the guidelines (Qs) were evaluated. ChatGPT demonstrated a higher accuracy rate for CQs than for Qs (80% vs. 36%, P value: 0.005). ChatGPT has the potential to be a valuable tool for clinicians in the management of hypertension. (Tokushima University Institutional Repository) ● Metadata: 118375 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-23-030 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37286486 ● Search Scopus @ Elsevier (PMID): 37286486 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-23-030 (Tokushima University Institutional Repository: 118375, DOI: 10.1253/circj.CJ-23-030, PubMed: 37286486)
27.	Natsumi Yamaguchi, Yoshitaka Kosaka, Akihiro Haga, Masataka Sata and Kenya Kusunose : Artificial intelligence-assisted interpretation of systolic function by echocardiogram, Open Heart, Vol.10, No.2, e002287., 2023. (Summary) Precise and reliable echocardiographic assessment of left ventricular ejection fraction (LVEF) is needed for clinical decision-making. Recently, artificial intelligence (AI) models have been developed to estimate LVEF accurately. The aim of this study was to evaluate whether an AI model could estimate an expert read of LVEF and reduce the interinstitutional variability of level 1 readers with the AI-LVEF displayed on the echocardiographic screen. This prospective, multicentre echocardiographic study was conducted by five cardiologists of level 1 echocardiographic skill (minimum level of competency to interpret images) from different hospitals. Protocol 1: Visual LVEFs for the 48 cases were measured without input from the AI-LVEF. Protocol 2: the 48 cases were again shown to all readers with inclusion of AI-LVEF data. To assess the concordance and accuracy with or without AI-LVEF, each visual LVEF measurement was compared with an average of the estimates by five expert readers as a reference. A good correlation was found between AI-LVEF and reference LVEF (r=0.90, p<0.001) from the expert readers. For the classification LVEF, the area under the curve was 0.95 on heart failure with preserved EF and 0.96 on heart failure reduced EF. For the precision, the SD was reduced from 6.1±2.3 to 2.5±0.9 (p<0.001) with AI-LVEF. For the accuracy, the root-mean squared error was improved from 7.5±3.1 to 5.6±3.2 (p=0.004) with AI-LVEF. AI can assist with the interpretation of systolic function on an echocardiogram for level 1 readers from different institutions. (Keyword) Humans / Ventricular Function, Left / Stroke Volume / Artificial Intelligence / Prospective Studies / Echocardiography / Heart Failure (Tokushima University Institutional Repository) ● Metadata: 118454 (Link to Publication Site) ● Publication site (DOI): 10.1136/openhrt-2023-002287 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37460267 ● Summary page in Scopus @ Elsevier: 2-s2.0-85165601733 (Tokushima University Institutional Repository: 118454, DOI: 10.1136/openhrt-2023-002287, PubMed: 37460267, Elsevier: Scopus)
28.	Shusuke Yagi, Tomoya Hara, Hirotsugu Yamada, Kenya Kusunose, Takayuki Ise and Masataka Sata : Intimal Sarcoma of the Pulmonary Artery as an Embolic Cause of Sudden Death, Circulation Journal, Vol.87, No.7, 1036, 2023. (Tokushima University Institutional Repository) ● Metadata: 118374 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-23-0029 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37245990 ● Search Scopus @ Elsevier (PMID): 37245990 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-23-0029 (Tokushima University Institutional Repository: 118374, DOI: 10.1253/circj.CJ-23-0029, PubMed: 37245990)
29.	Kenya Kusunose, Yukina Hirata, Natsumi Yamaguchi, Y Kosaka, T Tsuji, J Kotoku and Masataka Sata : Deep learning approach for analyzing chest x-rays to predict cardiac events in heart failure, Frontiers in Cardiovascular Medicine, Vol.10, 1081628, 2023. (Summary) A deep learning (DL) model based on a chest x-ray was reported to predict elevated pulmonary artery wedge pressure (PAWP) as heart failure (HF). The aim of this study was to (1) investigate the role of probability of elevated PAWP for the prediction of clinical outcomes in association with other parameters, and (2) to evaluate whether probability of elevated PAWP based on DL added prognostic information to other conventional clinical prognostic factors in HF. We evaluated 192 patients hospitalized with HF. We used a previously developed AI model to predict HF and calculated probability of elevated PAWP. Readmission following HF and cardiac mortality were the primary endpoints. Probability of elevated PAWP was associated with diastolic function by echocardiography. During a median follow-up period of 58 months, 57 individuals either died or were readmitted. Probability of elevated PAWP appeared to be associated with worse clinical outcomes. After adjustment for readmission score and laboratory data in a Cox proportional-hazards model, probability of elevated PAWP at pre-discharge was associated with event free survival, independent of elevated left atrial pressure (LAP) based on echocardiographic guidelines ( < 0.001). In sequential Cox models, a model based on clinical data was improved by elevated LAP (= 0.005), and increased further by probability of elevated PAWP (< 0.001). In contrast, the addition of pulmonary congestion interpreted by a doctor did not statistically improve the ability of a model containing clinical variables (compared = 0.086). This study showed the potential of using a DL model on a chest x-ray to predict PAWP and its ability to add prognostic information to other conventional clinical prognostic factors in HF. The results may help to enhance the accuracy of prediction models used to evaluate the risk of clinical outcomes in HF, potentially resulting in more informed clinical decision-making and better care for patients. (Tokushima University Institutional Repository) ● Metadata: 118373 (Link to Publication Site) ● Publication site (DOI): 10.3389/fcvm.2023.1081628 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37273880 ● Search Scopus @ Elsevier (PMID): 37273880 ● Search Scopus @ Elsevier (DOI): 10.3389/fcvm.2023.1081628 (Tokushima University Institutional Repository: 118373, DOI: 10.3389/fcvm.2023.1081628, PubMed: 37273880)
30.	T Tsuji, Yukina Hirata, Kenya Kusunose, Masataka Sata, S Kumagai, K Shiraishi and J Kotoku : Classification of chest X-ray images by incorporation of medical domain knowledge into operation branch networks., BMC Medical Imaging, Vol.23, No.1, 62, 2023. (Summary) This study was conducted to alleviate a common difficulty in chest X-ray image diagnosis: The attention region in a convolutional neural network (CNN) does not often match the doctor's point of focus. The method presented herein, which guides the area of attention in CNN to a medically plausible region, can thereby improve diagnostic capabilities. The model is based on an attention branch network, which has excellent interpretability of the classification model. This model has an additional new operation branch that guides the attention region to the lung field and heart in chest X-ray images. We also used three chest X-ray image datasets (Teikyo, Tokushima, and ChestX-ray14) to evaluate the CNN attention area of interest in these fields. Additionally, after devising a quantitative method of evaluating improvement of a CNN's region of interest, we applied it to evaluation of the proposed model. Operation branch networks maintain or improve the area under the curve to a greater degree than conventional CNNs do. Furthermore, the network better emphasizes reasonable anatomical parts in chest X-ray images. The proposed network better emphasizes the reasonable anatomical parts in chest X-ray images. This method can enhance capabilities for image interpretation based on judgment. (Keyword) Humans / X-Rays / Thorax / Heart / Neural Networks, Computer (Tokushima University Institutional Repository) ● Metadata: 118875 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12880-023-01019-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37161392 ● Summary page in Scopus @ Elsevier: 2-s2.0-85158935839 (Tokushima University Institutional Repository: 118875, DOI: 10.1186/s12880-023-01019-0, PubMed: 37161392, Elsevier: Scopus)
31.	U Munkhjargal, Daiju Fukuda, B Ganbaatar, Kumiko Suto, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : A Selective Mineralocorticoid Receptor Blocker, Esaxerenone, Attenuates Vascular Dysfunction in Diabetic C57BL/6 Mice, Journal of Atherosclerosis and Thrombosis, Vol.30, No.4, 326-334, 2023. (Summary) Pharmacological blockade of mineralocorticoid receptors (MRs) is a potential therapeutic approach to reduce cardiovascular complications since MRs play a crucial role in cardiovascular regulation. Recent studies suggest that MR antagonists affect several extrarenal tissues, including vessel function. We investigated the effect of a novel nonsteroidal selective MR blocker, esaxerenone, on diabetes-induced vascular dysfunction. Diabetes was induced by a single dose of streptozotocin in 8-week-old male C57BL/6 mice. Esaxerenone (3 mg/kg/day) or a vehicle was administered by gavage to diabetic mice for 3 weeks. Metabolic parameters, plasma aldosterone levels, and parameters related to renal function were measured. Endothelium-dependent or -independent vascular responses of the aortic segments were analyzed with acetylcholine or sodium nitroprusside, respectively. Human umbilical vein endothelial cells (HUVECs) were used for the in vitro study. Induction of diabetes elevated plasma aldosterone level (P<0.05) and impaired endothelium-dependent vascular relaxation (P<0.05). The administration of esaxerenone ameliorated the endothelial dysfunction (P<0.01) without the alteration of metabolic parameters, blood pressure, and renal function. Esaxerenone improved the eNOS phosphorylation in the aorta obtained from diabetic mice (P<0.05) compared with that in the vehicle-treated group. Furthermore, a major MR agonist, aldosterone, decreased eNOS phosphorylation and increased eNOS phosphorylation in HUVECs, which recovered with esaxerenone. Esaxerenone ameliorated the endothelium-dependent vascular relaxation caused by aldosterone in the aortic segments obtained from C57BL/6 mice (P<0.001). Esaxerenone attenuates the development of diabetes-induced endothelial dysfunction in mice. These results suggest that esaxerenone has potential vascular protective effects in individuals with diabetes. (Tokushima University Institutional Repository) ● Metadata: 118690 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.63382 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35732424 ● Search Scopus @ Elsevier (PMID): 35732424 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.63382 (Tokushima University Institutional Repository: 118690, DOI: 10.5551/jat.63382, PubMed: 35732424)
32.	A Kudo, N Machii, T Ono, H Saito, Y Oshiro, R Takahashi, K Oshiro, Y Taneda, M Higa, K Nakachi, Shusuke Yagi, H Masuzaki, Masataka Sata and Michio Shimabukuro : Effect of dapagliflozin on 24-hour glycemic variables in Japanese patients with type 2 diabetes mellitus receiving basal insulin supported oral therapy (DBOT): a multicenter, randomized, open-label, parallel-group study, BMJ Open Diabetes Research & Care, Vol.11, No.2, e003302, 2023. (Summary) This study aimed to evaluate the impacts of dapagliflozin on 24-hour glucose variability and diabetes-related biochemical variables in Japanese patients with type 2 diabetes who had received basal insulin supported oral therapy (BOT). Changes in mean daily blood glucose level before and after 48-72 hours of add-on or no add-on of dapagliflozin (primary end point) and diabetes-related biochemical variables and major safety variables during the 12 weeks (secondary end point) were evaluated in the multicenter, randomized, two-arm, open-label, parallel-group comparison study. Among 36 participants, 18 were included in the no add-on group and 18 were included in the dapagliflozin add-on group. Age, gender, and body mass index were comparable between the groups. There were no changes in continuous glucose monitoring metrics in the no add-on group. In the dapagliflozin add-on group, mean glucose (183-156 mg/dL, p=0.001), maximum glucose (300-253, p<0.01), and SD glucose (57-45, p<0.05) decreased. Time in range increased (p<0.05), while time above the range decreased in the dapagliflozin add-on group but not in the no add-on group. After 12-week treatment with dapagliflozin add-on, 8-hydroxy-2'-deoxyguanosine (8OHdG), as well as hemoglobin A1c (HbA1c), decreased. This study showed that the mean daily blood glucose and other daily glucose profiles were amended after 48-72 hours of dapagliflozin add-on in Japanese patients with type 2 diabetes who received BOT. The diabetes-related biochemical variables such as HbA1c and urinary 8OHdG were also obtained during the 12 weeks of dapagliflozin add-on without major adverse events. A preferable 24-hour glucose profile in 'time in ranges' and an improvement in reactive oxygen species by dapagliflozin warrant us to evaluate these benefits in larger clinical studies. UMIN000019457. (Keyword) Humans / Diabetes Mellitus, Type 2 / Blood Glucose / Hypoglycemic Agents / Glycated Hemoglobin / Blood Glucose Self-Monitoring / 8-Hydroxy-2'-Deoxyguanosine / East Asian People / Treatment Outcome / Insulins (Tokushima University Institutional Repository) ● Metadata: 118567 (Link to Publication Site) ● Publication site (DOI): 10.1136/bmjdrc-2022-003302 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37028805 ● Search Scopus @ Elsevier (PMID): 37028805 ● Search Scopus @ Elsevier (DOI): 10.1136/bmjdrc-2022-003302 (Tokushima University Institutional Repository: 118567, DOI: 10.1136/bmjdrc-2022-003302, PubMed: 37028805)
33.	Noritake Matsuda, Hideki Otsuka, Tamaki Otani, Shota Azane, Yamato Kunikane, Yoichi Otomi, Yuya Ueki, Masahiro Kubota, Masafumi Amano, Shusuke Yagi, Masataka Sata and Masafumi Harada : New quantitative indices of cardiac amyloidosis with 99mTc-pyrophosphate scintigraphy, Japanese Journal of Radiology, Vol.41, No.4, 428-436, 2023. (Summary) Amyloid light chain (AL) and transthyretin (ATTR) are the major subtypes of cardiac amyloidosis (CA). Tc-pyrophosphate (PYP) scintigraphy is used to differentiate ATTR from other CA subtypes. We adapted the standardized uptake value (SUV) for Tc-PYP and proposed two quantitative indices, amyloid deposition volume (AmyDV) and total amyloid uptake (TAU). This study aimed to evaluate the utility of these quantitative indices in differentiating ATTR from non-ATTRs. Before the SUV measurement, the Becquerel calibration factor (BCF) of Tc was obtained by a phantom experiment. Thirty-two patients who had undergone hybrid SPECT/CT imaging 3 h after injection of Tc-PYP (370 MBq) were studied. CT attenuation correction for image reconstruction was applied in all. We calculated SUV, AmyDV, and TAU using a quantitative analysis software program for bone SPECT (GI-BONE) and analyzed AmyDV using two methods: threshold method (set 40%); and constant value method (average SUV of ribs). We assessed the diagnostic ability of heart-to-contralateral lung (H/CL) ratio, SUV, AmyDV, and TAU to differentiate ATTR from non-ATTR using receiver operating characteristic (ROC) analysis. Statistically significant differences in all quantitative indices were observed between ATTR and non-ATTR. The area under the curve of each quantitative index for discriminating between ATTR and non-ATTR were as follows: H/CL, 0.997; SUV, 0.953; SUV (M1), 0.964; SUV (M2), 0.969; AmyDV (M1), 0.875; AmyDV (M2), 0.974; and TAU, 0.974. The AmyDV (M2) had higher diagnostic ability than AmyDV (M1). Thus, TAU was calculated as AmyDV (M2) × SUV (M2). In the ROC curve, SUV, AmyDV, and TAU had almost the same diagnostic ability as H/CL in distinguishing ATTR from non-ATTRs. We propose two novel 3D-based quantitative parameters (AmyDV and TAU) that have almost equal ability to discriminate ATTR from non-ATTR. (Tokushima University Institutional Repository) ● Metadata: 117912 (Link to Publication Site) ● Publication site (DOI): 10.1007/s11604-022-01364-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36449252 ● Summary page in Scopus @ Elsevier: 2-s2.0-85143121783 (Tokushima University Institutional Repository: 117912, DOI: 10.1007/s11604-022-01364-0, PubMed: 36449252, Elsevier: Scopus)
34.	Tomoya Hara, Masataka Sata and Daiju Fukuda : Emerging roles of Protease-Activated Receptors in Cardiometabolic Disorders, Journal of Cardiology, Vol.81, No.4, 337-346, 2023. (Summary) Cardiometabolic disorders, including obesity-related insulin resistance and atherosclerosis, share sterile chronic inflammation as a major cause; however, the precise underlying mechanisms of chronic inflammation in cardiometabolic disorders are not fully understood. Accumulating evidence suggests that several coagulation proteases, including thrombin and activated factor X (FXa), play an important role not only in the coagulation cascade but also in the proinflammatory responses through protease-activated receptors (PARs) in many cell types. Four members of the PAR family have been cloned (PAR 1-4). For instance, thrombin activates PAR-1, PAR-3, and PAR-4. FXa activates both PAR-1 and PAR-2, while it has no effect on PAR-3 or PAR-4. Previous studies demonstrated that PAR-1 and PAR-2 activated by thrombin or FXa promote gene expression of inflammatory molecules mainly via the NF-κB and ERK1/2 pathways. In obese adipose tissue and atherosclerotic vascular tissue, various stresses increase the expression of tissue factor and procoagulant activity. Recent studies indicated that the activation of PARs in adipocytes and vascular cells by coagulation proteases promotes inflammation in these tissues, which leads to the development of cardiometabolic diseases. This review briefly summarizes the role of PARs and coagulation proteases in the pathogenesis of inflammatory diseases and describes recent findings (including ours) on the potential participation of this system in the development of cardiometabolic disorders. New insights into PARs may ensure a better understanding of cardiometabolic disorders and suggest new therapeutic options for these major health threats. (Tokushima University Institutional Repository) ● Metadata: 117567 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jjcc.2022.09.013 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36195252 ● Search Scopus @ Elsevier (PMID): 36195252 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jjcc.2022.09.013 (Tokushima University Institutional Repository: 117567, DOI: 10.1016/j.jjcc.2022.09.013, PubMed: 36195252)
35.	Ryota Miyamoto, Takayuki Ise, Tomoya Yoshida and Masataka Sata : Endomyocardial biopsy-proven fulminant lymphocytic myocarditis presenting with mid-apical ballooning, European Heart Journal. Case Reports, Vol.7, No.3, ytad123, 2023. (Tokushima University Institutional Repository) ● Metadata: 118932 (Link to Publication Site) ● Publication site (DOI): 10.1093/ehjcr/ytad123 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37006797 ● Search Scopus @ Elsevier (PMID): 37006797 ● Search Scopus @ Elsevier (DOI): 10.1093/ehjcr/ytad123 (Tokushima University Institutional Repository: 118932, DOI: 10.1093/ehjcr/ytad123, PubMed: 37006797)
36.	TOMONORI Takahashi, Kenya Kusunose, S Hayashi, Robert Zheng, Natsumi Yamaguchi, Sae Morita, Yukina Hirata, Susumu Nishio, Yoshihito Saijyo, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Isoproterenol loading transesophageal echocardiography in atrial fibrillation, The International Journal of Cardiovascular Imaging, Vol.39, No.3, 511-518, 2023. (Summary) In patients with sludge or severe spontaneous echo contrast (SEC) in the left atrial appendage (LAA), cases with isoproterenol loading transesophageal echocardiography (ISP-TEE) have been reported to identify the presence of thrombus in the LAA. This study aimed to assess the validity and hemodynamic changes of ISP-TEE in the LAA. We prospectively enrolled patients with atrial fibrillation (AF) who underwent ISP-TEE. The degree of sludge/SEC was categorized as being either absent (grade 0), mild SEC (grade 1), moderate SEC (grade 2), severe SEC or sludge (grade 3). The hemodynamic evaluation was performed by measuring LAA flow velocity, LAA tissue Doppler imaging (LAA-TDI) velocity, and pulmonary vein systolic forward flow velocity (PVS). In total, 35 patients (mean age 71 ± 7 years; 71% male) underwent ISP-TEE. Among 35 patients, 30 patients had grade 3 or 2 SEC, 5 patients had grade 1 SEC. After ISP loading, 23 patients (66% of all patients) showed improved sludge/SEC and one patient was diagnosed with thrombus in the LAA. There were 25 patients with grade 1 SEC, or no SEC (classified as Group1), 10 patients had residual sludge or grade 2 to 3 SEC (classified as Group2) after ISP administration. LAA flow, LAA-TDI, and PVS velocities were significantly higher in group 1 than in group 2 after ISP administration. There was no complication during the examination and after 24 h and 3 months. ISP infusion may be a potential tool to recognize LAA thrombus under the sludge/SEC during TEE in AF. (Keyword) Humans / Male / Middle Aged / Aged / Female / Atrial Fibrillation / Echocardiography, Transesophageal / Isoproterenol / Sewage / Atrial Appendage / Predictive Value of Tests / Thrombosis (Tokushima University Institutional Repository) ● Metadata: 118275 (Link to Publication Site) ● Publication site (DOI): 10.1007/s10554-022-02749-y (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36357528 ● Search Scopus @ Elsevier (PMID): 36357528 ● Search Scopus @ Elsevier (DOI): 10.1007/s10554-022-02749-y (Tokushima University Institutional Repository: 118275, DOI: 10.1007/s10554-022-02749-y, PubMed: 36357528)
37.	A Tanaka, Masataka Sata, Y Okada, H Teragawa, K Eguchi, Michio Shimabukuro, I Taguchi, K Matsunaga, Y Kanzaki, H Yoshida, T Ishizu, S Ueda, M Kitakaze, T Murohara and K Node : Effect of ipragliflozin on carotid intima-media thickness in patients with type 2 diabetes: a multicenter, randomized, controlled trial, European Heart Journal. Cardiovascular Pharmacotherapy, Vol.9, No.2, 165-172, 2023. (Summary) To examine the effects of a 24-month treatment with ipragliflozin on carotid intima-media thickness (IMT) in type 2 diabetes patients. In this multicenter, prospective, randomized, open-label, and blinded-endpoint investigator-initiated clinical trial, adults with type 2 diabetes and haemoglobin A1C (HbA1c) of 6.0-10.0% (42-86 mmol/mol) were randomized equally to ipragliflozin (50 mg daily) and non-sodium-glucose cotransporter-2 (SGLT2) inhibitor use of standard-care (control group) for type 2 diabetes and were followed-up to 24 months. The primary endpoint was the change in mean common carotid artery IMT (CCA-IMT) from baseline to 24 months. A total of 482 patients were equally allocated to the ipragliflozin (N = 241) and control (N = 241) groups, and 464 patients (median age 68 years, female 31.7%, median type 2 diabetes duration 8 years, median HbA1c 7.3%) were included in the analyses. For the primary endpoint, the changes in the mean CCA-IMT from baseline to 24 months were 0.0013 [95% confidence interval (CI), -0.0155-0.0182] mm and 0.0015 (95% CI, -0.0155-0.0184) mm in the ipragliflozin and control groups, respectively, with an estimated group difference (ipragliflozin-control) of -0.0001 mm (95% CI, -0.0191-0.0189; P = 0.989). A group difference in HbA1c change at 24 months was also non-significant between the treatment groups [-0.1% (95% CI, -0.2-0.1); P = 0.359]. Twenty-four months of ipragliflozin treatment did not affect carotid IMT status in patients with type 2 diabetes recruited in the PROTECT study, relative to the non-SGLT2 inhibitor-use standard care for type 2 diabetes. (Keyword) Adult / Humans / Female / Aged / Diabetes Mellitus, Type 2 / Carotid Intima-Media Thickness / Glycated Hemoglobin / Prospective Studies / Treatment Outcome (Tokushima University Institutional Repository) ● Metadata: 117974 (Link to Publication Site) ● Publication site (DOI): 10.1093/ehjcvp/pvac059 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36308299 ● Search Scopus @ Elsevier (PMID): 36308299 ● Search Scopus @ Elsevier (DOI): 10.1093/ehjcvp/pvac059 (Tokushima University Institutional Repository: 117974, DOI: 10.1093/ehjcvp/pvac059, PubMed: 36308299)
38.	Kenya Kusunose, Yuichiro Okushi, Y Okayama, Robert Zheng, M Nakai, Y Sumita, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Benefits of guideline-directed medical therapy to loop diuretics in management of heart failure, The Journal of Medical Investigation : JMI, Vol.70, No.1.2, 41-53, 2023. (Keyword) heart failure / angiotensin-converting enzyme inhibitor / angiotensin receptor blocker / β-blockers / mineralocorticoid receptor antagonists (Tokushima University Institutional Repository) ● Metadata: 118306 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.70.41 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37164742 ● CiNii @ National Institute of Informatics (CRID): 1390296055446303872 ● Search Scopus @ Elsevier (PMID): 37164742 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.70.41 (Tokushima University Institutional Repository: 118306, DOI: 10.2152/jmi.70.41, PubMed: 37164742, CiNii: 1390296055446303872)
39.	Y Higashikuni, W Liu, G Numata, K Tanaka, Daiju Fukuda, Y Tanaka, Y Hirata, T Imamura, E Takimoto, I Komuro and Masataka Sata : NLRP3 Inflammasome Activation Through Heart-Brain Interaction Initiates Cardiac Inflammation and Hypertrophy During Pressure Overload, Circulation, Vol.147, No.4, 338-355, 2023. (Summary) Mechanical stress on the heart, such as high blood pressure, initiates inflammation and causes hypertrophic heart disease. However, the regulatory mechanism of inflammation and its role in the stressed heart remain unclear. IL-1β (interleukin-1β) is a proinflammatory cytokine that causes cardiac hypertrophy and heart failure. Here, we show that neural signals activate the NLRP3 (nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing 3) inflammasome for IL-1β production to induce adaptive hypertrophy in the stressed heart. C57BL/6 mice, knockout mouse strains for NLRP3 and P2RX7 (P2X purinoceptor 7), and adrenergic neuron-specific knockout mice for SLC17A9, a secretory vesicle protein responsible for the storage and release of ATP, were used for analysis. Pressure overload was induced by transverse aortic constriction. Various animal models were used, including pharmacological treatment with apyrase, lipopolysaccharide, 2'(3')--(4-benzoylbenzoyl)-ATP, MCC950, anti-IL-1β antibodies, clonidine, pseudoephedrine, isoproterenol, and bisoprolol, left stellate ganglionectomy, and ablation of cardiac afferent nerves with capsaicin. Cardiac function and morphology, gene expression, myocardial IL-1β and caspase-1 activity, and extracellular ATP level were assessed. In vitro experiments were performed using primary cardiomyocytes and fibroblasts from rat neonates and human microvascular endothelial cell line. Cell surface area and proliferation were assessed. Genetic disruption of NLRP3 resulted in significant loss of IL-1β production, cardiac hypertrophy, and contractile function during pressure overload. A bone marrow transplantation experiment revealed an essential role of NLRP3 in cardiac nonimmune cells in myocardial IL-1β production and cardiac phenotype. Pharmacological depletion of extracellular ATP or genetic disruption of the P2X7 receptor suppressed myocardial NLRP3 inflammasome activity during pressure overload, indicating an important role of ATP/P2X7 axis in cardiac inflammation and hypertrophy. Extracellular ATP induced hypertrophic changes of cardiac cells in an NLRP3- and IL-1β-dependent manner in vitro. Manipulation of the sympathetic nervous system suggested sympathetic efferent nerves as the main source of extracellular ATP. Depletion of ATP release from sympathetic efferent nerves, ablation of cardiac afferent nerves, or a lipophilic β-blocker reduced cardiac extracellular ATP level, and inhibited NLRP3 inflammasome activation, IL-1β production, and adaptive cardiac hypertrophy during pressure overload. Cardiac inflammation and hypertrophy are regulated by heart-brain interaction. Controlling neural signals might be important for the treatment of hypertensive heart disease. (Keyword) Mice / Rats / Humans / Animals / Inflammasomes / NLR Family, Pyrin Domain-Containing 3 Protein / Mice, Inbred C57BL / Myocytes, Cardiac / Inflammation / Arrhythmias, Cardiac / Brain / Cardiomegaly / Adenosine Triphosphate / Interleukin-1beta / Nucleotide Transport Proteins (Tokushima University Institutional Repository) ● Metadata: 117970 (Link to Publication Site) ● Publication site (DOI): 10.1161/CIRCULATIONAHA.122.060860 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36440584 ● Search Scopus @ Elsevier (PMID): 36440584 ● Search Scopus @ Elsevier (DOI): 10.1161/CIRCULATIONAHA.122.060860 (Tokushima University Institutional Repository: 117970, DOI: 10.1161/CIRCULATIONAHA.122.060860, PubMed: 36440584)
40.	Yutaka Kawabata, Tetsuzo Wakatsuki, Koji Yamaguchi, Daiju Fukuda, Hiroyuki Ito, Tomomi Matsuura, Kenya Kusunose, Takayuki Ise, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Y Tsuruo and Masataka Sata : Association of Microluminal Structures Assessed by Optical Coherence Tomography With Local Inflammation in Adjacent Epicardial Adipose Tissue and Coronary Plaque Characteristics in Fresh Cadavers, Circulation Journal, Vol.87, No.2, 329-335, 2023. (Summary) Coronary intraplaque microluminal structures (MS) are associated with plaque vulnerability, and the inward progression of vascular inflammation from the adventitia towards the media and intima has also been demonstrated. Therefore, in the present study we investigated the relationships among MS, local inflammation in adjacent epicardial adipose tissue (EAT), and coronary plaque characteristics.Methods and Results: Optical coherence tomography (OCT) revealed MS in the left anterior descending coronary artery in 10 fresh cadaveric hearts. We sampled 30 lesions and subdivided them based on the presence of MS: MS (+) group (n=19) and MS (-) group (n=11). We measured inflammatory molecule levels in the adjacent EAT and percentage lipid volume assessed by integrated backscatter intravascular ultrasound in each lesion. The expression levels of vascular endothelial growth factor B and C-C motif chemokine ligand 2 were significantly higher in the MS (+) group than in the MS (-) group (0.9±0.7 vs. 0.2±0.2 arbitrary units (AU), P=0.04 and 1.5±0.5 vs. 0.6±0.7 AU, P=0.02, respectively). Percentage lipid volume was significantly higher in the MS (+) group than in the MS (-) group (38.7±16.5 vs. 23.7±10.9%, P=0.03). Intraplaque MS observed on OCT were associated with lipid-rich plaques and local inflammation in the adjacent EAT. Collectively, these results suggest that local inflammation in the EAT is associated with coronary plaque vulnerability via MS. (Tokushima University Institutional Repository) ● Metadata: 117602 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-22-0299 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36244741 ● Search Scopus @ Elsevier (PMID): 36244741 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-22-0299 (Tokushima University Institutional Repository: 117602, DOI: 10.1253/circj.CJ-22-0299, PubMed: 36244741)
41.	石井亜由美, Takayuki Ise, 西川孝治, Hirokazu Ohminami, Muneyuki Kadota, Shusuke Yagi, Tetsuya Matsuura and Masataka Sata : TAVI後の認知機能低下に関わる因子の検討, 心臓リハビリテーション(JJCR), Vol.29, No.3,4, 242-208, 2023.
42.	Tomonori Takahashi, Kenya Kusunose, Robert Zheng, Natsumi Yamaguchi, Yukina Hirata, Susumu Nishio, Yoshihito Saijyo, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Association between cardiovascular risk factors and left ventricular strain distribution in patients without previous cardiovascular disease, Journal of Echocardiography, Vol.20, No.4, 208-215, 2022. (Summary) Some cardiovascular (CV) risk factors, such as hypertension and diabetes mellitus, have been reported to reduce left ventricular (LV) longitudinal strain (LS) even in patients with preserved LV ejection fraction. We hypothesized that multiple CV risk factors might cause changes in myocardial strain. Our study aimed to assess the association between multiple CV risk factors and strain in patients without previous CV disease (CVD). We retrospectively evaluated 137 patients without CVD, who underwent echocardiography at our institution between May 2017 and February 2020. They were divided into four groups based on the number of risk factors (group 0: no risk factor, group 1: one risk factor, group 2: two risk factors, and groups 3: three or four risk factors). Risk factors were hypertension, dyslipidemia, diabetes mellitus, and chronic kidney disease. Absolute values of global LS (GLS) and relative apical LS ratio (RALSR) defined using the equation: average apical LS/(average basal LS + average mid LS) and was used as a marker of strain distribution. Out of 137 patients, group 0 had 35 patients, group 1 had 35 patients, group 2 had 32 patients, and group 3 had 35 patients. GLS was 22.4 ± 2.0%, 21.7 ± 2.1%, 21.3 ± 1.8%, 20.7 ± 2.2%, and RALSR was 0.64 ± 0.06, 0.66 ± 0.06, 0.68 ± 0.08, 0.69 ± 0.07 in groups 0-3, respectively. The one-way ANOVA detected significant differences between groups in GLS (p = 0.005) and RALSR (p = 0.037), respectively. Group 3 had a significantly lower GLS and higher RALSR than group 0 (p < 0.05). In patients without previous CVD, LS decreased especially from the basal segment as the number of cardiovascular risks increased. The segmental LS may be markers of occult LV dysfunction in patients with CV risk factors. (Keyword) Humans / Cardiovascular Diseases / Retrospective Studies / Risk Factors / Stroke Volume / Ventricular Function, Left / Ventricular Dysfunction, Left / Heart Disease Risk Factors / Hypertension (Link to Publication Site) ● Publication site (DOI): 10.1007/s12574-022-00576-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35562627 ● Search Scopus @ Elsevier (PMID): 35562627 ● Search Scopus @ Elsevier (DOI): 10.1007/s12574-022-00576-7 (DOI: 10.1007/s12574-022-00576-7, PubMed: 35562627)
43.	Atsushi Tanaka, Takumi Imai, Michio Shimabukuro, Ikuko Nakamura, Kazuo Matsunaga, Yukio Ozaki, Tohru Minamino, Masataka Sata and Koichi Node : Effect of canagliflozin on white blood cell counts in patients with type 2 diabetes and heart failure: A subanalysis of the randomized CANDLE trial, Journal of Diabetes Investigation, Vol.13, No.12, 1990-1999, 2022. (Summary) Clinical evidence is lacking about the influence of sodium-glucose cotransporter 2 inhibitors on white blood cell (WBC) counts, a commonly used and widely available marker of inflammation. The aim of the present analysis was to assess the effect of canagliflozin relative to glimepiride on WBC counts. This was a post-hoc subanalysis of the CANDLE trial (Effects of Canagliflozin in Patients with Type 2 Diabetes and Chronic Heart Failure: A Randomized Trial; UMIN000017669), an investigator-initiated, multicenter, open-label, randomized, controlled trial. A total of 233 patients with type 2 diabetes and concomitant heart failure were randomly assigned to either canagliflozin (n = 113) or glimepiride (n = 120) treatment for 24 weeks. Overall, patient baseline characteristics were as follows: mean ± standard deviation age, 68.6 ± 10.1 years; hemoglobin A1c, 7.0 ± 0.9%; left ventricular ejection fraction, 56.7 ± 14.4%; and median N-terminal pro-brain natriuretic peptide, 252 pg/mL (interquartile range 96-563 pg/mL). The mean baseline WBC counts were 6704 cells/μL (95% confidence interval 6,362-7,047) in the canagliflozin group and 6322 cells/μL (95% confidence interval 5,991-6,654) in the glimepiride group. There were no significant differences between treatment groups in terms of changes in WBC counts from baseline to weeks 4 and 12. In contrast, a group difference (canagliflozin minus glimepiride) from baseline to week 24 was significant (mean difference - 456 cells/μL [95% confidence interval -774 to -139, P = 0.005]). Our findings suggest that 24 weeks of treatment with canagliflozin, relative to glimepiride, reduced WBC counts in patients with type 2 diabetes and heart failure. (Tokushima University Institutional Repository) ● Metadata: 117489 (Link to Publication Site) ● Publication site (DOI): 10.1111/jdi.13899 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36114704 ● Search Scopus @ Elsevier (PMID): 36114704 ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.13899 (Tokushima University Institutional Repository: 117489, DOI: 10.1111/jdi.13899, PubMed: 36114704)
44.	O Bavuu, Daiju Fukuda, B Ganbaatar, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Esaxerenone, a selective mineralocorticoid receptor blocker, improves insulin sensitivity in mice consuming high-fat diet., European Journal of Pharmacology, 175190, 2022. (Summary) Esaxerenone is a novel, non-steroidal selective mineralocorticoid receptor (Csige et al.) blocker. MR activation plays a crucial role in the development of cardiovascular and metabolic diseases. In this study, we investigated the effects of esaxerenone on various metabolic parameters in mice. Esaxerenone (3 mg/kg/day) was orally administered to high-fat diet (HFD)-fed male C57BL/6 mice. Mice fed a normal diet (ND) served as controls. Glucose and insulin tolerance, plasma lipid levels, and transaminase levels were assessed as metabolic parameters. Macrophage accumulation in the adipose tissue was evaluated using histological analysis. 3T3-L1 adipocytes, HepG2 cells, and C2C12 myotubes were used for in vitro experiments. Gene expression and insulin signaling were examined using quantitative RT-PCR and western blotting, respectively. HFD successfully induced insulin resistance compared with that in ND. Esaxerenone ameliorated insulin resistance (P < 0.05) without altering other metabolic parameters, such as the lipid profile. Esaxerenone administration tended to decrease plasma transaminase levels compared with those in the non-treated group. In the adipose tissue, esaxerenone decreased macrophage accumulation (P < 0.05) and increased the expression levels of adiponectin and PPARγ. Aldosterone significantly decreased the expression levels of PPARγ and adiponectin in 3T3-L1 adipocytes. Furthermore, aldosterone attenuated insulin-induced Akt phosphorylation in 3T3-L1 adipocytes, HepG2 cells, and C2C12 myotubes in a dose-dependent manner (P < 0.01). These effects were ameliorated by pretreatment with esaxerenone. Esaxerenone ameliorated insulin resistance in HFD-fed mice. Reduction of inflammation and improvement in insulin signaling may underlie the beneficial effects of esaxerenone. (Tokushima University Institutional Repository) ● Metadata: 117375 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2022.175190 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35961594 ● Search Scopus @ Elsevier (PMID): 35961594 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2022.175190 (Tokushima University Institutional Repository: 117375, DOI: 10.1016/j.ejphar.2022.175190, PubMed: 35961594)
45.	Sachiko Nishimoto, Masataka Sata and Daiju Fukuda : Expanding role of deoxyribonucleic acid-sensing mechanism in the development of lifestyle-related diseases, Frontiers in Cardiovascular Medicine, Vol.9, 881181, 2022. (Summary) In lifestyle-related diseases, such as cardiovascular, metabolic, respiratory, and kidney diseases, chronic inflammation plays a causal role in their pathogenesis; however, underlying mechanisms of sterile chronic inflammation are not well-understood. Previous studies have confirmed the damage of cells in these organs in the presence of various risk factors such as diabetes, dyslipidemia, and cigarette smoking, releasing various endogenous ligands for pattern recognition receptors. These studies suggested that nucleic acids released from damaged tissues accumulate in these tissues, acting as an endogenous ligand. Undamaged DNA is an integral factor for the sustenance of life, whereas, DNA fragments, especially those from pathogens, are potent activators of the inflammatory response. Recent studies have indicated that inflammatory responses such as the production of type I interferon (IFN) induced by DNA-sensing mechanisms which contributes to self-defense system in innate immunity participates in the progression of inflammatory diseases by the recognition of nucleic acids derived from the host, including mitochondrial DNA (mtDNA). The body possesses several types of DNA sensors. Toll-like receptor 9 (TLR9) recognizes DNA fragments in the endosomes. In addition, the binding of DNA fragments in the cytosol activates cyclic guanosine monophosphate (GMP)-adenosine monophosphate (AMP) synthase (cGAS), resulting in the synthesis of the second messenger cyclic GMP-AMP (cGAMP). The binding of cGAMP to stimulator of interferon genes (STING) activates NF-κB and TBK-1 signaling and consequently the production of many inflammatory cytokines including IFNs. Numerous previous studies have demonstrated the role of DNA sensors in self-defense through the recognition of DNA fragments derived from pathogens. Beyond the canonical role of TLR9 and cGAS-STING, this review describes the role of these DNA-sensing mechanism in the inflammatory responses caused by endogenous DNA fragments, and in the pathogenesis of lifestyle-related diseases. (Tokushima University Institutional Repository) ● Metadata: 118561 (Link to Publication Site) ● Publication site (DOI): 10.3389/fcvm.2022.881181 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36176986 ● Search Scopus @ Elsevier (PMID): 36176986 ● Search Scopus @ Elsevier (DOI): 10.3389/fcvm.2022.881181 (Tokushima University Institutional Repository: 118561, DOI: 10.3389/fcvm.2022.881181, PubMed: 36176986)
46.	Kenya Kusunose, Hirotsugu Yamada, Y Saijo, Susumu Nishio, Yukina Hirata, Takayuki Ise, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Clinical course and decision-making in heart failure by preload stress echocardiography: a preliminary study, ESC Heart Failure, Vol.9, No.6, 4020-4029, 2022. (Summary) Abnormal left ventricular diastolic response to preload stress can be an early marker of heart failure (HF). The aim of this study was to assess clinical course in patients with HF with preserved ejection fraction (HFpEF) who underwent preload stress echocardiography. In the subgroup analysis, we assessed the prognosis of patients with unstable signs during preload stress classified by treatment strategies. We prospectively conducted preload stress echocardiographic studies between January 2006 and December 2013 in 211 patients with HFpEF. Fifty-eight patients had abnormal diastolic reserve during preload stress (unstable impaired relaxation: unstable IR). Of 58 patients with unstable IR, 19 patients were assigned to additional therapy by increased or additional therapy and 39 patients were assigned to standard therapy. Composite outcomes were prespecified as the primary endpoint of death and hospitalization for deteriorating HF. During a median period of 6.9 years, 19 patients (33%) reached the composite outcome. Unstable group with standard therapy had significantly shorter event-free survival than stable group. Patients with uptitration of therapy had longer event-free survival than those with standard therapy group after adjustment of laboratory data (hazard ratio, 0.20, 95% confidence interval, 0.05-0.90; P = 0.036); the 10 year event-free survival in patients with and without uptitration of therapy was 93% and 51%, respectively (P = 0.023). Patients with unstable sign had significantly shorter event-free survival than patients with stable sign. After additional therapy, the prognosis of patients with unstable signs improved. This technique may impact decision-making for improving their prognosis. (Tokushima University Institutional Repository) ● Metadata: 118008 (Link to Publication Site) ● Publication site (DOI): 10.1002/ehf2.14127 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36017722 ● Search Scopus @ Elsevier (PMID): 36017722 ● Search Scopus @ Elsevier (DOI): 10.1002/ehf2.14127 (Tokushima University Institutional Repository: 118008, DOI: 10.1002/ehf2.14127, PubMed: 36017722)
47.	S Abe, Y Haruyama, G Kobashi, S Toyoda, T Inoue, H Tomiyama, T Ishizu, T Kohro, Y Higashi, B Takase, T Suzuki, S Ueda, T Yamazaki, T Furumoto, K Kario, S Koba, Y Takemoto, T Hano, Masataka Sata, Y Ishibashi, K Node, K Maemura, Y Ohya, T Furukawa, H Ito and A Yamashina : Effect of Novel Stratified Lipid Risk by "LDL-Window" and Flow-Mediated Dilation on the Prognosis of Coronary Artery Disease Using the FMD-J Study A Data, Circulation Journal, Vol.86, No.9, 1444-1454, 2022. (Summary) Elevated levels of triglyceride (TG) and non-high-density lipoprotein cholesterol (non-HDL-C) are regarded as a residual lipid risk in low-density lipoprotein cholesterol (LDL-C)-lowering therapy. This study investigated the association between lipid risk stratified by TG and non-HDL-C and the prognosis of patients with coronary artery disease (CAD), and the association between stratified lipid risk and flow-mediated dilatation (FMD) index.Methods and Results: The 624 CAD patients enrolled in flow-mediated dilation (FMD)-J study A were divided into 4 groups: low-risk group (n=413) with TG <150 mg/dL and non-HDL-C <170 mg/dL; hyper-TG group (n=180) with TG 150 mg/dL and non-HDL-C <170 mg/dL; hyper-non-HDL group (n=12) with TG <150 mg/dL and non-HDL-C 170 mg/dL; and high-risk group (n=19) with TG 150 mg/dL and non-HDL-C 170 mg/dL. Comparison of the groups showed the cumulative incidence of a 3-point major adverse cardiovascular event (MACE) was different and highest in the high-risk group in all the patients (P=0.009), and in patients with a FMD index 7.0% (P=0.021), but not in those with a FMD index <7.0%. Multivariable regression analysis showed that high lipid risk (P=0.019) and FMD <7.0% (P=0.040) were independently correlated with the incidence of a 3-point MACE. Novel stratification of lipid risk, simply using TG and non-HDL-C levels, combined with FMD measurement, is useful for predicting cardiovascular outcomes in patients with CAD. (Tokushima University Institutional Repository) ● Metadata: 117809 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-21-1068 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35871575 ● Search Scopus @ Elsevier (PMID): 35871575 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-21-1068 (Tokushima University Institutional Repository: 117809, DOI: 10.1253/circj.CJ-21-1068, PubMed: 35871575)
48.	A Sezai, A Tanaka, T Imai, K Kida, H Sekino, T Murohara, Masataka Sata, N Suzuki and K Node : Comparing the Effects of Canagliflozin vs. Glimepiride by Body Mass Index in Patients with Type 2 Diabetes and Chronic Heart Failure: A Subanalysis of the CANDLE Trial, Biomedicines, Vol.10, No.7, 1656, 2022. (Summary) We present results of a 24-week comparative study of the effects of the sodium-glucose cotransporter 2 (SGLT2) inhibitor canagliflozin vs. the sulfonylurea glimepiride, by baseline body mass index (BMI), in patients with type 2 diabetes and chronic heart failure. We conducted a post hoc analysis of the CANDLE trial. This subanalysis evaluated NT-proBNP, BMI, and other laboratory parameters, according to the subgroups stratified by BMI ≥ 25 kg/m vs. BMI < 25 kg/m. A group ratio of proportional changes in the geometric means of NT-proBNP was 0.99 ( = 0.940) for the subgroup with BMI ≥ 25 kg/m and 0.85 ( = 0.075) for the subgroup with BMI < 25 kg/m, respectively. When baseline BMI was modeled as a continuous variable, results for patients with BMI < 30 kg/m showed a slightly smaller increase in NT-proBNP in the canagliflozin group vs. the glimepiride group ( = 0.295); that difference was not seen among patients with BMI ≥30 kg/m ( = 0.948). Irrespective of obesity, the canagliflozin group was associated with significant reduction in BMI compared to the glimepiride group. There was no significant difference in the effects of canagliflozin, relative to glimepiride, on NT-proBNP concentrations irrespective of baseline obesity. UMIN clinical trial registration number: UMIN000017669. (Tokushima University Institutional Repository) ● Metadata: 117802 (Link to Publication Site) ● Publication site (DOI): 10.3390/biomedicines10071656 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35884961 ● Search Scopus @ Elsevier (PMID): 35884961 ● Search Scopus @ Elsevier (DOI): 10.3390/biomedicines10071656 (Tokushima University Institutional Repository: 117802, DOI: 10.3390/biomedicines10071656, PubMed: 35884961)
49.	Y Higashikuni, W Liu and Masataka Sata : Give a Leg Up: Screening for Peripheral Artery Disease after Acute Myocardial Infarction, Journal of Atherosclerosis and Thrombosis, Vol.29, No.7, 989-991, 2022. (Tokushima University Institutional Repository) ● Metadata: 117321 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.ED186 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34853214 ● Search Scopus @ Elsevier (PMID): 34853214 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.ED186 (Tokushima University Institutional Repository: 117321, DOI: 10.5551/jat.ED186, PubMed: 34853214)
50.	Koji Yamaguchi, Tetsuzo Wakatsuki, Tomomi Matsuura, Kazuhisa Matsumoto, Yutaka Kawabata, Muneyuki Kadota, Kenya Kusunose, Takayuki Ise, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Drug-coated balloon angioplasty for severe pulmonary vein stenosis resulting from cryoballoon ablation for atrial fibrillation, Journal of Cardiology Cases, Vol.26, 35-38, 2022. (Tokushima University Institutional Repository) ● Metadata: 117234 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jccase.2022.02.009 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85127324683 (Tokushima University Institutional Repository: 117234, DOI: 10.1016/j.jccase.2022.02.009, Elsevier: Scopus)
51.	Y Okushi, Kenya Kusunose, M Nakai, Y Sumita, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Comparison of Direct Oral Anticoagulants for Acute Hospital Mortality in Venous Thromboembolism, American Journal of Cardiovascular Drugs, Vol.22, No.4, 407-416, 2022. (Summary) The choice of direct oral anticoagulants (DOACs) for venous thromboembolism (VTE) is at the physician's discretion; however, it is useful to know the differences in the clinical data of DOACs to help physicians choose. We aimed to compare the mortality associated with the use of rivaroxaban, edoxaban, and apixaban in clinical practice. We identified 38,245 patients with first hospitalization for VTE from the Diagnosis Procedure Combination database in the Japanese Registry of All Cardiac and Vascular Datasets (JROAD-DPC). We classified patients into three groups by DOAC (rivaroxaban and edoxaban group, rivaroxaban and apixaban group, and edoxaban and apixaban group) and compared the in-hospital mortality and bleeding risk by propensity score (PS) matching in each group. After PS matching, patients with rivaroxaban use had significantly lower total in-hospital mortality (1.2% vs. 2.1%; odds ratio [OR] 0.55, p = 0.012) and in-hospital mortality within 21 days (0.4% vs. 1.0%; OR 0.41, p = 0.020) and 28 days (0.7% vs. 1.3%; OR 0.53, p = 0.042) than patients with apixaban use. In the subanalysis, significant differences were only observed in patients younger than 80 years of age, patients with pulmonary embolism, and patients without heart failure. There was no significant difference in in-hospital mortality in the other groups and in the rate of bleeding events among the three groups. On PS-matched analysis, there was a difference in in-hospital mortality, especially in the rivaroxaban and apixaban group. Identifying the clinical characteristics of patients associated with each DOAC, as well as prognosis, will be useful in determining treatment strategies for VTE. (Link to Publication Site) ● Publication site (DOI): 10.1007/s40256-021-00514-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34927214 ● Search Scopus @ Elsevier (PMID): 34927214 ● Search Scopus @ Elsevier (DOI): 10.1007/s40256-021-00514-5 (DOI: 10.1007/s40256-021-00514-5, PubMed: 34927214)
52.	Kenya Kusunose, Yukina Hirata, Natsumi Yamaguchi, Y Kosaka, T Tsuji, J Kotoku and Masataka Sata : Deep Learning for Detection of Exercise-Induced Pulmonary Hypertension Using Chest X-Ray Images, Frontiers in Cardiovascular Medicine, Vol.9, 891703, 2022. (Summary) Stress echocardiography is an emerging tool used to detect exercise-induced pulmonary hypertension (EIPH). However, facilities that can perform stress echocardiography are limited by issues such as cost and equipment. We evaluated the usefulness of a deep learning (DL) approach based on a chest X-ray (CXR) to predict EIPH in 6-min walk stress echocardiography. The study enrolled 142 patients with scleroderma or mixed connective tissue disease with scleroderma features who performed a 6-min walk stress echocardiographic test. EIPH was defined by abnormal cardiac output (CO) responses that involved an increase in mean pulmonary artery pressure (mPAP). We used the previously developed AI model to predict PH and calculated PH probability in this cohort. EIPH defined as ΔmPAP/ΔCO >3.3 and exercise mPAP >25 mmHg was observed in 52 patients, while non-EIPH was observed in 90 patients. The patients with EIPH had a higher mPAP at rest than those without EIPH. The probability of PH based on the DL model was significantly higher in patients with EIPH than in those without EIPH. Multivariate analysis showed that gender, mean PAP at rest, and the probability of PH based on the DL model were independent predictors of EIPH. A model based on baseline parameters (age, gender, and mPAP at rest) was improved by adding the probability of PH predicted by the DL model (AUC: from 0.65 to 0.74; = 0.046). Applying the DL model based on a CXR may have a potential for detection of EIPH in the clinical setting. (Tokushima University Institutional Repository) ● Metadata: 117225 (Link to Publication Site) ● Publication site (DOI): 10.3389/fcvm.2022.891703 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35783826 ● Search Scopus @ Elsevier (PMID): 35783826 ● Search Scopus @ Elsevier (DOI): 10.3389/fcvm.2022.891703 (Tokushima University Institutional Repository: 117225, DOI: 10.3389/fcvm.2022.891703, PubMed: 35783826)
53.	W Liu, Y Higashikuni and Masataka Sata : Linking RNA dynamics to heart disease: the lncRNA/miRNA/mRNA axis in myocardial ischemia-reperfusion injury, Hypertension Research, Vol.45, No.6, 1067-1069, 2022. (Link to Publication Site) ● Publication site (DOI): 10.1038/s41440-022-00905-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35365797 ● Search Scopus @ Elsevier (PMID): 35365797 ● Search Scopus @ Elsevier (DOI): 10.1038/s41440-022-00905-4 (DOI: 10.1038/s41440-022-00905-4, PubMed: 35365797)
54.	Yasuhiro Mitsui, Mai Yagi, Sho Muraki, Tomomi Matsuura, Yoshimi Bando, Shota Fujimoto, Shinji Kitamura, Koichi Okamoto, Naoki Muguruma, Masataka Sata and Tetsuji Takayama : Pulmonary Tumor Thrombotic Microangiopathy Due to Gastric Cancer Diagnosed Antemortem by a Cytological Examination of Aspirated Pulmonary Artery Blood., Internal Medicine, Vol.61, No.10, 1491-1495, 2022. (Tokushima University Institutional Repository) ● Metadata: 118012 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.8313-21 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34670901 ● Search Scopus @ Elsevier (PMID): 34670901 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.8313-21 (Tokushima University Institutional Repository: 118012, DOI: 10.2169/internalmedicine.8313-21, PubMed: 34670901)
55.	A Mizuno, Kenya Kusunose, T Kishi, J Rewley, C Matsumoto, Y Sahashi, M Ishida, S Sanada, M Fukuda, T Sugimoto, M Hirano, D Yoneoka, Masataka Sata, T Anzai and K Node : Impact of Tweeting Summaries by the Japanese Circulation Society Official Account on Article Viewership - Pilot Trial, Circulation Journal, Vol.86, No.4, 715-720, 2022. (Summary) The impact of promotional tweets from the official journal account (forCirculation JournalandCirculation Reports) on article viewership has not been thoroughly evaluated.Methods and Results:We retrospectively collected journal viewership data forCirculation JournalandCirculation Reportsfrom March 2021 to August 2021. We compared viewership between articles with (n=15) and without (n=250) tweets. After 1 : 4 propensity score matching (15 tweeted articles and 60 non-tweeted matched controls), journal viewership metrics within 7 days of the tweeting date (and the hypothetical tweeting date), was larger in tweeted articles than non-tweeted articles (median [interquartile range] Abstract page views 89 [60-104] vs. 18 [8-41]). This pilot study suggests a positive relationship between journal-posted promotional tweets and article viewership. (Keyword) Benchmarking / Humans / Japan / Pilot Projects / Retrospective Studies / Social Media (Tokushima University Institutional Repository) ● Metadata: 117213 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-21-0944 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35283367 ● Search Scopus @ Elsevier (PMID): 35283367 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-21-0944 (Tokushima University Institutional Repository: 117213, DOI: 10.1253/circj.CJ-21-0944, PubMed: 35283367)
56.	Daiju Fukuda, PT Pham and Masataka Sata : Emerging Roles of the Innate Immune System Regulated by DNA Sensors in the Development of Vascular and Metabolic Diseases, Journal of Atherosclerosis and Thrombosis, Vol.29, No.3, 297-307, 2022. (Summary) Sterile chronic inflammation causes cardiometabolic disorders; however, the mechanisms are not fully understood. Previous studies have demonstrated the degradation of cells/tissues in the vasculature and metabolic organs in lifestyle-associated diseases, such as diabetes and hyperlipidemia, suggesting the release and/or accumulation of nucleic acids from damaged cells. DNA is indispensable for life; however, DNA fragments, especially those from pathogens, strongly induce inflammation by the activation of DNA sensors. Growing evidence suggests that DNA-sensing mechanisms, which are normally involved in self-defense against pathogens as the innate immune system, are associated with the progression of inflammatory diseases in response to endogenous DNA fragments. There are several types of DNA sensors in our bodies. Toll-like receptor 9 (TLR9)-one of the most studied DNA sensors-recognizes DNA fragments in endosome. In addition, stimulator of interferon genes (STING), which has recently been extensively investigated, recognizes cyclic GMP-AMP (cGAMP) generated from DNA fragments in the cytosol. Both TLR9 and STING are known to play pivotal roles in host defense as the innate immune system. However, recent studies have indicated that the activation of these DNA sensors in immune cells, such as macrophages, promotes inflammation leading to the development of vascular and metabolic diseases associated with lifestyle. In this review, we discuss recent advances in determining the roles of DNA sensors in these disease contexts. Revealing a novel mechanism of sterile chronic inflammation regulated by DNA sensors might facilitate clinical interventions for these health conditions. (Keyword) Animals / DNA / Humans / Immunity, Innate / Metabolic Diseases / Signal Transduction / Vascular Diseases (Tokushima University Institutional Repository) ● Metadata: 116996 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.RV17059 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34248111 ● Search Scopus @ Elsevier (PMID): 34248111 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.RV17059 (Tokushima University Institutional Repository: 116996, DOI: 10.5551/jat.RV17059, PubMed: 34248111)
57.	Kazuhisa Matsumoto, Takeshi Tobiume, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Tetsuzo Wakatsuki, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Evaluation of the input site and characteristics of the antegrade fast pathway based on three-dimensional bi-atrial stimulus-ventricle mapping, Journal of Interventional Cardiac Electrophysiology, Vol.63, No.2, 417-424, 2022. (Summary) Previous studies examined the right atrial (RA) input site of the antegrade fast pathway (AFp) (AFpI). However, the left atrial (LA) input to the atrioventricular (AV) node has not been extensively evaluated. In this study, we created three-dimensional (3-D) bi-atrial stimulus-ventricle (St-V) maps and analyzed the input site and characteristics of the AFp in both the RA and LA. Forty-four patients diagnosed with atrial fibrillation or WPW syndrome were included in this study. Three-dimensional bi-atrial St-V mapping was performed using an electroanatomical mapping system. Sites exhibiting the minimal St-V interval (MinSt-V) were defined as AFpIs and were classified into seven segments, four in the RA (F, S, M, and I) and three in the LA (M1, M2, and M3). By combining the MinSt-V in the RA and LA, the AFpIs were classified into three types: RA, LA, and bi-atrial (BA) types. The clinical and electrophysiological characteristics were compared. AFpIs were most frequently observed at site S in the RA (34%) and M2 in the LA (50%), and the BA type was the most common (57%). AFpIs in the LA were recognized in 75% of the patients. There were no clinical or electrophysiological indicators for predicting AFpI sites. Three-dimensional bi-atrial St-V maps could classify AFpIs in both the RA and LA. AFpIs in the LA were frequently recognized. There were no significant clinical or electrophysiological indicators for predicting AFpI sites, and 3-D bi-atrial St-V mapping was the only method to reveal the precise AFp input site. (Tokushima University Institutional Repository) ● Metadata: 116382 (Link to Publication Site) ● Publication site (DOI): 10.1007/s10840-021-01026-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34231099 ● Search Scopus @ Elsevier (PMID): 34231099 ● Search Scopus @ Elsevier (DOI): 10.1007/s10840-021-01026-7 (Tokushima University Institutional Repository: 116382, DOI: 10.1007/s10840-021-01026-7, PubMed: 34231099)
58.	Masato Nakamura, Hitoshi Yaku, Junya Ako, Hirokuni Arai, Tohru Asai, Taishiro Chikamori, Hiroyuki Daida, Kiyoshi Doi, Toshihiro Fukui, Toshiaki Ito, Kazushige Kadota, Junjiro Kobayashi, Tatsuhiko Komiya, Ken Kozuma, Yoshihisa Nakagawa, Koichi Nakao, Hiroshi Niinami, Takayuki Ohno, Yukio Ozaki, Masataka Sata, Shuichiro Takanashi, Hirofumi Takemura, Takafumi Ueno, Satoshi Yasuda, Hitoshi Yokoyama, Tomoyuki Fujita, Tokuo Kasai, Shun Kohsaka, Takashi Kubo, Susumu Manabe, Naoya Matsumoto, Shigeru Miyagawa, Tomohiro Mizuno, Noboru Motomura, Satoshi Numata, Hiroyuki Nakajima, Hirotaka Oda, Hiromasa Otake, Fumiyuki Otsuka, Ken-Ichiro Sasaki, Kazunori Shimada, Tomoki Shimokawa, Toshiro Shinke, Tomoaki Suzuki, Masao Takahashi, Nobuhiro Tanaka, Hiroshi Tsuneyoshi, Taiki Tojo, Dai Une, Satoru Wakasa, Koji Yamaguchi, Takashi Akasaka, Atsushi Hirayama, Kazuo Kimura, Takeshi Kimura, Yoshiro Matsui, Shunichi Miyazaki, Yoshitaka Okamura, Minoru Ono, Hiroki Shiomi and Kazuo Tanemoto : JCS/JSCVS 2018 Guideline on Revascularization of Stable Coronary Artery Disease, Circulation Journal, Vol.86, No.3, 477-588, 2022. (Keyword) Coronary Artery Bypass / Coronary Artery Disease / Humans / Myocardial Revascularization / Percutaneous Coronary Intervention / Treatment Outcome (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-20-1282 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35095031 ● Summary page in Scopus @ Elsevier: 2-s2.0-85125252399 (DOI: 10.1253/circj.CJ-20-1282, PubMed: 35095031, Elsevier: Scopus)
59.	Kenya Kusunose, Robert Zheng, Hirotsugu Yamada and Masataka Sata : How to standardize the measurement of left ventricular ejection fraction, Journal of Medical Ultrasonics, Vol.49, No.1, 35-43, 2022. (Link to Publication Site) ● Publication site (DOI): 10.1007/s10396-021-01116-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34322777 ● Summary page in Scopus @ Elsevier: 2-s2.0-85111531757 (DOI: 10.1007/s10396-021-01116-z, PubMed: 34322777, Elsevier: Scopus)
60.	Shusuke Yagi, Daiju Fukuda, Takayuki Ise, Koji Yamaguchi, Kenya Kusunose, Muneyuki Kadota, Yutaka Kawabata, Tomomi Matsuura, Tomohiro Soga, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Shinji Kawahito and Masataka Sata : Clinical clerkship students' preferences and satisfaction regarding online lectures during the COVID-19 pandemic, BMC Medical Education, Vol.22, No.1, 43, 2022. (Summary) The COVID-19 pandemic has caused an unprecedented disruption in medical education. Students and lecturers had to adapt to online education. The current study aimed to investigate the level of satisfaction and future preference for online lectures among clinical clerkship students and elucidated the factors that affect these outcomes. We selected a sample of 114 medical students undergoing clinical clerkship during the COVID-19 pandemic. We conducted onsite lectures before the pandemic and online lectures after the outbreak. A survey was conducted, and the sample included students and 17 lecturers. The average scores of total satisfaction and future preference related to online lectures were computed. Students' scores on total satisfaction with online lectures and their future preference were higher than those for onsite lectures. Scores on the ease of debating dimension were low and those on accessibility of lectures in online lectures were higher than those in onsite lectures. There was no difference between the two groups in the scores on the comprehensibility and ease of asking questions dimensions. Results of the multiple regression analysis revealed that accessibility determined total satisfaction, and future preference was determined by comprehensibility as well as accessibility. Contrary to students' future preferences, lecturers favored onsite lectures to online ones. Online lectures are an acceptable mode of teaching during the COVID-19 pandemic for students undergoing clinical clerkship. Online lectures are expected to become more pervasive to avoid the spread of COVID-19. (Keyword) COVID-19 / Clinical Clerkship / Humans / Pandemics / Personal Satisfaction / SARS-CoV-2 / Students, Medical (Tokushima University Institutional Repository) ● Metadata: 116989 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12909-021-03096-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35042505 ● Summary page in Scopus @ Elsevier: 2-s2.0-85123015852 (Tokushima University Institutional Repository: 116989, DOI: 10.1186/s12909-021-03096-7, PubMed: 35042505, Elsevier: Scopus)
61.	Nao Ishii, Kenya Kusunose, A Shono, K Matsumoto, Susumu Nishio, Natsumi Yamaguchi, Yukina Hirata, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Effects of Radiofrequency Catheter Ablation on Cardiac Reserve Using Preload Stress Echocardiography in Paroxysmal and Persistent Atrial Fibrillation, The American Journal of Cardiology, Vol.168, 71-77, 2022. (Summary) The effects of catheter ablation on exercise tolerance and quality of life in patients with atrial fibrillation (AF) have been reported. We assessed cardiac function in more detail using the leg positive pressure (LPP) technique and found that contractile reserve is particularly important in relation to exercise tolerance and prognosis. In this study, we used the LPP technique to examine changes in contractile reserve immediately after ablation and 6 months later. We prospectively enrolled patients who underwent catheter ablation for AF at 2 institutes. We performed LPP stress echocardiography 2 to 3 days after (FU-1) and 6 months after (FU-2) ablation to examine changes in cardiac function indexes. The primary end point was improvement in contractile reserve. Ultimately, 109 patients (mean age 67.4 ± 9.6 years; 70% men) underwent 2 sessions of LPP stress echocardiography. The median CHADS-VAS score was 2 (interquartile range 13). From FU-1 to FU-2, the change in the stroke volume index after the LPP maneuver increased in patients with paroxysmal and persistent AF with low CHADS-VAS scores (both p <0.05). Regardless of AF subtype, contractile reserve at FU-2 improved in patients with low CHADS-VAS scores compared with that at FU-1. In contrast, patients with high CHADS-VAS scores had no change. In conclusion, patients with AF with a low CHADS-VAS score had improved contractile reserve after ablation, whereas patients with high scores did not show any improvement. Aggressive interventions in patients with high scores may lead to better management after catheter ablation. (Keyword) Aged / Atrial Fibrillation / Catheter Ablation / Echocardiography, Stress / Female / Humans / Male / Middle Aged / Predictive Value of Tests / Quality of Life / Risk Assessment / Risk Factors / Treatment Outcome (Tokushima University Institutional Repository) ● Metadata: 116987 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.amjcard.2021.12.026 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35063270 ● Search Scopus @ Elsevier (PMID): 35063270 ● Search Scopus @ Elsevier (DOI): 10.1016/j.amjcard.2021.12.026 (Tokushima University Institutional Repository: 116987, DOI: 10.1016/j.amjcard.2021.12.026, PubMed: 35063270)
62.	Kenya Kusunose, H Yoshida, A Tanaka, H Teragawa, Y Akasaki, Y Fukumoto, K Eguchi, H Kamiya, K Kario, Hirotsugu Yamada, Masataka Sata, K Node and Munehide Matsuhisa : Effect of febuxostat on left ventricular diastolic function in patients with asymptomatic hyperuricemia: a sub analysis of the PRIZE Study, Hypertension Research, Vol.45, No.1, 106-115, 2022. (Tokushima University Institutional Repository) ● Metadata: 116992 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41440-021-00752-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34657137 ● Search Scopus @ Elsevier (PMID): 34657137 ● Search Scopus @ Elsevier (DOI): 10.1038/s41440-021-00752-9 (Tokushima University Institutional Repository: 116992, DOI: 10.1038/s41440-021-00752-9, PubMed: 34657137)
63.	Masataka Sata : 徳島県循環器病対策推進計画, Shikoku Acta Medica, Vol.77, No.5,6, 199-206, 2021. (Summary) Cerebrovascular diseases including stroke and cardiovascular diseases are the leading causes of death in Japan, which together account for 23.2% of the total number of deaths in 2018. The major causes of the need for long-term care in Japan are also cerebrovascular disease(16.1%)and cardiovascular disease(4.5%), which together account for more than one-fifth of the total. Medical expenses for both cerebrovascular and cardiovascular disease account for ≈20% of the total, which is the highest by injury/illness classification. The Cerebrovascular and Cardiovascular Disease Control Act, of Japanese national law, was promulgated by a legislative act on December 14, 2018, and enacted on December 1, 2019. On the basis of the Cerebrovascular and Cardiovascular Disease Control Act, the Ministry of Health, Labour and Welfare, Japan, published the Japanese National Plan for Promotion of Measures Against Cerebrovascular and Cardiovascular Disease on October 27, 2020. It has indicated both problems in the current situation and individual measures to address the problems. The Japanese National Plan includes 3 major measures : spreading awareness of prevention measures and accurate information on cerebrovascular and cardiovascular disease ; enhancing service provision systems related to health, medical care, and welfare services ; and promoting research on cerebrovascular and cardiovascular disease. The 2 main goals of the Japanese National Plan are to extend healthy life expectancy by 3 years by 2040 compared with 2016 and to decrease age-adjusted mortality of cerebrovascular and cardiovascular disease. The average life expectancy and healthy life expectancy for both men and women increased by 0.67 to 1.72 years from 2010 to 2016 in Japan. In 2016, the unhealthy period which is defined as differences between healthy life expectancy(men, 72.14 years ; women, 74.49 years)and average life expectancy(men, 80.98 years ; women, 87.14 years)was large : ≈8.8 years for men and ≈12.4 years for women. Therefore, extending healthy life expectancy is a primary goal of the Japanese National Plan. Based on this national plan, the Tokushima Plan for Promotion of Measures Against Cerebrovascular and Cardiovascular Diseases is developed through the meetings of the Tokushima Council for Promotion of Measures Against Cerebrovascular and Cardiovascular Diseases, parliamentary associated meetings, and public comments. The council is composed of patients with cerebrovascular or cardiovascular disease ; those engaged in emergency services and health, medical, or welfare services ; and those with academic experience. Here, we describe outline of the Tokushima Plan for Promotion of Measures Against Cerebrovascular and Cardiovascular Disease. (Keyword) Cardiovascular disease / Healthy life expectancy / Rehabilitation / Endovascular treatment (Tokushima University Institutional Repository) ● Metadata: 117131 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050855201331782272 (Tokushima University Institutional Repository: 117131, CiNii: 1050855201331782272)
64.	Kumiko Suto, Daiju Fukuda, Masakazu Shinohara, Byambasuren Ganbaatar, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, Ken-Ichi Hirata and Masataka Sata : Pemafibrate, A Novel Selective Peroxisome Proliferator-Activated Receptor α Modulator, Reduces Plasma Eicosanoid Levels and Ameliorates Endothelial Dysfunction in Diabetic Mice., Journal of Atherosclerosis and Thrombosis, Vol.28, No.12, 1349-1360, 2021. (Summary) Various pathological processes related to diabetes cause endothelial dysfunction. Eicosanoids derived from arachidonic acid (AA) have roles in vascular regulation. Fibrates have recently been shown to attenuate vascular complications in diabetics. Here we examined the effects of pemafibrate, a selective peroxisome proliferator-activated receptor α modulator, on plasma eicosanoid levels and endothelial function in diabetic mice. Diabetes was induced in 7-week-old male wild-type mice by a single injection of streptozotocin (150 mg/kg). Pemafibrate (0.3 mg/kg/day) was administered orally for 3 weeks. Untreated mice received vehicle. Circulating levels of eicosanoids and free fatty acids were measured using both gas and liquid chromatography-mass spectrometry. Endothelium-dependent and endothelium-independent vascular responses to acetylcholine and sodium nitroprusside, respectively, were analyzed. Pemafibrate reduced both triglyceride and non-high-density lipoprotein -cholesterol levels (P<0.01), without affecting body weight. It also decreased circulating levels of AA (P<0.001), thromboxane B (P<0.001), prostaglandin E, leukotriene B (P<0.05), and 5-hydroxyeicosatetraenoic acid (P<0.001), all of which were elevated by the induction of diabetes. In contrast, the plasma levels of 15-deoxy-Δ-prostaglandin J, which declined following diabetes induction, remained unaffected by pemafibrate treatment. In diabetic mice, pemafibrate decreased palmitic acid (PA) and stearic acid concentrations (P<0.05). Diabetes induction impaired endothelial function, whereas pemafibrate ameliorated it (P<0.001). The results of ex vivo experiments indicated that eicosanoids or PA impaired endothelial function. Pemafibrate diminished the levels of vasoconstrictive eicosanoids and free fatty acids accompanied by a reduction of triglyceride. These effects may be associated with the improvement of endothelial function by pemafibrate in diabetic mice. (Tokushima University Institutional Repository) ● Metadata: 116054 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.61101 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33775978 ● Search Scopus @ Elsevier (PMID): 33775978 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.61101 (Tokushima University Institutional Repository: 116054, DOI: 10.5551/jat.61101, PubMed: 33775978)
65.	Yuichi Kimura, Yasuhiro Izumiya, Satoshi Araki, Satoru Yamamura, Shinsuke Hanatani, Yoshiro Onoue, Toshifumi Ishida, Yuichiro Arima, Taishi Nakamura, Eiichiro Yamamoto, Takafumi Senokuchi, Tatsuya Yoshizawa, Masataka Sata, Shokei Kim-Mitsuyama, Naomi Nakagata, Eva Bober, Thomas Braun, Koichi Kaikita, Kazuya Yamagata and Kenichi Tsujita : Sirt7 Deficiency Attenuates Neointimal Formation Following Vascular Injury by Modulating Vascular Smooth Muscle Cell Proliferation, Circulation Journal, Vol.85, No.12, 2232-2240, 2021. (Summary) Sirt7 is a recently identified sirtuin and has important roles in various pathological conditions, including cancer progression and metabolic disorders. It has previously been reported that Sirt7 is a key molecule in acute myocardial wound healing and pressure overload-induced cardiac hypertrophy. In this study, the role of Sirt7 in neointimal formation after vascular injury is investigated.Methods and Results:Systemic (Sirt7) and smooth muscle cell-specific Sirt7-deficient mice were subjected to femoral artery wire injury. Primary vascular smooth muscle cells (VSMCs) were isolated from the aorta of wild type (WT) and Sirt7mice and their capacity for cell proliferation and migration was compared. Sirt7 expression was increased in vascular tissue at the sites of injury. Sirt7mice demonstrated significant reduction in neointimal formation compared to WT mice. In vitro, Sirt7 deficiency attenuated the proliferation of serum-induced VSMCs. Serum stimulation-induced upregulation of cyclins and cyclin-dependent-kinase 2 (CDK2) was significantly attenuated in VSMCs of Sirt7compared with WT mice. These changes were accompanied by enhanced expression of the microRNA 290-295 cluster, the translational negative regulator of CDK2, in VSMCs of Sirt7mice. It was confirmed that smooth muscle cell-specific Sirt7-deficient mice showed significant reduction in neointima compared with control mice. Sirt7 deficiency attenuates neointimal formation after vascular injury. Given the predominant role in vascular neointimal formation, Sirt7 is a potentially suitable target for treatment of vascular diseases. (Tokushima University Institutional Repository) ● Metadata: 116725 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-20-0936 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33678753 ● Search Scopus @ Elsevier (PMID): 33678753 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-20-0936 (Tokushima University Institutional Repository: 116725, DOI: 10.1253/circj.CJ-20-0936, PubMed: 33678753)
66.	Kenya Kusunose, Miharu Arase, Robert Zheng, Yukina Hirata, Susumu Nishio, Takayuki Ise, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Clinical Utility of Overlap Time for Incomplete Relaxation to Predict Cardiac Events in Heart Failure: Incomplete relaxation in heart failure, Journal of Cardiac Failure, Vol.27, No.11, 1222-1230, 2021. (Summary) The overlap time of transmitral flow can be a novel marker of subclinical left ventricular (LV) dysfunction for predicting adverse events in heart failure (HF). We aimed to 1) investigate the role of overlap time of E-A wave in association with clinical parameters, and 2) evaluate whether the overlap time could add prognostic information with respect to other conventional clinical prognosticators in HF. We prospectively evaluated 153 patients hospitalized with HF (mean age 68±15 years; 63% male). The primary endpoint was readmission following HF and cardiac death. During a median period of 25 months, 43 patients were either readmitted or died. Overlap time appeared to be associated with worse outcomes. After adjustment for readmission score and ratio of diastolic filling period and cardiac cycle length in a Cox proportional-hazards model, overlap time was associated with event free survival, independent of elevated left atrial pressure (LAP) based on guidelines. When overlap time was added to the model based on clinical variables and elevated LAP, the C-statistic significantly improves from 0.70 (95% CI: 0.63-0.77) to 0.77 (95% CI: 0.69-0.83, compared P=0.035). This preliminary study suggested that prolonged overlap time may have potential for predicting readmission and cardiac mortality risk assessment in HF. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cardfail.2021.05.018 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34129950 ● Search Scopus @ Elsevier (PMID): 34129950 ● Search Scopus @ Elsevier (DOI): 10.1016/j.cardfail.2021.05.018 (DOI: 10.1016/j.cardfail.2021.05.018, PubMed: 34129950)
67.	Y Higashikuni, W Liu, T Obana and Masataka Sata : Pathogenic Basis of Thromboinflammation and Endothelial Injury in COVID-19: Current Findings and Therapeutic Implications, International Journal of Molecular Sciences, Vol.22, No.21, 12081, 2021. (Summary) Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic with a great impact on social and economic activities, as well as public health. In most patients, the symptoms of COVID-19 are a high-grade fever and a dry cough, and spontaneously resolve within ten days. However, in severe cases, COVID-19 leads to atypical bilateral interstitial pneumonia, acute respiratory distress syndrome, and systemic thromboembolism, resulting in multiple organ failure with high mortality and morbidity. SARS-CoV-2 has immune evasion mechanisms, including inhibition of interferon signaling and suppression of T cell and B cell responses. SARS-CoV-2 infection directly and indirectly causes dysregulated immune responses, platelet hyperactivation, and endothelial dysfunction, which interact with each other and are exacerbated by cardiovascular risk factors. In this review, we summarize current knowledge on the pathogenic basis of thromboinflammation and endothelial injury in COVID-19. We highlight the distinct contributions of dysregulated immune responses, platelet hyperactivation, and endothelial dysfunction to the pathogenesis of COVID-19. In addition, we discuss potential therapeutic strategies targeting these mechanisms. (Keyword) Angiotensin-Converting Enzyme 2 / Antiviral Agents / Blood Coagulation / COVID-19 / Endothelium, Vascular / Humans / Immunity, Innate / Platelet Activation / SARS-CoV-2 / Thrombosis (Tokushima University Institutional Repository) ● Metadata: 116739 (Link to Publication Site) ● Publication site (DOI): 10.3390/ijms222112081 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34769508 ● Search Scopus @ Elsevier (PMID): 34769508 ● Search Scopus @ Elsevier (DOI): 10.3390/ijms222112081 (Tokushima University Institutional Repository: 116739, DOI: 10.3390/ijms222112081, PubMed: 34769508)
68.	Robert Zheng, Kenya Kusunose, Y Okushi, Y Okayama, M Nakai, Y Sumita, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Impact of cancer on short-term in-hospital mortality after primary acute myocardial infarction, Open Heart, Vol.8, No.2, e00186, 2021. (Tokushima University Institutional Repository) ● Metadata: 116972 (Link to Publication Site) ● Publication site (DOI): 10.1136/openhrt-2021-001860 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34810277 ● Summary page in Scopus @ Elsevier: 2-s2.0-85120377378 (Tokushima University Institutional Repository: 116972, DOI: 10.1136/openhrt-2021-001860, PubMed: 34810277, Elsevier: Scopus)
69.	Kenya Kusunose, Hironori Takahashi, Susumu Nishio, Yukina Hirata, Robert Zheng, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Kenji Shimada, Yasuhisa Kanematsu, Yasushi Takagi and Masataka Sata : Predictive value of left atrial function for latent paroxysmal atrial fibrillation as the cause of embolic stroke of undetermined source, Journal of Cardiology, Vol.78, No.5, 355-361, 2021. (Summary) In patients with embolic stroke of undetermined source (ESUS), paroxysmal atrial fibrillation (AF) is often diagnosed, however, the risk of paroxysmal AF in ESUS has not been well described. Several studies have suggested a linkage between left atrial (LA) functional parameters and risk of AF in stroke patients. The aim of this study was to assess the role of LA functional parameters as predictors of latent paroxysmal AF in ESUS on admission. Between January 2015 and December 2019, consecutive stroke patients with suspected ESUS at admission were prospectively included in this study. They were under hospital electrocardiographic monitoring for detection of new-onset AF. Various echocardiographic parameters including left atrial strain were assessed for association with new-onset AF. We gathered 1082 consecutive patients with ischemic stroke. After exclusions, 121 patients with suspected ESUS at admission formed the study cohort. New-onset AF was detected in 46 (38%) patients during hospital electrocardiographic monitoring (median follow-up: 18 days). LA pump and reservoir strains were significantly and independently associated with new-onset AF. Receiver operating characteristic analysis for the association with new-onset AF showed that the areas under the curve (AUCs) of clinical parameters plus one of each strain (LA pump strain: AUC: 0.86±0.04 and LA reservoir strain: AUC: 0.76±0.05) models were significantly better than plus LA volume index (AUC: 0.68±0.04, compared p-values <0.05). LA strain was significantly associated with new development of AF. Patients with impaired LA function at admission should be carefully monitored to find AF. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jjcc.2021.05.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34119401 ● Search Scopus @ Elsevier (PMID): 34119401 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jjcc.2021.05.005 (DOI: 10.1016/j.jjcc.2021.05.005, PubMed: 34119401)
70.	Rie Tsutsumi, Yuki Yamasaki, Jiro Takeo, Hiroko Miyahara, Mayu Sebe, Masahiro Bando, Yousuke Tanba, Yuna Mishima, Kana Takeji, Nanako Ueshima, Masashi Kuroda, Saeko Masumoto, Nagakatsu Harada, Daiju Fukuda, Ryoko Yoshimoto, Yasuo M. Tsutsumi, Ken-ichi Aihara, Masataka Sata and Hiroshi Sakaue : Long-chain monounsaturated fatty acids improve endothelial function with altering microbial flora, Translational Research : The Journal of Laboratory and Clinical Medicine, Vol.237, 16-30, 2021. (Summary) Fish oil-derived long-chain monounsaturated fatty acids (LCMUFAs) with a carbon chain length longer than 18 units ameliorate cardiovascular risk in mice. In this study, we investigated whether LCMUFAs could improve endothelial functions in mice and humans. In a double-blind, randomized, placebo-controlled, parallel-group, multi-center study, healthy subjects were randomly assigned to either an LCMUFA oil (saury oil) or a control oil (olive and tuna oils) group. Sixty subjects were enrolled and administrated each oil for 4 weeks. For the animal study, ApoE mice were fed a Western diet supplemented with 3% of either gadoleic acid (C20:1) or cetoleic acid (C22:1) for 12 weeks. Participants from the LCMUFA group showed improvements in endothelial function and a lower trimethylamine-N-oxide level, which is a predictor of coronary artery disease. C20:1 and C22:1 oils significantly improved atherosclerotic lesions and plasma levels of several inflammatory cytokines, including IL-6 and TNF-α. These beneficial effects were consistent with an improvement in the gut microbiota environment, as evident from the decreased ratio of Firmicutes and/ or Bacteroidetes, increase in the abundance of Akkermansia, and upregulation of short-chain fatty acid (SCFA)-induced glucagon-like peptide-1 (GLP-1) expression and serum GLP-1 level. These data suggest that LCMUFAs alter the microbiota environment that stimulate the production of SCFAs, resulting in the induction of GLP-1 secretion. Fish oil-derived long-chain monounsaturated fatty acids might thus help to protect against cardiovascular disease. (Tokushima University Institutional Repository) ● Metadata: 116689 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.trsl.2021.03.016 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33775867 ● Summary page in Scopus @ Elsevier: 2-s2.0-85114290883 (Tokushima University Institutional Repository: 116689, DOI: 10.1016/j.trsl.2021.03.016, PubMed: 33775867, Elsevier: Scopus)
71.	Kenya Kusunose, Yuichiro Okushi, Yoshihiro Okayama, Robert Zheng, Michikazu Nakai, Yoko Sumita, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Use of Echocardiography and Heart Failure In-Hospital Mortality from Registry Data in Japan., Journal of Cardiovascular Development and Disease, Vol.8, No.10, 124, 2021. (Summary) Echocardiography requires a high degree of skill on the part of the examiner, and the skill may be more improved in larger volume centers. This study investigated trends and outcomes associated with the use and volume of echocardiographic exams from a real-world registry database of heart failure (HF) hospitalizations. This study was based on the Diagnosis Procedure Combination database in the Japanese Registry of All Cardiac and Vascular Datasets (JROAD-DPC). A first analysis was performed to assess the trend of echocardiographic examinations between 2012 and 2016. A secondary analysis was performed to assess whether echocardiographic use was associated with in-hospital mortality in 2015. During this period, the use of echocardiography grew at an average annual rate of 6%. Patients with echocardiography had declining rates of hospital mortality, and these trends were associated with high hospitalization costs. In the 2015 sample, a total of 52,832 echocardiograms were examined, corresponding to 65.6% of all HF hospital admissions for that year. We found that the use and volume of echocardiography exams were associated with significantly lower odds of all-cause hospital mortality in heart failure (adjusted odds ratio (OR): 0.48 for use of echocardiography and 0.78 for the third tertile; both < 0.001). The use of echocardiography was associated with decreased odds of hospital mortality in HF. The volumes of echocardiographic examinations were also associated with hospital mortality. (Tokushima University Institutional Repository) ● Metadata: 117323 (Link to Publication Site) ● Publication site (DOI): 10.3390/jcdd8100124 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34677193 ● Summary page in Scopus @ Elsevier: 2-s2.0-85116636823 (Tokushima University Institutional Repository: 117323, DOI: 10.3390/jcdd8100124, PubMed: 34677193, Elsevier: Scopus)
72.	Shusuke Yagi, T Takahashi, K Murakami, M Azuma, M Sugano, R Miyamoto, M Niki, Hirotsugu Yamada, Yutaka Kawabata, Tani Akihiro, Daiju Fukuda, Muneyuki Kadota, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Tomomi Matsuura, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki, H Hata and Masataka Sata : Infective Endocarditis from Furuncle with Meningitis Complication Caused by Methicillin-resistant Staphylococcus aureus, Internal Medicine, Vol.60, No.20, 3251-3255, 2021. (Tokushima University Institutional Repository) ● Metadata: 118014 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.6902-20 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33867390 ● Search Scopus @ Elsevier (PMID): 33867390 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.6902-20 (Tokushima University Institutional Repository: 118014, DOI: 10.2169/internalmedicine.6902-20, PubMed: 33867390)
73.	Kenya Kusunose, T Imai, A Tanaka, K Dohi, K Shiina, T Yamada, K Kida, K Eguchi, H Teragawa, Y Takeishi, N Ohte, Hirotsugu Yamada, Masataka Sata and K Node : Effects of canagliflozin on NT-proBNP stratified by left ventricular diastolic function in patients with type 2 diabetes and chronic heart failure: a sub analysis of the CANDLE trial, Cardiovascular Diabetology, Vol.20, No.1, 186, 2021. (Summary) Identification of the effective subtypes of treatment for heart failure (HF) is an essential topic for optimizing treatment of the disorder. We hypothesized that the beneficial effect of SGLT2 inhibitors (SGLT2i) on the levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) might depend on baseline diastolic function. To elucidate the effects of SGLT2i in type 2 diabetes mellitus (T2DM) and chronic HF we investigated, as a post-hoc sub-study of the CANDLE trial, the effects of canagliflozin on NT-proBNP levels from baseline to 24 weeks, with the data stratified by left ventricular (LV) diastolic function at baseline. Patients (n = 233) in the CANDLE trial were assigned randomly to either an add-on canagliflozin (n = 113) or glimepiride treatment groups (n = 120). The primary endpoint was a comparison between the two groups of the changes from baseline to 24 weeks in NT-pro BNP levels, stratified according to baseline ventricular diastolic function. The change in the geometric mean of NT-proBNP level from baseline to 24 weeks was 0.98 (95% CI 0.89-1.08) in the canagliflozin group and 1.07 (95% CI 0.97-1.18) in the glimepiride group. The ratio of change with canagliflozin/glimepiride was 0.93 (95% CI 0.82-1.05). Responder analyses were used to investigate the response of an improvement in NT-proBNP levels. Although the subgroup analyses for septal annular velocity (SEP-e') showed no marked heterogeneity in treatment effect, the subgroup with an SEP-e' < 4.7 cm/s indicated there was an association with lower NT-proBNP levels in the canagliflozin group compared with that in the glimepiride group (ratio of change with canagliflozin/glimepiride (0.83, 95% CI 0.66-1.04). In the subgroup with a lower LV diastolic function, canagliflozin showed a trend of reduced NT-pro BNP levels compared to that observed with glimepiride. This study suggests that the beneficial effects of canagliflozin treatment may be different in subgroups classified by the severity of LV diastolic dysfunction. (Tokushima University Institutional Repository) ● Metadata: 116720 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12933-021-01380-w (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34521417 ● Summary page in Scopus @ Elsevier: 2-s2.0-85115075981 (Tokushima University Institutional Repository: 116720, DOI: 10.1186/s12933-021-01380-w, PubMed: 34521417, Elsevier: Scopus)
74.	Yuta Torii, Kenya Kusunose, Yukina Hirata, Susumu Nishio, Takayuki Ise, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Left Atrial Strain Associated with Functional Recovery in Patients Receiving Optimal Treatment for Heart Failure, Journal of the American Society of Echocardiography, Vol.34, No.9, 966-975, 2021. (Summary) Heart failure with recovered ejection fraction (HFrecEF) has been reported in several previous studies to have a better prognosis than heart failure with reduced ejection fraction (HFrEF). However, the factors associated with HFrecEF have not been identified. The aim of this study was to test the hypothesis that left atrial (LA) strain could help identify patients with recovered ejection fraction (EF) among those with heart failure (HF) with low EF on admission. One hundred consecutive patients hospitalized for the first time for new-onset HF were enrolled. Patients were clinically diagnosed with HFrEF on admission (left ventricular EF < 40%) and received optimal treatment for HF. Twenty-eight patients improved to HFrecEF during 6 months of follow-up. Regarding clinical background, there were significantly more women and a lower rate of atrial fibrillation in the HFrecEF group than in the HFrEF group. In a multivariate logistic regression analysis, LA strain was an independent predictor of HFrecEF, even after adjustment for gender and left ventricular EF (odds ratio: 4.06; 95% CI: 2.04-8.07; P < .001). A cutoff value of 10.8% for LA strain showed high sensitivity (96%) and specificity (82%) in identifying HFrecEF in patients with HF presenting with low EF on admission. During a follow-up period of 24 ± 13 months, 31 patients (31%) had cardiovascular death or readmission for HF. Patients with reduced LA strain (<10.8%) had significantly shorter event-free survival than those with preserved LA strain (P = .02). LA strain is a useful indicator for predicting HFrecEF and should be considered as a routine measurement in patients with HFrEF on admission. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.echo.2021.03.016 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33852960 ● Search Scopus @ Elsevier (PMID): 33852960 ● Search Scopus @ Elsevier (DOI): 10.1016/j.echo.2021.03.016 (DOI: 10.1016/j.echo.2021.03.016, PubMed: 33852960)
75.	Moriaki Yamanaka, Shoichiro Takao, Hideki Otsuka, Youichi Otomi, Saho Irahara, Yamato Kunikane, Satoru Takashi, Airi Yamamoto, Masataka Sata and Masafumi Harada : The Utility of a Combination of <sup>99m</sup>Tc-MIBI Washout Imaging and Cardiac Magnetic Resonance Imaging in the Evaluation of Cardiomyopathy, Annals of Nuclear Cardiology, Vol.7, No.1, 8-16, 2021. (Summary) Background: In cardiomyopathy, 99mTc-MIBI washout can reflect mitochondrial dysfunction and late gadolinium enhancement (LGE) on cardiac magnetic imaging (MRI) is associated with tissue fibrosis. We sought to determine the relationship between 99mTc-MIBI uptake, 99mTc-MIBI washout, and LGE on MRI in patients with cardiomyopathy. Methods: Twenty-one patients underwent rest myocardial perfusion scintigraphy at 45 minutes (early) and 4 hours (delayed) after intravenous 99mTc-MIBI administration and cardiac MRI. We assessed myocardial perfusion, 99mTc-MIBI washout, and LGE. We divided the left ventricle (LV) wall into 16 segments using a polar map. Then, we classified each segment into 5 groups according to 99mTc-MIBI uptake in early-rest images and washout. Additionally, we created a contingency table based on LGE presence/absence in the groups. Results: We evaluated 336 segments in 21 patients. 99mTc-MIBI uptake was decreased in 168 segments in the early-rest 99mTc-MIBI images. 99mTc-MIBI washout was observed in 108 segments with either normal perfusion or reduced perfusion in the early-rest 99mTc-MIBI images. LGE was positive in 104 segments. A contingency table analysis with Fisher窶冱 exact test showed that LGE was observed significantly more frequently in the segments with decreased 99mTc-MIBI uptake (p < 0.001). In segments without a decreased 99mTc-MIBI uptake, there was a significant correlation between increased 99mTc-MIBI washout and the presence of LGE (p = 0.033). Conclusions: In cardiomyopathy, the mitochondrial dysfunction in the early stage is shown as 99mTc-MIBI washout, and fibrotic changes in the myocardium in advanced stages are shown as LGE on cardiac MRI. The severity of myocardial damage and the clinical stage of cardiomyopathy can be evaluated using multimodal imaging. (Keyword) <sup>99m</sup>Tc-MIBI / Cardiomyopathy / Late gadolinium enhancement (LGE) / Washout (Link to Publication Site) ● Publication site (DOI): 10.17996/anc.21-00124 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390007750045919616 ● Search Scopus @ Elsevier (DOI): 10.17996/anc.21-00124 (DOI: 10.17996/anc.21-00124, CiNii: 1390007750045919616)
76.	Sae X. Morita, Kenya Kusunose, Akihiro Haga, Masataka Sata, Kohei Hasegawa, Yoshihiko Raita, Muredach P. Reilly, Michael A. Fifer, Mathew S. Maurer and Yuichi J. Shimada : Deep Learning Analysis of Echocardiographic Images to Predict Positive Genotype in Patients With Hypertrophic Cardiomyopathy., Frontiers in Cardiovascular Medicine, Vol.8, 669860, 2021. (Summary) Genetic testing provides valuable insights into family screening strategies, diagnosis, and prognosis in patients with hypertrophic cardiomyopathy (HCM). On the other hand, genetic testing carries socio-economical and psychological burdens. It is therefore important to identify patients with HCM who are more likely to have positive genotype. However, conventional prediction models based on clinical and echocardiographic parameters offer only modest accuracy and are subject to intra- and inter-observer variability. We therefore hypothesized that deep convolutional neural network (DCNN, a type of deep learning) analysis of echocardiographic images improves the predictive accuracy of positive genotype in patients with HCM. In each case, we obtained parasternal short- and long-axis as well as apical 2-, 3-, 4-, and 5-chamber views. We employed DCNN algorithm to predict positive genotype based on the input echocardiographic images. We performed 5-fold cross-validations. We used 2 reference models-the Mayo HCM Genotype Predictor score (Mayo score) and the Toronto HCM Genotype score (Toronto score). We compared the area under the receiver-operating-characteristic curve (AUC) between a combined model using the reference model plus DCNN-derived probability and the reference model. We calculated the -value by performing 1,000 bootstrapping. We calculated sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV). In addition, we examined the net reclassification improvement. We included 99 adults with HCM who underwent genetic testing. Overall, 45 patients (45%) had positive genotype. The new model combining Mayo score and DCNN-derived probability significantly outperformed Mayo score (AUC 0.86 [95% CI 0.79-0.93] vs. 0.72 [0.61-0.82]; < 0.001). Similarly, the new model combining Toronto score and DCNN-derived probability exhibited a higher AUC compared to Toronto score alone (AUC 0.84 [0.76-0.92] vs. 0.75 [0.65-0.85]; = 0.03). An improvement in the sensitivity, specificity, PPV, and NPV was also achieved, along with significant net reclassification improvement. In conclusion, compared to the conventional models, our new model combining the conventional and DCNN-derived models demonstrated superior accuracy to predict positive genotype in patients with HCM. (Link to Publication Site) ● Publication site (DOI): 10.3389/fcvm.2021.669860 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34513940 ● Search Scopus @ Elsevier (PMID): 34513940 ● Search Scopus @ Elsevier (DOI): 10.3389/fcvm.2021.669860 (DOI: 10.3389/fcvm.2021.669860, PubMed: 34513940)
77.	Tomomi Matsuura, Takeshi Soeki, Daiju Fukuda, Etsuko Uematsu, Takeshi Tobiume, Tomoya Hara, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Activated Factor X Signaling Pathway via Protease-Activated Receptor 2 Is a Novel Therapeutic Target for Preventing Atrial Fibrillation, Circulation Journal, Vol.85, No.8, 1383-1391, 2021. (Summary) Activated factor X (FXa), which contributes to chronic inflammation via protease-activated receptor 2 (PAR2), might play an important role in atrial fibrillation (AF) arrhythmogenesis. This study aimed to assess whether PAR2 signaling contributes to AF arrhythmogenesis and whether rivaroxaban ameliorates atrial inflammation and prevents AF.Methods and Results:In Study 1, PAR2 deficient (PAR2-/-) and wild-type mice were infused with angiotensin II (Ang II) or a vehicle via an osmotic minipump for 2 weeks. In Study 2, spontaneously hypertensive rats (SHRs) were treated with rivaroxaban, warfarin, or vehicle for 2 weeks after 8 h of right atrial rapid pacing. The AF inducibility and atrial remodeling in both studies were examined. Ang II-treated PAR2-/- mice had a lower incidence of AF and less mRNA expression of collagen1 and collagen3 in the atrium compared to wild-type mice treated with Ang II. Rivaroxaban significantly reduced AF inducibility compared with warfarin or vehicle. In SHRs treated with a vehicle, rapid atrial pacing promoted gene expression of inflammatory and fibrosis-related biomarkers in the atrium. Rivaroxaban, but not warfarin, significantly reduced expression levels of these genes. The FXa-PAR2 signaling pathway might contribute to AF arrhythmogenesis associated with atrial inflammation. A direct FXa inhibitor, rivaroxaban, could prevent atrial inflammation and reduce AF inducibility, probably by inhibiting the pro-inflammatory activation. (Tokushima University Institutional Repository) ● Metadata: 116065 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-20-1006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33746155 ● Summary page in Scopus @ Elsevier: 2-s2.0-85111576585 (Tokushima University Institutional Repository: 116065, DOI: 10.1253/circj.CJ-20-1006, PubMed: 33746155, Elsevier: Scopus)
78.	Pham Tran Phuong, Daiju Fukuda, Sachiko Nishimoto, JR Kim-Kaneyama, XF Lei, Yutaka Takahashi, Tomohito Sato, Kimie Tanaka, Kumiko Suto, Yutaka Kawabata, Koji Yamaguchi, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Kenji Shimada, Yasuhisa Kanematsu, Yasushi Takagi, Michio Shimabukuro, Mitsutoshi Setou, Glen N Barber and Masataka Sata : STING, a cytosolic DNA sensor, plays a critical role in atherogenesis: a link between innate immunity and chronic inflammation caused by lifestyle-related diseases, European Heart Journal, Vol.42, No.42, 4336-4348, 2021. (Summary) Lifestyle-related diseases promote atherosclerosis, a chronic inflammatory disease; however, the molecular mechanism remains largely unknown. Endogenous DNA fragments released under over-nutrient condition provoke sterile inflammation through the recognition by DNA sensors. Here, we investigated the role of stimulator of interferon genes (STING), a cytosolic DNA sensor, in atherogenesis. Apolipoprotein E-deficient (Apoe-/-) mice fed a western-type diet (WTD), a hypercholesterolaemic mouse model, showed higher STING expression and markers for DNA damage such as γH2AX, p53, and single-stranded DNA (ssDNA) accumulation in macrophages in the aorta compared with wild-type (WT) mice. The level of cGAMP, a STING agonist, in the aorta was higher in Apoe-/- mice. Genetic deletion of Sting in Apoe-/- mice reduced atherosclerotic lesions in the aortic arch, lipid, and macrophage accumulation in plaques, and inflammatory molecule expression in the aorta compared with the control. Pharmacological blockade of STING using a specific inhibitor, C-176, ameliorated atherogenesis in Apoe-/- mice. In contrast, bone marrow-specific STING expression in Apoe-/- mice stimulated atherogenesis. Expression or deletion of STING did not affect metabolic parameters and blood pressure. In vitro studies revealed that STING activation by cGAMP or mitochondrial DNA accelerated inflammatory molecule expression (e.g. TNF-α or IFN-β) in mouse and human macrophages. Activation of nuclear factor-κB and TANK binding kinase 1 was involved in STING-associated vascular inflammation and macrophage activation. Furthermore, human atherosclerotic lesions in the carotid arteries expressed STING and cGAMP. Stimulator of interferon genes stimulates pro-inflammatory activation of macrophages, leading to the development of atherosclerosis. Stimulator of interferon genes signalling may serve as a potential therapeutic target for atherosclerosis. (Link to Publication Site) ● Publication site (DOI): 10.1093/eurheartj/ehab249 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34226923 ● Summary page in Scopus @ Elsevier: 2-s2.0-85120384111 (DOI: 10.1093/eurheartj/ehab249, PubMed: 34226923, Elsevier: Scopus)
79.	B Ganbaatar, Daiju Fukuda, M Shinohara, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, KI Hirata and Masataka Sata : Inhibition of S1P Receptor 2 Attenuates Endothelial Dysfunction and Inhibits Atherogenesis in Apolipoprotein E-Deficient Mice, Journal of Atherosclerosis and Thrombosis, Vol.28, No.6, 630-642, 2021. (Summary) The bioactive lipid, sphingosine-1-phosphate (S1P), has various roles in the physiology and pathophysiology of many diseases. There are five S1P receptors; however, the role of each S1P receptor in atherogenesis is still obscure. Here we investigated the contribution of S1P receptor 2 (S1P2) to atherogenesis by using a specific S1P2 antagonist, ONO-5430514, in apolipoprotein E-deficient (Apoe) mice. Apoe mice fed with a western-type diet (WTD) received ONO-5430514 (30 mg/kg/day) or vehicle. To examine the effect on atherogenesis, Sudan IV staining, histological analysis, qPCR, and vascular reactivity assay was performed. Human umbilical vein endothelial cells (HUVEC) were used for in vitro experiments. WTD-fed Apoe mice had significantly higher S1P2 expression in the aorta compared with wild-type mice. S1P2 antagonist treatment for 20 weeks reduced atherosclerotic lesion development (p<0.05). S1P2 antagonist treatment for 8 weeks ameliorated endothelial dysfunction (p<0.05) accompanied with significant reduction of lipid deposition, macrophage accumulation, and inflammatory molecule expression in the aorta compared with vehicle. S1P2 antagonist attenuated the phosphorylation of JNK in the abdominal aorta compared with vehicle (p<0.05). In HUVEC, S1P promoted inflammatory molecule expression such as MCP-1 and VCAM-1 p<0.001), which was attenuated by S1P2 antagonist or a JNK inhibitor (p<0.01). S1P2 antagonist also inhibited S1P-induced JNK phosphorylation in HUVEC (p<0.05). Our results suggested that an S1P2 antagonist attenuates endothelial dysfunction and prevents atherogenesis. S1P2, which promotes inflammatory activation of endothelial cells, might be a therapeutic target for atherosclerosis. (Tokushima University Institutional Repository) ● Metadata: 116449 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.54916 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32879149 ● Search Scopus @ Elsevier (PMID): 32879149 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.54916 (Tokushima University Institutional Repository: 116449, DOI: 10.5551/jat.54916, PubMed: 32879149)
80.	Y Okushi, Kenya Kusunose, Y Okayama, Robert Zheng, M Nakai, Y Sumita, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Acute Hospital Mortality of Venous Thromboembolism in Patients With Cancer From Registry Data, Journal of the American Heart Association, Vol.10, No.11, e019373, 2021. (Summary) Background The prognosis of patients with cancer-venous thromboembolism (VTE) is not well known because of a lack of registry data. Moreover, there is also no knowledge on how specific types are related to prognosis. We sought to evaluate the clinical characteristics and outcomes of patients with cancer-associated VTE, compared with a matched cohort without cancer using real-world registry data of VTE. Methods and Results This study was based on the Diagnosis Procedure Combination database in the JROAD-DPC (Japanese Registry of All Cardiac and Vascular Diseases and the Diagnosis Procedure Combination). Of 5 106 151 total patients included in JROAD-DPC, we identified 49 580 patients who were first hospitalized with VTE from April 2012 to March 2017. Propensity score was estimated with a logistic regression model, with cancer as the dependent variable and 18 clinically relevant covariates. After propensity matching, there were 25 148 patients with VTE with or without cancer. On propensity score-matched analysis with 25 148 patients with VTE, patients with cancer had higher total in-hospital mortality within 7 days (1.3% versus 1.1%, odds ratio [OR], 1.66; 95% CI, 1.31-2.11; <0.0001), 14 days (2.5% versus 1.5%, OR, 2.07; 95% CI, 1.72-2.49; <0.0001), and 30 days (4.8% versus 2.0%, OR, 2.85; 95% CI, 2.45-3.31; <0.0001). On analysis for each type of cancer, in-hospital mortality in 11 types of cancer was significantly high, especially pancreas (OR, 12.96; 95% CI, 6.41-26.20), biliary tract (OR, 8.67; 95% CI, 3.00-25.03), and liver (OR, 7.31; 95% CI, 3.05-17.50). Conclusions Patients with cancer had a higher in-hospital acute mortality for VTE than those without cancer, especially in pancreatic, biliary tract, and liver cancers. (Tokushima University Institutional Repository) ● Metadata: 116140 (Link to Publication Site) ● Publication site (DOI): 10.1161/JAHA.120.019373 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34027673 ● Search Scopus @ Elsevier (PMID): 34027673 ● Search Scopus @ Elsevier (DOI): 10.1161/JAHA.120.019373 (Tokushima University Institutional Repository: 116140, DOI: 10.1161/JAHA.120.019373, PubMed: 34027673)
81.	T Ogata, H Shimada, T Inoue, S Takeshita, Y Tsuboi, N Uesugi, M Fujiwara, Masataka Sata and Hirotsugu Yamada : Quantification of Carotid Plaque Histology Using iPlaque Software, Ultrasound in Medicine & Biology, Vol.47, No.4, 928-931, 2021. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ultrasmedbio.2020.12.002 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85098957691 (DOI: 10.1016/j.ultrasmedbio.2020.12.002, Elsevier: Scopus)
82.	Daiju Fukuda and Masataka Sata : Frontiers of inflammatory disease research: inflammation in cardiovascular-cerebral diseases, Inflammation and Regeneration, Vol.41, No.1, 10, 2021. (Tokushima University Institutional Repository) ● Metadata: 116335 (Link to Publication Site) ● Publication site (DOI): 10.1186/s41232-021-00160-z (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1186/s41232-021-00160-z (Tokushima University Institutional Repository: 116335, DOI: 10.1186/s41232-021-00160-z)
83.	Yukina Hirata, Kenya Kusunose, Takumasa Tsuji, Kohei Fujimori, Jun'ichi Kotoku and Masataka Sata : Deep Learning for Detection of Elevated Pulmonary Artery Wedge Pressure using Standard Chest X-Ray, The Canadian Journal of Cardiology, Vol.37, No.8, 1198-1206, 2021. (Summary) To accurately diagnose and control heart failure (HF), it is important to carry out a simple assessment of elevated pulmonary arterial wedge pressure (PAWP). The aim of this study was to develop and validate an objective method for detecting elevated PAWP by applying deep learning (DL) to a chest x-ray (CXR). We enrolled 1013 consecutive patients with a right-heart catheter between October 2009 and February 2020. We developed a convolutional neural network to identify patients with elevated PAWP (> 18 mm Hg) as the actual value of PAWP to be used in the dataset for training. In the prospective validation dataset used to detect elevated PAWP, the area under the receiver operating characteristic curve (AUC) was calculated using the DL model that evaluated the CXR. In the prospective validation dataset, the AUC of the DL model with CXR was not significantly different from the AUC produced by brain natriuretic peptide (BNP) and the echocardiographic left-ventricular diastolic dysfunction (DD) algorithm (DL model: 0.77 vs BNP: 0.77 vs DD algorithm: 0.70; respectively; P = NS for all comparisons); it was, however, significantly higher than the AUC of the cardiothoracic ratio (DL model vs cardiothoracic ratio [CTR]: 0.66, P = 0.044). The model based on 3 parameters (BNP, DD algorithm, and CTR) was improved by adding the DL model (AUC: from 0.80 to 0.86; P = 0.041). Applying the DL model based on a CXR (a classical, universal, and low-cost test) is useful for screening for elevated PAWP. (Keyword) Aged / Algorithms / Cardiac Catheterization / Datasets as Topic / deep learning / Echocardiography / female / Humans / male / Natriuretic Peptide, Brain / Prospective Studies / Pulmonary Wedge Pressure / Radiography, Thoracic (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cjca.2021.02.007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33609716 ● Summary page in Scopus @ Elsevier: 2-s2.0-85108436549 (DOI: 10.1016/j.cjca.2021.02.007, PubMed: 33609716, Elsevier: Scopus)
84.	Miharu Arase, Kenya Kusunose, N Yamaguchi, Yukina Hirata, Susumu Nishio, Y Okushi, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Cardiac reserve by 6-minute walk stress echocardiography in systemic sclerosis., Open Heart, Vol.8, No.1, e001559, 2021. (Tokushima University Institutional Repository) ● Metadata: 116465 (Link to Publication Site) ● Publication site (DOI): 10.1136/openhrt-2020-001559 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1136/openhrt-2020-001559 (Tokushima University Institutional Repository: 116465, DOI: 10.1136/openhrt-2020-001559)
85.	Kenya Kusunose, Y Okushi, Y Okayama, Robert Zheng, M Abe, M Nakai, Y Sumita, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Association between Vitamin D and Heart Failure Mortality in 10,974 Hospitalized Individuals., Nutrients, Vol.13, No.2, 335, 2021. (Summary) A broad range of chronic conditions, including heart failure (HF), have been associated with vitamin D deficiency. Existing clinical trials involving vitamin D supplementation in chronic HF patients have been inconclusive. We sought to evaluate the outcomes of patients with vitamin D supplementation, compared with a matched cohort using real-world big data of HF hospitalization. This study was based on the Diagnosis Procedure Combination database in the Japanese Registry of All Cardiac and Vascular Datasets (JROAD-DPC). After exclusion criteria, we identified 93,692 patients who were first hospitalized with HF between April 2012 and March 2017 (mean age was 79 ± 12 years, and 52.2% were male). Propensity score (PS) was estimated with logistic regression model, with vitamin D supplementation as the dependent variable and clinically relevant covariates. On PS-matched analysis with 10,974 patients, patients with vitamin D supplementation had lower total in-hospital mortality (6.5 vs. 9.4%, odds ratio: 0.67, < 0.001) and in-hospital mortality within 7 days and 30 days (0.9 vs. 2.5%, OR, 0.34, and 3.8 vs. 6.5%, OR: 0.56, both < 0.001). In the sub-group analysis, mortalities in patients with age < 75, diabetes, dyslipidemia, atrial arrhythmia, cancer, renin-angiotensin system blocker, and β-blocker were not affected by vitamin D supplementation. Patients with vitamin D supplementation had a lower in-hospital mortality for HF than patients without vitamin D supplementation in the propensity matched cohort. The identification of specific clinical characteristics in patients benefitting from vitamin D may be useful for determining targets of future randomized control trials. (Tokushima University Institutional Repository) ● Metadata: 116464 (Link to Publication Site) ● Publication site (DOI): 10.3390/nu13020335 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33498709 ● Summary page in Scopus @ Elsevier: 2-s2.0-85099832739 (Tokushima University Institutional Repository: 116464, DOI: 10.3390/nu13020335, PubMed: 33498709, Elsevier: Scopus)
86.	Gulinu Maimaituxun, Kenya Kusunose, Hirotsugu Yamada, Daiju Fukuda, Shusuke Yagi, Yuta Torii, Nao Yamada, Takeshi Soeki, H Masuzaki, Masataka Sata and Michio Shimabukuro : Deleterious Effects of Epicardial Adipose Tissue Volume on Global Longitudinal Strain in Patients With Preserved Left Ventricular Ejection Fraction, Frontiers in Cardiovascular Medicine, Vol.7, 607825, 2021. (Link to Publication Site) ● Publication site (DOI): 10.3389/fcvm.2020.607825 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33521062 ● Search Scopus @ Elsevier (PMID): 33521062 ● Search Scopus @ Elsevier (DOI): 10.3389/fcvm.2020.607825 (DOI: 10.3389/fcvm.2020.607825, PubMed: 33521062)
87.	Hironori Tanaka, Yoshihito Saijyo, Tetsu Tomonari, Takahiro Tanaka, Tatsuya Taniguchi, Shusuke Yagi, Koichi Okamoto, Hiroshi Miyamoto, Masahiro Sogabe, Yasushi Sato, Naoki Muguruma, Koichi Tsuneyama, Masataka Sata and Tetsuji Takayama : An Adult Case of Congenital Extrahepatic Portosystemic Shunt Successfully Treated with Balloon-occluded Retrograde Transvenous Obliteration, Internal Medicine, Vol.60, No.12, 1839-1845, 2021. (Summary) A 42-year-old woman visited our hospital due to syncope. Contrast-enhanced CT revealed portosystemic shunt, portal vein hypoplasia, and multiple liver nodules. The histological examination of a liver biopsy specimen exhibited portal vein hypoplasia and revealed that the liver tumor was positive for glutamine synthetase. The patient was therefore diagnosed with congenital extrahepatic portosystemic shunt type II, and with focal nodular hyperplasia (FNH)-like nodules. She had the complication of severe portopulmonary hypertension and underwent complete shunt closure by balloon-occluded retrograde transvenous obliteration (B-RTO). The intrahepatic portal vein was well developed at 1 year after B-RTO, and multiple liver nodules completely regressed. Her pulmonary hypertension also improved. (Tokushima University Institutional Repository) ● Metadata: 116336 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.5914-20 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33456037 ● Search Scopus @ Elsevier (PMID): 33456037 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.5914-20 (Tokushima University Institutional Repository: 116336, DOI: 10.2169/internalmedicine.5914-20, PubMed: 33456037)
88.	Akira Takashima, Shusuke Yagi, Koji Yamaguchi, Kiyoe Kurahashi, Yuko Kojima, Robert Zheng, Takayuki Ise, Kenya Kusunose, Sumiko Yoshida, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Ken-ichi Aihara, Masashi Akaike and Masataka Sata : Congenital Hypogonadotropic Hypogonadism with Early-Onset Coronary Artery Disease., The Journal of Medical Investigation : JMI, Vol.68, No.1.2, 189-191, 2021. (Summary) The patient with congenital hypogonadotropic hypogonadism (HH) shows low serum levels of androgen, which is a group of sex hormones including testosterone, caused by the decreased gonadotropin release in the hypothalamus. Recent reports showed androgens exert protective effects against insulin resistance or atherosclerotic diseases, such as diabetes mellitus or coronary artery disease. However, whether the juvenile hypogonadism affects the diabetes or cardiovascular disease is unclear. We report a case of a middle-aged man with congenital HH who had severe coronary artery disease complicated with metabolic disorders. J. Med. Invest. 68 : 189-191, February, 2021. (Tokushima University Institutional Repository) ● Metadata: 116019 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.68.189 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33994469 ● Search Scopus @ Elsevier (PMID): 33994469 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.68.189 (Tokushima University Institutional Repository: 116019, DOI: 10.2152/jmi.68.189, PubMed: 33994469)
89.	Yutaka Kawabata, Takeshi Soeki, Hiroyuki Ito, Tomomi Matsuura, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Takeshi Tobiume, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, M Kitani, K Kawano, Y Taketani and Masataka Sata : Effects of L-/N-Type Calcium Channel Blockers on Angiotensin II-Renin Feedback in Hypertensive Patients, International Journal of Hypertension, 6653851, 2020. (Tokushima University Institutional Repository) ● Metadata: 115937 (Link to Publication Site) ● Publication site (DOI): 10.1155/2020/6653851 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33489354 ● Summary page in Scopus @ Elsevier: 2-s2.0-85098701678 (Tokushima University Institutional Repository: 115937, DOI: 10.1155/2020/6653851, PubMed: 33489354, Elsevier: Scopus)
90.	Takeshi Tobiume, R Kato, Tomomi Matsuura, Kazuhisa Matsumoto, M Hara, N Takamori, Y Taketani, K Okwa, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Takeshi Soeki, Masataka Sata and K Matsumoto : Antegrade slow pathway mapping of typical atrioventricular nodal reentrant tachycardia based on direct slow pathway capture, Journal of Arrhythmia, Vol.37, No.1, 128-139, 2020. (Tokushima University Institutional Repository) ● Metadata: 116343 (Link to Publication Site) ● Publication site (DOI): 10.1002/joa3.12484 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33664895 ● Summary page in Scopus @ Elsevier: 2-s2.0-85099515348 (Tokushima University Institutional Repository: 116343, DOI: 10.1002/joa3.12484, PubMed: 33664895, Elsevier: Scopus)
91.	K Tanaka, Daiju Fukuda and Masataka Sata : Roles of Epicardial Adipose Tissue in the Pathogenesis of Coronary Atherosclerosis - An Update on Recent Findings, Circulation Journal, Vol.85, No.1, 2-8, 2020. (Summary) Adipose tissue serves not only as an energy store or a mechanical cushion, but also as an endocrine organ. Recent evidence revealed that perivascular adipose tissue is involved in vascular homeostasis and pathophysiology of adjacent arteries by producing various adipokines. Epicardial adipose tissue (EAT) is located between the surface of the heart and the visceral layer of the pericardium and surrounds the coronary arteries. Many clinical studies suggest that an increase in EAT volume is associated with coronary artery disease. It has been reported that exercise and some antidiabetic drugs can reduce EAT volume. In this review, we outline recent findings on the roles of EAT in the pathogenesis of coronary atherosclerosis. (Tokushima University Institutional Repository) ● Metadata: 116291 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-20-0935 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33268604 ● Summary page in Scopus @ Elsevier: 2-s2.0-85099089624 (Tokushima University Institutional Repository: 116291, DOI: 10.1253/circj.CJ-20-0935, PubMed: 33268604, Elsevier: Scopus)
92.	Eiichi Araki, Atsushi Tanaka, Nobuya Inagaki, Hiroshi Ito, Kohjiro Ueki, Toyoaki Murohara, Kenjiro Imai, Masataka Sata, Takehiro Sugiyama, Hideki Ishii, Shunsuke Yamane, Takashi Kadowaki, Issei Komuro and Koichi Node : Diagnosis, Prevention, and Treatment of Cardiovascular Diseases in People With Type 2 Diabetes and Prediabetes - A Consensus Statement Jointly From the Japanese Circulation Society and the Japan Diabetes Society, Circulation Journal, Vol.12, No.1, 1-51, 2020. (Tokushima University Institutional Repository) ● Metadata: 117214 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-20-0865 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33250455 ● Summary page in Scopus @ Elsevier: 2-s2.0-85099105428 (Tokushima University Institutional Repository: 117214, DOI: 10.1253/circj.CJ-20-0865, PubMed: 33250455, Elsevier: Scopus)
93.	Kenya Kusunose, Yukina Hirata, T Tsuji, J Kotoku and Masataka Sata : Deep learning to predict elevated pulmonary artery pressure in patients with suspected pulmonary hypertension using standard chest X ray, Scientific Reports, Vol.10, No.1, 19311, 2020. (Summary) Accurate diagnosis of pulmonary hypertension (PH) is crucial to ensure that patients receive timely treatment. We hypothesized that application of artificial intelligence (AI) to the chest X-ray (CXR) could identify elevated pulmonary artery pressure (PAP) and stratify the risk of heart failure hospitalization with PH. We retrospectively enrolled a total of 900 consecutive patients with suspected PH. We trained a convolutional neural network to identify patients with elevated PAP (> 20 mmHg) as the actual value of PAP. The endpoints in this study were admission or occurrence of heart failure with elevated PAP. In an independent evaluation set for detection of elevated PAP, the area under curve (AUC) by the AI algorithm was significantly higher than the AUC by measurements of CXR images and human observers (0.71 vs. 0.60 and vs. 0.63, all p < 0.05). In patients with AI predicted PH had 2-times the risk of heart failure with PH compared with those without AI predicted PH. This preliminary work suggests that applying AI to the CXR in high risk groups has limited performance when used alone in identifying elevated PAP. We believe that this report can serve as an impetus for a future large study. (Tokushima University Institutional Repository) ● Metadata: 115491 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-020-76359-w (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33203947 ● Search Scopus @ Elsevier (PMID): 33203947 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-020-76359-w (Tokushima University Institutional Repository: 115491, DOI: 10.1038/s41598-020-76359-w, PubMed: 33203947)
94.	Yoshihito Saijyo, Kenya Kusunose, Y Okushi, Hirotsugu Yamada, Hiroaki Toba and Masataka Sata : Relationship between regional left ventricular dysfunction and cancer-therapy-related cardiac dysfunction, Heart, Vol.106, No.22, 1752-1758, 2020. (Summary) The aim of our study was to assess the association between risk of cancer-therapy-related cardiac dysfunction (CTRCD) after first follow-up and the difference in echocardiographic measures from baseline to follow-up. We retrospectively enrolled 87 consecutive patients (58±14 years, 55 women) who received anthracycline and underwent echocardiographic examinations both before (baseline) and after initial anthracycline administration (first follow-up). We measured absolute values of global longitudinal strain (GLS), apical longitudinal strain (LS), mid-LS and basal-LS at baseline and first follow-up, and per cent changes (Δ) of these parameters were calculated. Among 61 patients who underwent further echocardiographic examinations (second follow-up, third follow-up, etc), we assessed the association between regional left ventricular (LV) systolic dysfunction from baseline to follow-up and development of CTRCD, defined as LV ejection fraction (LVEF) under 53% and more absolute decrease of 10% from baseline, after first follow-up. LVEF (65%±4% vs 63±4%, p=0.004), GLS (23.2%±2.6% vs 22.2±2.4%, p=0.005) and basal-LS (21.9%±2.5% vs 19.9±2.4%, p<0.001) at first follow-up significantly decreased compared with baseline. Among the 61 patients who had further follow-up echocardiographic examinations, 13% developed CTRCD. In the Cox-hazard model, worse Δbasal-LS was significantly associated with CTRCD. By Kaplan-Meier analysis, patients with Δbasal-LS decrease of more than the median value (-9.7%) had significantly worse event-free survival than those with a smaller decrease (p=0.015). Basal-LS significantly decreased prior to development of CTRCD, and worse basal-LS was associated with development of CTRCD in patients receiving anthracycline chemotherapy. (Keyword) Antibiotics, Antineoplastic / Cardiotoxicity / Echocardiography / Female / Follow-Up Studies / Heart Diseases / Humans / Male / Middle Aged / Neoplasms / Retrospective Studies / Risk Factors / Stroke Volume / Ventricular Dysfunction, Left / Ventricular Function, Left (Link to Publication Site) ● Publication site (DOI): 10.1136/heartjnl-2019-316339 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32209616 ● Search Scopus @ Elsevier (PMID): 32209616 ● Search Scopus @ Elsevier (DOI): 10.1136/heartjnl-2019-316339 (DOI: 10.1136/heartjnl-2019-316339, PubMed: 32209616)
95.	N Tanabe, K Fukuda, H Matsubara, N Nakanishi, N Tahara, S Ikeda, T Kishi, T Satoh, KI Hirata, T Inoue, H Kimura, Y Okano, O Okazaki, Masataka Sata, I Tsujino, S Ueno, N Yamada, A Yao and T Kuriyama : Selexipag for Chronic Thromboembolic Pulmonary Hypertension in Japanese Patients - A Double-Blind, Randomized, Placebo-Controlled, Multicenter Phase II Study, Circulation Journal, Vol.84, No.10, 1866-1874, 2020. (Summary) Selexipag is an oral prostacyclin receptor (IP receptor) agonist with a non-prostanoid structure. This study examined its efficacy and safety in Japanese patients with non-operated or persistent/recurrent chronic thromboembolic pulmonary hypertension (CTEPH).Methods and Results:This Phase II study was a randomized, double-blind, placebo-controlled parallel-group comparison. The primary endpoint was a change in pulmonary vascular resistance (PVR) from baseline to week 17. The main analysis involved a per-protocol set group of 28 subjects. The change in PVR (mean±SD) after 17 weeks of treatment in the selexipag group was -104±191 dyn·s/cm, whereas that in the placebo group was 26±180 dyn·s/cm. Thus, the treatment effect after 17 weeks of selexipag treatment was calculated as -130±189 dyn·s/cm(P=0.1553). Although the primary endpoint was not met, for the group not concomitantly using a pulmonary vasodilator the PVR in the selexipag group was significantly decreased compared with placebo group (P=0.0364). The selexipag group also showed improvement in total pulmonary resistance and cardiac index. Selexipag treatment improved pulmonary hemodynamics in Japanese patients with CTEPH, but PVR did not show a significant difference between the selexipag and placebo groups. (Trial registration: JAPIC Clinical Trials Information [JapicCTI-111667]). (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-20-0438 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32879152 ● Search Scopus @ Elsevier (PMID): 32879152 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-20-0438 (DOI: 10.1253/circj.CJ-20-0438, PubMed: 32879152)
96.	Kenya Kusunose, nao Yamada, Hirotsugu Yamada, Susumu Nishio, Yoshihito Saijoh, Yukina Hirata, Yuta Torii, Takayuki Ise, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Association between Right Ventricular Contractile Function and Cardiac Events in Isolated Post-capillary and Combined Pre- and Post-capillary Pulmonary Hypertension, Journal of Cardiac Failure, Vol.26, No.1, 43-51, 2020. (Summary) Recent studies have shown that patients with combined pre- and postcapillary pulmonary hypertension (CpcPH) had worse outcomes than those with isolated postcapillary pulmonary hypertension (IpcPH). However, the prognostic factors including right ventricular (RV) function have not been well documented. The aim of this study was to assess the differentiation of PH phenotypes, using echocardiography, and the association between RV longitudinal strain and cardiac events. We prospectively recruited consecutive patients who had undergone right heart catheterization. The primary endpoint was cardiovascular death or readmission due to heart failure. We included 137 patients with Group 2 PH. A RV longitudinal strain of 17% was sensitive (85%) and specific (70%) to determine the CpcPH. During a median period of 31 months, 43 patients experienced the primary endpoint during follow-up. In a multivariate analysis, RV longitudinal strain was associated with the primary endpoint in both CpcPH and IpcPH (HR: 0.84, P = 0.003; HR: 0.86, P = 0.001). Lower RV longitudinal strain was independently associated with worse outcomes in CpcPH and IpcPH. RV longitudinal strain may play a prognostic role in PH phenotypes. (Tokushima University Institutional Repository) ● Metadata: 114190 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cardfail.2019.08.021 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31487533 ● Summary page in Scopus @ Elsevier: 2-s2.0-85072539026 (Tokushima University Institutional Repository: 114190, DOI: 10.1016/j.cardfail.2019.08.021, PubMed: 31487533, Elsevier: Scopus)
97.	Yukina Hirata, Susumu Nishio, Kenya Kusunose, Yukina Fujita, Miharu Arase, Hirotsugu Yamada and Masataka Sata : Comparison of Global Longitudinal Strain Measurement Among Recent Version Echocardiographic Machines and Vendor Independent Strain Analysis Software, Japanese Journal of Medical Ultrasound Technology, Vol.45, No.4, 405-413, 2020. (Summary) <p><b>Purpose</b>: Global longitudinal strain (GLS) assessed using the two-dimensional (2D) speckle tracking method is considered to be an accurate and reproducible measurement method for assessing the LV contractility. However, the measurement variability across different ultrasonography machines has been discussed. This study aimed to determine whether the measurement variability among newer echocardiographic machines is lower than that reported in previous studies.</p><p><b>Subjects and Methods</b>: We enrolled 34 healthy volunteers. Apical images were acquired using three types of latest ultrasonography machines at the Tokushima University Hospital. The GLS values were assessed and compared using the latest version of the vendor-specific software and one vendor-independent software packages (EchoInsight ver. 2.2.6.2230, Epsilon).</p><p><b>Results and Discussion</b>: The upgraded vendor-specific software showed good correlation in GLS [GE vs. Philips (r=0.678, p<0.001, Bias 1.1%, 2SD ±2.9%), GE vs. Canon (r=0.690, p<0.001, Bias 0.4%, 2SD ±2.5%), Philips vs. Canon (r=0.551, p<0.001, Bias 1.5%, 2SD ±3.2%)]. The GLS measured using vendor-independent software provided greater degree of correlation than that with each software alone.</p><p><b>Conclusion</b>: The measurement variability of GLS between devices was superior than that reported previously. Moreover, the GLS measured using the images acquired using each device with EchoInsight showed good inter-device correlation.</p> (Keyword) intervendor variability / speckle-tracking echocardiography / 2D strain (Link to Publication Site) ● Publication site (DOI): 10.11272/jss.316 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390848250135697408 ● Search Scopus @ Elsevier (DOI): 10.11272/jss.316 (DOI: 10.11272/jss.316, CiNii: 1390848250135697408)
98.	Yuta Torii, Kenya Kusunose, Robert Zheng, Hirotsugu Yamada, Rie Amano, Rikizo Matsumoto, Yukina Hirata, Susumu Nishio, Nao Yamada, Takayuki Ise, Koji Yamaguchi, Takeshi Tobiume, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki, Yoshihiro Okayama and Masataka Sata : Association between Sarcopenia/Lower Muscle Mass and Short-Term Regression of Deep Vein Thrombosis Using Direct Oral Anticoagulants, International Heart Journal, Vol.61, No.4, 787-794, 2020. (Summary) Advanced age, obesity, and muscle weakness are independent factors in the onset of deep vein thrombosis (DVT). Recently, an association between sarcopenia and DVT has been reported. We hypothesized that sarcopenia related factors, observed by ultrasonography, are associated with the regression effect on the thrombus following anticoagulation therapy. The present study focused on gastrocnemius muscle (GCM) thickness and the GCM's internal echogenic brightness. We examined the association with DVT regression following direct oral anticoagulants (DOACs) treatment.The prospective cohort study period was between October 2017 and August 2018. We enrolled 46 patients diagnosed with DVT by ultrasonography, who were aged >60 years old and treated with DOACs. Sarcopenia was evaluated using the Asian Working Group for Sarcopenia flowchart. The average DOACs treatment period was 94 days, and 29 patients exhibited thrombus regression. On univariate logistic regression analysis, sarcopenia, average GCM diameter index, and gastrocnemius integrated backscatter index were significantly associated with thrombus regression. In a multivariate model, only the average GCM diameter index correlated with thrombus regression.The average GCM diameter index is associated with DVT regression treated with DOACs. Considering the GCM diameter during DVT treatment can be a marker to make a decision for the treatment of DVT. (Keyword) Aged / Aged, 80 and over / Factor Xa Inhibitors / female / Humans / male / Middle Aged / Muscle, Skeletal / Prospective Studies / Sarcopenia / Ultrasonography / Venous Thrombosis (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.20-032 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32684602 ● Summary page in Scopus @ Elsevier: 2-s2.0-85088879684 (DOI: 10.1536/ihj.20-032, PubMed: 32684602, Elsevier: Scopus)
99.	S Nishimoto, Daiju Fukuda and Masataka Sata : Emerging roles of Toll-like receptor 9 in cardiometabolic disorders, Inflammation and Regeneration, Vol.40, 18, 2020. (Summary) Growing evidence suggests that damage-associated molecule patterns (DAMPs) and their receptors, pattern recognition receptors (PRRs), are associated with the progression of cardiometabolic disorders, including obesity-related insulin resistance and atherosclerosis. Cardiometabolic disorders share sterile chronic inflammation as a major cause; however, the exact mechanisms are still obscure. Toll-like receptor 9 (TLR9), one of the nucleic acid-sensing TLRs, recognizes DNA fragments derived from pathogens and contributes to self-defense by activation of the innate immune system. In addition, previous studies demonstrated that TLR9 recognizes DNA fragments released from host cells, accelerating sterile inflammation, which is associated with inflammatory diseases such as autoimmune diseases. In obese adipose tissue and atherosclerotic vascular tissue, various stresses release DNA fragments and/or nuclear proteins as DAMPs from degenerated adipocytes and vascular cells. Recent studies indicated that the activation of TLR9 in immune cells including macrophages and dendritic cells by recognition of these DAMPs promotes inflammation in these tissues, which causes cardiometabolic disorders. This review discusses recent advances in understanding the role of sterile inflammation associated with TLR9 and its endogenous ligands in cardiometabolic disorders. New insights into innate immunity may provide better understanding of cardiometabolic disorders and new therapeutic options for these major health threats in recent decades. (Tokushima University Institutional Repository) ● Metadata: 115917 (Link to Publication Site) ● Publication site (DOI): 10.1186/s41232-020-00118-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32714475 ● Search Scopus @ Elsevier (PMID): 32714475 ● Search Scopus @ Elsevier (DOI): 10.1186/s41232-020-00118-7 (Tokushima University Institutional Repository: 115917, DOI: 10.1186/s41232-020-00118-7, PubMed: 32714475)
100.	Kenya Kusunose, M Fujiwara, Hirotsugu Yamada, Susumu Nishio, Y Saijo, N Yamada, Yukina Hirata, Yuta Torii, Takayuki Ise, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Deterioration of Biventricular Strain Is an Early Marker of Cardiac Involvement in Confirmed Sarcoidosis, European Heart Journal Cardiovascular Imaging, Vol.21, No.7, 796-804, 2020. (Summary) Risk assessment of developing cardiac involvement in systemic sarcoidosis can be challenging because of limited data. Recently, attention has been given to left ventricular and right ventricular (LV and RV) involvement in cardiac sarcoidosis (CS) and its prevalence, relevance, and prognostic value. The aim of this study was to assess the role of biventricular strain to predict prognosis in confirmed sarcoidosis patients. LV and RV longitudinal strains (LSs) were evaluated by 2D speckle tracking in 139 consecutive confirmed sarcoidosis patients without other pre-existing structural heart diseases, and 52 age- and gender-matched control subjects. The primary endpoint was CS-related events (cardiac death or development of cardiac involvement). Sarcoidosis without cardiac involvement had significantly lower LV and RV free wall LS compared with control subjects. Basal LS had a higher area under the curve for differentiation of sarcoidosis in patients without cardiac involvement compared to control (cut-off value: -18% with 89% sensitivity and 69% specificity). During a median period of 50 months, the occurrence of CS-related events was observed in 20 patients. In a multivariate analysis, basal LV LS and RV free wall LS were associated with the events [hazard ratio (HR) 0.72, P < 0.001 and HR: 0.83, P = 0.006, respectively]. Patients with impaired biventricular function had significantly shorter event-free survival than those with preserved biventricular function (P < 0.001). Deterioration of biventricular strain was associated with CS-related events. This information might be useful for clinical evaluation and follow-up in sarcoidosis. (Link to Publication Site) ● Publication site (DOI): 10.1093/ehjci/jez235 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31566217 ● Summary page in Scopus @ Elsevier: 2-s2.0-85086792785 (DOI: 10.1093/ehjci/jez235, PubMed: 31566217, Elsevier: Scopus)
101.	Hirofumi Tomiyama, Charalambos Vlachopoulos, Panagiotis Xaplanteris, Hiroki Nakano, Kazuki Shiina, Tomoko Ishizu, Takahide Kohro, Yukihito Higashi, Bonpei Takase, Toru Suzuki, Tsutomu Yamazaki, Tomoo Furumoto, Kazuomi Kario, Teruo Inoue, Shinji Koba, Yasuhiko Takemoto, Takuzo Hano, Masataka Sata, Yutaka Ishibashi, Koichi Node, Atsushi Tanaka, Koji Maemura, Yusuke Ohya, Taiji Furukawa, Hiroshi Ito, Toshiaki Ohkuma, Toshiharu Ninomiya, Taishiro Chikamori, Akira Yamashina and Shin-Ichiro Ueda : Usefulness of the SAGE Score to Predict Elevated Values of Brachial-Ankle Pulse Wave Velocity in Japanese Subjects With Hypertension, Hypertension Research, Vol.43, No.11, 1284-1294, 2020. (Summary) The score based on the office systolic blood pressure, age, fasting blood glucose level, and estimated glomerular filtration rate (SAGE score) has been proposed as a useful marker to identify elevated values of carotid-femoral pulse wave velocity (PWV). The present cross-sectional study was conducted to examine whether the SAGE score is also a useful marker to identify subjects with elevated brachial-ankle PWV values in Japanese subjects with hypertension. We measured the brachial-ankle PWV and calculated the SAGE score in a total of 1019 employees of a Japanese company with hypertension and 817 subjects with hypertension derived from a multicenter study cohort. The analyses in this study were based on data from these two study groups as well as on a composite population of the two (n = 1836). The receiver operating characteristic curve analysis showed that the area under the curve to identify subjects with brachial-ankle PWV values of 1800 cm/s was over 0.70 in each of the three study groups. Even after adjustments, a SAGE score 7 had a significant odds ratio for identifying subjects with brachial-ankle PWV values 1800 cm/s in the 1836 study subjects from the composite occupational and multicenter study cohort (odds ratio = 2.1, 95% confidence interval = 1.4-3.0, P < 0.01). Thus, in Japanese subjects with hypertension, the SAGE score may be a useful marker for identifying subjects with elevated brachial-ankle PWV values. (Link to Publication Site) ● Publication site (DOI): 10.1038/s41440-020-0472-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32457429 ● Summary page in Scopus @ Elsevier: 2-s2.0-85086387455 (DOI: 10.1038/s41440-020-0472-7, PubMed: 32457429, Elsevier: Scopus)
102.	Kenya Kusunose, Takashi Abe, Akihiro Haga, Daiju Fukuda, Hirotsugu Yamada, Masafumi Harada and Masataka Sata : A Deep Learning Approach for Assessment of Regional Wall Motion Abnormality From Echocardiographic Images, JACC. Cardiovascular Imaging, Vol.13, No.2, 374-381, 2020. (Summary) This study investigated whether a deep convolutional neural network (DCNN) could provide improved detection of regional wall motion abnormalities (RWMAs) and differentiate among groups of coronary infarction territories from conventional 2-dimensional echocardiographic images compared with that of cardiologists, sonographers, and resident readers. An effective intervention for reduction of misreading of RWMAs is needed. The hypothesis was that a DCNN trained using echocardiographic images would provide improved detection of RWMAs in the clinical setting. A total of 300 patients with a history of myocardial infarction were enrolled. From this cohort, 3 groups of 100 patients each had infarctions of the left anterior descending (LAD) artery, the left circumflex (LCX) branch, and the right coronary artery (RCA). A total of 100 age-matched control patients with normal wall motion were selected from a database. Each case contained cardiac ultrasonographs from short-axis views at end-diastolic, mid-systolic, and end-systolic phases. After the DCNN underwent 100 steps of training, diagnostic accuracies were calculated from the test set. Independently, 10 versions of the same model were trained, and ensemble predictions were performed using those versions. For detection of the presence of WMAs, the area under the receiver-operating characteristic curve (AUC) produced by the deep learning algorithm was similar to that produced by the cardiologists and sonographer readers (0.99 vs. 0.98, respectively; p = 0.15) and significantly higher than the AUC result of the resident readers (0.99 vs. 0.90, respectively; p = 0.002). For detection of territories of WMAs, the AUC by the deep learning algorithm was similar to the AUC by the cardiologist and sonographer readers (0.97 vs. 0.95, respectively; p = 0.61) and significantly higher than the AUC by resident readers (0.97 vs. 0.83, respectively; p = 0.003). From a validation group at an independent site (n = 40), the AUC by the deep learning algorithm was 0.90. The present results support the possibility of using DCNN for automated diagnosis of RWMAs in the field of echocardiography. (Tokushima University Institutional Repository) ● Metadata: 114196 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jcmg.2019.02.024 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31103590 ● Summary page in Scopus @ Elsevier: 2-s2.0-85070068493 (Tokushima University Institutional Repository: 114196, DOI: 10.1016/j.jcmg.2019.02.024, PubMed: 31103590, Elsevier: Scopus)
103.	A Tanaka, I Hisauchi, I Taguchi, A Sezai, S Toyoda, H Tomiyama, Masataka Sata, S Ueda, JI Oyama, M Kitakaze, T Murohara and K Node : Effects of canagliflozin in patients with type 2 diabetes and chronic heart failure: a randomized trial (CANDLE), ESC Heart Failure, Vol.7, No.4, 1585-159, 2020. (Tokushima University Institutional Repository) ● Metadata: 115096 (Link to Publication Site) ● Publication site (DOI): 10.1002/ehf2.12707 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32349193 ● Summary page in Scopus @ Elsevier: 2-s2.0-85083984977 (Tokushima University Institutional Repository: 115096, DOI: 10.1002/ehf2.12707, PubMed: 32349193, Elsevier: Scopus)
104.	Kenya Kusunose, Akihiro Haga, Mizuki Inoue, Daiju Fukuda, Hirotsugu Yamada and Masataka Sata : Clinically Feasible and Accurate View Classification of Echocardiographic Images Using Deep Learning, Biomolecules, Vol.10, No.5, E665, 2020. (Summary) A proper echocardiographic study requires several video clips recorded from different acquisition angles for observation of the complex cardiac anatomy. However, these video clips are not necessarily labeled in a database. Identification of the acquired view becomes the first step of analyzing an echocardiogram. Currently, there is no consensus whether the mislabeled samples can be used to create a feasible clinical prediction model of ejection fraction (EF). The aim of this study was to test two types of input methods for the classification of images, and to test the accuracy of the prediction model for EF in a learning database containing mislabeled images that were not checked by observers. We enrolled 340 patients with five standard views (long axis, short axis, 3-chamber view, 4-chamber view and 2-chamber view) and 10 images in a cycle, used for training a convolutional neural network to classify views (total 17,000 labeled images). All DICOM images were rigidly registered and rescaled into a reference image to fit the size of echocardiographic images. We employed 5-fold cross validation to examine model performance. We tested models trained by two types of data, averaged images and 10 selected images. Our best model (from 10 selected images) classified video views with 98.1% overall test accuracy in the independent cohort. In our view classification model, 1.9% of the images were mislabeled. To determine if this 98.1% accuracy was acceptable for creating the clinical prediction model using echocardiographic data, we tested the prediction model for EF using learning data with a 1.9% error rate. The accuracy of the prediction model for EF was warranted, even with training data containing 1.9% mislabeled images. The CNN algorithm can classify images into five standard views in a clinical setting. Our results suggest that this approach may provide a clinically feasible accuracy level of view classification for the analysis of echocardiographic data. (Tokushima University Institutional Repository) ● Metadata: 115024 (Link to Publication Site) ● Publication site (DOI): 10.3390/biom10050665 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32344829 ● Summary page in Scopus @ Elsevier: 2-s2.0-85083901945 (Tokushima University Institutional Repository: 115024, DOI: 10.3390/biom10050665, PubMed: 32344829, Elsevier: Scopus)
105.	Hiroyuki Ito, Tetsuzo Wakatsuki, Koji Yamaguchi, Daiju Fukuda, Yutaka Kawabata, Tomomi Matsuura, Kenya Kusunose, Takayuki Ise, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Yoshihiro Tsuruo and Masataka Sata : Atherosclerotic Coronary Plaque Is Associated With Adventitial Vasa Vasorum and Local Inflammation in Adjacent Epicardial Adipose Tissue in Fresh Cadavers, Circulation Journal, Vol.84, No.5, 769-775, 2020. (Tokushima University Institutional Repository) ● Metadata: 116640 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-19-0914 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32281556 ● Summary page in Scopus @ Elsevier: 2-s2.0-85083919450 (Tokushima University Institutional Repository: 116640, DOI: 10.1253/circj.CJ-19-0914, PubMed: 32281556, Elsevier: Scopus)
106.	A Tanaka, I Taguchi, H Teragawa, N Ishizaka, Y Kanzaki, H Tomiyama, Masataka Sata, A Sezai, K Eguchi, T Kato, S Toyoda, R Ishibashi, K Kario, T Ishizu, S Ueda, K Maemura, Y Higashi, H Yamada, M Ohishi, K Yokote, T Murohara, JI Oyama and K Node : Febuxostat does not delay progression of carotid atherosclerosis in patients with asymptomatic hyperuricemia: A randomized, controlled trial, PLoS Medicine, Vol.17, No.4, e1003095, 2020. (Summary) An elevated level of serum uric acid (SUA) is associated with an increased risk of cardiovascular disease. Pharmacological intervention with urate-lowering agents, such as the conventional purine analogue xanthine oxidase (XO) inhibitor, allopurinol, has been used widely for a long period of time in clinical practice to reduce SUA levels. Febuxostat, a novel non-purine selective inhibitor of XO, has higher potency for inhibition of XO activity and greater urate-lowering efficacy than conventional allopurinol. However, clinical evidence regarding the effects of febuxostat on atherosclerosis is lacking. The purpose of the study was to test whether treatment with febuxostat delays carotid intima-media thickness (IMT) progression in patients with asymptomatic hyperuricemia. The study was a multicenter, prospective, randomized, open-label, blinded-endpoint clinical trial undertaken at 48 sites throughout Japan between May 2014 and August 2018. Adults with both asymptomatic hyperuricemia (SUA >7.0 mg/dL) and maximum IMT of the common carotid artery (CCA) ≥1.1 mm at screening were allocated equally using a central web system to receive either dose-titrated febuxostat (10-60 mg daily) or as a control-arm, non-pharmacological lifestyle modification for hyperuricemia, such as a healthy diet and exercise therapy. Of the 514 enrolled participants, 31 were excluded from the analysis, with the remaining 483 people (mean age 69.1 years [standard deviation 10.4 years], female 19.7%) included in the primary analysis (febuxostat group, 239; control group, 244), based on a modified intention-to-treat principal. The carotid IMT images were recorded by a single sonographer at each site and read in a treatment-blinded manner by a single analyzer at a central core laboratory. The primary endpoint was the percentage change from baseline to 24 months in mean IMT of the CCA, determined by analysis of covariance using the allocation adjustment factors (age, gender, history of type 2 diabetes, baseline SUA, and baseline maximum IMT of the CCA) as the covariates. Key secondary endpoints included changes in other carotid ultrasonographic parameters and SUA and the incidence of clinical events. The mean values (± standard deviation) of CCA-IMT were 0.825 mm ± 0.173 mm in the febuxostat group and 0.832 mm ± 0.175 mm in the control group (mean between-group difference [febuxostat - control], -0.007 mm [95% confidence interval (CI) -0.039 mm to 0.024 mm; P = 0.65]) at baseline; 0.832 mm ± 0.182 mm in the febuxostat group and 0.848 mm ± 0.176 mm in the control group (mean between-group difference, -0.016 mm [95% CI -0.051 mm to 0.019 mm; P = 0.37]) at 24 months. Compared with the control group, febuxostat had no significant effect on the primary endpoint (mean percentage change 1.2% [95% CI -0.6% to 3.0%] in the febuxostat group (n = 207) versus 1.4% [95% CI -0.5% to 3.3%] in the control group (n = 193); mean between-group difference, -0.2% [95% CI -2.3% to 1.9%; P = 0.83]). Febuxostat also had no effect on the other carotid ultrasonographic parameters. The mean baseline values of SUA were comparable between the two groups (febuxostat, 7.76 mg/dL ± 0.98 mg/dL versus control, 7.73 mg/dL ± 1.04 mg/dL; mean between-group difference, 0.03 mg/dL [95% CI -0.15 mg/dL to 0.21 mg/dL; P = 0.75]). The mean value of SUA at 24 months was significantly lower in the febuxostat group than in the control group (febuxostat, 4.66 mg/dL ± 1.27 mg/dL versus control, 7.28 mg/dL ± 1.27 mg/dL; mean between-group difference, -2.62 mg/dL [95% CI -2.86 mg/dL to -2.38 mg/dL; P < 0.001]). Episodes of gout arthritis occurred only in the control group (4 patients [1.6%]). There were three deaths in the febuxostat group and seven in the control group during follow-up. A limitation of the study was the study design, as it was not a placebo-controlled trial, had a relatively small sample size and a short intervention period, and only enrolled Japanese patients with asymptomatic hyperuricemia. In Japanese patients with asymptomatic hyperuricemia, 24 months of febuxostat treatment did not delay carotid atherosclerosis progression, compared with non-pharmacological care. These findings do not support the use of febuxostat for delaying carotid atherosclerosis in this population. University Hospital Medical Information Network Clinical Trial Registry UMIN000012911. (Keyword) Aged / Aged, 80 and over / Asymptomatic Diseases / Carotid Artery Diseases / Carotid Intima-Media Thickness / Disease Progression / Febuxostat / Female / Gout Suppressants / Humans / Hyperuricemia / Male / Middle Aged / Prospective Studies / Single-Blind Method / Uric Acid (Tokushima University Institutional Repository) ● Metadata: 115247 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pmed.1003095 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32320401 ● Summary page in Scopus @ Elsevier: 2-s2.0-85083949564 (Tokushima University Institutional Repository: 115247, DOI: 10.1371/journal.pmed.1003095, PubMed: 32320401, Elsevier: Scopus)
107.	B Ganbaatar, Daiju Fukuda, M Shinohara, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, KI Hirata and Masataka Sata : Empagliflozin Ameliorates Endothelial Dysfunction and Suppresses Atherogenesis in Diabetic Apolipoprotein E-deficient Mice, European Journal of Pharmacology, Vol.15, No.875, 173040, 2020. (Summary) Recent studies reported cardioprotective effects of sodium glucose co-transporter 2 (SGLT2) inhibitors; however, the underlying mechanisms are still obscure. Here, we investigated whether empagliflozin attenuates atherogenesis and endothelial dysfunction in diabetic apolipoprotein E-deficient (ApoE) mice. Male streptozotocin (STZ) - induced diabetic ApoE mice were treated with empagliflozin for 12 or 8 weeks. Empagliflozin lowered blood glucose (P < 0.001) and lipid levels in diabetic ApoE mice. Empagliflozin treatment for 12 weeks significantly decreased atherosclerotic lesion size in the aortic arch (P < 0.01) along with reduction of lipid deposition (P < 0.05), macrophage accumulation (P < 0.001), and inflammatory molecule expression in plaques compared with the untreated group. Empagliflozin treatment for 8 weeks significantly ameliorated diabetes-induced endothelial dysfunction as determined by the vascular response to acetylcholine (P < 0.001). Empagliflozin reduced RNA expression of a macrophage marker, CD68, and inflammatory molecules such as MCP-1 (P < 0.05) and NADPH oxidase subunits in the aorta compared with the untreated group. Empagliflozin also reduced plasma levels of vasoconstrictive eicosanoids, prostaglandin E and thromboxane B (P < 0.001), which were elevated in diabetic condition. Furthermore, empagliflozin attenuated RNA expression of inflammatory molecules in perivascular adipose tissue (PVAT), suggesting the reduction of inflammation in PVAT. In in vitro studies, methylglyoxal (MGO), a precursor of AGEs, significantly increased the expression of inflammatory molecules such as MCP-1 and TNF-α in a murine macrophage cell line, RAW264.7. Our results indicated that empagliflozin attenuated endothelial dysfunction and atherogenesis in diabetic ApoE mice. Reduction of vasoconstrictive eicosanoids and inflammation in the vasculature and PVAT may have a role as underlying mechanisms at least partially. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2020.173040 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32114052 ● Summary page in Scopus @ Elsevier: 2-s2.0-85080985939 (DOI: 10.1016/j.ejphar.2020.173040, PubMed: 32114052, Elsevier: Scopus)
108.	T Maruhashi, J Soga, N Fujimura, N Idei, S Mikami, Y Iwamoto, A Iwamoto, M Kajikawa, T Matsumoto, N Oda, S Kishimoto, S Matsui, H Hashimoto, Y Takaeko, T Yamaji, T Harada, Y Han, Y Aibara, F Yusoff Mohamad, T Hidaka, Y Kihara, K Chayama, K Noma, A Nakashima, C Goto, H Tomiyama, B Takase, T Kohro, T Suzuki, T Ishizu, S Ueda, T Yamazaki, T Furumoto, K Kario, T Inoue, S Koba, K Watanabe, Y Takemoto, T Hano, Masataka Sata, Y Ishibashi, K Node, K Maemura, Y Ohya, T Furukawa, H Ito, H Ikeda, A Yamashina and Y Higashi : Increased arterial stiffness and cardiovascular risk prediction in controlled hypertensive patients with coronary artery disease: post hoc analysis of FMD-J (Flow-mediated Dilation Japan) Study A, Hypertension Research, Vol.43, No.8, 781-790, 2020. (Summary) The usefulness of brachial-ankle pulse wave velocity (baPWV), an index of arterial stiffness, is not fully known for the management of treated hypertensive patients with a history of coronary artery disease (CAD) who have blood pressure less than 130/80 mmHg, a recommended blood pressure target in the updated major hypertension guidelines. We analyzed data for 447 treated hypertensive patients with CAD enrolled in FMD-J Study A for assessment of the predictive value of baPWV for future cardiovascular events. The primary outcome was a composite of coronary events, stroke, heart failure, and sudden death. During a median follow-up period of 47.6 months, the primary outcome occurred in 64 patients. Blood pressure less than 130/80 mmHg was significantly associated with a lower risk of the composite outcome independent of other cardiovascular risk factors in treated hypertensive patients with CAD (hazard ratio, 0.59; 95% confidence interval (CI), 0.35-0.99; P = 0.04). In treated hypertensive patients with CAD who had blood pressure less than 130/80 mmHg, baPWV above the cutoff value of 1731 cm/s, derived from receiver-operator characteristic curve analysis for the composite outcome was significantly associated with a higher risk of the composite outcome independent of conventional risk factors (hazard ratio, 2.83; 95% CI, 1.02-7.91; P = 0.04). baPWV was an independent predictor of cardiovascular events in treated hypertensive patients with CAD who had blood pressure less than 130/80 mmHg, for whom measurement of baPWV is recommended for cardiovascular risk assessment. (Link to Publication Site) ● Publication site (DOI): 10.1038/s41440-020-0420-6 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32152482 ● Summary page in Scopus @ Elsevier: 2-s2.0-85081661351 (DOI: 10.1038/s41440-020-0420-6, PubMed: 32152482, Elsevier: Scopus)
109.	Yoshihito Saijo, Kenya Kusunose, Nao Yamada, Hirotsugu Yamada, Susumu Nishio, Yukina Hirata and Masataka Sata : Sequential speckle tracking imaging to detect early stage of cancer therapeutics-related cardiac dysfunction in a patient with breast cancer, Journal of Echocardiography, Vol.18, No.2, 134-135, 2020. (Tokushima University Institutional Repository) ● Metadata: 113232 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12574-019-00423-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30810909 ● Summary page in Scopus @ Elsevier: 2-s2.0-85062643604 (Tokushima University Institutional Repository: 113232, DOI: 10.1007/s12574-019-00423-2, PubMed: 30810909, Elsevier: Scopus)
110.	K Tanaka, Daiju Fukuda, Y Higashikuni, Y Hirata, I Komuro, T Saotome, Y Yamashita, T Asakura and Masataka Sata : Biodegradable Extremely-Small-Diameter Vascular Graft Made of Silk Fibroin can be Implanted in Mice, Journal of Atherosclerosis and Thrombosis, Vol.27, 1299-1309, 2020. (Summary) Synthetic vascular grafts are widely used in surgical revascularization, mainly for medium- to large-sized vessels. However, synthetic grafts smaller than 6 mm in diameter are associated with a high incidence of thrombosis. In this study, we evaluated silk fibroin, a major protein of silk, with high biocompatibility and biodegradability, as a useful material for extremely-small-diameter vascular grafts. A small-sized (0.9 mm inner diameter) graft was braided from a silk fibroin thread. The right carotid arteries of 8- to 14-week-old male C57BL/6 mice were cut at the midpoint, and fibroin grafts (5- to 7-mm in length) were transplanted using a cuff technique with polyimide cuffs. The grafts were harvested at different time points and analyzed histologically. CD31+ endothelial cells had already started to proliferate at 2 weeks after implantation. At 4 weeks, neointima had formed with α-smooth muscle actin+ cells, and the luminal surface was covered with CD31+endothelial cells. Mac3+ macrophages were accumulated in the grafts. Graft patency was confirmed at up to 6 months after implantation. This mouse model of arterial graft implantation enables us to analyze the remodeling process and biocompatibility of extremely-small-diameter vascular grafts. Biodegradable silk fibroin might be applicable for further researches using genetically modified mice. (Tokushima University Institutional Repository) ● Metadata: 115927 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.52720 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32101838 ● Search Scopus @ Elsevier (PMID): 32101838 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.52720 (Tokushima University Institutional Repository: 115927, DOI: 10.5551/jat.52720, PubMed: 32101838)
111.	Arief Rahadian, Daiju Fukuda, HM Salim, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Canagliflozin Prevents Diabetes-Induced Vascular Dysfunction in ApoE-Deficient Mice, Journal of Atherosclerosis and Thrombosis, Vol.27, No.11, 1141-1151, 2020. (Summary) Recent studies have demonstrated that selective sodium-glucose cotransporter 2 inhibitors (SGLT2is) reduce cardiovascular events, although their mechanism remains obscure. We examined the effect of canagliflozin, an SGLT2i, on atherogenesis and investigated its underlying mechanism. Canagliflozin (30 mg/kg/day) was administered by gavage to streptozotocin-induced diabetic apolipoprotein E-deficient (ApoE) mice. Sudan IV staining was performed at the aortic arch. Immunostaining, quantitative RT-PCR, and vascular reactivity assay were performed using the aorta. In vitro experiments using human umbilical vein endothelial cells (HUVECs) were also performed. Canagliflozin decreased blood glucose (P<0.001) and total cholesterol (P<0.05) levels. Sudan IV staining showed that 12-week canagliflozin treatment decreased atherosclerotic lesions (P<0.05). Further, 8-week canagliflozin treatment ameliorated endothelial dysfunction, as determined by acetylcholine-induced vasodilation (P<0.05), and significantly reduced the expressions of inflammatory molecules such as ICAM-1 and VCAM-1 in the aorta at the RNA and protein levels. Canagliflozin also reduced the expressions of NADPH oxidase subunits such as NOX2 and p22phox in the aorta and reduced urinary excretion of 8-OHdG, suggesting a reduction in oxidative stress. Methylglyoxal, a precursor of advanced glycation end products, increased the expressions of ICAM-1 and p22phox in HUVECs (P<0.05, both). Methylglyoxal also decreased the phosphorylation of eNOS and Akt but increased the phosphorylation of eNOS and p38 MAPK in HUVECs. Canagliflozin prevents endothelial dysfunction and atherogenesis in diabetic ApoE mice. Anti-inflammatory and antioxidative potential due to reduced glucose toxicity to endothelial cells might be its underlying mechanisms. (Tokushima University Institutional Repository) ● Metadata: 115926 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.52100 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32101837 ● CiNii @ National Institute of Informatics (CRID): 1390286426514028416 ● Search Scopus @ Elsevier (PMID): 32101837 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.52100 (Tokushima University Institutional Repository: 115926, DOI: 10.5551/jat.52100, PubMed: 32101837, CiNii: 1390286426514028416)
112.	Kenya Kusunose, Akihiro Haga, Natsumi Yamaguchi, Takashi Abe, Daiju Fukuda, Hirotsugu Yamada, Masafumi Harada and Masataka Sata : Deep Learning for Assessment of Left Ventricular Ejection Fraction from Echocardiographic Images, Journal of the American Society of Echocardiography, Vol.33, No.5, 632-635, 2020. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.echo.2020.01.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32111541 ● Summary page in Scopus @ Elsevier: 2-s2.0-85080044447 (DOI: 10.1016/j.echo.2020.01.009, PubMed: 32111541, Elsevier: Scopus)
113.	Akihiro Tani, Kenya Kusunose, Kazuhisa Mastumoto, Hirotsugu Yamada and Masataka Sata : Diastolic Mitral Regurgitation on Color M-Mode Echocardiography in a Patient With Complete Atrioventricular Block., Circulation Reports, Vol.2, No.3, 207-208, 2020. (Link to Publication Site) ● Publication site (DOI): 10.1253/circrep.CR-20-0002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33693230 ● Search Scopus @ Elsevier (PMID): 33693230 ● Search Scopus @ Elsevier (DOI): 10.1253/circrep.CR-20-0002 (DOI: 10.1253/circrep.CR-20-0002, PubMed: 33693230)
114.	Gulinu Maimaituxun, Daiju Fukuda, Hirofumi Izaki, Y Hirata, HO Kanayama, H Masuzaki, Masataka Sata and Michio Shimabukuro : Levels of Adiponectin Expression in Peri-Renal and Subcutaneous Adipose Tissue and Its Determinants in Human Biopsied Samples, Frontiers in Endocrinology, No.10, 897, 2020. (Tokushima University Institutional Repository) ● Metadata: 115257 (Link to Publication Site) ● Publication site (DOI): 10.3389/fendo.2019.00897 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32117043 ● Summary page in Scopus @ Elsevier: 2-s2.0-85079782281 (Tokushima University Institutional Repository: 115257, DOI: 10.3389/fendo.2019.00897, PubMed: 32117043, Elsevier: Scopus)
115.	平田有紀奈, 西尾進, 原田修, 宮里尚美, 原國督, Kenya Kusunose, 伊藤敦彦, Hirotsugu Yamada and Masataka Sata : Validation of Epicardial Adipose Tissue Thickness by Echocardiography for Predicting Coronary Artery Disease: a Multicenter Study, Japanese Journal of Medical Ultrasound Technology, Vol.45, No.1, 11-20, 2020. (Link to Publication Site) ● Publication site (DOI): 10.11272/jss.302 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.11272/jss.302 (DOI: 10.11272/jss.302)
116.	Maimaituxun Gulinu, Hirotsugu Yamada, Daiju Fukuda, Shusuke Yagi, Kenya Kusunose, Hirata Yukina, Nishio Susumu, Takeshi Soeki, Masuzaki Hiroaki, Masataka Sata and Michio Shimabukuro : Association of Local Epicardial Adipose Tissue Depots and Left Ventricular Diastolic Performance in Patients With Preserved Left Ventricular Ejection Fraction, Circulation Journal, Vol.84, No.2, 203-216, 2020. (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-19-0793 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31956209 ● Summary page in Scopus @ Elsevier: 2-s2.0-85079208017 (DOI: 10.1253/circj.CJ-19-0793, PubMed: 31956209, Elsevier: Scopus)
117.	Tatsuya Maruhashi, Masato Kajikawa, Shinji Kishimoto, Haruki Hashimoto, Yuji Takaeko, Takayuki Yamaji, Takahiro Harada, Yiming Han, Yoshiki Aibara, Farina Mohamad Yusoff, Takayuki Hidaka, Yasuki Kihara, Kazuaki Chayama, Ayumu Nakashima, Chikara Goto, Hirofumi Tomiyama, Bonpei Takase, Takahide Kohro, Toru Suzuki, Tomoko Ishizu, Shinichiro Ueda, Tsutomu Yamazaki, Tomoo Furumoto, Kazuomi Kario, Teruo Inoue, Shinji Koba, Kentaro Watanabe, Yasuhiko Takemoto, Takuzo Hano, Masataka Sata, Yutaka Ishibashi, Koichi Node, Koji Maemura, Yusuke Ohya, Taiji Furukawa, Hiroshi Ito, Hisao Ikeda, Akira Yamashina and Yukihito Higashi : Diagnostic Criteria of FlowMediated Vasodilation for Normal Endothelial Function and NitroglycerinInduced Vasodilation for Normal Vascular Smooth Muscle Function of the Brachial Artery, Journal of the American Heart Association, Vol.9, No.8, e013915, 2020. (Summary) Background Diagnostic criteria of flow-mediated vasodilation (FMD), an index of endothelial function, and nitroglycerin-induced vasodilation (NID), an index of vascular smooth muscle function, of the brachial artery have not been established. The purpose of this study was to propose diagnostic criteria of FMD and NID for normal endothelial function and normal vascular smooth muscle function. Methods and Results We investigated the cutoff values of FMD and NID in subjects with (risk group) and those without cardiovascular risk factors or cardiovascular diseases (no-risk group) in 7277 Japanese subjects (mean age 51.4±10.8 years) from the Flow-Mediated Dilation Japan study and the Flow-Mediated Dilatation Japan Registry study for analysis of the cutoff value of FMD and in 1764 Japanese subjects (62.2±16.1 years) from the registry of Hiroshima University Hospital for analysis of the cutoff value of NID. Receiver-operator characteristic curve analysis of FMD to discriminate subjects in the no-risk group from patients in the risk group showed that the optimal cutoff value of FMD to diagnose subjects in the no-risk group was 7.1%. Receiver-operator characteristic curve analysis of NID to discriminate subjects in the no-risk group from patients in the risk group showed that the optimal cutoff value of NID to diagnose subjects in the no-risk group was 15.6%. Conclusions We propose that the cutoff value for normal endothelial function assessed by FMD of the brachial artery is 7.1% and that the cutoff value for normal vascular smooth muscle function assessed by NID of the brachial artery is 15.6% in Japanese subjects. Clinical Trial Registration www.umin.ac.jp Unique identifiers: UMIN000012950, UMIN000012951, UMIN000012952, and UMIN000003409. (Tokushima University Institutional Repository) ● Metadata: 114774 (Link to Publication Site) ● Publication site (DOI): 10.1161/JAHA.119.013915 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31910779 ● Summary page in Scopus @ Elsevier: 2-s2.0-85077720595 (Tokushima University Institutional Repository: 114774, DOI: 10.1161/JAHA.119.013915, PubMed: 31910779, Elsevier: Scopus)
118.	Arief Rahadian, Daiju Fukuda, HM Salim, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Thrombin inhibition by dabigatran attenuates endothelial dysfunction in diabetic mice, Vascular Pharmacology, Vol.124, 106632, 2020. (Summary) Diabetic patients have coagulation abnormalities, in which thrombin plays a key role. Whereas accumulating evidence suggests that it also contributes to the development of vascular dysfunction through the activation of protease-activated receptors (PARs). Here we investigated whether the blockade of thrombin attenuates endothelial dysfunction in diabetic mice. Induction of diabetes by streptozotocin (STZ) increased the expression of PAR1, PAR3, and PAR4 in the aorta. STZ-induced diabetic mice showed impairment of endothelial function, while the administration of dabigatran etexilate, a direct thrombin inhibitor, significantly attenuated endothelial dysfunction in diabetic mice with no alteration of metabolic parameters including blood glucose level. Dabigatran did not affect endothelium-independent vasodilation. Dabigatran decreased the expression of inflammatory molecules (e.g., MCP-1 and ICAM-1) in the aorta of diabetic mice. Thrombin increased the expression of these inflammatory molecules and the phosphorylation of IκBα, and decreased the phosphorylation of eNOS in human umbilical endothelial cells (HUVEC). Thrombin significantly impaired the endothelium-dependent vascular response of aortic rings obtained from wild-type mice. Inhibition of NF-κB attenuated thrombin-induced inflammatory molecule expression in HUVEC and ameliorated thrombin-induced endothelial dysfunction in aortic rings. Dabigatran attenuated the development of diabetes-induced endothelial dysfunction. Thrombin signaling may serve as a potential therapeutic target in diabetic condition. (Tokushima University Institutional Repository) ● Metadata: 114211 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.vph.2019.106632 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31759113 ● Search Scopus @ Elsevier (PMID): 31759113 ● Search Scopus @ Elsevier (DOI): 10.1016/j.vph.2019.106632 (Tokushima University Institutional Repository: 114211, DOI: 10.1016/j.vph.2019.106632, PubMed: 31759113)
119.	Sayuri Doi, A Tamura, Takako Minagawa, A Osaka and Masataka Sata : Classification of physical activity in patients with heart failure categorized as New York Heart Association class I or II, The Journal of Medical Investigation : JMI, Vol.67, No.1.2, 124-133, 2020. (Summary) This study aimed that we were classification of physical activity in patients with heart failure categorized as New York Heart Association (NYHA) class I or II. We were a survey using a researcher- administered questionnaire, SF-8, the Specific Activity Scale (SAS), and the Scale to Measure Self-Care Behavior of Patients with Heart Disease. We included 70 patients who were treated in the Department of Cardiovascular Medicine at Hospital A. Regarding patient characteristics and clinical information after the cluster analysis, there were significant differences in the NYHA class (p = 0.001), BNP level (p = 0.012), self-management of medication adherence (p = 0.000), and exercise habits (p = 0.005). We summarized characteristics of each group as follows : Group A showed high tolerance to physical activity and near-perfect self-management; Group B showed moderate tolerance to physical activity but was not willing to commit to daily exercise and self-management; and Group C showed low tolerance to physical activity and often requested others to handle medication management. We needed that tolerance to physical activity and proposals for tailored instruction according to patient conditions, and needed that instructions tailored to the characteristics of heart failure patients in groups A-C. J. Med. Invest. 67 : 124-133, February, 2020. (Tokushima University Institutional Repository) ● Metadata: 114645 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.67.124 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32378595 ● Summary page in Scopus @ Elsevier: 2-s2.0-85084219030 (Tokushima University Institutional Repository: 114645, DOI: 10.2152/jmi.67.124, PubMed: 32378595, Elsevier: Scopus)
120.	Tomiyama Hirofumi, Ohkuma Toshiaki, Ninomiya Toshiharu, Nakano Hiroki, Matsumoto Chisa, Avolio Alberto, Kohro Takahide, Higashi Yukihito, Maruhashi Tetsuya, Takase Bonpei, Suzuki Toru, Ishizu Tomoko, Ueta Shinichiro, Yamazaki Tsutomu, Furumoto Tomoo, Kario Kazuomi, Inoue Teruo, Koba Shinji, Takemoto Yasuhiko, Hano Takuzo, Masataka Sata, Ishibashi Yutaka, Node Koichi, Maemura Koji, Ohya Yusuke, Furukawa Taiji, Ito Hiroshi, Chikamori Taishiro and Yamashina Akira : Brachial-Ankle Pulse Wave Velocity Versus Its Stiffness Index β-Transformed Value as Risk Marker for Cardiovascular Disease, Journal of the American Heart Association, Vol.8, No.24, e013004, 2019. (Summary) Background The difference in the predictive ability of the brachial-ankle pulse wave velocity (baPWV) and its stiffness index β-transformed value (β-baPWV, ie, baPWV adjusted for the pulse pressure) for the development of pathophysiological abnormalities related to cardiovascular disease or future occurrence of cardiovascular disease was examined. Methods and Results In study 1, a 7-year prospective observational study in cohorts of 3274 men and 3490 men, the area under the curve in the receiver operator characteristic curve analysis was higher for baPWV than for β-baPWV for predicting the development of hypertension (0.73, 95% CI=0.70 to 0.75 versus 0.59, 95% CI=0.56 to 0.62; <0.01) and/or the development of retinopathy (0.78, 95% CI=0.73 to 0.82 versus 0.66, 95% CI=0.60 to 0.71; <0.01) by the end of the study period. During study 2, a 3-year observation period on 511 patients with coronary artery disease, 72 cardiovascular events were confirmed. The C statistics of both markers for predicting the development of cardiovascular events were similar. Conclusions Stiffness index β transformation of the baPWV may attenuate the significance of the baPWV as a risk marker for development of pathophysiological abnormalities related to cardiovascular disease in male subjects. (Tokushima University Institutional Repository) ● Metadata: 114188 (Link to Publication Site) ● Publication site (DOI): 10.1161/JAHA.119.013004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31822217 ● Search Scopus @ Elsevier (PMID): 31822217 ● Search Scopus @ Elsevier (DOI): 10.1161/JAHA.119.013004 (Tokushima University Institutional Repository: 114188, DOI: 10.1161/JAHA.119.013004, PubMed: 31822217)
121.	K Aini, Daiju Fukuda, K Tanaka, Y Higashikuni, Yukina Hirata, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Vildagliptin, a DPP-4 Inhibitor, Attenuates Endothelial Dysfunction and Atherogenesis in Nondiabetic Apolipoprotein E-Deficient Mice, International Heart Journal, Vol.60, No.6, 1421-1429, 2019. (Summary) Dipeptidyl peptidase-4 (DPP-4) inhibitors are novel antidiabetic agents with possible vascular protection effects. Endothelial dysfunction is an initiation step in atherogenesis. The purpose of this study was to investigate whether vildagliptin (Vilda) attenuates the development of endothelial dysfunction and atherosclerotic lesions in nondiabetic apolipoprotein E-deficient (ApoE) mice. Eight-week-old nondiabetic ApoE mice fed a Western-type diet received Vilda (50 mg/kg/day) for 20 weeks or 8 weeks. After 20 weeks of treatment, Vilda administration reduced atherogenesis in the aortic arch as determined by en face Sudan IV staining compared with the vehicle group (P < 0.05). Vilda also reduced lipid accumulation (P < 0.05) and vascular cell adhesion molecule-1 (VCAM-1) expression (P < 0.05) and tended to decrease macrophage infiltration (P = 0.05) into atherosclerotic plaques compared with vehicle. After 8 weeks of treatment, endothelium-dependent vascular reactivity was examined. Vilda administration significantly attenuated the impairment of endothelial function in nondiabetic ApoE mice compared with the vehicle group (P < 0.05). Vilda treatment did not alter metabolic parameters, including blood glucose level, in both study protocols. To investigate the mechanism, aortic segments obtained from wild-type mice were incubated with exendin-4 (Ex-4), a glucagon-like peptide-1 (GLP-1) analog, in the presence or absence of lipopolysaccharide (LPS). Ex-4 attenuated the impairment of endothelium-dependent vasodilation induced by LPS (P < 0.01). Furthermore, Ex-4 promoted phosphorylation of eNOS at Ser1177 which was decreased by LPS in human umbilical endothelial cells (P < 0.05). Vilda inhibited the development of endothelial dysfunction and prevented atherogenesis in nondiabetic ApoE mice. Our results suggested that GLP-1-dependent amelioration of endothelial dysfunction is associated with the atheroprotective effects of Vilda. (Keyword) Animals / Apolipoproteins E / Atherosclerosis / Cell Culture Techniques / Dipeptidyl-Peptidase IV Inhibitors / Disease Models, Animal / Endothelial Cells / Endothelium, Vascular / Mice / Mice, Inbred C57BL / Vascular Cell Adhesion Molecule-1 / Vildagliptin (Tokushima University Institutional Repository) ● Metadata: 114212 (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.19-117 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31735774 ● Summary page in Scopus @ Elsevier: 2-s2.0-85075961168 (Tokushima University Institutional Repository: 114212, DOI: 10.1536/ihj.19-117, PubMed: 31735774, Elsevier: Scopus)
122.	Kenya Kusunose, Yuta Torii, Hirotsugu Yamada, Susumu Nishio, Yukina Hirata, Yoshihito Saijoh, Takayuki Ise, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Association of Echocardiography Before Major Elective Non-Cardiac Surgery With Improved Postoperative Outcomes - Possible Implications for Patient Care., Circulation Journal, Vol.83, No.12, 2512-2519, 2019. (Summary) Whether preoperative echocardiography improves postoperative outcomes is not well established, so we examined the value of echocardiographic assessment on the onset of postoperative heart failure (HF), and determining which patients benefitted most from undergoing echocardiography prior to major elective non-cardiac surgery.Methods and Results:We identified all patients aged 50 years and older who had major elective non-cardiac surgery, and excluded patients with previously identified severe cardiovascular disease. The primary endpoint was the onset of HF during hospitalization. A total of 806 patients were included in the analysis. During hospitalization, 49 patients (6%) reached the primary endpoint. Within the matched cohort, preoperative echocardiography was associated with a statistically significant decrease in postoperative HF (hazard ratio: 0.46, P=0.01). In subgroup analyses, age, sex, body surface area, hypertension, diabetes mellitus, prior HF, surgical type, chronic kidney disease, pulmonary disease, and malignancy influenced the association of echocardiography with postoperative HF. The use of echocardiography in elderly patients with certain risk factors was associated with improved postoperative outcomes. The basis for this finding remains to be determined; particularly whether echocardiography is simply a marker of a population with better outcomes or whether it leads to better management that improves outcomes. (Keyword) Aged / Echocardiography / Female / Heart Failure / Humans / Incidence / Japan / Male / Middle Aged / Predictive Value of Tests / Preoperative Care / Retrospective Studies / Risk Assessment / Risk Factors / Surgical Procedures, Operative / Time Factors / Treatment Outcome (Tokushima University Institutional Repository) ● Metadata: 114189 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-19-0663 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31611537 ● Search Scopus @ Elsevier (PMID): 31611537 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-19-0663 (Tokushima University Institutional Repository: 114189, DOI: 10.1253/circj.CJ-19-0663, PubMed: 31611537)
123.	田中君枝, 平田陽一郎, Daiju Fukuda and Masataka Sata : Recent Advance in Atherosclerosis Research, The Journal of the Japanese Society of Internal Medicine, Vol.108, No.10, 1607-1615, 2019. (Keyword) 血管周囲脂肪組織(PVAT) / 心外膜脂肪組織(EAT) / 凝固第X因子 / プロテアーゼ活性型受容体2(PAR-2) / インターロイキン-1β(IL-1β) (Link to Publication Site) ● Publication site (DOI): 10.2169/naika.108.1607 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390848250135223424 ● Search Scopus @ Elsevier (DOI): 10.2169/naika.108.1607 (DOI: 10.2169/naika.108.1607, CiNii: 1390848250135223424)
124.	Kenya Kusunose, Hirotsugu Yamada, Susumu Nishio, Yukina Hirata, Yoshihito Saijoh, Yuta Torii, nao Yamada, Takayuki Ise, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Pulmonary Artery Hypertension-Specific Therapy Improves Exercise Tolerance and Outcomes in Exercise-Induced Pulmonary Hypertension, JACC. Cardiovascular Imaging, Vol.12, No.12, 2576-2579, 2019. (Tokushima University Institutional Repository) ● Metadata: 114191 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jcmg.2019.07.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31422131 ● Search Scopus @ Elsevier (PMID): 31422131 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jcmg.2019.07.002 (Tokushima University Institutional Repository: 114191, DOI: 10.1016/j.jcmg.2019.07.002, PubMed: 31422131)
125.	PT Pham, Daiju Fukuda, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Rivaroxaban, a specific FXa inhibitor, improved endothelium-dependent relaxation of aortic segments in diabetic mice, Scientific Reports, Vol.9, No.1, 11206, 2019. (Summary) Activated factor X (FXa) plays a central role in the coagulation cascade, while it also mediates vascular function through activation of protease-activated receptors (PARs). Here, we examined whether inhibition of FXa by rivaroxaban, a direct FXa inhibitor, attenuates endothelial dysfunction in streptozotocin (STZ)-induced diabetic mice. Induction of diabetes increased the expression of a major FXa receptor, PAR2, in the aorta (P < 0.05). Administration of rivaroxaban (10 mg/kg/day) to diabetic wild-type (WT) mice for 3 weeks attenuated endothelial dysfunction as determined by acetylcholine-dependent vasodilation compared with the control (P < 0.001), without alteration of blood glucose level. Rivaroxaban promoted eNOS phosphorylation in the aorta (P < 0.001). Induction of diabetes to PAR2-deficient (PAR2) mice did not affect endothelial function and eNOS phosphorylation in the aorta compared with non-diabetic PAR2 mice. FXa or a PAR2 agonist significantly impaired endothelial function in aortic rings obtained from WT mice, but not in those from PAR2 mice. FXa promoted JNK phosphorylation (P < 0.01) and reduced eNOS phosphorylation (P < 0.05) in human coronary artery endothelial cells (HCAEC). FXa-induced endothelial dysfunction in aortic rings (P < 0.001) and eNOS phosphorylation (P < 0.05) in HCAEC were partially ameliorated by a JNK inhibitor. Rivaroxaban ameliorated diabetes-induced endothelial dysfunction. Our results suggest that FXa or PAR2 is a potential therapeutic target. (Tokushima University Institutional Repository) ● Metadata: 114192 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-019-47474-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31371788 ● Search Scopus @ Elsevier (PMID): 31371788 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-019-47474-0 (Tokushima University Institutional Repository: 114192, DOI: 10.1038/s41598-019-47474-0, PubMed: 31371788)
126.	Yuta Torii, Kenya Kusunose, Hirotsugu Yamada, Susumu Nishio, Yukina Hirata, Amano Rie, Yamao Masami, Zheng Robert, Yoshihito Saijoh, nao Yamada, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Updated Left Ventricular Diastolic Function Recommendations and Cardiovascular Events in Patients with Heart Failure Hospitalization, Journal of the American Society of Echocardiography, Vol.32, No.10, 1286-1297, 2019. (Summary) Evaluation of diastolic dysfunction is crucial in determining elevated left atrial pressure. However, a validation of the long-term prognostic value of the newly proposed algorithm updated in 2016 has not been performed. The aim of the present study was to investigate the relative value of the updated 2016 diastolic dysfunction grading system for the incidence of readmission in patients with heart failure (HF) with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). Two hundred thirty-two patients hospitalized with HF were retrospectively evaluated. Subjects were divided into two subgroups: those with HFrEF (n = 127) and those with HFpEF (n = 105). Readmission risk scores were calculated using the Yale Center for Outcomes Research and Evaluation HF, LACE index, and HOSPITAL scores. The primary end point was readmission following HF and cardiac death. Over a period of 24 months, 86 patients were either readmitted or died. Multivariate Cox analysis was performed on both the HFrEF and HFpEF groups. In the HFrEF group, both the 2009 and 2016 algorithms had superior incremental value for the association of the primary end point to several readmission risk scores. In the HFpEF group, only the 2016 algorithm led to significant improvement in association with the primary end point. The 2016 algorithm had incremental value over several readmission risk scores alone. The recommendations of the 2016 algorithm can be useful for readmission and cardiac mortality risk assessment in patients with HFrEF and HFpEF. The use of echocardiography to estimate elevated left atrial pressure appears to identify a higher risk group and may allow a more tailored approach to therapy. (Tokushima University Institutional Repository) ● Metadata: 114193 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.echo.2019.06.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31378421 ● Summary page in Scopus @ Elsevier: 2-s2.0-85069976367 (Tokushima University Institutional Repository: 114193, DOI: 10.1016/j.echo.2019.06.006, PubMed: 31378421, Elsevier: Scopus)
127.	M Kajikawa, T Maruhashi, T Hidaka, S Matsui, H Hashimoto, Y Takaeko, Y Nakano, S Kurisu, Y Kihara, FM Yusoff, S Kishimoto, K Chayama, C Goto, K Noma, A Nakashima, T Hiro, A Hirayama, K Shiina, H Tomiyama, Shusuke Yagi, Amano Rie, Hirotsugu Yamada, Masataka Sata and Y Higashi : Effect of Saxagliptin on Endothelial Function in Patients with Type 2 Diabetes: A Prospective Multicenter Study, Scientific Reports, Vol.9, No.1, 10206, 2019. (Summary) The dipeptidyl peptidase-4 inhibitor saxagliptin is a widely used antihyperglycemic agent in patients with type 2 diabetes. The purpose of this study was to evaluate the effects of saxagliptin on endothelial function in patients with type 2 diabetes. This was a prospective, multicenter, interventional study. A total of 34 patients with type 2 diabetes were enrolled at four university hospitals in Japan. Treatment of patients was initially started with saxagliptin at a dose of 5 mg daily. Assessment of endothelial function assessed by flow-mediated vasodilation (FMD) and measurement of stromal cell-derived factor-1α (SDF-1α) were conducted at baseline and at 3 months after treatment with saxagliptin. A total of 31 patients with type 2 diabetes were included in the analysis. Saxagliptin significantly increased FMD from 3.1 ± 3.1% to 4.2 ± 2.4% (P = 0.032) and significantly decreased total cholesterol from 190 ± 24 mg/dL to 181 ± 25 mg/dL (P = 0.002), glucose from 160 ± 53 mg/dL to 133 ± 25 mg/dL (P < 0.001), HbA1c from 7.5 ± 0.6% to 7.0 ± 0.6% (P < 0.001), urine albumin-to-creatinine ratio from 63.8 ± 134.2 mg/g to 40.9 ± 83.0 mg/g (P = 0.043), and total SDF-1α from 2108 ± 243 pg/mL to 1284 ± 345 pg/mL (P < 0.001). These findings suggest that saxagliptin is effective for improving endothelial function. (Tokushima University Institutional Repository) ● Metadata: 114195 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-019-46726-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31308448 ● Summary page in Scopus @ Elsevier: 2-s2.0-85069056464 (Tokushima University Institutional Repository: 114195, DOI: 10.1038/s41598-019-46726-3, PubMed: 31308448, Elsevier: Scopus)
128.	Akinori Nakanishi, Jouji Shunto, Reiko Shunto, Masataka Sata and Hiroshi Bando : A case of subacute thyroiditis associated with complete occlusion of right coronary artery, Journal of Diabetes, Metabolic Disorders & Control, Vol.6, No.3, 54-58, 2019. (Tokushima University Institutional Repository) ● Metadata: 113864 (Link to Publication Site) ● Publication site (DOI): 10.15406/jdmdc.2019.06.00183 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050001338827789056 ● Search Scopus @ Elsevier (DOI): 10.15406/jdmdc.2019.06.00183 (Tokushima University Institutional Repository: 113864, DOI: 10.15406/jdmdc.2019.06.00183, CiNii: 1050001338827789056)
129.	Kenya Kusunose, Akihiro Haga, Takashi Abe and Masataka Sata : Utilization of Artificial Intelligence in Echocardiography, Circulation Journal, Vol.83, No.8, 1623-1629, 2019. (Summary) Echocardiography has a central role in the diagnosis and management of cardiovascular disease. Precise and reliable echocardiographic assessment is required for clinical decision-making. Even if the development of new technologies (3-dimentional echocardiography, speckle-tracking, semi-automated analysis, etc.), the final decision on analysis is strongly dependent on operator experience. Diagnostic errors are a major unresolved problem. Moreover, not only can cardiologists differ from one another in image interpretation, but also the same observer may come to different findings when a reading is repeated. Daily high workloads in clinical practice may lead to this error, and all cardiologists require precise perception in this field. Artificial intelligence (AI) has the potential to improve analysis and interpretation of medical images to a new stage compared with previous algorithms. From our comprehensive review, we believe AI has the potential to improve accuracy of diagnosis, clinical management, and patient care. Although there are several concerns about the required large dataset and "black box" algorithm, AI can provide satisfactory results in this field. In the future, it will be necessary for cardiologists to adapt their daily practice to incorporate AI in this new stage of echocardiography. (Tokushima University Institutional Repository) ● Metadata: 114194 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-19-0420 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31257314 ● Summary page in Scopus @ Elsevier: 2-s2.0-85070102118 (Tokushima University Institutional Repository: 114194, DOI: 10.1253/circj.CJ-19-0420, PubMed: 31257314, Elsevier: Scopus)
130.	Rie Ueno, Shusuke Yagi, Mika Bando and Masataka Sata : Long-surviving Anomalous Origin of the Right Pulmonary Artery from the Ascending Aorta Complicated with Pulmonary Arteriovenous Fistula, Internal Medicine, Vol.58, No.18, 2749-2750, 2019. (Tokushima University Institutional Repository) ● Metadata: 113417 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.2455-18 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31178488 ● Summary page in Scopus @ Elsevier: 2-s2.0-85072509638 (Tokushima University Institutional Repository: 113417, DOI: 10.2169/internalmedicine.2455-18, PubMed: 31178488, Elsevier: Scopus)
131.	Shusuke Yagi, Hiromu Yamazaki, Susumu Nishio, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : Simultaneous Pulmonary Arterial and Venous Round Structures in Pulmonary Aspergillosis., Circulation Journal, Vol.83, No.6, 1416, 2019. (Tokushima University Institutional Repository) ● Metadata: 113219 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-18-0898 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30393271 ● Summary page in Scopus @ Elsevier: 2-s2.0-85066748188 (Tokushima University Institutional Repository: 113219, DOI: 10.1253/circj.CJ-18-0898, PubMed: 30393271, Elsevier: Scopus)
132.	Daiju Fukuda, Sachiko Nishimoto, Kunduziayi Aini, Atsushi Tanaka, Tsuyoshi Nishiguchi, Joo-Ri Kim-Kaneyama, Xiao-Feng Lei, Kiyoshi Masuda, Takuya Naruto, Kimie Tanaka, Yasutomi Higashikuni, Yoichiro Hirata, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, Issei Imoto, Takashi Akasaka, Michio Shimabukuro and Masataka Sata : Toll-Like Receptor 9 Plays a Pivotal Role in Angiotensin II-Induced Atherosclerosis, Journal of the American Heart Association, Vol.8, No.7, e010860, 2019. (Summary) Background Toll-like receptor ( TLR ) 9 recognizes bacterial DNA , activating innate immunity, whereas it also provokes inflammation in response to fragmented DNA released from mammalian cells. We investigated whether TLR 9 contributes to the development of vascular inflammation and atherogenesis using apolipoprotein E-deficient ( Apoe ) mice. Methods and Results Tlr9-deficient Apoe ( Tlr9 Apoe ) mice and Apoe mice on a Western-type diet received subcutaneous angiotensin II infusion (1000 ng/kg per minute) for 28 days. Angiotensin II increased the plasma level of double-stranded DNA, an endogenous ligand of TLR 9, in these mice. Genetic deletion or pharmacologic blockade of TLR 9 in angiotensin II-infused Apoe mice attenuated atherogenesis in the aortic arch ( P<0.05), reduced the accumulation of lipid and macrophages in atherosclerotic plaques, and decreased RNA expression of inflammatory molecules in the aorta with no alteration of metabolic parameters. On the other hand, restoration of TLR 9 in bone marrow in Tlr9 Apoe mice promoted atherogenesis in the aortic arch ( P<0.05). A TLR 9 agonist markedly promoted proinflammatory activation of Apoe macrophages, partially through p38 mitogen-activated protein kinase signaling. In addition, genomic DNA extracted from macrophages promoted inflammatory molecule expression more effectively in Apoe macrophages than in Tlr9 Apoe macrophages. Furthermore, in humans, circulating double-stranded DNA in the coronary artery positively correlated with inflammatory features of coronary plaques determined by optical coherence tomography in patients with acute myocardial infarction ( P<0.05). Conclusions TLR 9 plays a pivotal role in the development of vascular inflammation and atherogenesis through proinflammatory activation of macrophages. TLR 9 may serve as a potential therapeutic target for atherosclerosis. (Keyword) Aged / Angiotensin II / Animals / Aorta, Thoracic / atherosclerosis / Bone Marrow Transplantation / Cell-Free Nucleic Acids / Chemokine CCL2 / female / Humans / In Vitro Techniques / inflammation / Lipids / Macrophages / Macrophages, Peritoneal / male / Mice / knockout mice / Mice, Knockout, ApoE / Microscopy, Electron / Myocardial Infarction / Percutaneous Coronary Intervention / Plaque, Atherosclerotic / RNA, Messenger / Reverse Transcriptase Polymerase Chain Reaction / Toll-Like Receptor 9 / Tomography, Optical Coherence / Tumor Necrosis Factor-alpha / Vasoconstrictor Agents (Tokushima University Institutional Repository) ● Metadata: 113231 (Link to Publication Site) ● Publication site (DOI): 10.1161/JAHA.118.010860 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30905257 ● Summary page in Scopus @ Elsevier: 2-s2.0-85063712345 (Tokushima University Institutional Repository: 113231, DOI: 10.1161/JAHA.118.010860, PubMed: 30905257, Elsevier: Scopus)
133.	Yukina Hirata, Kenya Kusunose, Hirotsugu Yamada, Sae Morita, Yuta Torii, Susumu Nishio, Robert Zheng, Yoshihito Saijo, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Left atrial functional response after a marathon in healthy amateur volunteers, The International Journal of Cardiovascular Imaging, Vol.35, No.4, 633-643, 2019. (Summary) Middle-aged marathon runners have an increased risk of developing atrial fibrillation (AF). A previous study described that repetitive marathon running was associated with left atrial (LA) dysfunction. However, whether this change is common in marathon runners and which runners are at risk of LA dysfunction remain unknown. The purpose of this study was to determine which factors could predict LA dysfunction. We prospectively examined 12 healthy amateur volunteers (9 males, 31 ± 8 years old) who participated in a full marathon. All echocardiographic measurements and speckle-tracking echocardiography were performed before and after the marathon. The endpoint was defined as reduced LA reservoir strain 1 day after the marathon (non-responder group). Seven participants were in the non-responder group. Age (35 ± 9 vs. 26 ± 2 years, p = 0.020), augmentation index (76 ± 12 vs. 55 ± 8, p = 0.002), and diastolic blood pressures (83 ± 11 vs. 70 ± 7 mmHg, p = 0.021) in the non-responder group were significantly higher compared with the responder group. In multivariate linear regression analysis, only the augmentation index was an independent predictor of reduced LA reservoir function after the marathon (β = - 0.646, p = 0.023). The augmentation index was a predictive marker for reduction in LA reservoir function after a marathon in healthy amateur volunteers. (Keyword) Adaptation, Physiological / Adult / Atrial Fibrillation / Atrial Function, Left / Atrial Remodeling / Echocardiography, Doppler / female / Healthy Volunteers / Humans / male / Middle Aged / Physical Endurance / Prospective Studies / Risk Factors / Running / Time Factors / Young Adult (Tokushima University Institutional Repository) ● Metadata: 113069 (Link to Publication Site) ● Publication site (DOI): 10.1007/s10554-018-1502-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30470971 ● Summary page in Scopus @ Elsevier: 2-s2.0-85057125051 (Tokushima University Institutional Repository: 113069, DOI: 10.1007/s10554-018-1502-2, PubMed: 30470971, Elsevier: Scopus)
134.	M Kajikawa, T Maruhashi, S Kishimoto, S Matsui, H Hashimoto, Y Takaeko, FM Yusoff, Y Kihara, K Chayama, C Goto, K Noma, A Nakashima, H Tomiyama, B Takase, T Kohro, T Suzuki, T Ishizu, S Ueda, T Yamazaki, T Furumoto, K Kario, T Inoue, S Koba, K Watanabe, Y Takemoto, T Hano, Masataka Sata, Y Ishibashi, K Node, K Maemura, Y Ohya, T Furukawa, H Ito, H Ikeda, A Yamashina and Y Higashi : Target of Triglycerides as Residual Risk for Cardiovascular Events in Patients With Coronary Artery Disease - Post Hoc Analysis of the FMD-J Study A., Circulation Journal, Vol.83, No.5, 1064-1071, 2019. (Summary) Circulating triglyceride (TG) levels are a current focus as a residual risk for cardiovascular (CV) events. We evaluated the relationship between circulating TG levels and future CV events in patients with coronary artery disease (CAD) who were treated with conventional therapy. Methods and Results: We analyzed data for 652 patients who were enrolled in the FMD-J Study A. We investigated the associations between serum TG levels and first major CV events (death from CV cause, nonfatal acute coronary syndrome (ACS), nonfatal stroke, and CAD) for a 3-year follow-up period. Patients were divided into 4 groups based on serum TG level: low-normal (<100 mg/dL), high-normal (100-149 mg/dL), borderline hypertriglyceridemia (150-199 mg/dL), and moderate hypertriglyceridemia (≥200 mg/dL). During a median follow-up period of 46.6 months, 14 patients died (9 from CV causes), 16 had nonfatal ACS, 6 had nonfatal stroke, and 54 had CAD. The Kaplan-Meier curves for first major CV event among the 4 groups were significantly different (P=0.04). After adjustment for various confounders, serum TG level ≥100 mg/dL were significantly associated with an increased risk of first major CV events compared with serum TG level <100 mg/dL. Serum TG level may be a surrogate marker for predicting CV events in patients with CAD. (Tokushima University Institutional Repository) ● Metadata: 114197 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-18-1082 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30918221 ● Summary page in Scopus @ Elsevier: 2-s2.0-85065217320 (Tokushima University Institutional Repository: 114197, DOI: 10.1253/circj.CJ-18-1082, PubMed: 30918221, Elsevier: Scopus)
135.	Shusuke Yagi, Daisuke Kondo, Takayuki Ise, Daiju Fukuda, Koji Yamaguchi, Tetsuzo Wakatsuki, Yutaka Kawabata, Hiroyuki Ito, Yoshihito Saijo, Hiromitsu Seno, Kumiko Sutou, Rie Ueno, Takafumi Todoroki, Kenya Kusunose, Tomomi Matsuura, Takeshi Tobiume, Hirotsugu Yamada, Takeshi Soeki, Michio Shimabukuro, Ken-ichi Aihara, Masashi Akaike and Masataka Sata : Association of Decreased Docosahexaenoic Acid Level After Statin Therapy and Low Eicosapentaenoic Acid Level with In-Stent Restenosis in Patients with Acute Coronary Syndrome, Journal of Atherosclerosis and Thrombosis, Vol.26, No.3, 272-281, 2019. (Summary) It is speculated that statin therapy modulates the synthesis of polyunsaturated fatty acids (PUFA), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). However, the data available on the effects of statin therapy on the serum levels of PUFA and the subsequent impact on in-stent restenosis (ISR) in patients with acute coronary syndrome (ACS) are limited. A total of 120 ACS patients who received emergent coronary stent implantation, follow-up coronary angiography to evaluate ISR, and new statin therapy were enrolled. We measured the serum levels of the PUFA and lipids at the onset of ACS and at the follow-up coronary angiography. The follow-up coronary angiography revealed 38 ISR cases. New statin therapy significantly reduced the serum levels of DHA and low-density lipoprotein cholesterol (LDL-C), while it did not affect EPA level. Single regression analysis revealed that a decreased serum level of LDL-C was associated with decreased DHA level. The multiple logistic regression analysis revealed that the decreased DHA level after statin therapy and low serum level of EPA on admission were determinants of prevalence of ISR. Statin therapy decreased the serum level of DHA with a parallel reduction in LDL-C level in patients with ACS. Decreased DHA level after statin therapy and low EPA level on admission are risk factors for ISR, indicating that in patients with ACS, decreased serum levels of DHA may be a residual target for the prevention of ISR. (Keyword) Acute Coronary Syndrome / Aged / Coronary Restenosis / Docosahexaenoic Acids / Eicosapentaenoic Acid / female / Follow-Up Studies / Humans / Hydroxymethylglutaryl-CoA Reductase Inhibitors / male / Prognosis / Retrospective Studies / Risk Factors / Stents (Tokushima University Institutional Repository) ● Metadata: 113220 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.44735 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30135329 ● Summary page in Scopus @ Elsevier: 2-s2.0-85062425735 (Tokushima University Institutional Repository: 113220, DOI: 10.5551/jat.44735, PubMed: 30135329, Elsevier: Scopus)
136.	Tamio Teramoto, Arihiro Kiyosue, Yasushi Ishigaki, Mariko Harada-Shiba, Yumiko Kawabata, Asuka Ozaki, Marie T. Baccara-Dinet and Masataka Sata : Efficacy and safety of alirocumab 150mg every 4 weeks in hypercholesterolemic patients on non-statin lipid-lowering therapy or lowest strength dose of statin: ODYSSEY NIPPON, Journal of Cardiology, Vol.73, No.3, 218-227, 2019. (Summary) Alirocumab, a fully human monoclonal antibody to proprotein convertase subtilisin/kexin type 9, given every 2 weeks (Q2W), significantly reduced low-density lipoprotein cholesterol (LDL-C) levels in Japanese hypercholesterolemic patients on background statin. We evaluated alirocumab 150mg every 4 weeks (Q4W) in patients on lowest-dose statin or non-statin lipid-lowering therapy (LLT). ODYSSEY NIPPON was a double-blind study conducted in Japanese patients with LDL-C ≥100mg/dL (heterozygous familial hypercholesterolemia or non-familial hypercholesterolemia with coronary heart disease) or ≥120mg/dL (non-familial hypercholesterolemia, Japan Atherosclerosis Society category III) on atorvastatin 5mg/day or non-statin LLT. Patients were randomized (1:1:1) to subcutaneous alirocumab 150mg Q4W, alirocumab 150mg Q2W, or placebo for the 12-week double-blind treatment period (DBTP), followed by a 52-week open-label treatment period (OLTP). At entry into the OLTP, patients received alirocumab 150mg Q4W, with possible up-titration to 150mg Q2W at Week 24. Least-square mean percent change in LDL-C from baseline at Week 12 (primary efficacy endpoint) was -43.8% for alirocumab Q4W, -70.1% for Q2W, and -4.3% for placebo. During the OLTP, mean LDL-C change from baseline was -45.1% at Week 20, with a further reduction at Week 36, with achieved levels maintained to Week 64. Percent of patients with ≥1 adverse event (DBTP) was 51.9% with alirocumab Q4W, 47.2% with Q2W, and 46.4% with placebo. Most common adverse events were infections and infestations (25.9%, 22.6%, 17.9%, respectively), gastrointestinal disorders (13.0%, 9.4%, 12.5%), nervous system disorders (5.6%, 7.5%, 10.7%), and general disorders and administration-site conditions (3.7%, 11.3%, 5.4%). Hypercholesterolemic Japanese patients who tolerate only lowest-strength dose statin or non-statin LLT can achieve robust LDL-C reduction with alirocumab 150mg Q4W, in addition to their current LLT. Alirocumab 150mg Q4W dosing was efficacious and generally well tolerated without new safety concerns. (ClinicalTrials.gov number: NCT02584504). (Tokushima University Institutional Repository) ● Metadata: 113230 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jjcc.2018.10.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30509509 ● Summary page in Scopus @ Elsevier: 2-s2.0-85057486666 (Tokushima University Institutional Repository: 113230, DOI: 10.1016/j.jjcc.2018.10.004, PubMed: 30509509, Elsevier: Scopus)
137.	Yuko Saito, Hirotsugu Yamada, Kenya Kusunose, Ken Saito and Masataka Sata : Noninvasive assessment of left-ventricular diastolic electromechanical coupling in hypertensive heart disease,, Journal of Echocardiography, Vol.17, No.4, 206-212, 2019. (Summary) There is a need to stratify patients who may develop heart failure because of the current "heart failure pandemic". We hypothesized that noninvasive assessment of diastolic electromechanical coupling by electrocardiography and Doppler echocardiography may be clinically useful for risk stratification of hypertensive patients who may develop heart failure. We measured the time from the peak to end of the T wave (TpTe) as an electrophysiological parameter, and peak early diastolic mitral flow (E) and lateral annular (e') velocities as mechanical parameters in 109 patients with hypertension. Relationships between these parameters and their association with the prognosis were evaluated. The e' was inversely correlated with TpTe (p < 0.001) and QTc (p < 0.014), whereas E/e' was positively correlated with TpTe (p < 0.001) and QTc (p < 0.001). The TpTe predicted patients with E/e' > 12. There were 24 cardiovascular events during follow-up (57 ± 20 months), and Kaplan-Meier analysis showed that outcome was worse (p = 0.003) in patients with higher E/e' than lower E/e'; however, there was no difference between patients with longer TpTe (≧72 ms) and shorter TpTe (< 72 ms). The correlation of TpTe with e' and E/e' in hypertensive patients suggests that these parameters reflect diastolic ventricular electromechanical coupling. The E/e' predicted outcome, and an elevated E/e' should be suspected when TpTe is prolonged (> 72 ms). Noninvasive evaluation of diastolic electromechanical coupling is clinically useful in patients with hypertension for predicting their outcome. (Tokushima University Institutional Repository) ● Metadata: 113350 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12574-019-00421-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30756346 ● Summary page in Scopus @ Elsevier: 2-s2.0-85061449967 (Tokushima University Institutional Repository: 113350, DOI: 10.1007/s12574-019-00421-4, PubMed: 30756346, Elsevier: Scopus)
138.	Atsuko Yoshida, Takashi Kaji, Hirotsugu Yamada, Naoto Yonetani, Eishi Sogawa, Masami Yamao, Kazuhisa Maeda, Masataka Sata and Minoru Irahara : Measurement of hemodynamics immediately after vaginal delivery in healthy pregnant women by electrical cardiometry., The Journal of Medical Investigation : JMI, Vol.66, No.1.2, 75-80, 2019. (Summary) Few reports have focused on hemodynamics around delivery in pregnant women because of the difficulty of continuous and noninvasive measurement. Electrical cardiometry allows noninvasive continuous monitoring of hemodynamics and has recently been used in non-pregnant subjects. We compared the use of electrical cardiometry versus transthoracic echocardiography in healthy pregnant women and evaluated hemodynamics immediately after vaginal delivery. In Study 1, electrical cardiometry and transthoracic echocardiography were used to measure cardiac output in 20 pregnant women with threatened premature delivery. A significant correlation was found between the two methods, with electrical cardiometry showing the higher cardiac output. In Study 2, heart rate, stroke volume, and cardiac output were continuously measured in 15 women during vaginal delivery up to 2 h postpartum. Cardiac output increased markedly because of an increased heart rate and stroke volume at the time of newborn delivery. The heart rate then immediately returned to baseline, while cardiac output remained elevated for at least 2 h after delivery because of a sustained high stroke volume. Electrical cardiometry was as readily available as transthoracic echocardiography for evaluating hemodynamics and allowed for continuous measurement during labor. High intrapartum cardiac output was sustained for at least 2 h after vaginal delivery. J. Med. Invest. 66 : 75-80, February, 2019. (Tokushima University Institutional Repository) ● Metadata: 113325 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.66.75 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31064959 ● Search Scopus @ Elsevier (PMID): 31064959 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.66.75 (Tokushima University Institutional Repository: 113325, DOI: 10.2152/jmi.66.75, PubMed: 31064959)
139.	Shusuke Yagi, Seiichi Nishiyama, Toshio Abe and Masataka Sata : Recurrent venous thromboembolism after discontinuation of rivaroxaban therapy in a patient with antiphospholipid syndrome, BMJ Case Reports, Vol.12, No.1, e227663, 2019. (Summary) Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterised by thromboembolic events including venous thromboembolism (VTE) in association with the presence of antiphospholipid antibodies. The standard treatment of VTE historically consists of anticoagulation therapy with warfarin, a vitamin K antagonist. Recently, direct oral anticoagulants, including rivaroxaban have become available for the treatment of VTE. However, the choice of anticoagulant, and the duration of anticoagulation in patients with APS has not been determined yet due to lack of evidence. Here, we report a case of recurrent venous thrombosis after discontinuation of rivaroxaban therapy and avoiding sedentary lifestyle in a patient with APS. We suggest that indefinite anticoagulation therapy might be needed even in low-risk APS cases. (Keyword) Aftercare / Antiphospholipid Syndrome / Factor Xa Inhibitors / Fibrin Fibrinogen Degradation Products / Humans / Male / Middle Aged / Pulmonary Embolism / Recurrence / Rivaroxaban / Tomography, X-Ray Computed / Treatment Outcome / Venous Thromboembolism / Venous Thrombosis (Tokushima University Institutional Repository) ● Metadata: 114198 (Link to Publication Site) ● Publication site (DOI): 10.1136/bcr-2018-227663 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30635311 ● Summary page in Scopus @ Elsevier: 2-s2.0-85059843315 (Tokushima University Institutional Repository: 114198, DOI: 10.1136/bcr-2018-227663, PubMed: 30635311, Elsevier: Scopus)
140.	Mina Takahashi, Takeshi Tobiume, Kazuhisa Matsumoto, Tomomi Matsuura, Takeshi Soeki, 藤本裕太, 原田貴文, Zengu Robahto, 數藤久美子, 西條良仁, 上野理絵, Yutaka Kawabata, Mika Bando, nao Yamada, Hiroyuki Ito, 轟貴史, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : A successful case of catheter ablation against ventricular tachycardia storm due to old myocardial infarction in a patient with aortic valve replacement, Shikoku Acta Medica, Vol.74, No.56, 201-208, 2019. (Summary) A 68-year-old woman with VT storm and frequent appropriate ICD therapy was referred for catheter ablation. Her past history was notable for aortic valve replacement by mechanical valve due to infectious endocarditis 17 years prior to presentation and left ventricular apical old myocardial infarction with unknown onset. At 67 years old, She admitted to the prior hospital due to ventricular tachycardia with LBBB and superior axis at heart rate of 210 per minutes. Administration of amiodarone and magnesium sulfate was ineffective and cardioversion of 200J was successfully terminated the tachycardia. Intra-cardiac defibrillator was implanted and the administration of amiodarone and mexiletine was started. 5 months after, she admitted to the hospital due to the frequent appropriate shock against the same ventricular tachycardia. Administration of lidocaine, sotalol, pilsicainide, and magnesium sulfate could not control the tachycardia and she was referred to our hospital for catheter ablation. During the first session, ventricular tachycardia was easily induced and electroanatomical mapping was performed both during tachycardia and during sinus rhythm. Late diastolic potential preceding the onset of QRS wave by 45ms was detected at the infero-septal side of the apical aneurysm. 7 5s of the RF energy application at this site could terminate the tachycardia and thereafter no ventricular tachycardia was induced. But after dose-reduction or cessation of some anti-arrhythmic drugs, ventricular tachycardia was recurred and second session was performed. This time, no ventricular tachycardia was induced, then we performed isthmus transection and core isolation against the apical aneurysm. Thereafter no ventricular tachycardia was occurred in spite of dose-reduction or cessation of some anti-arrhythmic drugs. (Keyword) ventricular tachycardia / storm / old myocardial infarction / catheter ablation / aortic valve replacement (Tokushima University Institutional Repository) ● Metadata: 112988 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050001338015711104 (Tokushima University Institutional Repository: 112988, CiNii: 1050001338015711104)
141.	平田有紀奈, 西尾進, 原田修, 宮里尚美, 原國督, Kenya Kusunose, 伊藤敦彦, Hirotsugu Yamada and Masataka Sata : 超音波検査を用いた心外膜下脂肪厚の検査者間誤差の検討, Japanese Journal of Medical Ultrasound Technology, Vol.44, No.4, 456-463, 2019. (Link to Publication Site) ● Publication site (DOI): 10.11272/jss.290 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390845713087095296 ● Search Scopus @ Elsevier (DOI): 10.11272/jss.290 (DOI: 10.11272/jss.290, CiNii: 1390845713087095296)
142.	松本力三, 西尾進, 平田有紀奈, 湯浅麻美, Yuta Torii, 天野里江, 山尾雅美, Miharu Arase, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 糖尿病性腎症の各病期における超音波指標の比較, Japanese Journal of Medical Ultrasound Technology, Vol.44, No.4, 447-455, 2019. (Link to Publication Site) ● Publication site (DOI): 10.11272/jss.288 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390845713087255168 ● Search Scopus @ Elsevier (DOI): 10.11272/jss.288 (DOI: 10.11272/jss.288, CiNii: 1390845713087255168)
143.	Shusuke Yagi, Robert Zheng, Seiichi Nishiyama, Yutaka Kawabata, Takayuki Ise, Kosuke Sugiura, Haruhiko Yoshinari, Toshihiko Nishisho, Yoshimi Bando, Kumiko Kagawa, Daiju Fukuda, Tomohiro Soga, Yoshihito Saijoh, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Shinji Kawahito, Masashi Akaike and Masataka Sata : Osteolytic primary bone lymphoma in the multiple bones, The Journal of Medical Investigation : JMI, Vol.66, No.3,4, 347-350, 2019. (Summary) Primary non-Hodgkin bone lymphoma (PBL) can involve solitary or multiple destructive bone lesions such as those of the femur or pelvis humerus, and some cases have osteolytic lesions. PBL is a rare disease in adults. Thus, PBL is rarely considered a differential diagnosis of the osteolytic tumor. In addition, PBL can be underdiagnosed because patients do not experience symptoms or show objective abnormalities in the early stage. Here, we reported an elderly patient with PBL in multiple bones, including the cranial and femoral bones that were fractured due to falling. J. Med. Invest. 66 : 347-350, August, 2019. (Tokushima University Institutional Repository) ● Metadata: 114167 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.66.347 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31656303 ● Summary page in Scopus @ Elsevier: 2-s2.0-85074142443 (Tokushima University Institutional Repository: 114167, DOI: 10.2152/jmi.66.347, PubMed: 31656303, Elsevier: Scopus)
144.	Shusuke Yagi, Itsuro Endo, Taichi Murakami, Tetsuya Hida, Yousuke Yamamoto, Tomohiro Soga, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Shinji Kawahito and Masataka Sata : Adult onset of Immunoglobulin A vasculitis - A case report,, The Journal of Medical Investigation : JMI, Vol.66, No.3,4, 344-346, 2019. (Summary) Immunoglobulin A vasculitis (IgAV), formerly known as Henoch-Schönlein purpura, primarily occurs during childhood between the ages of 3 and 15 years and is the most common form of systemic vasculitis in children ; its occurrence in adults has been rarely reported. Such low incidence could be attributable to either under-diagnosis or misdiagnosis. Thus, not only pediatricians but also physicians should be able to diagnose IgAV accurately to manage the patients appropriately and avoid its associated complications. In addition, treatment of adult onset IgAV with renal involvement has not been fully established yet. We describe here a case of adult onset IgAV complicated by proteinuria and pharyngitis, which was cured by no specific treatment. J. Med. Invest. 66 : 344-346, August, 2019. (Keyword) Acetaminophen / Adult / Factor XIII / Humans / Immunoglobulin A / Male / Pharyngitis / Proteinuria / Purpura, Schoenlein-Henoch (Tokushima University Institutional Repository) ● Metadata: 114166 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.66.344 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31656302 ● Search Scopus @ Elsevier (PMID): 31656302 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.66.344 (Tokushima University Institutional Repository: 114166, DOI: 10.2152/jmi.66.344, PubMed: 31656302)
145.	Shusuke Yagi, Kumiko Kagawa, Eiki Fujimoto, Masataka Sata and Yoshihito Saijoh : Recurrent venous thrombosis during direct oral anticoagulant therapy in a patient with protein S deficiency, The Journal of Medical Investigation : JMI, Vol.66, No.1,2, 182-184, 2019. (Summary) Protein S (PS) deficiency is an inherited thrombophilia associated with an increased risk of venous thromboembolism (VTE). In Japan, unfractionated heparin followed by warfarin has been historically applied for the treatment of VTE. Recent evidence showed that direct oral anticoagulants (DOACs) were non-inferior to standard therapy with warfarin, with significantly less bleeding in patients with VTE. However, it is unknown whether DOACs are effective for the treatment of VTE in patients with thrombophilia, including protein S deficiency, due to lack of evidence. Here, we report a case of recurrent venous thrombosis during edoxaban therapy in a patient with protein S deficiency, which was successfully treated using high-dose apixaban therapy. J.Med. Invest. 66 : 182-184, February, 2019. (Tokushima University Institutional Repository) ● Metadata: 113418 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.66.182 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31064935 ● Summary page in Scopus @ Elsevier: 2-s2.0-85065794702 (Tokushima University Institutional Repository: 113418, DOI: 10.2152/jmi.66.182, PubMed: 31064935, Elsevier: Scopus)
146.	Shusuke Yagi, Rie Ueno, Kumiko Sutou, Tetsuzo Wakatsuki, Koji Yamaguchi, Yoshihito Saijo, Tomoya Hara, Takayuki Ise, Kenya Kusunose, Mika Bando, Tomomi Matsuura, Takeshi Tobiume, Hirotsugu Yamada, Daiju Fukuda, Takeshi Soeki, Masashi Akaike and Masataka Sata : Lambda-like J wave due to acute myocardial infarction of the diagonal branch, The Journal of Medical Investigation : JMI, Vol.66, No.1,2, 185-187, 2019. (Summary) The culprit lesion of acute myocardial infarction could be predicted by electrocardiogram findings. However, we experienced some cases with coronary angiographic finding in the area of ST-T elevation that was different from that predicted. The lambda-like J wave could be caused by ischemia although the mechanism has not been fully elucidated. We report a case of acute myocardial infarction that showed discrepancy between ST-T elevation with lambda-like ischemic J wave in a broad area and coronary angiographical finding of diagonal branch occlusion. J. Med. Invest. 66 : 185-187, February, 2019. (Tokushima University Institutional Repository) ● Metadata: 113420 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.66.185 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31064936 ● Summary page in Scopus @ Elsevier: 2-s2.0-85065772885 (Tokushima University Institutional Repository: 113420, DOI: 10.2152/jmi.66.185, PubMed: 31064936, Elsevier: Scopus)
147.	Shusuke Yagi, Yoshihito Saijo, Taku Matsuda, Yasuhisa Kanematsu and Masataka Sata : Spontaneous arteriovenous fistula of the superficial temporal artery, The Journal of Medical Investigation : JMI, Vol.66, No.1,2, 209-210, 2019. (Summary) An arteriovenous fistula of the superficial temporal artery (STA) is a direct and abnormal communication between the STA, feeding artery, and superficial temporal vein, draining veins that bypass the capillary network. Several cases of trauma-induced or iatrogenic-induced arteriovenous fistula (AVF) of the STA have been reported ; however, spontaneous AVF of the STA not associated with trauma or medical treatment are extremely rare. Herein, we present a case of spontaneous AVF of the STA diagnosed in old age. J. Med. Invest. 66 : 209-210, February, 2019. (Tokushima University Institutional Repository) ● Metadata: 113475 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.66.209 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31064944 ● Summary page in Scopus @ Elsevier: 2-s2.0-85065788300 (Tokushima University Institutional Repository: 113475, DOI: 10.2152/jmi.66.209, PubMed: 31064944, Elsevier: Scopus)
148.	Shusuke Yagi and Masataka Sata : Rupture of pes anserine bursa in a patient with pes anserine pain syndrome due to osteoarthritis, The Journal of Medical Investigation : JMI, Vol.66, No.1,2, 211-212, 2019. (Summary) Pes anserinus pain syndrome is a common, clinically defined condition that is characterized by pain around the medial knee and tenderness over the upper medial tibia. The anserine bursa could be the site of proliferative and inflammatory conditions due to knee osteoarthritis, leading to pain and fluid retention. However, rupture of the pes anserinus is rare. Herein, we present a case of rupture of the pes anserine bursa in a patient with pes anserine pain syndrome and osteoarthritis. Physicians should consider rupture of the pes anserine bursa as a differential diagnosis of acute unilateral lower leg swelling. J. Med. Invest. 66 : 211-212, February, 2019. (Tokushima University Institutional Repository) ● Metadata: 113476 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.66.211 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31064945 ● Summary page in Scopus @ Elsevier: 2-s2.0-85065766564 (Tokushima University Institutional Repository: 113476, DOI: 10.2152/jmi.66.211, PubMed: 31064945, Elsevier: Scopus)
149.	Yuishin Izumi, Ryosuke Miyamoto, Koji Fujita, Yuki Yamamoto, Hirotsugu Yamada, Tomoyasu Matsubara, Yuki Unai, Ai Tsukamoto, Naoko Takamatsu, Hiroyuki Nodera, Shinya Hayashi, Masaya Oda, Atsuko Mori, Yoshihiko Nishida, Shunsuke Watanabe, Hirohisa Ogawa, Hisanori Uehara, Shigeo Murayama, Masataka Sata and Ryuji Kaji : Distinct Incidence of Takotsubo Syndrome Between Amyotrophic Lateral Sclerosis and Synucleinopathies: A Cohort Study., Frontiers in Neurology, Vol.9, 1099, 2018. (Summary) Takotsubo syndrome (TTS) is an acute cardiac syndrome characterized by regional left ventricular dysfunction with a peculiar circumferential pattern, which typically results in apical ballooning. Evidence indicates a pivotal role of catecholamines in TTS, and researchers have discussed multiple hypotheses on the etiology, including multivessel coronary spasm, myocardial stunning, excessive transient ventricular afterload, and cardiac sympathetic overactivity with local noradrenaline spillover. Although central nervous system disorders, such as stroke and epilepsy, are known to trigger TTS, the incidence and clinical features of TTS in neurodegenerative disorders are poorly understood. Here, we retrospectively examined TTS cases in a single-center cohort composed of 250 patients with amyotrophic lateral sclerosis (ALS) and 870 patients with synucleinopathies [582 patients with Parkinson's disease (PD), 125 patients with dementia with Lewy bodies (DLB), and 163 patients with multiple system atrophy (MSA)] and identified 4 (1.6%, including 2 women) cases with ALS and no cases with synucleinopathies. Two ALS patients underwent autopsy and the pathological findings were compatible with the chronological changes identified in catecholamine-induced cardiomyopathy. A literature review identified 16 TTS cases with ALS, 1 case each with PD and DLB, and no cases with MSA. When current and previous TTS cases with ALS were concatenated: 55% (11/20) were female; 35% (7/20) had a bulbar-onset and 45% (9/20) had a limb-onset; the mean age of TTS onset was 63.3 ± 9.0 years and the mean interval time from ALS onset to TTS development was 4.9 ± 3.0 years; no (0/16) patients developed TTS within 12 months after ALS onset; 50% (10/20) underwent artificial ventilations; the mortality was 17% (3/18); and most cases had precipitating factors, and TTS development was associated with gastrostomy, tracheostomy, or infections in 45% (9/20) of the patients. This study demonstrated that ALS is a considerable predisposing factor of TTS and that synucleinopathies rarely cause TTS. The distinct TTS incidence between ALS and synucleinopathies may be due to cardiac sympathetic overactivity in ALS and may also be affected by cardiac sympathetic denervation in synucleinopathies. Moreover, the etiology of TTS in ALS may be reasonably explained by the two-hit theory. (Tokushima University Institutional Repository) ● Metadata: 113228 (Link to Publication Site) ● Publication site (DOI): 10.3389/fneur.2018.01099 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30619056 ● Search Scopus @ Elsevier (PMID): 30619056 ● Search Scopus @ Elsevier (DOI): 10.3389/fneur.2018.01099 (Tokushima University Institutional Repository: 113228, DOI: 10.3389/fneur.2018.01099, PubMed: 30619056)
150.	Sachiko Nishimoto, Kunduziayi Aini, Daiju Fukuda, Yasutomi Higashikuni, Kimie Tanaka, Yoichiro Hirata, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Activation of Toll-Like Receptor 9 Impairs Blood Flow Recovery After Hind-Limb Ischemia, Frontiers in Cardiovascular Medicine, Vol.5, 144, 2018. (Summary) Peripheral artery disease causes significant functional disability and results in impaired quality of life. Ischemic tissue injury releases various endogenous ligands for Toll-like receptors (TLRs), suggesting the involvement of TLRs in blood flow recovery. However, the role of TLR9, which was originally known as a sensor for bacterial DNA, remains unknown. This study investigated the role of TLR9 in blood flow recovery in the ischemic limb using a mouse hind-limb ischemia model. Unilateral femoral artery ligation was performed in TLR9-deficient () mice and wild-type mice. In wild-type mice, femoral artery ligation significantly increased mRNA expression of TLR9 in the ischemic limb ( < 0.001) and plasma levels of cell-free DNA (cfDNA) as determined by single-stranded DNA (ssDNA) ( < 0.05) and double-stranded DNA (dsDNA) ( < 0.01), which are endogenous ligands for TLR9, compared with the sham-operated group. Laser Doppler perfusion imaging demonstrated significantly improved ratio of blood flow in the ischemic to non-ischemic limb in mice compared with wild-type mice at 2 weeks after ligation ( < 0.05). mice showed increased capillary density and reduced macrophage infiltration in ischemic limb. Genetic deletion of TLR9 reduced the expression of TNF-α, and attenuated NF-κB activation in ischemic muscle compared with wild-type mice ( < 0.05, respectively) at 3 days after the surgery. ODN1826, a synthetic agonistic oligonucleotide for TLR9, or plasma obtained from mice with ischemic muscle promoted the expression of TNF-α in wild-type macrophages ( < 0.05), but not in macrophages. ODN1826 also activated NF-κB signaling as determined by the degradation of IκBα in wild-type macrophages ( < 0.05), but not in macrophages. In vitro experiments using human umbilical vein endothelial cells demonstrated that TNF-α, or conditioned medium obtained from wild-type macrophages treated with ODN1826 accelerated cell death as determined by MTS assay ( < 0.05 and < 0.01, respectively). Our results suggest that ischemic muscle releases cfDNA, which activates TLR9 and enhances inflammation, leading to impairment of blood flow recovery in the ischemic limb. cfDNA-TLR9 signaling may serve as a potential therapeutic target in ischemic limb disease. (Tokushima University Institutional Repository) ● Metadata: 113226 (Link to Publication Site) ● Publication site (DOI): 10.3389/fcvm.2018.00144 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30460242 ● Search Scopus @ Elsevier (PMID): 30460242 ● Search Scopus @ Elsevier (DOI): 10.3389/fcvm.2018.00144 (Tokushima University Institutional Repository: 113226, DOI: 10.3389/fcvm.2018.00144, PubMed: 30460242)
151.	Noriko Sugasawa, Ayako Katagi, Hirotsugu Kurobe, Taisuke Nakayama, Chika Nishio, Hiroko Takumi, Fumiharu Higashiguchi, Ken-ichi Aihara, Michio Shimabukuro, Masataka Sata and Tetsuya Kitagawa : Inhibition of Atherosclerotic Plaque Development by Oral Administration of α-Glucosyl Hesperidin and Water-Dispersible Hesperetin in Apolipoprotein E Knockout Mice., Journal of the American College of Nutrition, 1-8, 2018. (Summary) Hesperidin, an abundant flavonoid in citrus fruit, and its aglycone, hesperetin, have been reported to possess various physiological activities, including antioxidant, anti-inflammatory, hypolipidemic, and antihypertensive activities. In this study, we investigated whether α-glucosyl hesperidin and water-dispersible hesperetin have protective effects on atherosclerotic progression in apolipoprotein E knockout (Apo-E KO) mice. Ten-week-old male Apo-E KO mice were randomly assigned a regular high-fat diet, a high-fat diet with 0.5% α-glucosyl hesperidin, or a high-fat diet with 0.1% water-dispersible hesperetin for 12 weeks. Measurement of plasma total cholesterol levels, histological staining of aortic root, and immunohistochemistry for macrophages were performed to evaluate atherosclerotic plaque formation. Vascular reactivity of mouse aortic rings was also measured. Both α-glucosyl hesperidin and water-dispersible hesperetin reduced plasma total cholesterol level. They also reduced plaque formation area, adipose deposition, and macrophage infiltration into atherosclerotic lesion. Vascular-endothelium-dependent relaxation in response to acetylcholine was improved in both experimental diet groups compared to the high-fat diet group. Our study suggests that both α-glucosyl hesperidin and water-dispersible hesperetin exert protective effects on atherosclerotic progression in Apo-E KO mice because they exhibit hypolipidemic activity, reduce inflammation through macrophages, and prevent endothelial dysfunction. (Link to Publication Site) ● Publication site (DOI): 10.1080/07315724.2018.1468831 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30321103 ● Summary page in Scopus @ Elsevier: 2-s2.0-85055024782 (DOI: 10.1080/07315724.2018.1468831, PubMed: 30321103, Elsevier: Scopus)
152.	Yukina Hirata, Hirotsugu Yamada and Masataka Sata : Epicardial Fat and Pericardial Fat Surrounding the Heart Have Different Characteristics., Circulation Journal, Vol.82, No.10, 2475-2476, 2018. (Tokushima University Institutional Repository) ● Metadata: 114199 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-18-0923 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30185691 ● Summary page in Scopus @ Elsevier: 2-s2.0-85054095916 (Tokushima University Institutional Repository: 114199, DOI: 10.1253/circj.CJ-18-0923, PubMed: 30185691, Elsevier: Scopus)
153.	Minetaka Maeda, Kageyuki Oba, Satoshi Yamaguchi, Osamu Arasaki, Masataka Sata, Hiroaki Masuzaki and Michio Shimabukuro : Usefulness of Epicardial Adipose Tissue Volume to Predict Recurrent Atrial Fibrillation After Radiofrequency Catheter Ablation, The American Journal of Cardiology, Vol.122, No.10, 1694-1700, 2018. (Summary) Although increasing evidence suggests that epicardial adipose tissue volume (EATV) is associated with post-ablation atrial fibrillation (AF), ranges of EATV predictive of post-ablation recurrence of AF remain unclear. In this study, we evaluated: (1) relationships between EATV and characteristics of AF, (2) impact of EATV on recurrent AF after radiofrequency ablation; , and (3) cut-off point for recurrent AF using a receiver operating characteristic curve. In 218 consecutive symptomatic patients undergoing who underwent ablation for AF (143 paroxysmal AF; 78 persistent AF), the EATV index (EATVI: EATV/body surface area, mL/m) was measured using 320-row multidetector computed tomography. The high EATV group showed specific cardiometabolic derangements as well as left atrial dilatation and left ventricular dysfunction. Multivariate regression analysis showed that the EATVI was an independent predictor of recurrent AF after catheter ablation. High EATV (EATVI 85 mL/m) or EATVI cutoff 116 mL/m can predict recurrent AF after catheter ablation, independent of other risk factors. In conclusion, EATVI was an independent predictor of recurrent AF after catheter ablation; a high EATV tertile or EATVI cutoff may be useful for prediction of recurrent AF after catheter ablation. Future studies should determine the utility of the EATVI in the clinical setting of AF ablation. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.amjcard.2018.08.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30244845 ● Summary page in Scopus @ Elsevier: 2-s2.0-85053732191 (DOI: 10.1016/j.amjcard.2018.08.005, PubMed: 30244845, Elsevier: Scopus)
154.	Kimie Tanaka and Masataka Sata : Possible Roles of Epicardial Adipose Tissue in the Pathogenesis of Coronary Atherosclerosis., Annals of Nuclear Cardiology, Vol.4, No.1, 5-10, 2018. (Tokushima University Institutional Repository) ● Metadata: 114202 (Link to Publication Site) ● Publication site (DOI): 10.17996/anc.18-00079 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.17996/anc.18-00079 (Tokushima University Institutional Repository: 114202, DOI: 10.17996/anc.18-00079)
155.	B Ganbaatar, Daiju Fukuda, HM Salim, Sachiko Nishimoto, K Tanaka, Y Higashikuni, Y Hirata, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Ticagrelor, a P2Y12 antagonist, attenuates vascular dysfunction and inhibits atherogenesis in apolipoprotein-E-deficient mice., Atherosclerosis, Vol.275, 124-132, 2018. (Summary) Ticagrelor reduces cardiovascular events in patients with acute coronary syndrome (ACS). Recent studies demonstrated the expression of P2Y12 on vascular cells including endothelial cells, as well as platelets, and suggested its contribution to atherogenesis. We investigated whether ticagrelor attenuates vascular dysfunction and inhibits atherogenesis in apolipoprotein E-deficient (apoe) mice. Eight-week-old male apoe mice were fed a western-type diet (WTD) supplemented with 0.1% ticagrelor (approximately 120 mg/kg/day). Non-treated animals on WTD served as control. Atherosclerotic lesions were examined by en-face Sudan IV staining, histological analyses, quantitative RT-PCR analysis, and western blotting. Endothelial function was analyzed by acetylcholine-dependent vasodilation using aortic rings. Human umbilical vein endothelial cells (HUVEC) were used for in vitro experiments. Ticagrelor treatment for 20 weeks attenuated atherosclerotic lesion progression in the aortic arch compared with control (p < 0.05). Ticagrelor administration for 8 weeks attenuated endothelial dysfunction (p < 0.01). Ticagrelor reduced the expression of inflammatory molecules such as vascular cell adhesion molecule-1, macrophage accumulation, and lipid deposition. Ticagrelor decreased the phosphorylation of JNK in the aorta compared with control (p < 0.05). Ticagrelor and a JNK inhibitor ameliorated impairment of endothelium-dependent vasodilation by adenosine diphosphate (ADP) in wild-type mouse aortic segments. Furthermore, ticagrelor inhibited the expression of inflammatory molecules which were promoted by ADP in HUVEC (p < 0.001). Ticagrelor also inhibited ADP-induced JNK activation in HUVEC (p < 0.05). Ticagrelor attenuated vascular dysfunction and atherogenesis through the inhibition of inflammatory activation of endothelial cells. These effects might be a potential mechanism by which ticagrelor decreases cardiovascular events in patients with ACS. (Tokushima University Institutional Repository) ● Metadata: 114201 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2018.05.053 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29902700 ● Search Scopus @ Elsevier (PMID): 29902700 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2018.05.053 (Tokushima University Institutional Repository: 114201, DOI: 10.1016/j.atherosclerosis.2018.05.053, PubMed: 29902700)
156.	Yoshihito Saijo, Hirotsugu Yamada, Kenya Kusunose, Mika Bando, Susumu Nishio, Yuta Torii, Yukina Hirata, Hiromitsu Seno, Tomomi Matsuura, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : A clinical application of preload stress echocardiography for predicting future hemodynamic worsening in patients with early-stage heart failure., Echocardiography, Vol.35, No.10, 1587-1595, 2018. (Summary) To improve the prognosis of patients with heart failure, risk stratification in their early stage is important. We assessed whether the change in transmitral flow (TMF) velocity pattern during preload augmentation can predict future hemodynamic worsening in early-stage heart failure patients with impaired relaxation TMF pattern. We designed a prospective cohort study that included 155 consecutive patients with impaired relaxation (IR) pattern at rest. Preload stress echocardiography was achieved using leg-positive pressure (LPP), and changes in TMF pattern during the LPP was observed during baseline echocardiographic examination. The patients whose TMF pattern developed to pseudonormal (PN) pattern throughout the study period were classified into the change to PN group, and patients whose TMF pattern stayed in IR pattern were classified into the stay in IR group. The median follow-up period was 17 months. The average age was 68 ± 11 years old, and 97 patients (63%) were male. Among 155 patients, 27 were classified into the change to PN group. A Cox proportional hazard analysis confirmed that the change in the peak atrial systolic TMF velocity during the LPP (ΔA, hazard ratio = 0.58 per 1SD; 95% CI = 0.39-0.88, P = 0.010) was the powerful independent predictor of change into PN pattern. Kaplan-Meier analysis revealed that the patients with ΔA -7 cm/s had more likely to develop into PN pattern than patients with ΔA > -7 cm/s (P = 0.001). Evaluation of a response in TMF during the LPP might provide an incremental diagnostic value to detect future overt heart failure in patients with early-stage heart failure. (Tokushima University Institutional Repository) ● Metadata: 112877 (Link to Publication Site) ● Publication site (DOI): 10.1111/echo.14098 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30005132 ● Summary page in Scopus @ Elsevier: 2-s2.0-85054773574 (Tokushima University Institutional Repository: 112877, DOI: 10.1111/echo.14098, PubMed: 30005132, Elsevier: Scopus)
157.	Tatsuya Maruhashi, Junko Soga, Noritaka Fujimura, Naomi Idei, Shinsuke Mikami, Yumiko Iwamoto, Akimichi Iwamoto, Masato Kajikawa, Takeshi Matsumoto, Nozomu Oda, Shinji Kishimoto, Shogo Matsui, Haruki Hashimoto, Yoshiki Aibara, Farina Yusoff Mohamad, Takayuki Hidaka, Yasuki Kihara, Kazuaki Chayama, Kensuke Noma, Ayumu Nakashima, Chikara Goto, Hirofumi Tomiyama, Bonpei Takase, Takahide Kohro, Toru Suzuki, Tomoko Ishizu, Shinichiro Ueda, Tsutomu Yamazaki, Tomoo Furumoto, Kazuomi Kario, Teruo Inoue, Shinji Koba, Kentaro Watanabe, Yasuhiko Takemoto, Takuzo Hano, Masataka Sata, Yutaka Ishibashi, Koichi Node, Koji Maemura, Yusuke Ohya, Taiji Furukawa, Hiroshi Ito, Hisao Ikeda, Akira Yamashina and Yukihito Higashi : Endothelial Dysfunction, Increased Arterial Stiffness, and Cardiovascular Risk Prediction in Patients With Coronary Artery Disease FMD-J (Flow-Mediated Dilation Japan) Study, Journal of the American Heart Association, Vol.7, 14, 2018. (Summary) The usefulness of vascular function tests for management of patients with a history of coronary artery disease is not fully known. We measured flow-mediated vasodilation (FMD) and brachial-ankle pulse wave velocity (baPWV) in 462 patients with coronary artery disease for assessment of the predictive value of FMD and baPWV for future cardiovascular events in a prospective multicenter observational study. The first primary outcome was coronary events, and the second primary outcome was a composite of coronary events, stroke, heart failure, and sudden death. During a median follow-up period of 49.2 months, the first primary outcome occurred in 56 patients and the second primary outcome occurred in 66 patients. FMD above the cutoff value of 7.1%, derived from receiver-operator curve analyses for the first and second primary outcomes, was significantly associated with lower risk of the first (hazard ratio, 0.27; 95% confidence interval, 0.06-0.74; =0.008) and second (hazard ratio, 0.32; 95% confidence interval, 0.09-0.79; =0.01) primary outcomes. baPWV above the cutoff value of 1731 cm/s was significantly associated with higher risk of the first (hazard ratio, 1.86; 95% confidence interval, 1.01-3.44; =0.04) and second (hazard ratio, 2.19; 95% confidence interval, 1.23-3.90; =0.008) primary outcomes. Among 4 groups stratified according to the combination of cutoff values of FMD and baPWV, stepwise increases in the calculated risk ratio for the first and second primary outcomes were observed. In patients with coronary artery disease, both FMD and baPWV were significant predictors of cardiovascular events. The combination of FMD and baPWV provided further cardiovascular risk stratification. URL: www.umin.ac.jp. Unique identifier: UMIN000012950. (Tokushima University Institutional Repository) ● Metadata: 113035 (Link to Publication Site) ● Publication site (DOI): 10.1161/JAHA.118.008588 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30005558 ● Summary page in Scopus @ Elsevier: 2-s2.0-85050474129 (Tokushima University Institutional Repository: 113035, DOI: 10.1161/JAHA.118.008588, PubMed: 30005558, Elsevier: Scopus)
158.	Kenya Kusunose, Hiromitsu Seno, Hirotsugu Yamada, Susumu Nishio, Yuta Torii, Yukina Hirata, Y Saijo, Takayuki Ise, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Right Ventricular Function and Beneficial Effects of Cardiac Rehabilitation in Patients With Systolic Chronic Heart Failure., The Canadian Journal of Cardiology, Vol.34, No.10, 1307-1315, 2018. (Summary) It has been recognized that a comprehensive cardiac rehabilitation (CR) program improves mortality in patients with chronic heart failure. On the other hand, the magnitude of the improvement in exercise capacity after CR differs among individuals. The aim of this study was to assess the echocardiographic determinants of responders to CR using preload stress echocardiography. We prospectively enrolled 58 chronic heart failure patients with reduced left ventricular ejection fraction (aged 62 ± 11 years; 69% male; left ventricular ejection fraction 43% ± 7%) who had received optimized medical treatment in a CR program for 5 months. We performed preload echocardiographic studies using leg positive pressure (LPP) to assess the echocardiographic parameters during preload augmentation. We defined 41 patients as a development cohort to assess the predictive value of echocardiographic variables. Next, we validated results in the remaining 17 patients as a validation cohort. In the development cohort, significant improvement in peak oxygen uptake (VO) (>10%) after CR was observed in 58% patients. In a multivariable logistic regression model, the significant predictor of improvement in exercise capacity was right ventricular (RV) strain during LPP (odds ratio: 3.96 per 1 standard deviation; P = 0.01). An RV strain value of -16% during LPP had a good sensitivity of 0.79 and a specificity of 0.71 to identify patients with improvement in peak VO. In the validation cohort, an optimal cutoff value of RV strain value was the same (area under the curve: 0.77, sensitivity: 0.78, specificity: 0.65). RV strain during LPP may be an echocardiographic parameter for assessing beneficial effects of CR. (Tokushima University Institutional Repository) ● Metadata: 114204 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cjca.2018.06.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30146462 ● Summary page in Scopus @ Elsevier: 2-s2.0-85052061274 (Tokushima University Institutional Repository: 114204, DOI: 10.1016/j.cjca.2018.06.003, PubMed: 30146462, Elsevier: Scopus)
159.	Atsushi Tanaka, Atsushi Kawaguchi, Hirofumi Tomiyama, Tomoko Ishizu, Chisa Matsumoto, Yukihito Higashi, Bonpei Takase, Toru Suzuki, Shinichiro Ueda, Tsutomu Yamazaki, Tomoo Furumoto, Kazuomi Kario, Teruo Inoue, Shinji Koba, Yasuhiko Takemoto, Takuzo Hano, Masataka Sata, Yutaka Ishibashi, Koji Maemura, Yusuke Ohya, Taiji Furukawa, Hiroshi Ito, Akira Yamashina and Koichi Node : Cross-sectional and longitudinal associations between serum uric acid and endothelial function in subjects with treated hypertension., International Journal of Cardiology, Vol.272, 308-313, 2018. (Summary) The endothelial dysfunction-arterial stiffness-atherosclerosis continuum plays an important pathophysiological role in hypertension. The aim of this study was to investigate the cross-sectional association between serum uric acid (SUA) and vascular markers related to this continuum, and to assess the longitudinal association between SUA and endothelial function that represents the initial step of the continuum. We evaluated the baseline associations between SUA levels and vascular markers that included flow-mediated vasodilatation (FMD), brachial-ankle pulse wave velocity (baPWV), and common carotid artery intima-media thickness (CCA-IMT) in 648 subjects receiving antihypertensive treatment. The longitudinal association between baseline SUA levels and FMD measured at 1.5 and 3 yr of follow-up was also investigated. At baseline, modest, but significant correlations were observed between SUA and FMD in females (r = -0.171), baPWV in males with SUA >368.78 μmol/L (r = -0.122) and in females with a SUA level 362.83 μmol/L (r = 0.217), mean CCA-IMT in females with a SUA level 333.09 μmol/L (r = 0.139), and max CCA-IMT in females with SUA level 333.09 μmol/L (r = 0.138). A longitudinal association between SUA and FMD was less observed in males. In females, the baseline SUA was associated significantly with FMD values at 1.5 yr (r = -0.211), and SUA levels >237.92 μmol/L were associated significantly and independently with FMD values at 3 yr (r = -0.166). Lower SUA levels were associated with better vascular markers of the continuum, especially in females. Furthermore, we observed a longitudinal association between SUA and endothelial function, suggesting SUA level may be a potential marker of the continuum in hypertension. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijcard.2018.06.017 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29895425 ● Summary page in Scopus @ Elsevier: 2-s2.0-85048476487 (DOI: 10.1016/j.ijcard.2018.06.017, PubMed: 29895425, Elsevier: Scopus)
160.	Takeshi Soeki, Tomomi Matsuura, Takeshi Tobiume, Sachiko Bando, Matsumoto Kazuhisa, Hiromi Nagano, Etsuko Uematsu, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Clinical, Electrocardiographic, and Echocardiographic Parameter Combination Predicts the Onset of Atrial Fibrillation., Circulation Journal, Vol.82, No.9, 2253-2258, 2018. (Summary) The ability to identify risk markers for new-onset atrial fibrillation (AF) is critical to the development of preventive strategies, but it remains unknown whether a combination of clinical, electrocardiographic, and echocardiographic parameters predicts the onset of AF. In the present study, we evaluated the predictive value of a combined score that includes these parameters.Methods and Results:We retrospectively studied 1,040 patients without AF who underwent both echocardiography and 24-h Holter electrocardiography between May 2005 and December 2010. During a median follow-up period of 68.4 months (IQR, 49.9-93.3 months), we investigated the incidence of new-onset AF. Of the 1,040 patients, 103 (9.9%) developed AF. Patients who developed AF were older than patients who did not. Total heart beats, premature atrial contraction (PAC) count, maximum RR interval, and frequency of sinus pause quantified on 24-h electrocardiography were associated with new-onset AF. LA diameter (LAD) on echocardiography was also associated with the development of AF. On multivariate Cox analysis, age 58 years, PAC count 80 beats/day, maximum RR interval 1.64 s, and LAD 4.5 cm were independently associated with the development of AF. The incidence rate of new-onset AF significantly increased as the combined score (i.e., the sum of the risk score determined using hazard ratios) increased. A combined score that includes age, PAC count, maximum RR interval, and LAD could help characterize the risk of new-onset AF. (Tokushima University Institutional Repository) ● Metadata: 113221 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-17-0758 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29848884 ● Summary page in Scopus @ Elsevier: 2-s2.0-85052204332 (Tokushima University Institutional Repository: 113221, DOI: 10.1253/circj.CJ-17-0758, PubMed: 29848884, Elsevier: Scopus)
161.	Kageyuki Oba, Minetaka Maeda, Gulinu Maimaituxun, Satoshi Yamaguchi, Osamu Arasaki, Daiju Fukuda, Shusuke Yagi, Hirata Yukina, Susumu Nishio, Takashi Iwase, Shoichiro Takao, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masafumi Harada, Hiroaki Masuzaki, Masataka Sata and Michio Shimabukuro : Effect of the Epicardial Adipose Tissue Volume on the Prevalence of Paroxysmal and Persistent Atrial Fibrillation., Circulation Journal, Vol.82, No.7, 1778-1787, 2018. (Summary) Although increasing evidence suggests that epicardial adipose tissue volume (EATV) is associated with atrial fibrillation (AF), it is controversial whether there is a dose-response relationship of increasing EATV along the continuum of AF. We evaluated the effect of the EATV on the prevalence of paroxysmal AF (PAF) and persistent AF (PeAF) and the relationships with cardiac structure and functional remodeling.Methods and Results:Subjects who underwent multidetector computed tomography (MDCT) coronary angiography because of symptoms suggestive of coronary artery disease were divided into sinus rhythm (SR) (n=112), PAF (n=133), and PeAF (n=71) groups. The EATV index (EATV/body surface area, mL/m) was strongly associated with the prevalence of PAF and PeAF on the model adjusted for known AF risk factors. The effect of the EATV index on the prevalence of PeAF, but not on that of PAF, was modified by the left atrial (LA) dimension, suggesting that extension of the LA dimension is related to EATV expansion in PeAF. The cutoff value of the EATV index for the prevalence was higher in PeAF than in PAF (64 vs. 55 mL/m, P<0.01). The EATV index is associated with the prevalence of PAF and PeAF, and its cutoff values are predictive for PAF and PeAF development independently of other AF risk factors. (Tokushima University Institutional Repository) ● Metadata: 113224 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-18-0021 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29806623 ● Summary page in Scopus @ Elsevier: 2-s2.0-85049036945 (Tokushima University Institutional Repository: 113224, DOI: 10.1253/circj.CJ-18-0021, PubMed: 29806623, Elsevier: Scopus)
162.	Kenya Kusunose, Y Okushi, Hirotsugu Yamada, Susumu Nishio, Yuta Torii, Yukina Hirata, Y Saijo, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Prognostic Value of Frailty and Diastolic Dysfunction in Elderly Patients., Circulation Journal, Vol.82, No.8, 2103-2110, 2018. (Summary) High prevalence of frailty and of diastolic dysfunction (DD) in heart failure and high mortality in frail adults have been noted. We characterized frailty by quantifying differences on echocardiography, and assessed the added prognostic utility of frailty and DD grade in an elderly population. One hundred and ninety-one patients 65 years who had at least 1 cardiovascular risk factor were prospectively recruited for clinically indicated echocardiography at the present institute. Weight loss, exhaustion, and deficits in physical activity, gait speed, and handgrip strength were used to categorize patients as frail (3 features), intermediately frail (1 or 2 features), or non-frail (0 features). DD grade 2 was defined as severe. Frailty was associated with larger left atrial volume, smaller stroke volume, and worse DD grade after adjustment for age. In a period of 14 months, 29 patients (15%) had cardiovascular events. The addition of frailty score and severe DD significantly improved the prognostic power of a model containing male gender (model 1, male gender, χ=6.4; model 2, model 1 plus frailty score, χ=16.7, P=0.004; model 3, model 2 plus severe DD, χ=25.5, P=0.015). Both frailty and DD grade were significantly associated with future cardiovascular events in an elderly population with preserved ejection fraction and 1 risk factor of cardiovascular disease. (Tokushima University Institutional Repository) ● Metadata: 113222 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-18-0017 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29709994 ● Summary page in Scopus @ Elsevier: 2-s2.0-85050588123 (Tokushima University Institutional Repository: 113222, DOI: 10.1253/circj.CJ-18-0017, PubMed: 29709994, Elsevier: Scopus)
163.	Tomoya Hara, Pham Tran Phuong, Daiju Fukuda, Koji Yamaguchi, Chie Murata, Sachiko Nishimoto, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Soeki Takeshi, Tetsuzo Wakatsuki, Issei Imoto, Michio Shimabukuro and Masataka Sata : Protease-Activated Receptor-2 Plays a Critical Role in Vascular Inflammation and Atherosclerosis in Apolipoprotein E-Deficient Mice., Circulation, Vol.138, No.16, 1706-1719, 2018. (Summary) -The coagulation system is closely linked with vascular inflammation, although the underlying mechanisms are still obscure. Recent studies show that protease-activated receptor (PAR)-2, a major receptor of activated factor X (FXa), are expressed in both vascular cells and leukocytes, suggesting that PAR-2 may contribute to the pathogenesis of inflammatory diseases. Here we investigated the role of PAR-2 in vascular inflammation and atherogenesis. -We generated apolipoprotein E-deficient ( ) mice lacking systemic PAR-2 expression ( ). mice which lack or express PAR-2 only in bone-marrow (BM) cells were also generated by BM transplantation. Atherosclerotic lesions were investigated after 20 weeks on a western-type diet (WTD) by histological analyses, quantitative RT-PCR, and western blotting. In vitro experiments using BM-derived macrophages were performed to confirm pro-inflammatory roles of PAR-2. The association between plasma FXa level and the severity of coronary atherosclerosis was also examined in humans who underwent coronary intervention. - mice showed reduced atherosclerotic lesions in the aortic arch (<0.05) along with features of stabilized atherosclerotic plaques such as less lipid deposition (<0.05), collagen loss (<0.01), macrophage accumulation (<0.05), and inflammatory molecule expression (<0.05) compared with mice. Systemic PAR2 deletion in mice significantly decreased the expression of inflammatory molecules in the aorta. The results of BM transplantation experiments demonstrated that PAR-2 in hematopoietic cells contributed to atherogenesis in mice. PAR-2 deletion did not alter metabolic parameters. In vitro experiments demonstrated that FXa or a specific peptide agonist of PAR-2 significantly increased expression of inflammatory molecules and lipid uptake in BM-derived macrophages from wild-type mice compared with those from PAR-2-deficient mice. Activation of NF- κB signaling was involved in PAR-2-associated vascular inflammation and macrophage activation. In humans who underwent coronary intervention, plasma FXa level independently correlated with the severity of coronary atherosclerosis as determined by Gensini score (<0.05) and plaque volume (<0.01). -PAR-2 signaling activates macrophages and promotes vascular inflammation, increasing atherosclerosis in mice. This signaling pathway may also participate in atherogenesis in humans. (Tokushima University Institutional Repository) ● Metadata: 112891 (Link to Publication Site) ● Publication site (DOI): 10.1161/CIRCULATIONAHA.118.033544 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29700120 ● Summary page in Scopus @ Elsevier: 2-s2.0-85055611443 (Tokushima University Institutional Repository: 112891, DOI: 10.1161/CIRCULATIONAHA.118.033544, PubMed: 29700120, Elsevier: Scopus)
164.	Gulinu Maimaituxun, Michio Shimabukuro, Daiju Fukuda, Shusuke Yagi, Yukina Hirata, Takashi Iwase, Shoichiro Takao, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masafumi Harada and Masataka Sata : Local Thickness of Epicardial Adipose Tissue Surrounding the Left Anterior Descending Artery Is a Simple Predictor of Coronary Artery Disease - New Prediction Model in Combination With Framingham Risk Score., Circulation Journal, Vol.82, No.5, 1369-1378, 2018. (Summary) Compared with global cardiac adiposity, the local accumulation of fat surrounding coronary arteries might have a more direct impact on coronary artery disease (CAD). Here, we compared the local epicardial adipose tissue (EAT) thickness and global cardiac adiposity volumes for predicting CAD.Methods and Results:A total of 197 consecutive subjects underwent 320-slice multi-detector computed tomography coronary angiography and were segregated into CAD (1 coronary artery branch stenosis 50%) and non-CAD groups. EAT thickness was measured at the right coronary artery (EAT), the left anterior descending artery (EAT), and the left circumflex artery (EAT). Although EATand EATwere similar between the 2 groups, EATwas larger in the CAD group than in the non-CAD group (5.45±2.16 mm vs. 6.86±2.19 mm, P<0.001). EAT, after correcting for confounding factors, was strongly associated with CAD (r=0.276, P<0.001) and Gensini score (r=0.239, P<0.001). On multiple regression analysis, Framingham risk score combined with EATwas a strong predictor of CAD (adjusted R=0.121; P<0.001). The local fat thickness surrounding the LAD is a simple and useful surrogate marker for estimating the presence, severity, and extent of CAD, independent of classical cardiovascular risk factors. (Tokushima University Institutional Repository) ● Metadata: 112879 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-17-1289 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29563352 ● Summary page in Scopus @ Elsevier: 2-s2.0-85045965929 (Tokushima University Institutional Repository: 112879, DOI: 10.1253/circj.CJ-17-1289, PubMed: 29563352, Elsevier: Scopus)
165.	清水郁子, 瀬野弘光, Koji Yamaguchi, Kenya Kusunose, Hirotsugu Yamada, Tetsuzo Wakatsuki, Takeshi Soeki, Masataka Sata, Takashi Iwase, Hirotsugu Kurobe and Tetsuya Kitagawa : Calcified Amorphous Tumorに対し腫瘍摘出術を行った一例, Shikoku Acta Medica, Vol.74, No.1-2, 84, 2018.
166.	Shusuke Yagi, Y. Yamamoto, S. Nishiyama and Masataka Sata : An Occluded Hooklet of an Embedded Inferior Vena Cava Filter, Internal Medicine, Vol.57, No.15, 2275-2276, 2018. (Tokushima University Institutional Repository) ● Metadata: 114206 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.0505-17 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29526958 ● CiNii @ National Institute of Informatics (CRID): 1390001288050194688 ● Search Scopus @ Elsevier (PMID): 29526958 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.0505-17 (Tokushima University Institutional Repository: 114206, DOI: 10.2169/internalmedicine.0505-17, PubMed: 29526958, CiNii: 1390001288050194688)
167.	H Tomiyama, . T Ishizu, T Kohro, C Matsumoto, Y Higashi, B Takase, T Suzuki, . S Ueda, T Yamazaki, T Furumoto, K Kario, T Inoue, S Koba, Y Takemoto, T Hano, Masataka Sata, M Sata, Y Ishibashi, K Node, K Maemura, Y Ohya, T Furukawa, H Ito and A Yamashina : Longitudinal association among endothelial function, arterial stiffness and subclinical organ damage in hypertension., International Journal of Cardiology, Vol.15, No.253, 161-166, 2018. (Summary) To examine the longitudinal mutual association between endothelial dysfunction and arterial stiffness, and also to determine which of the two variables was more closely associated with the progression of subclinical organ damage. The brachial-ankle pulse wave velocity (baPWV), carotid intima-media thickness (CIMT), estimated glomerular filtration rate, microalbuminuria and flow-mediated vasodilatation of the brachial artery (FMD) were measured three times at 1.5-year intervals in 674 Japanese patients receiving antihypertensive treatment. The change of the baPWV during the study period was larger in the subjects with baseline FMD values in the lowest tertile as compared to those with baseline FMD values in the highest tertile. The change of the CIMT was smaller in the subjects with baseline baPWV values in the lowest tertile than in those with baseline baPWV values in the highest tertile. After the adjustment, the FMD value at the baseline was inversely associated with the baPWV at the end of the study period (beta=-0.07, p=0.01), although, the reverse association was not significant. The baPWV, but not the FMD value, at the baseline was associated with the CIMT (beta=0.06, p=0.04) measured at the end of the study period. In hypertension, endothelial dysfunction was associated with the progression of arterial stiffness, although the reverse association was not confirmed. The increased arterial stiffness rather than endothelial dysfunction may be more closely associated with the progression of atherosclerotic vascular damage, and the endothelial dysfunction-arterial stiffness-atherosclerosis continuum may be important in hypertension. (Tokushima University Institutional Repository) ● Metadata: 115151 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijcard.2017.11.022 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29174285 ● Summary page in Scopus @ Elsevier: 2-s2.0-85035071196 (Tokushima University Institutional Repository: 115151, DOI: 10.1016/j.ijcard.2017.11.022, PubMed: 29174285, Elsevier: Scopus)
168.	K Tanaka and Masataka Sata : Roles of Perivascular Adipose Tissue in the Pathogenesis of Atherosclerosis., Frontiers in Physiology, Vol.9, No.3, 3, 2018. (Summary) Traditionally, it is believed that white adipose tissues serve as energy storage, heat insulation, and mechanical cushion, whereas non-shivering thermogenesis occurs in brown adipose tissue. Recent evidence revealed that adipose tissue secretes many types of cytokines, called as adipocytokines, which modulate glucose metabolism, lipid profile, appetite, fibrinolysis, blood pressure, and inflammation. Most of the arteries are surrounded by perivascular adipose tissue (PVAT). PVAT has been thought to be simply a structurally supportive tissue for vasculature. However, recent studies showed that PVAT influences vasodilation and vasocontraction, suggesting that PVAT regulates vascular tone and diameter. Adipocytokines secreted from PVAT appear to have direct access to the adjacent arterial wall by diffusion or via vasa vasorum. In fact, PVAT around atherosclerotic lesions and mechanically-injured arteries displayed inflammatory cytokine profiles, suggesting that PVAT functions to promote vascular lesion formation. Many clinical studies revealed that increased accumulation of epicardial adipose tissue (EAT), which surrounds coronary arteries, is associated with coronary artery disease. In this review article, we will summarize recent findings about potential roles of PVAT in the pathogenesis of atherosclerosis, particularly focusing on a series of basic and clinical studies from our laboratory. (Tokushima University Institutional Repository) ● Metadata: 114208 (Link to Publication Site) ● Publication site (DOI): 10.3389/fphys.2018.00003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29487532 ● Summary page in Scopus @ Elsevier: 2-s2.0-85041922780 (Tokushima University Institutional Repository: 114208, DOI: 10.3389/fphys.2018.00003, PubMed: 29487532, Elsevier: Scopus)
169.	Tomoya Hara, Daiju Fukuda, K Tanaka, Y Higashikuni, Yukina Hirata, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Inhibition of activated factor X by rivaroxaban attenuates neointima formation after wire-mediated vascular injury., European Journal of Pharmacology, Vol.5, No.820, 222-228, 2018. (Summary) Accumulating evidence suggests that activated factor X (FXa), a key coagulation factor, plays an important role in the development of vascular inflammation through activation of many cell types. Here, we investigated whether pharmacological blockade of FXa attenuates neointima formation after wire-mediated vascular injury. Transluminal femoral artery injury was induced in C57BL/6 mice by inserting a straight wire. Rivaroxaban (5mg/kg/day), a direct FXa inhibitor, was administered from one week before surgery until killed. At four weeks after surgery, rivaroxaban significantly attenuated neointima formation in the injured arteries compared with control (P<0.01). Plasma lipid levels and blood pressure were similar between the rivaroxaban-treated group and non-treated group. Quantitative RT-PCR analyses demonstrated that rivaroxaban reduced the expression of inflammatory molecules (e.g., IL-1β and TNF-α) in injured arteries at seven days after surgery (P<0.05, respectively). In vitro experiments using mouse peritoneal macrophages demonstrated that FXa increased the expression of inflammatory molecules (e.g., IL-1β and TNF-α), which was blocked in the presence of rivaroxaban (P<0.05). Also, in vitro experiments using rat vascular smooth muscle cells (VSMC) demonstrated that FXa promoted both proliferation and migration of this cell type (P<0.05), which were blocked in the presence of rivaroxaban. Inhibition of FXa by rivaroxaban attenuates neointima formation after wire-mediated vascular injury through inhibition of inflammatory activation of macrophages and VSMC. (Tokushima University Institutional Repository) ● Metadata: 114209 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2017.12.037 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29269019 ● Summary page in Scopus @ Elsevier: 2-s2.0-85039155853 (Tokushima University Institutional Repository: 114209, DOI: 10.1016/j.ejphar.2017.12.037, PubMed: 29269019, Elsevier: Scopus)
170.	Yukina Hirata, Hirotsugu Yamada, Kenya Kusunose, Susumu Nishio, Yuta Torii, Yuki Horike and Masataka Sata : Provocation of clinically significant left ventricular outflow tract obstruction by postural change in patients with sigmoid septum., Journal of Echocardiography, Vol.16, No.4, 173-174, 2018. (Tokushima University Institutional Repository) ● Metadata: 114210 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12574-018-0372-x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29388159 ● Summary page in Scopus @ Elsevier: 2-s2.0-85045145878 (Tokushima University Institutional Repository: 114210, DOI: 10.1007/s12574-018-0372-x, PubMed: 29388159, Elsevier: Scopus)
171.	Akira Hirono, Kenya Kusunose, Norihito Kageyama, Masayuki Sumitomo, Masahiro Abe, Hiroyuki Fujinaga and Masataka Sata : Development and validation of optimal cut-off value in inter-arm systolic blood pressure difference for prediction of cardiovascular events, Journal of Cardiology, Vol.71, No.20, 24-30, 2018. (Summary) An inter-arm systolic blood pressure difference (IAD) is associated with cardiovascular disease. The aim of this study was to develop and validate the optimal cut-off value of IAD as a predictor of major adverse cardiac events in patients with arteriosclerosis risk factors. From 2009 to 2014, 1076 patients who had at least one cardiovascular risk factor were included in the analysis. We defined 700 randomly selected patients as a development cohort to confirm that IAD was the predictor of cardiovascular events and to determine optimal cut-off value of IAD. Next, we validated outcomes in the remaining 376 patients as a validation cohort. The blood pressure (BP) of both arms measurements were done simultaneously using the ankle-brachial blood pressure index (ABI) form of automatic device. The primary endpoint was the cardiovascular event and secondary endpoint was the all-cause mortality. During a median period of 2.8 years, 143 patients reached the primary endpoint in the development cohort. In the multivariate Cox proportional hazards analysis, IAD was the strong predictor of cardiovascular events (hazard ratio: 1.03, 95% confidence interval: 1.01-1.05, p=0.005). The receiver operating characteristic curve revealed that 5mmHg was the optimal cut-off point of IAD to predict cardiovascular events (p<0.001). In the validation cohort, the presence of a large IAD (IAD ≥5mmHg) was significantly associated with the primary endpoint (p=0.021). IAD is significantly associated with future cardiovascular events in patients with arteriosclerosis risk factors. The optimal cut-off value of IAD is 5mmHg. (Keyword) Aged / Aged, 80 and over / Arm / blood pressure / Blood Pressure Determination / Cardiovascular Diseases / Female / Humans / Male / Middle Aged / Risk Factors / Systole (Tokushima University Institutional Repository) ● Metadata: 110959 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jjcc.2017.06.010 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28830651 ● Summary page in Scopus @ Elsevier: 2-s2.0-85027682866 (Tokushima University Institutional Repository: 110959, DOI: 10.1016/j.jjcc.2017.06.010, PubMed: 28830651, Elsevier: Scopus)
172.	工藤萌宏, 待井典剛, 小野利夫, 大城義人, 高橋隆, 種田嘉信, 比嘉盛丈, Shusuke Yagi, 仲地健, 小林淳, 及川雅啓, Hirotsugu Yamada, 竹石恭知, Masataka Sata and Michio Shimabukuro : 時効型インスリン療法中の2型糖尿病患者におけるダパグリフロジンの血糖日内変動に及ぼす効果, Journal of Japan Society for the Study of Obesity, Vol.24, No.Suppl, 222, 2018.
173.	Kiyoshi Hibi, Shinjo Sonoda, Masanori Kawasaki, Yutaka Otsuji, Toyoaki Murohara, Hideki Ishii, Katsuhiko Sato, Ryoji Koshida, Yukio Ozaki, Masataka Sata, Yoshihiro Morino, Tadashi Miyamoto, Tetsuya Amano, Satoshi Morita, Ken Kozuma, Kazuo Kimura and Hisayoshi Fujiwara : Effects of Ezetimibe-Statin Combination Therapy on Coronary Atherosclerosis in Acute Coronary Syndrome., Circulation Journal, Vol.82, No.3, 757-766, 2017. (Summary) The results of previous clinical trials on the effects of ezetimibe-statin combination therapy on atherosclerosis are inconsistent, and the anti-atherosclerotic effect of ezetimibe remains controversial.Methods and Results:We conducted a prospective, randomized open-label study at 10 centers. One hundred and twenty-eight statin-naïve patients with acute coronary syndrome (ACS) undergoing intravascular ultrasound (IVUS)-guided percutaneous coronary intervention were randomized to receive either 2 mg/day pitavastatin plus 10 mg/day ezetimibe, or 2 mg/day pitavastatin. One hundred and 3 patients had evaluable IVUS of non-culprit coronary lesions at baseline and at follow-up. The primary endpoint was the percentage change in non-culprit coronary plaque volume (PV) and lipid PV on integrated backscatter IVUS. Mean low-density lipoprotein cholesterol was reduced from 123 mg/dL to 64 mg/dL in the combination therapy group (n=50) and 126 mg/dL to 87 mg/dL in the statin alone group (n=53; between-group difference, 16.9%, P<0.0001). The percent change in PV was -5.1% in the combination therapy group and -6.2% in the statin alone group (P=0.66), although both groups had reduction of PV compared with baseline (both P<0.01). The percent change in lipid PV did not differ between the groups (4.3 vs. -3.0%, P=0.37). In statin-naïve patients with ACS, combined therapy with ezetimibe and statin did not result in a significant change in coronary plaque regression or tissue component compared with statin alone. [Clinical Trial Registration: www.clinicaltrials.gov (NCT00549926)]. (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-17-0598 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29212965 ● Summary page in Scopus @ Elsevier: 2-s2.0-85042510747 (DOI: 10.1253/circj.CJ-17-0598, PubMed: 29212965, Elsevier: Scopus)
174.	Tomoya Kinouchi, Keiko T. Kitazato, Kenji Shimada, Kenji Yagi, Yoshiteru Tada, Nobuhisa Matsushita, Yoshitaka Kurashiki, Junichiro Satomi, Masataka Sata and Shinji Nagahiro : Correction to: Treatment with the PPARγ Agonist Pioglitazone in the Early Post-ischemia Phase Inhibits Pro-inflammatory Responses and Promotes Neurogenesis Via the Activation of Innate- and Bone Marrow-Derived Stem Cells in Rats., Translational Stroke Research, Vol.9, No.3, 317, 2017. (Summary) In the original publication of the article, the second author (Keiko T. Kitazato) was missing. (Link to Publication Site) ● Publication site (DOI): 10.1007/s12975-017-0589-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29177991 ● Summary page in Scopus @ Elsevier: 2-s2.0-85035015467 (DOI: 10.1007/s12975-017-0589-4, PubMed: 29177991, Elsevier: Scopus)
175.	Tatsuya Maruhashi, Junko Soga, Noritaka Fujimura, Naomi Idei, Shinsuke Mikami, Yumiko Iwamoto, Akimichi Iwamoto, Masato Kajikawa, Takeshi Matsumoto, Nozomu Oda, Shinji Kishimoto, Shogo Matsui, Haruki Hashimoto, Yoshiki Aibara, Farina Mohamad Yusoff, Takayuki Hidaka, Yasuki Kihara, Kazuaki Chayama, Kensuke Noma, Ayumu Nakashima, Chikara Goto, Hirofumi Tomiyama, Bonpei Takase, Takahide Kohro, Toru Suzuki, Tomoko Ishizu, Shinichiro Ueda, Tsutomu Yamazaki, Tomoo Furumoto, Kazuomi Kario, Teruo Inoue, Shinji Koba, Kentaro Watanabe, Yasuhiko Takemoto, Takuzo Hano, Masataka Sata, Yutaka Ishibashi, Koichi Node, Koji Maemura, Yusuke Ohya, Taiji Furukawa, Hiroshi Ito, Hisao Ikeda, Akira Yamashina and Yukihito Higashi : Brachial artery diameter as a marker for cardiovascular risk assessment: FMD-J study., Atherosclerosis, Vol.268, 92-98, 2017. (Summary) Baseline brachial artery (BBA) diameter has been reported to be a potential confounding factor of flow-mediated vasodilation (FMD). The purpose of this study was to evaluate the relationships between BBA diameter and cardiovascular risk factors and compare the diagnostic accuracy of BBA diameter in subjects without cardiovascular risk factors and patients with cardiovascular disease (CVD) with that of FMD. We measured BBA diameter and FMD in 5695 male subjects. In addition, we retrospectively investigated the incidence of cardiovascular events using another population sample consisting of 440 male subjects, to compare the accuracy of BBA diameter with that of FMD in predicting cardiovascular events. BBA diameter and FMD significantly correlated with age, body mass index, systolic blood pressure, diastolic blood pressure, triglycerides, high-density lipoprotein cholesterol, and glucose as well as Framingham risk score. The prevalence of cardiovascular risk factors and CVD increased with the increase in BBA diameter and FMD. Area under the curve (AUC) value of the receiver operating characteristic (ROC) curve for BBA diameter to diagnose subjects without cardiovascular risk factors (0.59 vs. 0.62, p = 0.001) or patients with CVD (0.58 vs. 0.64, p < 0.001) was significantly lower than that for FMD. In the retrospective study, the AUC value of the ROC curve for BBA diameter to predict first major cardiovascular events was significantly lower than that of FMD (0.50 vs. 0.62, p = 0.03). In men, BBA diameter was inferior to FMD for assessment of cardiovascular risk. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2017.11.022 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29195110 ● Summary page in Scopus @ Elsevier: 2-s2.0-85035801160 (DOI: 10.1016/j.atherosclerosis.2017.11.022, PubMed: 29195110, Elsevier: Scopus)
176.	Tomoya Kinouchi, Keiko T. Kitazato, Kenji Shimada, Kenji Yagi, Yoshiteru Tada, Nobuhisa Matsushita, Yoshitaka Kurashiki, Junichiro Satomi, Masataka Sata and Shinji Nagahiro : Treatment with the PPAR Agonist Pioglitazone in the Early Post-ischemia Phase Inhibits Pro-inflammatory Responses and Promotes Neurogenesis Via the Activation of Innate- and Bone Marrow-Derived Stem Cells in Rats., Translational Stroke Research, Vol.9, No.3, 306-316, 2017. (Summary) Neurogenesis is essential for a good post-stroke outcome. Exogenous stem cells are currently being tested to promote neurogenesis after stroke. Elsewhere, we demonstrated that treatment with the PPARγ agonist pioglitazone (PGZ) before cerebral ischemia induction reduced brain damage and activated survival-related genes in ovariectomized (OVX) rats. Here, we tested our hypothesis that post-ischemia treatment with PGZ inhibits brain damage and contributes to neurogenesis via activated stem cells. Bone marrow (BM) cells of 7-week-old Wistar female rats were replaced with BM cells from green fluorescent protein-transgenic (GFP) rats. Three weeks later, they were ovariectomized (OVX/GFP rats). We subjected 7-week-old Wistar male and 13-week-old OVX/GFP rats to 90-min cerebral ischemia. Male and OVX/GFP rats were divided into two groups, one was treated with PGZ (2.5 mg/kg/day) and the other served as the vehicle control (VC). In both male and OVX/GFP rats, post-ischemia treatment with PGZ reduced neurological deficits and the infarct volume. In male rats, PGZ decreased the mRNA level of IL-6 and M1-like macrophages after 24 h. In OVX/GFP rats, PGZ augmented the proliferation of resident stem cells in the subventricular zone (SVZ) and the recruitment of GFP stem cells on days 7-14. Both types of proliferated stem cells migrated from the SVZ into the peri-infarct area. There, they differentiated into mature neurons, glia, and blood vessels in association with activated Akt, MAP2, and VEGF. Post-ischemia treatment with PGZ may offer a new avenue for stroke treatment through contribution to neuroprotection and neurogenesis. (Keyword) Animals / Bone Marrow Cells / Brain Ischemia / Disease Models, Animal / Female / Male / Neural Stem Cells / Neurogenesis / Neuroprotective Agents / PPAR gamma / Pioglitazone / Rats / Rats, Wistar / Stroke / Thiazolidinediones (Tokushima University Institutional Repository) ● Metadata: 115816 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12975-017-0577-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29110250 ● Summary page in Scopus @ Elsevier: 2-s2.0-85033492212 (Tokushima University Institutional Repository: 115816, DOI: 10.1007/s12975-017-0577-8, PubMed: 29110250, Elsevier: Scopus)
177.	Hiromu Yamazaki, Shusuke Yagi, Yuta Torii, Rie Amano, Yasuyuki Oomichi, Teruaki Sangawa, Daiju Fukuda, Muneyuki Kadota, Takayuki Ise, Rie Ueno, Tomoya Hara, Kenya Kusunose, Tomomi Matsuura, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Edoxaban improves acute venous thromboembolism while preserving protein C and protein S levels, Journal of Cardiology, Vol.71, No.3, 305-309, 2017. (Summary) It is well known that warfarin inhibits the synthesis of vitamin K-dependent anticoagulants, including thrombin, protein C and S, and factor Xa, leading, paradoxically, to an initial hypercoagulable state. Edoxaban, a direct inhibitor of activated factor X is widely used for the treatment of acute venous thromboembolism (VTE). However, the effect of edoxaban on circulating coagulation factors, in patients with acute VTE, remains unknown. We enrolled 57 patients with acute VTE with/without pulmonary embolism treated with edoxaban (n=37) or warfarin (n=20) in a clinical setting. Before treatment and 2 weeks after treatment, we evaluated thrombotic burden using ultrasound or computed tomography angiography. We also evaluated thrombin generation, represented by prothrombin fragment F1+2; thrombus degradation, represented by D-dimer; and levels of anticoagulants, including protein C, protein S, and antithrombin III. Both edoxaban and warfarin treatment improved thrombotic burden and decreased prothrombin fragment F1+2, and D-dimer. Edoxaban treatment preserved protein C and protein S levels. In contrast, warfarin decreased protein C and protein S levels. Neither treatment affected antithrombin III. Edoxaban improves VTE while preserving protein C and protein S levels, thereby indicating that edoxaban improves thrombotic burden while maintaining levels of anticoagulants. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jjcc.2017.09.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29100817 ● Summary page in Scopus @ Elsevier: 2-s2.0-85032912457 (DOI: 10.1016/j.jjcc.2017.09.009, PubMed: 29100817, Elsevier: Scopus)
178.	Shusuke Yagi, Ken-ichi Aihara, Takeshi Kondo, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Daiju Fukuda, Yutaka Nakaya, Kin-Ichiro Suwaki, Takashi Takeji, Toshihiro Wada, Masdan Hotimah Salim, Saori Hama, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Takeshi Tobiume, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Munehide Matsuhisa, Michio Shimabukuro, Masashi Akaike and Masataka Sata : Predictors for the Treatment Effect of Sodium Glucose Co-transporter 2 Inhibitors in Patients with Type 2 Diabetes Mellitus., Advances in Therapy, Vol.35, No.1, 124-134, 2017. (Summary) Predictors for the effect of sodium glucose co-transporter 2 (SGLT2) inhibitors at lowering hemoglobin A1c (HbA1c) levels in type 2 diabetes mellitus patients remain unclear. We therefore aimed to elucidate these predictors in type 2 diabetes patients after 3 months of SGLT2 treatment. A total of 302 consecutive type 2 diabetes patients who had been treated with SGLT2 inhibitors as monotherapy or add-on therapy to existing antidiabetic treatments were enrolled retrospectively. After excluding 27 patients whose HbA1c levels could not be evaluated 3 months after treatment, the glucose-lowering effects of SGLT2 inhibitors were assessed in 275 patients by measuring HbA1c levels before and 3 months after treatment. The predictors for changes in HbA1c levels after 3 months of treatment were evaluated. SGLT2 inhibitor treatment for 3 months decreased HbA1c levels from 7.8 ± 1.2% to 7.4 ± 1.0% (p < 0.0001). A multiple regression analysis showed that the independent determinants for SGLT2 inhibitor treatment effect included decreased HbA1c levels after 1 month of treatment, high baseline HbA1c levels, and a high estimated glomerular filtration rate (eGFR). We show that type 2 diabetes patients who received the greatest glucose-lowering effect with SGLT2 inhibitor treatment were those with preserved renal function (high baseline eGFR) and high baseline HbA1c levels. Moreover, SGLT2 inhibitor treatment efficacy could be predicted by the patients' initial response to treatment. (Link to Publication Site) ● Publication site (DOI): 10.1007/s12325-017-0639-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29185199 ● Summary page in Scopus @ Elsevier: 2-s2.0-85035102977 (DOI: 10.1007/s12325-017-0639-z, PubMed: 29185199, Elsevier: Scopus)
179.	Shusuke Yagi, Takeshi Soeki, Ken-Ichi Aihara, Daiju Fukuda, Takayuki Ise, Muneyuki Kadota, Sachiko Bando, Tomomi Matsuura, Takeshi Tobiume, Koji Yamaguchi, Kenya Kusunose, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro, Masashi Akaike and Masataka Sata : Low Serum Levels of Eicosapentaenoic Acid and Docosahexaenoic Acid are Risk Factors for Cardiogenic Syncope in Patients with Brugada Syndrome, International Heart Journal, Vol.58, No.5, 720-723, 2017. (Summary) The n-3 polyunsaturated fatty acids (PUFAs), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have antiarrhythmic effects, possibly via modulation of the cardiac ion channels. Nevertheless, it is unknown whether low serum levels of n-3 PUFAs are risk factors for ventricular fibrillation in patients with Brugada syndrome (BrS). We retrospectively reviewed data from 62 men with BrS and evaluated their serum levels of EPA and DHA, and the risk factors for sudden cardiac death, including a history of cardiogenic syncope. Nineteen patients had a history of cardiogenic syncope, and their EPA and DHA levels were significantly lower than those of the patients without syncope. Multivariate logistic regression analysis revealed that low EPA and DHA levels were associated with the incidence of syncope. The receiver-operator characteristic curve showed the area under the curves of EPA and DHA for history of syncope were 0.84 and 0.72, respectively. In conclusion, low levels of EPA and DHA are risk factors for cardiogenic syncope in patients with BrS, which suggests that n-3 PUFAs play important roles in preventing ventricular fibrillation in BrS. (Keyword) Adult / Aged / Aged, 80 and over / Biomarkers / Brugada Syndrome / Chromatography, Gas / Docosahexaenoic Acids / Eicosapentaenoic Acid / Electrocardiography / Follow-Up Studies / Humans / Incidence / Japan / Male / Middle Aged / Prevalence / ROC Curve / Retrospective Studies / Risk Assessment / Risk Factors / Syncope / Young Adult (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.16-278 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28966307 ● CiNii @ National Institute of Informatics (CRID): 1390282680202467328 ● Summary page in Scopus @ Elsevier: 2-s2.0-85032215381 (DOI: 10.1536/ihj.16-278, PubMed: 28966307, CiNii: 1390282680202467328, Elsevier: Scopus)
180.	Yuriko Takagawa, Shusuke Yagi, Takayuki Ise, Ayumi Ishii, Koji Nishikawa, Daiju Fukuda, Kenya Kusunose, Tomomi Matsuura, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Shinsuke Katoh, Ken-ichi Aihara, Masashi Akaike and Masataka Sata : Improved Exercise Capacity After Cardiac Rehabilitation Is Associated with Reduced Visceral Fat in Patients with Chronic Heart Failure., International Heart Journal, Vol.58, No.5, 746-751, 2017. (Summary) Participation in a comprehensive cardiac rehabilitation (CR) program has been shown to reduce mortality and improve exercise capacity and symptoms in patients with chronic heart failure (CHF). Reduced exercise capacity leads to a concomitant reduction of skeletal muscle mass and accumulation of body fat. However, it is currently unknown whether CR reduces visceral adipose tissue (VAT) and/or subcutaneous abdominal adipose tissue (SAT) in patients with CHF. In addition, the body composition associated with improved exercise capacity after CR in patients with CHF has not been previously studied. Nineteen CHF patients who were categorized as NYHA functional class II or III and had received optimal medical treatment including a CR program for 5 months were enrolled in this study. The CR program significantly increased peak VO and reduced B-type natriuretic peptide. In addition, fat and body composition analysis showed reductions in the visceral fat tissue (VAT) area, subcutaneous abdominal adipose tissue (SAT) area, body weight, and total fat weight after CR. There were no changes in total water weight and total muscle weight. Single regression analysis revealed that the amelioration of reduced exercise capacity seen after CR is associated with reduced VAT area but not with SAT area or body weight. In conclusion, CR reduces VAT and improves exercise capacity in patients with CHF. This suggests that reducing VAT is important for CR to be most effective in the treatment of CHF. (Keyword) Body Composition / Cardiac Rehabilitation / Exercise Tolerance / Female / Follow-Up Studies / heart failure / Humans / Intra-Abdominal Fat / Male / Middle Aged / obesity / oxygen consumption / Prognosis / Retrospective Studies / Weight Loss (Tokushima University Institutional Repository) ● Metadata: 110111 (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.16-454 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28966316 ● Summary page in Scopus @ Elsevier: 2-s2.0-85032221042 (Tokushima University Institutional Repository: 110111, DOI: 10.1536/ihj.16-454, PubMed: 28966316, Elsevier: Scopus)
181.	Shusuke Yagi, Yukina Hirata, Takayuki Ise, Kenya Kusunose, Hirotsugu Yamada, Daiju Fukuda, Salim Masdan Hotimah, G Maimaituxun, Susumu Nishio, Yuriko Takagawa, Saori Hama, Tomomi Matsuura, Koji Yamaguchi, Takeshi Tobiume, Takeshi Soeki, Tetsuzo Wakatsuki, Ken-ichi Aihara, Masashi Akaike, Michio Shimabukuro and Masataka Sata : Canagliflozin reduces epicardial fat in patients with type 2 diabetes mellitus., Diabetology & Metabolic Syndrome, Vol.9, 78, 2017. (Summary) It is unknown whether canagliflozin, a selective sodium glucose co-transporter 2 inhibitor, reduces epicardial adipose tissue (EAT) thickness, which is associated with insulin resistance and is a risk factor for coronary artery disease. We administered 100 mg of canagliflozin for 6 months to 13 patients with type 2 diabetes mellitus. We evaluated glycemic control, visceral adipose tissue (VAT) area and subcutaneous adipose tissue (SAT) area, and skeletal muscle mass by using impedance methods, and EAT thickness by using echocardiography. Canagliflozin treatment for 6 months decreased hemoglobin A1c level from 7.1 ± 0.5% to 6.7 ± 0.6% (P < 0.05) and decreased EAT thickness from 9.3 ± 2.5 to 7.3 ± 2.0 mm (P < 0.001), along with a trend of decreasing VAT and SAT area. No association was found between any of these changes. Canagliflozin reduced EAT thickness in patients with type 2 diabetes mellitus independent of its effect on lowering blood glucose, suggesting that canagliflozin may have an effect in preventing cardiovascular events in these patients (UMIN000021327). (Tokushima University Institutional Repository) ● Metadata: 114544 (Link to Publication Site) ● Publication site (DOI): 10.1186/s13098-017-0275-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29034006 ● Summary page in Scopus @ Elsevier: 2-s2.0-85030465923 (Tokushima University Institutional Repository: 114544, DOI: 10.1186/s13098-017-0275-4, PubMed: 29034006, Elsevier: Scopus)
182.	Shusuke Yagi, Daiju Fukuda, KI Aihara, Masashi Akaike, Michio Shimabukuro and Masataka Sata : n-3 Polyunsaturated Fatty Acids: Promising Nutrients for Preventing Cardiovascular Disease., Journal of Atherosclerosis and Thrombosis, Vol.24, No.10, 999-1010, 2017. (Summary) The adoption of the Western-style diet, with decreased fish intake and lack of exercise, has increased the prevalence of cardiovascular disease (CVD) in Japan. Statin treatment has been established to reduce the risk of cardiovascular events; however, 60%-70% of these events occur despite its use. Thus, the residual risk for CVD should be identified and resolved to reduce further cardiovascular events. The serum levels of n-3 polyunsaturated fatty acids (PUFAs), including eicosapentaenoic acid and docosahexaenoic acid, are reportedly associated with an increased incidence of cardiovascular events and mortality, whereas the addition of n-3 PUFA treatment to the statin treatment decreases cardiovascular events. Similar to statins, n-3 PUFAs have pleiotropic effects in addition to lipid-modifying effects. Pre-clinical and clinical studies have shown that n-3 PUFAs prevent cardiovascular events by ameliorating endothelial function and attenuating lipid accumulation, vascular inflammation, and macrophage recruitment, thereby causing coronary plaque development and rupture. Taken together, n-3 PUFAs are comprehensively able to attenuate the atherogenic response. Therefore, n-3 PUFA intake is recommended to prevent cardiovascular events, particularly in patients with multiple cardiovascular risk factors. (Tokushima University Institutional Repository) ● Metadata: 115484 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.RV17013 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28835582 ● Summary page in Scopus @ Elsevier: 2-s2.0-85030703516 (Tokushima University Institutional Repository: 115484, DOI: 10.5551/jat.RV17013, PubMed: 28835582, Elsevier: Scopus)
183.	Kenya Kusunose, Hirotsugu Yamada, Susumu Nishio, Yuta Torii, Yukina Hirata, Hiromitsu Seno, Yoshihito Saijo, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Preload Stress Echocardiography Predicts Outcomes in Patients With Preserved Ejection FractionandLow-GradientAorticStenosis, Circulation. Cardiovascular Imaging, Vol.10, No.10, 2017. (Summary) The projected aortic valve area (AVA) at a normal transvalvular flow rate using dobutamine is helpful to determine the actual severity of aortic stenosis (AS) and to predict risk of adverse events in low-gradient AS cases with unclear surgical indication. Our study aimed to identify the independent and incremental value of preload stress echocardiography-derived AVA to predict outcomes in patients with preserved ejection fraction and low-gradient AS. We prospectively performed echocardiographic studies in 79 patients with low-gradient AS (age, 77±7 years; 30% men) with preload stress echocardiography using leg positive pressure. AVA was calculated using AVA and transvalvular flow rate at baseline and during leg positive pressure. The primary end point was the decision for aortic valve surgery or cardiac death. During a median period of 19 months, 23 patients had the decision for aortic valve surgery, and none died during follow-up. In a stepwise multivariable analysis, indexed AVA (AVAi; hazard ratio, 2.00 per 0.1 cm/m decrease; 95% confidence interval, 1.36-2.96; <0.001) was associated with the primary end point. Using a receiver operating characteristic curve analysis, the best cutoff value of AVAi for predicting cardiac events was <0.72 cm/m. By incorporating AVAi into AVAi at baseline, continuous net reclassification index for cardiac events was 0.48 (=0.04). In patients with low-gradient AS, indexed AVA derived from preload stress echocardiography can be useful to predict risk of adverse events. The present article should be considered as a proof of concept study, and we think that larger multicenter studies are warranted. (Keyword) Aged / Aged, 80 and over / Aortic Valve / Aortic Valve Stenosis / Area Under Curve / Disease Progression / Disease-Free Survival / Echocardiography, Stress / Female / Humans / Kaplan-Meier Estimate / Male / Models, Cardiovascular / Predictive Value of Tests / Prospective Studies / ROC Curve / Severity of Illness Index / Stroke Volume / Time Factors / Ventricular Function, Left (Link to Publication Site) ● Publication site (DOI): 10.1161/CIRCIMAGING.117.006690 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29021259 ● Summary page in Scopus @ Elsevier: 2-s2.0-85031850278 (DOI: 10.1161/CIRCIMAGING.117.006690, PubMed: 29021259, Elsevier: Scopus)
184.	Susumu Nishio, Kenya Kusunose, Hirotsugu Yamada, Yukina Hirata, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Echocardiographic Epicardial Adipose Tissue Thickness Is Associated with Symptomatic Coronary Vasospasm during Provocative Testing., Journal of the American Society of Echocardiography, Vol.30, No.10, 1021-1027, 2017. (Summary) Epicardial adipose tissue (EAT) is the ectopic visceral fat surrounding the heart, which plays an important role in atherosclerosis of the coronary arteries via endothelial damage. Several studies have also suggested that vasospasm with angina (VSA) causes endothelial dysfunction in the coronary arteries. The aim of this study was to evaluate the thickness of EAT in the anterior interventricular groove (EAT-AIG) using echocardiography in patients who had no obstructive coronary artery disease and were suspected of having VSA. Sixty-five patients who underwent intracoronary acetylcholine provocation testing for clinical indications were prospectively enrolled. VSA was diagnosed by coronary artery stenosis increase of >90% and the presentation of chest pain with ischemic changes on electrocardiography. Subjects were divided into two groups, with and without significant coronary spasm (VSA group, 30 patients; non-VSA group, 35 patients), consistent with acetylcholine provocation testing. EAT-AIG thickness was significantly greater in the VSA group than in the non-VSA group (8.2 2.7 vs 6.1 2.5 mm, P = .002). By receiver operating characteristic analysis, EAT-AIG thickness had a high C statistic (area under the curve = 0.81, P < .001) after adjustment for conventional risk factors (smoking, diabetes mellitus, and dyslipidemia). EAT-AIG thickness had incremental diagnostic value over other conventional risk factors (area under the curve = 0.81 vs 0.64, P for comparison = .020). EAT-AIG thickness, which is noninvasively and easily measured using transthoracic echocardiography, can be one of multiple clinical variables associated with VSA. (Tokushima University Institutional Repository) ● Metadata: 110928 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.echo.2017.06.024 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28843368 ● Search Scopus @ Elsevier (PMID): 28843368 ● Search Scopus @ Elsevier (DOI): 10.1016/j.echo.2017.06.024 (Tokushima University Institutional Repository: 110928, DOI: 10.1016/j.echo.2017.06.024, PubMed: 28843368)
185.	Tatsuya Maruhashi, Junko Soga, Noritaka Fujimura, Naomi Idei, Shinsuke Mikami, Yumiko Iwamoto, Akimichi Iwamoto, Masato Kajikawa, Takeshi Matsumoto, Nozomu Oda, Shinji Kishimoto, Shogo Matsui, Haruki Hashimoto, Yoshiki Aibara, Farina Binti Mohamad Yusoff, Takayuki Hidaka, Yasuki Kihara, Kazuaki Chayama, Kensuke Noma, Ayumu Nakashima, Chikara Goto, Hirofumi Tomiyama, Bonpei Takase, Takahide Kohro, Toru Suzuki, Tomoko Ishizu, Shinichiro Ueda, Tsutomu Yamazaki, Tomoo Furumoto, Kazuomi Kario, Teruo Inoue, Shinji Koba, Kentaro Watanabe, Yasuhiko Takemoto, Takuzo Hano, Masataka Sata, Yutaka Ishibashi, Koichi Node, Koji Maemura, Yusuke Ohya, Taiji Furukawa, Hiroshi Ito, Hisao Ikeda, Akira Yamashina and Yukihito Higashi : Endothelial Function Is Impaired in Patients Receiving Antihypertensive Drug Treatment Regardless of Blood Pressure Level: FMD-J Study (Flow-Mediated Dilation Japan), Hypertension, Vol.70, No.4, 790-797, 2017. (Summary) Hypertension is associated with endothelial dysfunction. Blood pressure significantly correlates with endothelial function in antihypertensive drug-naive subjects. The purpose of this study was to determine whether treatment status affects the relationship between blood pressure and endothelial function. We measured flow-mediated vasodilation (FMD) in 2297 subjects, including 1822 antihypertensive drug-naive subjects and 475 treated hypertensive patients. FMD significantly decreased in relation to increase in systolic blood pressure (8.2±3.1% in subjects with systolic blood pressure of <120 mm Hg, 7.5±2.8% for 120-129 mm Hg, 7.1±2.8% for 130-139 mm Hg, and 6.7±2.6% for ≥140 mm Hg; <0.001). Systolic blood pressure was independently associated with FMD in untreated subjects. In contrast, there was no significant relationship between systolic blood pressure and FMD in treated hypertensive patients (4.6±3.1% in treated hypertensives with systolic blood pressure of <120 mm Hg, 4.8±2.7% for 120-129 mm Hg, 4.9±2.8% for 130-139 mm Hg, and 4.5±2.3% for ≥140 mm Hg; =0.77). Propensity score matching analysis revealed that the prevalence of endothelial dysfunction defined as FMD of less than the division point for the lowest tertile, and the middle tertile of FMD was significantly higher in treated hypertensive patients than in untreated subjects in all systolic blood pressure categories. Endothelial function assessed by FMD was impaired regardless of the level of blood pressure achieved by antihypertensive drug treatment in hypertensive patients. (Keyword) Adult / Aged / Antihypertensive Agents / blood pressure / Blood Pressure Determination / Endothelium, Vascular / female / Humans / hypertension / Japan / male / Medication Therapy Management / Middle Aged / Vasodilation (Link to Publication Site) ● Publication site (DOI): 10.1161/HYPERTENSIONAHA.117.09612 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28808069 ● Summary page in Scopus @ Elsevier: 2-s2.0-85030614940 (DOI: 10.1161/HYPERTENSIONAHA.117.09612, PubMed: 28808069, Elsevier: Scopus)
186.	Yukina Hirata, Kenya Kusunose, Hirotsugu Yamada, Rikuto Shimizu, Yuta Torii, Susumu Nishio, Yoshihito Saijo, Shoichiro Takao, Takeshi Soeki and Masataka Sata : Age-related changes in morphology of left atrial appendage in patients with atrial fibrillation., The International Journal of Cardiovascular Imaging, Vol.34, No.2, 321-328, 2017. (Summary) The purpose of this study was to evaluate the relationship between age and frequency of left atrial appendage (LAA) morphology in patients with atrial fibrillation (AF) compared with sinus rhythm (SR). We enrolled 145 AF patients, and 199 SR patients for the control group without any cardiovascular disease. LAA volume index (LAAVi) and morphology were assessed by electrocardiogram-gated computed tomography angiography. LAA morphology was classified into "chicken wing" or "non-chicken wing" according to the previously described classification. There was no significant trend in frequency of non-chicken wing morphology among ages in the SR group (p = 0.36 for trend), whereas the frequency was negatively related to age in the AF group (p = 0.002 for trend). In multivariable logistic regression, age > 65 (odds ratio [OR] 0.42, p = 0.002) and duration of AF (OR 0.53, p = 0.010) and LAAVi (OR 0.62, p = 0.017) were independent factors of non-chicken wing LAA morphology in the AF group. LAA morphology is affected by age, especially in patients with AF. When we utilize non-chicken wing LAA morphology as a stroke risk factor in patients with AF, we should pay attention to their age. (Link to Publication Site) ● Publication site (DOI): 10.1007/s10554-017-1232-x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28808846 ● Search Scopus @ Elsevier (PMID): 28808846 ● Search Scopus @ Elsevier (DOI): 10.1007/s10554-017-1232-x (DOI: 10.1007/s10554-017-1232-x, PubMed: 28808846)
187.	Masanori Asakura, Jiyoong Kim, Hiroshi Asanuma, Toshimitsu Hamasaki, Kengo Tsukahara, Yorihiko Higashino, Tetsuya Ishikawa, Yasuharu Nakama, Shinji Koba, Yasuyuki Maruyama, Mitsuru Tsujimoto, Hideo Himeno, Takanori Ohkusa, Susumu Fujino, Makoto Shimizu, Tsutomu Endo, Shunichi Yoda, Takahiro Muroya, Toyoaki Murohara, Nobuyuki Ohte, Hiroshi Suzuki, Tohru Kohno, Kazuki Fukui, Takaaki Shiono, Hiroyuki Takase, Hiroyasu Uzui, Yoshiyuki Nagai, Yuji Hashimoto, Shuntaro Ikeda, Sumio Mizuno, Koichi Tamita, Masashi Fujita, Kazuo Satake, Yoshihiko Kinoshita, Tatsuya Nunohiro, Satoru Sakagami, Jitsuo Higaki, Isao Morii, Reimin Sawada, Yoshikazu Hiasa, Tomohiko Shigemasa, Makoto Nakahama, Masataka Sata, Osamu Doi, Tetsuro Ueda, Takahisa Yamada, Takayoshi Yamanouchi, Hajime Yamaguchi, Yukiko Morita, Hideki Hayashi and Masafumi Kitakaze : Does Treatment of Impaired Glucose Tolerance Improve Cardiovascular Outcomes in Patients with Previous Myocardial Infarction?, Cardiovascular Drugs and Therapy, Vol.31, No.4, 401-411, 2017. (Summary) We evaluated the effects of an alpha-glucosidase inhibitor, voglibose, on cardiovascular events in patients with a previous myocardial infarction (MI) and impaired glucose tolerance (IGT). This prospective, randomized, open, blinded-endpoint study was conducted in 112 hospitals and clinics in Japan in 3000 subjects with both previous MI and IGT receiving voglibose (0.6 mg/day, n = 424) or no drugs (n = 435) for 2 years. The Data and Safety Monitoring Board (DSMB) recommended discontinuation of the study in June 2012 after an interim analysis when the outcomes of 859 subjects were obtained. The primary endpoint was cardiovascular events including cardiovascular death, nonfatal MI, nonfatal unstable angina, nonfatal stroke, and percutaneous coronary intervention/coronary artery bypass graft. Secondary endpoints included individual components of the primary endpoint in addition to all-cause mortality and hospitalization due to heart failure. The age, ratio of males, and HbA1C were 65 vs. 65 years, 86 vs. 87%, and 5.6 vs. 5.5% in the groups with and without voglibose, respectively. Voglibose improved IGT; however, Kaplan-Meier analysis showed no significant between-group difference with respect to cardiovascular events [12.5% with voglibose vs. 10.1% without voglibose for the primary endpoint (95% confidence interval, 0.82-1.86)]; there were no significant differences in secondary endpoints. Although voglibose effectively treated IGT, no additional benefits for cardiovascular events in patients with previous MI and IGT were observed. Voglibose may not be a contributing therapy to the secondary prevention in patients with MI and IGT. Clinicaltrials.gov number: NCT00212017. (Keyword) Aged / Cardiovascular Diseases / Female / Glucose Intolerance / Glycoside Hydrolase Inhibitors / Humans / Hypoglycemic Agents / Inositol / Japan / Kaplan-Meier Estimate / Male / Middle Aged / Myocardial Infarction / Prospective Studies / Secondary Prevention / Treatment Outcome (Link to Publication Site) ● Publication site (DOI): 10.1007/s10557-017-6740-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28779371 ● Summary page in Scopus @ Elsevier: 2-s2.0-85026840711 (DOI: 10.1007/s10557-017-6740-3, PubMed: 28779371, Elsevier: Scopus)
188.	Shusuke Yagi, Minoru Mitsugi, Teruaki Sanagawa, Masashi Akaike and Masataka Sata : Paget-Schroetter Syndrome in a Baseball Pitcher., International Heart Journal, Vol.58, No.4, 637-640, 2017. (Summary) Paget-Schroetter syndrome (PSS) is thrombosis of the deep veins draining the upper extremity due to anatomic abnormalities of the thoracic outlet that cause subclavian compression and subsequent thrombosis, leading to thrombus formation in the subclavian vein. Vigorous arm activity in sports is a known risk factor. Here, we report a case of Paget-Schroetter syndrome in a 31-year-old male non-professional baseball pitcher. (Keyword) Adult / Baseball / Fibrinolytic Agents / Humans / Male / Thrombolytic Therapy / Tomography, X-Ray Computed / Upper Extremity Deep Vein Thrombosis (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.16-447 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28701678 ● Summary page in Scopus @ Elsevier: 2-s2.0-85026825932 (DOI: 10.1536/ihj.16-447, PubMed: 28701678, Elsevier: Scopus)
189.	Tamio Teramoto, Akira Kondo, Arihiro Kiyosue, Mariko Harada-Shiba, Yasushi Ishigaki, Kimimasa Tobita, Yumiko Kawabata, Asuka Ozaki, Marie T. Baccara-Dinet and Masataka Sata : Efficacy and safety of alirocumab in patients with hypercholesterolemia not adequately controlled with non-statin lipid-lowering therapy or the lowest strength of statin: ODYSSEY NIPPON study design and rationale., Lipids in Health and Disease, Vol.16, No.1, 121, 2017. (Summary) Statins are generally well-tolerated and serious side effects are infrequent, but some patients experience adverse events and reduce their statin dose or discontinue treatment altogether. Alirocumab is a highly specific, fully human monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), which can produce substantial and sustained reductions of low-density lipoprotein cholesterol (LDL-C). The randomized, double-blind, placebo-controlled, parallel-group, phase 3 ODYSSEY NIPPON study will explore alirocumab 150 mg every 4 weeks (Q4W) in 163 Japanese patients with hypercholesterolemia who are on the lowest-strength dose of atorvastatin (5 mg/day) or are receiving a non-statin lipid-lowering therapy (LLT) (fenofibrate, bezafibrate, ezetimibe, or diet therapy alone). Hypercholesterolemia is defined as LDL-C ≥ 100 mg/dL (2.6 mmol/L) in patients with heterozygous familial hypercholesterolemia or non-familial hypercholesterolemia with a history of documented coronary heart disease, or ≥120 mg/dL (3.1 mmol/L) in patients with non-familial hypercholesterolemia classified as primary prevention category III (i.e. high-risk patients). During the 12-week double-blind treatment period, patients will be randomized (1:1:1) to receive alirocumab subcutaneously (SC) 150 mg Q4W alternating with placebo for alirocumab Q4W, or alirocumab 150 mg SC every 2 weeks (Q2W), or SC placebo Q2W. The primary efficacy endpoint is the percentage change in calculated LDL-C from baseline to week 12. The long-term safety and tolerability of alirocumab will also be investigated. The ODYSSEY NIPPON study will provide insights into the efficacy and safety of alirocumab 150 mg Q4W or 150 mg Q2W among Japanese patients with hypercholesterolemia who are on the lowest-strength dose of atorvastatin, or are receiving a non-statin LLT (including diet therapy alone). ClinicalTrials.gov number: NCT02584504. (Keyword) Adult / Antibodies, Monoclonal / Atorvastatin / Cholesterol, LDL / Double-Blind Method / Female / Humans / Hydroxymethylglutaryl-CoA Reductase Inhibitors / Hypercholesterolemia / Male / Proprotein Convertase 9 / Young Adult (Tokushima University Institutional Repository) ● Metadata: 114527 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12944-017-0513-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28623954 ● Summary page in Scopus @ Elsevier: 2-s2.0-85027879484 (Tokushima University Institutional Repository: 114527, DOI: 10.1186/s12944-017-0513-7, PubMed: 28623954, Elsevier: Scopus)
190.	Kenya Kusunose, Hirotsugu Yamada, Susumu Nishio, Yukina Hirata, Hiromitsu Seno, Y Saijo, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Echocardiographic Predictors for Worsening of Six-Minute Walk Distances in Patients With Systemic Sclerosis (Scleroderma), The American Journal of Cardiology, Vol.120, No.2, 315-321, 2017. (Summary) Change in 6-minute walk distance (6MWD) has been used as a clinical marker in pulmonary hypertension. Determinants and worsening of 6MWD remain a matter of debate because nonpulmonary factors have an impact on the 6MWD. We hypothesized that future reduction of 6MWD in patients with systemic sclerosis (SSc) was more closely associated with cardiac dysfunction. We prospectively performed standard clinical and echocardiographic evaluations in SSc patients with the 6-minute walk test at enrollment. Features associated with the 6MWD were sought in a multiple linear regression analysis and compared using standardized . Worsening of the 6MWD was defined as a 15% reduction and served as the primary outcome. Eighty-one patients were included. In the multivariate analysis, baseline 6MWD was related to SSc severity score ( = -0.250, p = 0.024), left atrial volume index ( = -0.222, p = 0.046), right ventricular fractional area change ( = 0.252, p = 0.025), and the ratio of mean pulmonary artery pressure and cardiac output ( = -0.31, p = 0.002). During follow-up, 20 patients reached the primary outcome. In sequential Cox models, a model based on right ventricular fractional area change at baseline (chi-square 4.8) was improved by left atrial volume index (chi-square 10.3, p = 0.007). In conclusion, determinants and worsening of 6MWD are explained by cardiac factors. When using the 6MWD as a clinical marker in pulmonary hypertension patients, their left ventricular diastolic function and right ventricular systolic function should be taken into consideration. (Keyword) Diastole / Disease Progression / Echocardiography, Doppler / Female / Follow-Up Studies / Humans / Hypertension, Pulmonary / Male / Middle Aged / Predictive Value of Tests / Prospective Studies / Scleroderma, Systemic / Stroke Volume / Systole / Time Factors / Ventricular Function, Left / Ventricular Function, Right / Walking (Link to Publication Site) ● Publication site (DOI): 10.1016/j.amjcard.2017.04.024 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28532772 ● Search Scopus @ Elsevier (PMID): 28532772 ● Search Scopus @ Elsevier (DOI): 10.1016/j.amjcard.2017.04.024 (DOI: 10.1016/j.amjcard.2017.04.024, PubMed: 28532772)
191.	Kenya Kusunose, Hirotsugu Yamada, Susumu Nishio, Ayumi Ishii, Yukina Hirata, Hiromitsu Seno, Yoshihito Saijo, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : RV Myocardial Strain During Pre-Load Augmentation Is Associated With Exercise Capacity in Patients With Chronic HF, JACC. Cardiovascular Imaging, Vol.10, No.10, 1240-1249, 2017. (Summary) The aim of this study was to assess the relationship between right ventricular (RV) function during pre-load augmentation and exercise tolerance. Peak oxygen uptake (VO2) is a strong predictor of mortality in chronic heart failure. Cardiac function during pre-load augmentation is an important part of the phenomenon in the evaluation of exercise capacity. We prospectively performed echocardiographic studies in 68 chronic heart failure patients with cardiopulmonary exercise testing (mean age 60 ± 12 years; 69% male). After resting evaluations, echocardiographic parameters were repeated during leg positive pressure (LPP). Exercise capacity was assessed by peak VO2 in all patients (left ventricular ejection fraction: 43 ± 15%). Patients with severely reduced exercise capacity (peak VO2 <14 ml/kg/min) had significantly lower stroke volume index, left ventricular global longitudinal strain and RV strain and higher filling pressure (E/e' and pulmonary arterial systolic pressure) than the remainder. Stroke volume index ( = 0.49), global longitudinal strain ( = -0.61), E/e' ( = -0.32), pulmonary arterial systolic pressure ( = -0.57), and RV strain ( = -0.66) during LPP were independently correlated to peak VO2 (all p < 0.01). RV strain during LPP was the most powerful predictor in identifying patients with severely reduced exercise capacity (cut off value: -17%; sensitivity: 81%; specificity: 88%; areas under the curve: 0.88; p < 0.001) compared with other variables including resting parameters. RV strain during pre-load augmentation correlated independently to peak VO2 and was a powerful predictor in identifying patients with severely reduced exercise capacity. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jcmg.2017.03.022 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28734918 ● Summary page in Scopus @ Elsevier: 2-s2.0-85025467938 (DOI: 10.1016/j.jcmg.2017.03.022, PubMed: 28734918, Elsevier: Scopus)
192.	Akihiro Tokushige, Shinichiro Ueda, Hirofumi Tomiyama, Mituru Ohishi, Takahide Kohro, Yukihito Higashi, Bonpei Takase, Toru Suzuki, Tomoko Ishizu, Tsutomu Yamazaki, Tomoo Furumoto, Kazuomi Kario, Teruo Inoue, Shinji Koba, Yasuhiko Takemoto, Takuzo Hano, Masataka Sata, Yutaka Ishibashi, Koichi Node, Koji Maemura, Yusuke Ohya, Taiji Furukawa, Hiroshi Ito and Akira Yamashina : Association Between Waist-to-Height Ratio and Endothelial Dysfunction in Patients With Morbidity A Report From the FMD-J Study, Circulation Journal, Vol.81, No.12, 1911-1918, 2017. (Summary) Waist circumference (WC), waist-to-height ratio (WHtR) and body mass index (BMI) are known as easy anthropometric markers of abnormal obesity and screening tools for predicting cardiovascular outcomes, but which indices are best is unclear. We therefore investigated the superiority and association between each index and low flow-mediated dilatation (FMD) as a surrogate marker for cardiovascular outcomes in patients with morbidity in a large Japanese prospective cohort.Methods and Results:A total of 1,645 Japanese patients who had coronary artery disease and hypertension or diabetes mellitus were enrolled, and 1,087 of them were analyzed. The high-WHtR group (≥0.5) showed greater morbidity and increased inflammation in association with atherosclerosis compared with the low-WHtR group. High WHtR and advanced age were identified as predictors of low FMD (odds ratio (OR) 1.39, 95% confidence interval (CI) 1.02-1.88, P=0.037 and OR 1.55, 95% CI 1.19-2.01, P=0.001, respectively). However, WC was not associated with that risk in either sex (male: OR 1.37, 95% CI 0.97-1.93, P=0.076; female: OR 1.08, 95% CI 0.68-1.73, P=0.74), and no association was evident between high BMI and low FMD (OR 0.92, 95% CI 0.71-1.19, P=0.54). WHtR offers a superior predictor of decreased FMD than other anthropometric indices, and progression of arteriosclerosis might be detected more sensitively. Further study is needed to investigate the relationship between cardiovascular mortality and WHtR. (Keyword) Aged / Asian Continental Ancestry Group / atherosclerosis / Dilatation / Disease Progression / Endothelium / Female / Humans / Male / Middle Aged / Morbidity / Prospective Studies / Waist-Height Ratio (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-17-0211 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28690284 ● Summary page in Scopus @ Elsevier: 2-s2.0-85035216086 (DOI: 10.1253/circj.CJ-17-0211, PubMed: 28690284, Elsevier: Scopus)
193.	Michio Shimabukuro, Atsushi Tanaka, Masataka Sata, Kazuoki Dai, Yoshisato Sibata, Yohei Inoue, Hiroki Ikenaga, Shinji Kishimoto, Kozue Ogasawara, Akira Takashima, Toshiyuki Niki, Osamu Arasaki, Koichi Oshiro, Yutaka Mori, Masaharu Ishihara and Koichi Nobe : α-Glucosidase inhibitor miglitol attenuates glucose fluctuation, heart rate variability and sympathetic activity in patients with type 2 diabetes and acute coronary syndrome: a multicenter randomized controlled (MACS) study., Cardiovascular Diabetology, Vol.16, No.1, 86, 2017. (Summary) Little is known about clinical associations between glucose fluctuations including hypoglycemia, heart rate variability (HRV), and the activity of the sympathetic nervous system (SNS) in patients with acute phase of acute coronary syndrome (ACS). This pilot study aimed to evaluate the short-term effects of glucose fluctuations on HRV and SNS activity in type 2 diabetes mellitus (T2DM) patients with recent ACS. We also examined the effect of suppressing glucose fluctuations with miglitol on these variables. This prospective, randomized, open-label, blinded-endpoint, multicenter, parallel-group comparative study included 39 T2DM patients with recent ACS, who were randomly assigned to either a miglitol group (n = 19) or a control group (n = 20). After initial 24-h Holter electrocardiogram (ECG) (Day 1), miglitol was commenced and another 24-h Holter ECG (Day 2) was recorded. In addition, continuous glucose monitoring (CGM) was performed throughout the Holter ECG. Although frequent episodes of subclinical hypoglycemia (≤4.44 mmo/L) during CGM were observed on Day 1 in the both groups (35% of patients in the control group and 31% in the miglitol group), glucose fluctuations were decreased and the minimum glucose level was increased with substantial reduction in the episodes of subclinical hypoglycemia to 7.7% in the miglitol group on Day 2. Holter ECG showed that the mean and maximum heart rate and mean LF/HF were increased on Day 2 in the control group, and these increases were attenuated by miglitol. When divided 24-h time periods into day-time (0700-1800 h), night-time (1800-0000 h), and bed-time (0000-0700 h), we found increased SNS activity during day-time, increased maximum heart rate during night-time, and glucose fluctuations during bed-time, which were attenuated by miglitol treatment. In T2DM patients with recent ACS, glucose fluctuations with subclinical hypoglycemia were associated with alterations of HRV and SNS activity, which were mitigated by miglitol, suggesting that these pathological relationships may be a residual therapeutic target in such patients. Trial registration Unique Trial Number, UMIN000005874 ( https://upload.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000006929 ). (Keyword) 1-Deoxynojirimycin / Acute Coronary Syndrome / Adult / Aged / Blood Glucose / Diabetes Mellitus, Type 2 / Female / glucose / Glycoside Hydrolase Inhibitors / Heart Rate / Humans / Hypoglycemic Agents / Male / Middle Aged / Treatment Outcome (Tokushima University Institutional Repository) ● Metadata: 114510 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12933-017-0571-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28683829 ● Summary page in Scopus @ Elsevier: 2-s2.0-85022075532 (Tokushima University Institutional Repository: 114510, DOI: 10.1186/s12933-017-0571-1, PubMed: 28683829, Elsevier: Scopus)
194.	Akira Takashima, Tatsuro Ogata, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Intracardiac echocardiography-guided biopsy of a lipomatous cardiac tumor arising from the interatrial septum., Circulation Journal, Vol.81, No.10, 1553-1555, 2017. (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-17-0138 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28367861 ● Summary page in Scopus @ Elsevier: 2-s2.0-85030104785 (DOI: 10.1253/circj.CJ-17-0138, PubMed: 28367861, Elsevier: Scopus)
195.	Maimaituxun Gulinu, Michio Shimabukuro, Hotimah Masdan Salim, Minoru Tabata, Daisuke Yuji, Yoshihisa Morimoto, Takeshi Akasaka, Tomomi Matsuura, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Takaki Sugimoto, Masashi Tanaka, Shuichiro Takanashi and Masataka Sata : Gender-linked impact of epicardial adipose tissue volume in patients who underwent coronary artery bypass graft surgery or non-coronary valve surgery, PLoS ONE, Vol.12, No.6, e0177170, 2017. (Summary) Traditional and non-traditional risk factors for atherosclerotic cardiovascular disease (ASCVD) are different between men and women. Gender-linked impact of epicardial adipose tissue volume (EATV) in patients undergoing coronary artery bypass grafting (CABG) remains unknown. Gender-linked impact of EATV, abdominal fat distribution and other traditional ASCVD risk factors were compared in 172 patients (men: 115; women: 57) who underwent CABG or non-coronary valvular surgery (non-CABG). In men, EATV, EATV index (EATV/body surface area) and the markers of adiposity such as body mass index, waist circumference and visceral fat area were higher in the CABG group than in the non-CABG group. Traditional ASCVD risk factors were also prevalent in the CABG group. In women, EATV and EATV index were higher in the CABG group, but other adiposity markers were comparable between CABG and non-CABG groups. Multivariate logistic regression analysis showed that in men, CABG was determined by EATV Index and other ASCVD risk factors including hypertension, dyslipidemia, adiponectin, high sensitive C-reactive protein (hsCRP) and type 2 diabetes mellitus (Corrected R2 = 0.262, p < 0.0001), while in women, type 2 diabetes mellitus is a single strong predictor for CABG, excluding EATV Index (Corrected R2 = 0.266, p = 0.005). Our study found that multiple risk factors, including epicardial adipose tissue volume and traditional ASCVD factors are determinants for CABG in men, but type 2 diabetes mellitus was the sole determinant in women. Gender-specific disparities in risk factors of CABG prompt us to evaluate new diagnostic and treatment strategies and to seek underlying mechanisms. (Tokushima University Institutional Repository) ● Metadata: 112321 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0177170 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28594865 ● Summary page in Scopus @ Elsevier: 2-s2.0-85020391442 (Tokushima University Institutional Repository: 112321, DOI: 10.1371/journal.pone.0177170, PubMed: 28594865, Elsevier: Scopus)
196.	S Bando, Takeshi Soeki, Tomomi Matsuura, Takeshi Tobiume, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro, Naoki Muguruma, Tetsuji Takayama, I Kishimoto, Kenji Kangawa and Masataka Sata : Plasma brain natriuretic peptide levels are elevated in patients with cancer, PLoS ONE, Vol.12, No.6, e0178607, 2017. (Summary) Natriuretic peptides have been proposed as biomarkers of cardiovascular disease, especially heart failure. Brain natriuretic peptide (BNP) has also been shown to be upregulated at the transcriptional and translational levels by pro-inflammatory cytokines in cardiac myocytes. Although we often measure plasma BNP levels in cancer patients, it remains unknown whether cancer-related inflammation affects the plasma BNP levels. We investigated the relationship between the BNP and human cancers. We retrospectively studied 2,923 patients in whom the plasma BNP levels and serum C-reactive protein (CRP) were measured and echocardiography was performed. Patients with clinically evident heart failure (NYHA II or higher), heart disease requiring medical treatment or surgery, renal dysfunction, and inflammatory disease were excluded. There were 234 patients in the final analysis. Blood sampling was performed before surgery and chemotherapy. In addition, we evaluated the relationship between the inflammation and plasma BNP levels in mouse models of colon cancer. Of the 234 patients, 80 were diagnosed with cancer. Both the plasma BNP and serum CRP levels were significantly higher in cancer patients than those without. There were no significant differences in the echocardiographic parameters. There was a significant positive correlation between the plasma BNP and serum CRP levels in cancer patients (r = 0.360, P<0.01) but not in those without. In cancer patients, only the CRP correlated with the BNP independent of the age, creatinine level, hypertension, and body mass index. In addition, in nude mice with subcutaneous colon cancer, the plasma BNP level was elevated compared with that in non-cancer mice, and there was a significant relationship between the plasma BNP and serum levels of the inflammatory markers. In cancer patients, as well as colon cancer model mice, the plasma BNP levels were elevated, possibly due to cancer-related inflammation. The effect of cancer on the BNP levels should be considered when using BNP as an indicator of heart failure in cancer patients. (Tokushima University Institutional Repository) ● Metadata: 112318 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0178607 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28570595 ● Search Scopus @ Elsevier (PMID): 28570595 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0178607 (Tokushima University Institutional Repository: 112318, DOI: 10.1371/journal.pone.0178607, PubMed: 28570595)
197.	Salim Masdan Hotimah, Daiju Fukuda, Yasutomi Higashikuni, Kimie Tanaka, Yoichiro Hirata, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Teneligliptin, a dipeptidyl peptidase-4 inhibitor, attenuated pro-inflammatory phenotype of perivascular adipose tissue and inhibited atherogenesis in normoglycemic apolipoprotein-E-deficient mice., Vascular Pharmacology, Vol.96-98, No.16, 19-25, 2017. (Summary) Dipeptidyl peptidase-4 (DPP-4) inhibitors have various cellular effects that are associated with vascular protection. Here, we examined whether teneligliptin alters the pro-inflammatory phenotype of perivascular adipose tissue (PVAT) and inhibits atherogenesis. Teneligliptin (60mg/kg/day) was administered orally to apolipoprotein-E-deficient (ApoE(-/-)) mice for 20weeks. Teneligliptin significantly inhibited the development of atherosclerosis in the aortic arch compared with vehicle (P<0.05), without alteration of blood glucose level or blood pressure. Histological analyses demonstrated that teneligliptin decreased lipid deposition and MCP-1 expression (P<0.05, respectively), and tended to decrease macrophage accumulation in atherosclerotic plaques. The results of quantitative RT-PCR analysis demonstrated that teneligliptin reduced the expression of inflammatory molecules such as TNF- and MCP-1 in the abdominal aorta. Furthermore, teneligliptin reduced the expression of a macrophage marker and Nox-4, a major NADPH oxidase subunit in adipocytes, in PVAT around the aortic arch. Administration of teneligliptin for 8weeks ameliorated endothelium-dependent vasodilation and reduced oxidative stress as determined by urinary 8-OHdG excretion (P<0.05) compared with vehicle. In vitro experiments demonstrated that exendin-4 (Ex-4), a GLP-1 analog, decreased the expression of inflammatory molecules in RAW264.7 cells. Also, Ex-4 decreased Nox4 expression in 3T3-L1 adipocytes. Teneligliptin inhibited atherogenesis with attenuation of the inflammatory phenotype in PVAT. A GLP-1 analog suppressed pro-inflammatory activation of macrophages and adipocytes. Suppression of the pro-inflammatory phenotype of PVAT might contribute, at least partially, to the cardioprotective effects of teneligliptin. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.vph.2017.03.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28347868 ● Summary page in Scopus @ Elsevier: 2-s2.0-85016431523 (DOI: 10.1016/j.vph.2017.03.003, PubMed: 28347868, Elsevier: Scopus)
198.	Hirotsugu Yamada, Atsushi Tanaka, Kenya Kusunose, Rie Amano, Munehide Matsuhisa, Hiroyuki Daida, Masaaki Ito, Hiroyuki Tsutsui, Mamoru Nanasato, Haruo Kamiya, K Yasuko Bando, Masato Odawara, Hisako Yoshida, Toyoaki Murohara, Masataka Sata and Koichi Node : Effect of sitagliptin on the echocardiographic parameters of left ventricular diastolic function in patients with type 2 diabetes: a subgroup analysis of the PROLOGUE study., Cardiovascular Diabetology, Vol.16, No.1, 63, 2017. (Summary) Diabetes is associated closely with an increased risk of cardiovascular events, including diastolic dysfunction and heart failure that leads to a shortening of life expectancy. It is therefore extremely valuable to evaluate the impact of antidiabetic agents on cardiac function. However, the influence of dipeptidyl peptidase 4 inhibitors on cardiac function is controversial and a major matter of clinical concern. We therefore evaluated the effect of sitagliptin on echocardiographic parameters of diastolic function in patients with type 2 diabetes as a sub-analysis of the PROLOGUE study. (Tokushima University Institutional Repository) ● Metadata: 114509 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12933-017-0546-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28490337 ● Search Scopus @ Elsevier (PMID): 28490337 ● Search Scopus @ Elsevier (DOI): 10.1186/s12933-017-0546-2 (Tokushima University Institutional Repository: 114509, DOI: 10.1186/s12933-017-0546-2, PubMed: 28490337)
199.	Yutaka Nakaya, Daiju Fukuda, Takashi Oyamada, Kazuo Ogawa, Nagakatsu Harada, Hironori Nakagami, Ryuichi Morishita, Masataka Sata and Hiroshi Sakaue : A novel lipoprotein (a) lowering drug, D-47, decreases neointima thickening after vascular injury., The Journal of Medical Investigation : JMI, Vol.64, No.1, 2, 64-67, 2017. (Summary) Although Lp(a) have been thought to be a cardiovascular risk factor, it is unclear whether lowering Lp(a) levels reduces the risk of cardiovascular diseases. No pharmacological agents which selectively reduce serum Lp(a) levels, and Lp(a) is present in primate but absent in common laboratory animals such as mice and pigs. In the present study we used transgenic mice of human Lp(a) and tested effect a novel Lp(a) lowering drug D-47 on neointima formation after vascular injury. D-47 successfully decreased plasma levels of Lp(a) and possibly inhibited neointima formation in Lp(a) transgenic mice. The results indicate that we can modulate plasma Lp(a) levels by pharmacologic agents and inhibit atherogenic properties of Lp(a) by reducing plasma levels of Lp(a). J. Med. Invest. 64: 64-67, February, 2017. (Keyword) lipoprotein a / atherosclerosis / cardiovascular events / low density lipoprotein (Tokushima University Institutional Repository) ● Metadata: 111083 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.64.64 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28373630 ● Search Scopus @ Elsevier (PMID): 28373630 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.64.64 (Tokushima University Institutional Repository: 111083, DOI: 10.2152/jmi.64.64, PubMed: 28373630)
200.	Kenya Kusunose, Yuta Torii, Hirotsugu Yamada, Susumu Nishio, Yukina Hirata, Hiromitsu Seno, Yoshihito Saijo, Takayuki Ise, Koji Yamaguchi, Takeshi Tobiume, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Clinical Utility of Longitudinal Strain to Predict Functional Recovery in Patients With Tachyarrhythmia and Reduced LVEF., JACC. Cardiovascular Imaging, Vol.10, No.2, 118-126, 2017. (Summary) Objectives: The aim of this study was to assess the time course of presumptive TIC and the predictors of LV functional recovery in such patients.Background: Tachycardia-induced cardiomyopathy (TIC) is a potentially reversible cardiomyopathy with effective treatment of the tachyarrhythmia. However, cases without improvement of left ventricular (LV) systolic function were found occasionally. The diagnosis of TIC can be challenging, and the role of echocardiographic imaging in the prediction of LV functional recovery is limited.Methods: LV segmental longitudinal strains (LS) were evaluated by 2-dimensional speckle tracking in 71 consecutive patients (65±16 years; 61% men) with tachyarrhythmia and reduced LV ejection fraction (EF) without any other known cardiovascular disease, and 30 age and gender matched control subjects. Relative apical LS ratio (RALSR) was defined using the equation: average apical LS / (average basal LS + average mid LS) as a marker of strain distribution.Results: Compared to control subjects, patients with tachyarrhythmia had significantly lower global LS. Improvement in LVEF within 6 months after treatment of index arrhythmia was observed in 41 patients, and LVEF did not improve in 30 patients. In univariate analysis, lower LVEF at baseline (hazard ratio: HR: 0.59 per 1SD, p=0.04) and higher RALSR (HR: 11.2 per 1SD, p <0.001) were associated with no recovery in LVEF during follow-up. In a multivariate logistic regression model, the significant predictor of LV systolic functional recovery was RALSR (HR: 22.9 per 1SD, p=0.001). A RALSR of 0.61 was sensitive (71%) and specific (90%) in differentiating LV systolic functional recovery (area under the curve: 0.88).Conclusions: The RALSR was associated with LV systolic functional recovery. This information might be useful for clinical evaluation and follow-up in patients with reduced LVEF. (Keyword) tachycardia induced cardiomyopathy / strain imaging / functional recovery (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jcmg.2016.03.019 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27665160 ● Summary page in Scopus @ Elsevier: 2-s2.0-84994494325 (DOI: 10.1016/j.jcmg.2016.03.019, PubMed: 27665160, Elsevier: Scopus)
201.	鳥居裕太, 西尾進, 松本力三, 平田有紀奈, 天野里江, 山尾雅美, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 超音波検査が診断に有用であった右5指動静脈奇形の1例, Japanese Journal of Medical Ultrasound Technology, Vol.42, No.6, 726, 2017.
202.	Masataka Sata : 巻頭総説冠動脈硬化における心外膜脂肪の役割血管, 日本心脈管作動物質学会, Vol.40, No.4, 2017.
203.	K Sai, K Kajinami, H Akao, M Iwadare, R Sato-Ishida, Y Kawai, K Takeda, T Tanimoto, T Yamano, T Akasaka, T Ishida, K Hirata, K Saku, Shusuke Yagi, Takeshi Soeki, Masataka Sata, M Ueno, S Miyazaki, A Shiraki, J Oyama, K Node, K Sugamura, H Ogawa, K Kurose, K Maekawa, Y Matsuzawa, T Imatoh, R Hasegawa, Consortium Pharmacogenomics Data Science Japanese and Y Saito : A possible role for HLA-DRB1*04:06 in statin-related myopathy in Japanese patients., Drug Metabolism and Pharmacokinetics, Vol.31, No.6, 467-470, 2016. (Keyword) Genetic polymorphism / HLA / Myopathy / Rhabdomyolysis / Statin (Link to Publication Site) ● Publication site (DOI): 10.1016/j.dmpk.2016.09.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27839692 ● Search Scopus @ Elsevier (PMID): 27839692 ● Search Scopus @ Elsevier (DOI): 10.1016/j.dmpk.2016.09.002 (DOI: 10.1016/j.dmpk.2016.09.002, PubMed: 27839692)
204.	Hirofumi Tomiyama, Takashi Miwa, Kenshi Kan, Munehide Matsuhisa, Haruo Kamiya, Mamoru Nanasato, Tomoki Kitano, Hiroaki Sano, Jun Ohno, Masato Iida, Masataka Sata, Hirotsugu Yamada, Koji Maemura, Atsushi Tanaka, Toyoaki Murohara and Koichi Node : Impact of glycemic control with sitagliptin on the 2-year progression of arterial stiffness: a sub-analysis of the PROLOGUE study., Cardiovascular Diabetology, Vol.15, No.1, 150, 2016. (Summary) No conclusive evidence has been obtained yet on the significance of the effects of dipeptidyl peptidase-4 (DPP-4 inhibitor) treatment on the arterial stiffness in clinical settings. In addition, the effects of good glycemic control on the arterial stiffness have also not been clarified yet. As a sub-analysis of the PROLOGUE study, we examined the effect of a DPP-4 inhibitor (sitagliptin) on the 2-year progression of the arterial stiffness and also to determine the effect of good glycemic control on the rate of progression of the arterial stiffness. In the PROLOGUE study, the study participants were either allocated to add-on sitagliptin treatment or to continued treatment with conventional anti-diabetic agents. Among the 463 participants of the PROLOGUE study, we succeeded in measuring the brachial-ankle pulse wave velocity (baPWV) at least two times during the 2-year study period in 96 subjects. The changes in the baPWV during the study period were similar between the both groups (i.e., with/without staglipitin), overall. On the other hand, when the study subjects were divided into two groups according to the glycemic control status during the study period {good glycemic control group (GC) = hemoglobin (Hb)A1c <7.0 at both 12 and 24 months after the treatment randomization; poor glycemic control group (PC) = HbA1c ≥7.0 at either 12 months, 24 months, or both}, the 2-year increase of the baPWV was marginally significantly larger in the PC group (144 ± 235 cm/s) as compared to that the GC group (-10 ± 282 cm/s) (p = 0.036). While the present study could not confirm the beneficial effect of sitagliptin per se on the arterial stiffness, the results suggested that good glycemic control appears to be beneficial for delaying the annual progression of the arterial stiffness. Trial registration University Hospital Medical Information Network Clinical Trials Registry UMIN000004490. (Tokushima University Institutional Repository) ● Metadata: 114508 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12933-016-0472-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27809848 ● Summary page in Scopus @ Elsevier: 2-s2.0-84994050554 (Tokushima University Institutional Repository: 114508, DOI: 10.1186/s12933-016-0472-8, PubMed: 27809848, Elsevier: Scopus)
205.	HM Salim, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Glycemic control with ipragliflozin, a novel selective SGLT2 inhibitor, ameliorated endothelial dysfunction in streptozotocin-induced diabetic mouse., Frontiers in Cardiovascular Medicine, Vol.3, 43, 2016. (Summary) BACKGROUND: Endothelial dysfunction caused by increased oxidative stress is a critical initiator of macro- and micro-vascular disease development in diabetic patients. Ipragliflozin, a selective sodium-glucose cotransporter 2 (SGLT2) inhibitor, offers a novel approach for the treatment of diabetes by enhancing urinary glucose excretion. The aim of this study was to examine whether ipragliflozin attenuates endothelial dysfunction in diabetic mice.METHODS: Eight-week-old male C57BL/6 mice were treated with streptozotocin (150mg/kg) by a single intraperitoneal injection to induce diabetes mellitus. At 3days of injection, ipragliflozin (3mg/kg/day) was administered via gavage for 3weeks. Vascular function was assessed by isometric tension recording. Human umbilical vein endothelial cells (HUVEC) were used for in vitro experiments. RNA and protein expression were examined by quantitative RT-PCR (qPCR) and western blot, respectively. Oxidative stress was determined by measuring urine 8-hydroxy-2'-deoxyguanosine (8-OHdG) level.RESULTS: Ipragliflozin administration significantly reduced blood glucose level (P<0.001) and attenuated the impairment of endothelial function in diabetic mice, as determined by acetylcholine-dependent vasodilation (P<0.001). Ipragliflozin did not alter metabolic parameters, such as body weight and food intake. Ipragliflozin administration ameliorated impaired phosphorylation of Akt and eNOSSer1177 in the abdominal aorta and reduced reactive oxygen species generation as determined by urinary excretion of 8-OHdG in diabetic mice. Furthermore, qPCR analyses demonstrated that ipragliflozin decreased the expression of inflammatory molecules [e.g., monocyte chemoattractant protein-1 (MCP-1) vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule (ICAM)-1] in the abdominal aorta (P<0.05). In in vitro studies, incubation with methylglyoxal, one of the advanced glycation end products, significantly impaired phosphorylation of Akt and eNOSSer1177 (P<0.01) and increased the expression of MCP-1, VCAM-1, and ICAM-1 in HUVEC.CONCLUSION: Ipragliflozin improved hyperglycemia and prevented the development of endothelial dysfunction under a hyperglycemic state, at least partially by attenuation of oxidative stress. (Keyword) SGLT2 inhibitor / endothelial function / hyperglycemia / inflammation / oxidative stress (Tokushima University Institutional Repository) ● Metadata: 114485 (Link to Publication Site) ● Publication site (DOI): 10.3389/fcvm.2016.00043 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27833913 ● Search Scopus @ Elsevier (PMID): 27833913 ● Search Scopus @ Elsevier (DOI): 10.3389/fcvm.2016.00043 (Tokushima University Institutional Repository: 114485, DOI: 10.3389/fcvm.2016.00043, PubMed: 27833913)
206.	A Takashima, Shusuke Yagi, Koji Yamaguchi, S Watanabe, N Yamamoto, H Ito, M Kadota, T Hara, H Yamazaki, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Purulent pericarditis accompanying pericardial abscess induced by nocardia in an immunocompromised patient., Circulation Journal, Vol.80, No.11, 2409-2411, 2016. (Keyword) Abscess / Aged, 80 and over / Echocardiography / Female / Humans / Immunocompromised Host / Nocardia / Nocardia Infections / Pericarditis / Pericardium / Tomography, X-Ray Computed (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-16-0531 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27628220 ● Summary page in Scopus @ Elsevier: 2-s2.0-84992462594 (DOI: 10.1253/circj.CJ-16-0531, PubMed: 27628220, Elsevier: Scopus)
207.	A Takashima, Daiju Fukuda, K Tanaka, Y Higashikuni, Y Hirata, S Nishimoto, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Yutaka Taketani, Michio Shimabukuro and Masataka Sata : Combination of n-3 polyunsaturated fatty acids reduces atherogenesis in apolipoprotein E-deficient mice by inhibiting macrophage activation., Atherosclerosis, Vol.254, 142-150, 2016. (Summary) BACKGROUND AND AIMS: Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are major components of n-3 polyunsaturated fatty acids (n-3 PUFAs) which inhibit atherogenesis, although few studies have examined the effects of the combination of EPA and DHA on atherogenesis. The aim of this study was to investigate whether DHA has additional anti-atherosclerotic effects when combined with EPA.METHODS: Male 8-week-old apolipoprotein E-deficient (Apoe-/-) mice were fed a western-type diet supplemented with different amounts of EPA and DHA; EPA (2.5%, w/w), low-dose EPA + DHA (2.5%, w/w), or high-dose EPA + DHA (5%, w/w) for 20 weeks. The control group was fed a western-type diet containing no n-3 PUFA. Histological and gene expression analysis were performed in atherosclerotic lesions in the aorta. To address the mechanisms, RAW264.7 cells were used.RESULTS: All n-3 PUFA treatments significantly attenuated the development and destabilization of atherosclerotic plaques compared with the control. The anti-atherosclerotic effects were enhanced in the high-dose EPA + DHA group (p < 0.001), whereas the pure EPA group and low-dose EPA + DHA group showed similar results. EPA and DHA additively attenuated the expression of inflammatory molecules in RAW264.7 cells stimulated with LPS. DHA or EPA + DHA suppressed LPS-induced toll-like receptor 4 (TLR4) expression in lipid rafts on RAW264.7 cells (p < 0.05). Lipid raft disruption by methyl--cyclodextrin suppressed mRNA expression of inflammatory molecules in LPS-stimulated macrophages.CONCLUSION: n-3 PUFAs suppressed atherogenesis. DHA combined with EPA had additional anti-inflammatory effects and inhibited atherogenesis in Apoe-/- mice. The reduction of TLR4 expression in lipid rafts in macrophages by DHA might be involved in this mechanism, at least partially. (Keyword) Atherosclerosis / Inflammation / Lipid raft / Macrophage / Toll-like receptor 4 / n-3 poly unsaturated fatty acid (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2016.10.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27744130 ● Summary page in Scopus @ Elsevier: 2-s2.0-84991678518 (DOI: 10.1016/j.atherosclerosis.2016.10.002, PubMed: 27744130, Elsevier: Scopus)
208.	鳥居裕太, 西尾進, 玉井佑里恵, 山崎宙, Shoichiro Takao, Kenya Kusunose, Koji Yamaguchi, Tetsuzo Wakatsuki, Hirotsugu Yamada and Masataka Sata : 解剖学的異常を認めない膝窩動脈捕捉症候群の1例, Japanese Journal of Medical Ultrasound Technology, Vol.41, No.5, 513-520, 2016. (Link to Publication Site) ● Publication site (DOI): 10.11272/jss.41.513 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001205281332224 ● Search Scopus @ Elsevier (DOI): 10.11272/jss.41.513 (DOI: 10.11272/jss.41.513, CiNii: 1390001205281332224)
209.	Zhi-Hong Yang, Masahiro Bando, Toshihiro Sakurai, Ye Chen, Beatrice Emma-Okon, Bree Wilhite, Daiju Fukuda, Boris Vaisman, Milton Pryor, Yoshiyuki Wakabayashi, Maureen Sampson, Zu-Xi Yu, Akiko Sakurai, Abdalrahman Zarzour, Hiroko Miyahara, Jiro Takeo, Hiroshi Sakaue, Masataka Sata and Alan T. Remaley : Long-chain monounsaturated fatty acid-rich fish oil attenuates the development of atherosclerosis in mouse models., Molecular Nutrition & Food Research, Vol.60, No.10, 2208-2218, 2016. (Summary) SCOPE: Fish oil-derived long-chain monounsaturated fatty acids (LCMUFA) containing chain lengths longer than 18 were previously shown to improve cardiovascular disease risk factors in mice. However, it is not known if LCMUFA also exerts anti-atherogenic effects. The main objective of the present study was to investigate the effect of LCMUFA on the development of atherosclerosis in mouse models.METHODS AND RESULTS: LDLR-KO mice were fed Western diet supplemented with 2% (w/w) of either LCMUFA concentrate, olive oil, or not (control) for 12 wk. LCMUFA, but not olive oil, significantly suppressed the development of atherosclerotic lesions and several plasma inflammatory cytokine levels, although there were no major differences in plasma lipids between the three groups. At higher doses 5% (w/w) LCMUFA supplementation was observed to reduce pro-atherogenic plasma lipoproteins and to also reduce atherosclerosis in ApoE-KO mice fed a Western diet. RNA sequencing and subsequent qPCR analyses revealed that LCMUFA upregulated PPAR signaling pathways in liver. In cell culture studies, apoB-depleted plasma from LDLR-K mice fed LCMUFA showed greater cholesterol efflux from macrophage-like THP-1 cells and ABCA1-overexpressing BHK cells.CONCLUSION: Our research showed for the first time that LCMUFA consumption protects against diet-induced atherosclerosis, possibly by upregulating the PPAR signaling pathway. (Keyword) Long-chain monounsaturated / atherosclerosis / PPAR signaling / cholesterol efflux, / inflammation (Link to Publication Site) ● Publication site (DOI): 10.1002/mnfr.201600142 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27273599 ● Summary page in Scopus @ Elsevier: 2-s2.0-85027917138 (DOI: 10.1002/mnfr.201600142, PubMed: 27273599, Elsevier: Scopus)
210.	Tatsuya Maruhashi, Yukihito Higashi, Yasuki Kihara, Hirotsugu Yamada, Masataka Sata, Shinichiro Ueda, Masato Odawara, Yasuo Terauchi, Kazuoki Dai, Jun Ohno, Masato Iida, Hiroaki Sano, Hirofumi Tomiyama, Teruo Inoue, Atsushi Tanaka, Toyoaki Murohara and Koichi Node : Long-term effect of sitagliptin on endothelial function in type 2 diabetes: a sub-analysis of the PROLOGUE study., Cardiovascular Diabetology, Vol.15, No.1, 134, 2016. (Summary) As a sub-analysis of the PROLOGUE study, we evaluated the long-term effect of sitagliptin, a dipeptidyl peptidase 4 inhibitor, on endothelial function in the conduit brachial artery in patients with type 2 diabetes. In the PROLOGUE study, patients were randomly assigned to either add-on sitagliptin treatment (sitagliptin group) or continued conventional antihyperglycemic treatment (conventional group). Among the 463 participants in the PROLOGUE study, FMD was measured in 17 patients in the sitagliptin group and 18 patients in the conventional group at the beginning and after 12 and 24 months of treatment. HbA1c levels were significantly decreased after 12 and 24 months of treatment compared to baseline values in both groups (7.0 0.4 vs. 6.6 0.3 and 6.6 0.4 % in the sitagliptin group; 7.0 0.6 vs. 6.6 0.7 and 6.6 0.7 % in the conventional group; P < 0.05, respectively). There was no significant difference between FMD values at baseline and after 12 and 24 months in the sitagliptin group (4.3 2.6 vs. 4.4 2.1 and 4.4 2.3 %, P = 1.0, respectively). Although FMD had a tendency to increase from 4.3 2.4 % at baseline to 5.2 1.9 % after 12 months and 5.1 2.2 % after 24 months in the conventional group, there was no significant difference between FMD values at baseline and after 12 and 24 months (P = 0.36 and 0.33, respectively). Add-on sitagliptin to conventional antihyperglycemic drugs in patients with type 2 diabetes did not alter endothelial function in the conduit brachial artery measured by FMD during a 2-year study period. Sitagliptin may be used without concern for an adverse effect on endothelial function in patients with type 2 diabetes. University hospital Medical Information Network (UMIN) Center: ID UMIN000004490. (Keyword) Aged / Biomarkers / Blood Glucose / Brachial Artery / Diabetes Mellitus, Type 2 / Dipeptidyl-Peptidase IV Inhibitors / Drug Therapy, Combination / Endothelium, Vascular / Female / Glycated Hemoglobin A / Humans / Japan / Male / Middle Aged / Prospective Studies / Sitagliptin Phosphate / Time Factors / Treatment Outcome / Vasodilation (Tokushima University Institutional Repository) ● Metadata: 114511 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12933-016-0438-x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27624168 ● Summary page in Scopus @ Elsevier: 2-s2.0-84992361845 (Tokushima University Institutional Repository: 114511, DOI: 10.1186/s12933-016-0438-x, PubMed: 27624168, Elsevier: Scopus)
211.	A Tanaka, T Murohara, I Taguchi, K Eguchi, M Suzuki, M Kitakaze, Y Sato, T Ishizu, Y Higashi, Hirotsugu Yamada, M Nanasato, Michio Shimabukuro, H Teragawa, S Ueda, S Kodera, Munehide Matsuhisa, T Kadokami, K Kario, Y Nishio, T Inoue, K Maemura, J Oyama, M Ohishi, Masataka Sata, H Tomiyama, K Node and Investigators Study PROTECT : Rationale and design of a multicenter randomized controlled study to evaluate the preventive effect of ipragliflozin on carotid atherosclerosis: the PROTECT study., Cardiovascular Diabetology, Vol.15, No.1, 133, 2016. (Summary) BACKGROUND: Type 2 diabetes mellitus is associated strongly with an increased risk of micro- and macro-vascular complications, leading to impaired quality of life and shortened life expectancy. In addition to appropriate glycemic control, multi-factorial intervention for a wide range of risk factors, such as hypertension and dyslipidemia, is crucial for management of diabetes. A recent cardiovascular outcome trial in diabetes patients with higher cardiovascular risk demonstrated that a SGLT2 inhibitor markedly reduced mortality, but not macro-vascular events. However, to date there is no clinical evidence regarding the therapeutic effects of SGLT2 inhibitors on arteriosclerosis. The ongoing PROTECT trial was designed to assess whether the SGLT2 inhibitors, ipragliflozin, prevented progression of carotid intima-media thickness in Japanese patients with type 2 diabetes mellitus.METHODS: A total of 480 participants with type 2 diabetes mellitus with a HbA1c between 6 and 10 % despite receiving diet/exercise therapy and/or standard anti-diabetic agents for at least 3 months, will be randomized systematically (1:1) into either ipragliflozin or control (continuation of conventional therapy) groups. After randomization, ipragliflozin (50-100 mg once daily) will be added on to the background therapy in participants assigned to the ipragliflozin group. The primary endpoint of the study is the change in mean intima-media thickness of the common carotid artery from baseline to 24 months. Images of carotid intima-media thickness will be analyzed at a central core laboratory in a blinded manner. The key secondary endpoints include the change from baseline in other parameters of carotid intima-media thickness, various metabolic parameters, and renal function. Other cardiovascular functional tests are also planned for several sub-studies.DISCUSSION: The PROTECT study is the first to assess the preventive effect of ipragliflozin on progression of carotid atherosclerosis using carotid intima-media thickness as a surrogate marker. The study has potential to clarify the protective effects of ipragliflozin on atherosclerosis. Trial registration Unique Trial Number, UMIN000018440 ( https://upload.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000021348 ). (Keyword) Adult / Aged / Biomarkers / Carotid Artery Diseases / Carotid Artery, Common / Carotid Intima-Media Thickness / Clinical Protocols / Diabetes Mellitus, Type 2 / Diabetic Angiopathies / Drug Therapy, Combination / Female / Glucosides / Hemoglobin A, Glycosylated / Humans / Hypoglycemic Agents / Japan / Male / Middle Aged / Prospective Studies / Research Design / Sodium-Glucose Transporter 2 / Thiophenes / Time Factors / Treatment Outcome / Young Adult (Tokushima University Institutional Repository) ● Metadata: 114507 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12933-016-0449-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27619983 ● Search Scopus @ Elsevier (PMID): 27619983 ● Search Scopus @ Elsevier (DOI): 10.1186/s12933-016-0449-7 (Tokushima University Institutional Repository: 114507, DOI: 10.1186/s12933-016-0449-7, PubMed: 27619983)
212.	菅澤典子, Chika Nishio, 中山泰介, Hirotsugu Kurobe, 宅見央子, 東口文治, Ken-ichi Aihara, Michio Shimabukuro, Masataka Sata and Tetsuya Kitagawa : 糖転移ヘスペリジン/分散ヘスペレチンの動脈硬化病巣進展に対する抑制効果についての検討, The Journal of Metabolism and Clinical Nutrition, Vol.19, No.3, 351-360, 2016. (Keyword) 糖転移ヘスペリジン / 分散ヘスペレチン / atherosclerosis / マクロファージ / ApoEノックアウトマウス
213.	T Ueda, Y Nakata, N Yamasaki, H Oda, K Sentani, A Kanai, N Onishi, K Ikeda, Y Sera, Z Honda, K Tanaka, Masataka Sata, S Ogawa, W Yasui, H Saya, J Takita and H Honda : ALK^R1275Q perturbs extracellular matrix, enhances cell invasion and leads to the development of neuroblastoma in cooperation with MYCN., Oncogene, Vol.35, No.34, 4447-4458, 2016. (Summary) Overexpression of MYCN is a hallmark of neuroblastoma (NB). ALK(R1275Q), an activating mutation of ALK (anaplastic lymphoma kinase), has been found in sporadic and familial NB patients. In this report, we demonstrated that ALK(R1275Q) knock-in, MYCN transgenic compound mice developed NB with complete penetrance. Transcriptome analysis revealed that ALK(R1275Q) globally downregulated the expression of extracellular matrix (ECM)- and basement membrane (BM)-associated genes in both primary neuronal cells and NB tumors. Accordingly, ALK(R1275Q)/MYCN tumors exhibited reduced expression of ECM/BM-related proteins as compared with MYCN tumors. In addition, on MYCN transduction, ALK(R1275Q)-expressing neuronal cells exhibited increased migratory and invasive activities. Consistently, enhanced invasion and metastasis were demonstrated in ALK(R1275Q)/MYCN mice. These results collectively indicate that ALK(R1275Q) confers a malignant potential on neuronal cells that overexpress MYCN by impairing normal ECM/BM integrity and enhancing tumor growth and dissemination. Moreover, we found that crizotinib, an ALK inhibitor, almost completely inhibited the growth of ALK(R1275Q)/MYCN tumors in an allograft model. Our findings provided insights into the cooperative mechanism of the mutated ALK and overexpressed MYCN in the pathogenesis of NB and demonstrated the effectiveness of crizotinib on ALK(R1275Q)-positive tumors. (Link to Publication Site) ● Publication site (DOI): 10.1038/onc.2015.519 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26829053 ● Search Scopus @ Elsevier (PMID): 26829053 ● Search Scopus @ Elsevier (DOI): 10.1038/onc.2015.519 (DOI: 10.1038/onc.2015.519, PubMed: 26829053)
214.	M Kadota, Takayuki Ise, Shusuke Yagi, Takashi Iwase, Masashi Akaike, R Ueno, Y Kawabata, T Hara, K Ogasawara, Mika Bando, S Bando, Tomomi Matsuura, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Response prediction and influence of tolvaptan in chronic heart failure patients considering the interaction of the renin-angiotensin-aldosterone system and arginine vasopressin., International Heart Journal, Vol.57, No.4, 461-465, 2016. (Summary) The renin-angiotensin-aldosterone system (RAAS) and arginine vasopressin (AVP) regulate body fluids. Although conventional diuretics have been used for treating heart failure, they activate RAAS and exacerbate renal function. Tolvaptan, a newly developed vasopressin-2 receptor antagonist, elicits aquaresis and improves volume overload in heart failure patients, however, the predictors of tolvaptan effectiveness and the influence on the RAAS and renal function according to tolvaptan therapy are not established. We evaluated 26 chronic heart failure patients receiving therapy with 15 mg/day tolvaptan and examined their laboratory and urinary data before and after tolvaptan therapy. A response to tolvaptan was defined as a body weight decrease by more than 2 kg in a week and a urine volume increase by 500 mL/ day compared with that before tolvaptan administration. Body weight, urine volume, and brain natriuretic peptide levels significantly improved (P < 0.05), without any worsening of renal function represented by serum creatinine, sodium, and potassium. Moreover, no significant changes were observed in the plasma renin activity and plasma aldosterone concentration (PAC). In the responder group, urine osmolality before tolvaptan administration was significantly higher (P < 0.05) but declined significantly after tolvaptan administration (P < 0.05). The AVP/PAC ratio before administration was positively correlated with the efficacy of tolvaptan. Tolvaptan treatment could prevent RAAS activation in chronic heart failure patients. Moreover, monitoring the AVP/PAC ratio may be useful in predicting the tolvaptan response. (Keyword) Adult / Aged / Aged, 80 and over / Antidiuretic Hormone Receptor Antagonists / Arginine Vasopressin / Benzazepines / Body Mass Index / Female / Heart Failure / Humans / Male / Middle Aged / Prospective Studies / Renin-Angiotensin System / Treatment Outcome (Tokushima University Institutional Repository) ● Metadata: 109694 (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.15-491 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27357439 ● Summary page in Scopus @ Elsevier: 2-s2.0-84979587993 (Tokushima University Institutional Repository: 109694, DOI: 10.1536/ihj.15-491, PubMed: 27357439, Elsevier: Scopus)
215.	Michio Shimabukuro, H Sato, Hirofumi Izaki, Daiju Fukuda, E Uematsu, Y Hirata, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Hiro-omi Kanayama, H Masuzaki and Masataka Sata : Depot- and gender-specific expression of NLRP3 inflammasome and toll-like receptors in adipose tissue of cancer patients., BioFactors, Vol.42, No.4, 397-406, 2016. (Keyword) obesity / inflammation / gender (Link to Publication Site) ● Publication site (DOI): 10.1002/biof.1287 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27086574 ● Summary page in Scopus @ Elsevier: 2-s2.0-84982113330 (DOI: 10.1002/biof.1287, PubMed: 27086574, Elsevier: Scopus)
216.	Hirotsugu Yamada, 田中秀和, 宮原俊介, 尾形竜郎, Kenya Kusunose, 西尾進, 鳥居裕太, 平田有紀奈, 大北裕 and Masataka Sata : 表在エコー図検査と心エコー図検査のコラボレーションにより感染性心内膜炎が迅速に診断できた僧帽弁逸脱症の1例:Staphylococcus warneriによる自己弁への感染性心内膜炎, Japanese Journal of Medical Ultrasonics, Vol.43, No.4, 581-586, 2016. (Summary) 症例は，46歳男性，循環器内科医師，主訴は左足関節内果部と上腕の疼痛である．僧帽弁逸脱症による僧帽弁逆流と発作性心房細動の既往がある．足関節の疼痛は蜂窩織炎を疑って，血液検査と表在エコー図検査を行った．疼痛部は皮下浮腫が著明であったが，軟部組織の血流シグナルが乏しく，後脛骨動脈の血管壁を主体とした炎症と，同動脈の閉塞が確認された．一方，左手関節近位の尺骨動脈は逆行性血流を示しており，左尺骨動脈分岐部直後で閉塞していた．これらの所見から多発性血管閉塞性動脈炎と診断し，その原因究明のために直ちに心エコー図検査を施行した．その結果，僧帽弁に可動性を有する棍棒状の異常構造物を認め，僧帽弁逆流は高度に増悪しており，感染性心内膜炎と診断された．頭部MRI検査で異常を認めなかったため，外科的加療(疣腫摘除術，僧帽弁形成術，左房縫縮術，左心耳閉鎖術，Maze手術)が行われた．血液培養は陰性であったが，摘出した疣腫の培養からStaphylococcus warneriが同定された．Staphylococcus warneriは皮膚常在菌であり，本病原体による自己弁の感染性心内膜炎は報告が少ない．術後の経過は良好であり，抗生剤を6週間静脈投与した後に社会復帰した．患者が循環器内科医であり，自身の足関節および上腕の疼痛を契機に，表在エコー図検査と心エコー図検査を用いることで，感染性心内膜炎を迅速に診断した稀有な症例であり，かつ，感染性心内膜炎の起炎菌としては稀なStaphylococcus warneriが同定されたので，文献的な考察を加えて報告する． (Link to Publication Site) ● Publication site (DOI): 10.3179/jjmu.JJMU.A.63 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.3179/jjmu.JJMU.A.63 (DOI: 10.3179/jjmu.JJMU.A.63)
217.	J Oyama, T Murohara, M Kitakaze, T Ishizu, Y Sato, K Kitagawa, H Kamiya, M Ajioka, M Ishiara, K Dai, M Nanasato, Masataka Sata, K Maemura, H Tomiyama, Y Higashi, K Kaku, Hirotsugu Yamada, Munehide Matsuhisa, K Yamashita, YK Bando, N Kashihara, S Ueda, T Inoue, K Node and Investigators Study PROLOGUE : The Effect of Sitagliptin on Carotid Artery Atherosclerosis in Type 2 Diabetes: The PROLOGUE Randomized Controlled Trial., PLoS Medicine, Vol.13, No.6, e1002051, 2016. (Summary) BACKGROUND: Experimental studies have suggested that dipeptidyl peptidase-4 (DPP-4) inhibitors provide cardiovascular protective effects. We performed a randomized study to evaluate the effects of sitagliptin added on to the conventional therapy compared with conventional therapy alone (diet, exercise, and/or drugs, except for incretin-related agents) on the intima-media thickness (IMT) of the carotid artery, a surrogate marker for the evaluation of atherosclerotic cardiovascular disease, in people with type 2 diabetes mellitus (T2DM).METHODS AND FINDINGS: We used a multicenter PROBE (prospective, randomized, open label, blinded endpoint) design. Individuals aged 30 y with T2DM (6.2% HbA1c < 9.4%) were randomly allocated to receive either sitagliptin (25 to 100 mg/d) or conventional therapy. Carotid ultrasound was performed at participating medical centers, and all parameters were measured in a core laboratory. Of the 463 enrolled participants with T2DM, 442 were included in the primary analysis (sitagliptin group, 222; conventional therapy group, 220). Estimated mean (± standard error) common carotid artery IMT at 24 mo of follow-up in the sitagliptin and conventional therapy groups was 0.827 ± 0.007 mm and 0.837 ± 0.007 mm, respectively, with a mean difference of -0.009 mm (97.2% CI -0.028 to 0.011, p = 0.309). HbA1c level at 24 mo was significantly lower with sitagliptin than with conventional therapy (6.56% ± 0.05% versus 6.72% ± 0.05%, p = 0.008; group mean difference -0.159, 95% CI -0.278 to -0.041). Episodes of serious hypoglycemia were recorded only in the conventional therapy group, and the rate of other adverse events was not different between the two groups. As it was not a placebo-controlled trial and carotid IMT was measured as a surrogate marker of atherosclerosis, there were some limitations of interpretation.CONCLUSIONS: In the PROLOGUE study, there was no evidence that treatment with sitagliptin had an additional effect on the progression of carotid IMT in participants with T2DM beyond that achieved with conventional treatment.TRIAL REGISTRATION: University Hospital Medical Information Network Clinical Trials Registry UMIN000004490. (Tokushima University Institutional Repository) ● Metadata: 114321 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pmed.1002051 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27351380 ● Search Scopus @ Elsevier (PMID): 27351380 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pmed.1002051 (Tokushima University Institutional Repository: 114321, DOI: 10.1371/journal.pmed.1002051, PubMed: 27351380)
218.	Jun-Ichi Oyama, Atsushi Tanaka, Yasunori Sato, Hirofumi Tomiyama, Masataka Sata, Tomoko Ishizu, Isao Taguchi, Takanori Kuroyanagi, Hiroki Teragawa, Nobukazu Ishizaka, Yumiko Kanzaki, Mitsuru Ohishi, Kazuo Eguchi, Yukihito Higashi, Hirotsugu Yamada, Koji Maemura, Junya Ako, Yasuko K. Bando, Shinichiro Ueda, Teruo Inoue, Toyoaki Murohara and Koichi Node : Rationale and design of a multicenter randomized study for evaluating vascular function under uric acid control using the xanthine oxidase inhibitor, febuxostat: the PRIZE study., Cardiovascular Diabetology, Vol.15, No.1, 87, 2016. (Summary) BACKGROUND: Xanthine oxidase inhibitors are anti-hyperuricemic drugs that decrease serum uric acid levels by inhibiting its synthesis. Xanthine oxidase is also recognized as a pivotal enzyme in the production of oxidative stress. Excess oxidative stress induces endothelial dysfunction and inflammatory reactions in vascular systems, leading to atherosclerosis. Many experimental studies have suggested that xanthine oxidase inhibitors have anti-atherosclerotic effects by decreasing in vitro and in vivo oxidative stress. However, there is only limited evidence on the clinical implications of xanthine oxidase inhibitors on atherosclerotic cardiovascular disease in patients with hyperuricemia. We designed the PRIZE study to evaluate the effects of febuxostat on a surrogate marker of cardiovascular disease risk, ultrasonography-based intima-media thickness of the carotid artery in patients with hyperuricemia.METHODS: The study is a multicenter, prospective, randomized, open-label and blinded-endpoint evaluation (PROBE) design. A total of 500 patients with asymptomatic hyperuricemia (uric acid >7.0 mg/dL) and carotid intima-media thickness 1.1 mm will be randomized centrally to receive either febuxostat (10-60 mg/day) or non-pharmacological treatment. Randomization is carried out using the dynamic allocation method stratified according to age (<65, 65 year), gender, presence or absence of diabetes mellitus, serum uric acid (<8.0, 8.0 mg/dL), and carotid intima-media thickness (<1.3, 1.3 mm). In addition to administering the study drug, we will also direct lifestyle modification in all participants, including advice on control of body weight, sleep, exercise and healthy diet. Carotid intima-media thickness will be evaluated using ultrasonography performed by skilled technicians at a central laboratory. Follow-up will be continued for 24 months. The primary endpoint is percentage change in mean intima-media thickness of the common carotid artery 24 months after baseline, measured by carotid ultrasound imaging.CONCLUSIONS: PRIZE will be the first study to provide important data on the effects of febuxostat on atherosclerosis in patients with asymptomatic hyperuricemia. Trial Registration Unique trial Number, UMIN000012911 ( https://upload.umin.ac.jp/cgi-open-bin/ctr/ctr.cgi?function=brows&action=brows&type=summary&recptno=R000015081&language=E ). (Keyword) carotid artery / Febuxostat / Hyperuricemia / Intima-media thickness (IMT) / Xanthine oxidase inhibitor (Tokushima University Institutional Repository) ● Metadata: 114506 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12933-016-0409-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27317093 ● Summary page in Scopus @ Elsevier: 2-s2.0-84975229374 (Tokushima University Institutional Repository: 114506, DOI: 10.1186/s12933-016-0409-2, PubMed: 27317093, Elsevier: Scopus)
219.	Michio Shimabukuro, C Okawa, Hirotsugu Yamada, S Yanagi, E Uematsu, N Sugasawa, Hirotsugu Kurobe, Y Hirata, JR Kim-Kaneyama, XF Lei, S Takao, Y Tanaka, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki, Tetsuya Kitagawa, H Masuzaki, M Sato and Masataka Sata : The pathophysiological role of oxidized cholesterols in epicardial fat accumulation and cardiac dysfunction: A study in swine fed a high caloric diet with an inhibitor of intestinal cholesterol absorption, ezetimibe., The Journal of Nutritional Biochemistry, Vol.35, 66-73, 2016. (Summary) Oxidized cholesterols (oxycholesterols) in food have been recognized as strong atherogenic components, but their tissue distributions and roles in cardiovascular diseases remain unclear. To investigate whether accumulation of oxycholesterols is linked to cardiac morphology and function, and whether reduction of oxycholesterols can improve cardiac performance, domestic male swine were randomized to a control diet (C), high caloric diet (HCD) or HCD+Ezetimibe, an inhibitor of intestinal cholesterol absorption, group (HCD+E) and evaluated for: (1) distribution of oxycholesterol components in serum and tissues, (2) levels of oxycholesterol-related enzymes, (3) paracardial and epicardial coronary fat thickness, and (4) cardiac performance. Ezetimibe treatment for 8weeks attenuated increases in oxycholesterols in the HCD group almost completely in liver, but reduced only levels of 4β-hydroxycholesterol in left ventricular (LV) myocardium. Ezetimibe treatment altered the expression of genes for cholesterol and fatty acid metabolism and decreased the expression of CYP3A46, which catabolizes cholesterol to 4β-hydroxycholesterol, strongly in liver. An increase in epicardial fat thickness and impaired cardiac performance in the HCD group were improved by ezetimibe treatment, and the improvement was closely related to the reduction in levels of 4β-hydroxycholesterol in LV myocardium. In conclusion, an increase in oxycholesterols in the HCD group was closely related to cardiac hypertrophy and dysfunction, as well as an increase in epicardial fat thickness. Ezetimibe may directly reduce oxycholesterol in liver and LV myocardium, and improve cardiac morphology and function. (Keyword) Cardiac function / Cardiac hypertrophy / Epicardial fat / Obesity / Oxycholesterol (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jnutbio.2016.05.010 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27416363 ● Search Scopus @ Elsevier (PMID): 27416363 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jnutbio.2016.05.010 (DOI: 10.1016/j.jnutbio.2016.05.010, PubMed: 27416363)
220.	Michio Shimabukuro, N Higa, H Masuzaki, Masataka Sata and S Ueda : Impact of individual metabolic risk components or its clustering on endothelial and smooth muscle cell function in men., Cardiovascular Diabetology, Vol.15, No.1, 77, 2016. (Summary) Impaired vasoreactivity is often observed in subjects with metabolic syndrome, a condition that includes the presence of a specific cluster of risk factors for obesity and cardiovascular disease. However, hierarchical causes in the impaired vasoreactivity have not been clarified. We evaluated the impact of individual metabolic risk components or its clustering under the condition of insulin resistance on endothelial and smooth muscle cell function. Vascular reactivity to acetylcholine (Ach), with or without nitric oxide synthase (NOS) inhibitor N (G)-monomethyl-L-arginine (L-NMMA), or sodium nitroprusside (SNP) by forearm venous occlusion plethysmography and insulin sensitivity index (M mg/kg/min) in euglycemic clamp were measured in men without (n = 18, control group) or with (n = 19, metabolic syndrome group) metabolic syndrome. (1) Ach-induced maximal forearm blood flow (maxFBF) was impaired in subjects with metabolic syndrome. In particular, the NOS-dependent component of Ach-induced maxFBF was selectively decreased, while the NOS-independent component remained relatively unchanged. (2) Ach-induced maxFBF and ∆Ach-induced maxFBF with L-NMMA were correlated with waist circumference, glucose, and triglycerides, and most strongly correlated with visceral fat area, adiponectin, and M. (3) Multivariate regression analysis indicated that individual metabolic risk components explained Ach-induced maxFBF by 4-21 %. Clustering of all metabolic risk components increased this to 35 %, and the presence of metabolic syndrome explained 30 %, indicating that defining metabolic syndrome can effectively predict impairment of endothelial dysfunction. Endothelial dysfunction was correlated with individual metabolic risk components, but more strongly with clustering of the components under a condition with low insulin sensitivity. We suggest that in subjects with metabolic syndrome, endothelial function is impaired by multiple cardiovascular risk factors exclusively when under the condition of insulin insensitivity and also that defining metabolic syndrome can effectively predict impairment of endothelial dysfunction. (Tokushima University Institutional Repository) ● Metadata: 114505 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12933-016-0394-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27188597 ● Search Scopus @ Elsevier (PMID): 27188597 ● Search Scopus @ Elsevier (DOI): 10.1186/s12933-016-0394-5 (Tokushima University Institutional Repository: 114505, DOI: 10.1186/s12933-016-0394-5, PubMed: 27188597)
221.	Mika Bando, Hirotsugu Yamada, Kenya Kusunose, Daiju Fukuda, Rie Amano, Rina Tamai, Yuta Torii, Yukina Hirata, Susumu Nishio, Junichiro Satomi, Shinji Nagahiro and Masataka Sata : Noninvasive quantitative tissue characterization of carotid plaque using color-coded mapping based on ultrasound integrated backscatter., JACC. Cardiovascular Imaging, Vol.9, No.5, 625-627, 2016. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jcmg.2015.02.017 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26093930 ● Summary page in Scopus @ Elsevier: 2-s2.0-84931059223 (DOI: 10.1016/j.jcmg.2015.02.017, PubMed: 26093930, Elsevier: Scopus)
222.	A Tanaka, T Inoue, M Kitakaze, J Oyama, Masataka Sata, I Taguchi, W Shimizu, H Watada, J Ako, Y Sakata, T Anzai, M Uematsu, M Suzuki, K Eguchi, A Yamashina, Y Saito, Y Sato, S Ueda, T Murohara and K Node : Rationale and design of a randomized trial to test the safety and non-inferiority of canagliflozin in patients with diabetes with chronic heart failure: the CANDLE trial., Cardiovascular Diabetology, Vol.15, No.1, 57, 2016. (Summary) Because type 2 diabetes mellitus is associated strongly with an increased risk of cardiovascular diseases, the number of patients with diabetes with chronic heart failure is increasing steadily. However, clinical evidence of therapeutic strategies in such patients is still lacking. A recent randomized, placebo-controlled trial in patients with type 2 diabetes with high cardiovascular risk demonstrated that the SGLT2 inhibitor, empagliflozin, reduced the incidence of hospitalization for heart failure. Because SGLT2 inhibitors cause a reduction in body weight and blood pressure in addition to improving glycemic control, they have the potential to exert beneficial effects on the clinical pathophysiology of heart failure. The aim of the ongoing CANDLE trial is to test the safety and non-inferiority of canagliflozin, another SGLT2 inhibitor, compared with glimepiride, a sulfonylurea agent, in patients with type 2 diabetes mellitus and chronic heart failure. A total of 250 patients with type 2 diabetes who are drug-naïve or taking any anti-diabetic agents and suffering from chronic heart failure with a New York Heart Association classification I to III will be randomized centrally into either canagliflozin or glimepiride groups (1: 1) using the dynamic allocation method stratified by age (<65, ≥65 year), HbA1c level (<6.5, ≥6.5 %), and left ventricular ejection fraction (<40, ≥40 %). After randomization, all the participants will be given the add-on study drug for 24 weeks in addition to their background therapy. The primary endpoint is the percentage change from baseline in NT-proBNP after 24 weeks of treatment. The key secondary endpoints after 24 weeks of treatment are the change from baseline in glycemic control, blood pressure, body weight, lipid profile, quality of life score related to heart failure, and cardiac and renal function. The CANDLE trial is the first to assess the safety and non-inferiority of canagliflozin in comparison with glimepiride in patients with type 2 diabetes with chronic heart failure. This trial has the potential to evaluate the clinical safety and efficacy of canagliflozin on heart failure. Trial registration Unique trial Number, UMIN000017669. (Keyword) Adult / Aged / Aged, 80 and over / Benzhydryl Compounds / Blood Glucose / Blood Pressure / Canagliflozin / Chronic Disease / Diabetes Mellitus, Type 2 / Female / Glucosides / Heart Failure / Humans / Hypoglycemic Agents / Male / Metformin / Middle Aged / Quality of Life / Sulfonylurea Compounds (Tokushima University Institutional Repository) ● Metadata: 114504 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12933-016-0381-x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27044332 ● Search Scopus @ Elsevier (PMID): 27044332 ● Search Scopus @ Elsevier (DOI): 10.1186/s12933-016-0381-x (Tokushima University Institutional Repository: 114504, DOI: 10.1186/s12933-016-0381-x, PubMed: 27044332)
223.	HM Salim, Daiju Fukuda, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Dipeptidyl peptidase-4 inhibitor, linagliptin, ameliorates endothelial dysfunction and atherogenesis in normoglycemic apolipoprotein-E deficient mice., Vascular Pharmacology, Vol.79, 16-23, 2016. (Summary) Background; The dipeptidyl peptidase-4 (DPP-4) inhibitors have vasoprotective effects. This study investigated whether a recently approved DPP-4 inhibitor, linagliptin (Lina), suppresses atherogenesis in non-diabetic apolipoprotein-E deficient (ApoE-/-) mice and examined its effects on endothelial function. Methods and Results; Lina (10 mg/kg/day) was administered orally to ApoE-/- mice for 20 weeks. Lina reduced atherogenesis without the alteration of metabolic parameters including blood glucose level compared with the control (P<0.05). Results of immunohistochemistry and quantitative RT-PCR demonstrated that Lina significantly decreased inflammatory molecule expression and macrophage infiltration in atherosclerotic aorta. Lina administration to ApoE-/- mice for 9 weeks ameliorated endothelium-dependent vasodilation compared with non-treated mice. Plasma active glucagon-like peptide-1 (GLP-1) level was significantly higher in the treated group (P<0.05). Exendin-4 (Ex-4), a GLP-1 analogue, ameliorated endothelium-dependent vasodilation impaired by palmitic acid (PA) in wild-type mouse aortic segments. Ex-4 promoted phosphorylation of eNOSSer1177 and Akt which are abrogated by PA in human umbilical vein endothelial cells. In addition, Lina administration to ApoE-/- mice decreased oxidative stress as determined by urinary 8-OHdG secretion and NADPH oxidase subunit expression in the abdominal aorta.Conclusion; Lina inhibited atherogenesis in non-diabetic ApoE-/- mice. Amelioration of endothelial dysfunction associated with the reduction of oxidative stress by GLP-1 contributes to the atheroprotective effects of Lina. (Keyword) DPP-4 inhibitor / linagliptin / GLP-1 / endothelial function / inflammation / oxidative stress (Tokushima University Institutional Repository) ● Metadata: 110139 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.vph.2015.08.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26277250 ● Search Scopus @ Elsevier (PMID): 26277250 ● Search Scopus @ Elsevier (DOI): 10.1016/j.vph.2015.08.011 (Tokushima University Institutional Repository: 110139, DOI: 10.1016/j.vph.2015.08.011, PubMed: 26277250)
224.	Sachiko Nishimoto, Daiju Fukuda, Yasutomi Higashikuni, Kimie Tanaka, Yoichiro Hirata, Chie Murata, Joo-Ri Kim-Kaneyama, Fukiko Sato, Masahiro Bando, Shusuke Yagi, Takeshi Soeki, Tetsuya Hayashi, Issei Imoto, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata : Obesity-induced DNA released from adipocytes stimulates chronic adipose tissue inflammation and insulin resistance., Science Advances, Vol.2, No.3, e1501332, 2016. (Summary) Obesity stimulates chronic inflammation in adipose tissue, which is associated with insulin resistance, although the underlying mechanism remains largely unknown. Here we showed that obesity-related adipocyte degeneration causes release of cell-free DNA (cfDNA), which promotes macrophage accumulation in adipose tissue via Toll-like receptor 9 (TLR9), originally known as a sensor of exogenous DNA fragments. Fat-fed obese wild-type mice showed increased release of cfDNA, as determined by the concentrations of single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) in plasma. cfDNA released from degenerated adipocytes promoted monocyte chemoattractant protein-1 (MCP-1) expression in wild-type macrophages, but not in TLR9-deficient (Tlr9 (-/-) ) macrophages. Fat-fed Tlr9 (-/-) mice demonstrated reduced macrophage accumulation and inflammation in adipose tissue and better insulin sensitivity compared with wild-type mice, whereas bone marrow reconstitution with wild-type bone marrow restored the attenuation of insulin resistance observed in fat-fed Tlr9 (-/-) mice. Administration of a TLR9 inhibitory oligonucleotide to fat-fed wild-type mice reduced the accumulation of macrophages in adipose tissue and improved insulin resistance. Furthermore, in humans, plasma ssDNA level was significantly higher in patients with computed tomography-determined visceral obesity and was associated with homeostasis model assessment of insulin resistance (HOMA-IR), which is the index of insulin resistance. Our study may provide a novel mechanism for the development of sterile inflammation in adipose tissue and a potential therapeutic target for insulin resistance. (Tokushima University Institutional Repository) ● Metadata: 110123 (Link to Publication Site) ● Publication site (DOI): 10.1126/sciadv.1501332 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27051864 ● Summary page in Scopus @ Elsevier: 2-s2.0-84986905526 (Tokushima University Institutional Repository: 110123, DOI: 10.1126/sciadv.1501332, PubMed: 27051864, Elsevier: Scopus)
225.	Kenya Kusunose, M Sato, Hirotsugu Yamada, Y Saijo, Mika Bando, Y Hirata, S Nishio, S Hayashi and Masataka Sata : Prognostic implications of non-invasive vascular function tests in high-risk atherosclerosis patients., Circulation Journal, Vol.80, No.4, 1034-1040, 2016. (Summary) BACKGROUND: The aim of this study was to assess the role of clinically available vascular function tests as predictors of cardiovascular events and decline in kidney function.MethodsandResults:One hundred and fourteen patients who had at least 2 cardiovascular risk factors were recruited for vascular function assessment including ankle-brachial blood pressure index (ABI), brachial-ankle pulse wave velocity (baPWV), cardio-ankle vascular index (CAVI) and flow-mediated vasodilatation (%FMD). During a median period of 51 months, 35 patients reached the primary endpoint (29 cardiovascular events and 6 cardiac deaths), and 30 patients reached the secondary endpoint (decline in kidney function: defined as a 5% per year decline of estimated glomerular filtration rate). In sequential Cox models, a model on the basis of the Framingham risk score, hemoglobin, and high-sensitivity C-reactive protein (chi-squared, 16.6) was improved by the ABI (chi-squared: 21.5; P=0.047). The baPWV (hazard ratio: 1.42 per 1 SD increase; P=0.025) and the CAVI (hazard ratio: 1.52 per 1 SD increase; P=0.040) were associated with the secondary endpoint. The %FMD was only slightly associated with the primary and secondary endpoints.CONCLUSIONS: Both ABI and baPWV are significantly associated with future cardiovascular events in high-risk patients with cardiovascular disease. The predictive capabilities of these parameters are greater than that of other parameters in this cohort. (Keyword) Cardiovascular event / Endothelial function / Kidney function / Vascular function (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-15-1356 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26936237 ● Summary page in Scopus @ Elsevier: 2-s2.0-84961625684 (DOI: 10.1253/circj.CJ-15-1356, PubMed: 26936237, Elsevier: Scopus)
226.	Takeshi Soeki and Masataka Sata : Inflammatory biomarkers and atherosclerosis., International Heart Journal, Vol.57, No.2, 134-139, 2016. (Summary) Atherosclerosis has been regarded as a form of chronic vascular inflammation. Numerous biomarkers associated with inflammation have been identified as novel targets to monitor atherosclerosis and cardiovascular risk. C-reactive protein (CRP) is one of the most actively studied and established inflammatory biomarkers for cardiovascular events. However, CRP response is triggered by many disorders unrelated to cardiovascular disease, which interferes with the clinical application. This review describes established and traditional inflammatory biomarkers including CRP as well as novel inflammatory biomarkers reflective of local atherosclerotic inflammation. In addition, we focus on the potential usefulness of inflammatory biomarkers in developing anti-atherosclerotic therapeutic approaches. (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.15-346 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26973275 ● Summary page in Scopus @ Elsevier: 2-s2.0-84961564419 (DOI: 10.1536/ihj.15-346, PubMed: 26973275, Elsevier: Scopus)
227.	Takeshi Soeki, Tomomi Matsuura, Sachiko Bando, Takeshi Tobiume, Etsuko Uematsu, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Relationship between local production of microRNA-328 and atrial substrate remodeling in atrial fibrillation., Journal of Cardiology, Vol.68, No.6, 472-477, 2016. (Summary) BACKGROUND: The underlying mechanism of atrial substrate remodeling in atrial fibrillation (AF) remains unknown. In this study, we investigated whether local and systemic levels of microRNA (miR) might be associated with the presence of AF and with left atrial (LA) substrate properties.METHODS: Blood from the periphery, pulmonary vein (PV), and left atrial appendage (LAA) was sampled from 30 patients with AF undergoing PV isolation, and from 10 control subjects with Wolff-Parkinson-White syndrome and without AF. We measured peripheral, PV, and LAA plasma levels of miR-1, -26, -133a, -328, and -590 by reverse transcription-polymerase chain reaction. LA global contact mapping during sinus rhythm was performed before PV isolation.RESULTS: Plasma levels of miR-328 were higher in patients with AF than in control subjects. Plasma miR-328 levels were significantly higher in the LAA than in the periphery and PV in patients with AF, but not in control subjects. Plasma miR-1 levels were also higher in the LAA than in the PV in AF patients. Interestingly, LAA plasma levels of miR-328 showed a positive correlation with the LA voltage zone index (area with voltage <0.5mV divided by total LA surface area) and a weak correlation with LA volume.CONCLUSION: Local production of miR-328 in the left atrium may be involved in the process of atrial remodeling in patients with AF. (Keyword) Atrial fibrillation / Left atrium / MicroRNA / Remodeling / Substrate (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jjcc.2015.12.007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26987792 ● Summary page in Scopus @ Elsevier: 2-s2.0-84960969355 (DOI: 10.1016/j.jjcc.2015.12.007, PubMed: 26987792, Elsevier: Scopus)
228.	Yuta Torii, Hirotsugu Yamada, Susumu Matsukuma, Susumu Nishio, Kenya Kusunose, Miho Abe and Masataka Sata : Left Ventricular lipomatous hamartoma mimicking a calcified amorphous tumor., Circulation, Vol.133, No.8, e408-e410, 2016. (Link to Publication Site) ● Publication site (DOI): 10.1161/CIRCULATIONAHA.115.019252 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26903022 ● Search Scopus @ Elsevier (PMID): 26903022 ● Search Scopus @ Elsevier (DOI): 10.1161/CIRCULATIONAHA.115.019252 (DOI: 10.1161/CIRCULATIONAHA.115.019252, PubMed: 26903022)
229.	Yoshihiro Hayakawa, Manabu Kawada, Hiroyoshi Nishikawa, Takahiro Ochiya, Hideyuki Saya, Hiroyuki Seimiya, Ryoji Yao, Masahiro Hayashi, Chieko Kai, Akira Matsuda, Tomoki Naoe, Atsushi Ohtsu, Taku Okazaki, Hideo Saji, Masataka Sata, Haruhiko Sugimura, Yuichi Sugiyama, Masakazu Toi and Tatsuro Irimura : Report on the use of non-clinical studies in the regulatory evaluation of oncology drugs., Cancer Science, Vol.107, No.2, 189-202, 2016. (Summary) Non-clinical studies are necessary at each stage of the development of oncology drugs. Many experimental cancer models have been developed to investigate carcinogenesis, cancer progression, metastasis, and other aspects in cancer biology and these models turned out to be useful in the efficacy evaluation and the safety prediction of oncology drugs. While the diversity and the degree of engagement in genetic changes in the initiation of cancer cell growth and progression are widely accepted, it has become increasingly clear that the roles of host cells, tissue microenvironment, and the immune system also play important roles in cancer. Therefore, the methods used to develop oncology drugs should continuously be revised based on the advances in our understanding of cancer. In this review, we extensively summarize the effective use of those models, their advantages and disadvantages, ranges to be evaluated and limitations of the models currently used for the development and for the evaluation of oncology drugs. (Keyword) Animals / Antineoplastic Agents / Disease Models, Animal / Drug Discovery / Humans / Medical Oncology / Neoplasms (Tokushima University Institutional Repository) ● Metadata: 112369 (Link to Publication Site) ● Publication site (DOI): 10.1111/cas.12857 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26919617 ● Search Scopus @ Elsevier (PMID): 26919617 ● Search Scopus @ Elsevier (DOI): 10.1111/cas.12857 (Tokushima University Institutional Repository: 112369, DOI: 10.1111/cas.12857, PubMed: 26919617)
230.	Michio Shimabukuro, T Saito, H Masuzaki and Masataka Sata : Screening of coronary artery disease in diabetic patients: who and how? -reply-, Circulation Journal, Vol.80, No.2, 544, 2016. (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-15-1377 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26781270 ● Summary page in Scopus @ Elsevier: 2-s2.0-84955469675 (DOI: 10.1253/circj.CJ-15-1377, PubMed: 26781270, Elsevier: Scopus)
231.	Toshiyuki Niki, Tetsuzo Wakatsuki, Koji Yamaguchi, Yoshio Taketani, Hiroyasu Oeduka, Kenya Kusunose, Takayuki Ise, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Effects of the addition of eicosapentaenoic acid to strong statin therapy on inflammatory cytokines and coronary plaque components assessed by integrated backscatter intravascular ultrasound., Circulation Journal, Vol.80, No.2, 450-460, 2016. (Summary) BACKGROUND: The effects of eicosapentaenoic acid (EPA) on coronary artery disease have been previously reported; however, those of the addition of EPA to strong statins on coronary plaque components and local inflammatory cytokines are not known.METHODSANDRESULTS: A total of 95 patients who had been treated with strong statin for at least 6 months were randomized into 2 groups: an EPA group (additional treatment with EPA at 1,800 mg/day, n=48) or a control group (no additional treatment, n=47), for 6 months. The tissue characteristics of target coronary plaque in each patient were analyzed using IB-IVUS before and after treatment. We also measured plasma levels of inflammatory cytokines sampled in the coronary sinus (CS) and peripheral vein.A significant reduction in lipid volume (18.5±1.3 to 15.0±1.5 mm(3), P=0.007) and a significant increase in fibrous volume (22.9±0.8 to 25.6±1.1 mm(3), P=0.01) were observed in IB-IVUS image analyses in the EPA group, but no significant changes in the plaque components in the control group. CS levels of pentraxin 3 and monocyte chemoattractant protein-1 were lower after than before treatment with EPA (3.3±2.1 to 2.6±1.2 ng/ml, 120.4±26.2 to 110.2±26.8 pg/ml, P=0.015 and P=0.008, respectively); however, there were no significant changes in those inflammatory cytokines between pre- and post-treatment in the control group.CONCLUSIONS: The addition of EPA was associated with reduced lipid volume in coronary plaques and decreased inflammatory cytokines. (Circ J 2016; 80: 450-460). (Keyword) Coronary plaque / Eicosapentaenoic acid / Inflammatory cytokines / Integrated backscatter intravascular ultrasound / Strong statins (Tokushima University Institutional Repository) ● Metadata: 109653 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-15-0813 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26667367 ● Summary page in Scopus @ Elsevier: 2-s2.0-84955453337 (Tokushima University Institutional Repository: 109653, DOI: 10.1253/circj.CJ-15-0813, PubMed: 26667367, Elsevier: Scopus)
232.	Yuta Torii, Kenya Kusunose, Hirotsugu Yamada, Susumu Nishio, Yukina Hirata, Rie Amano, Masami Yamao, Mika Bando, Shuji Hayashi and Masataka Sata : Comparison of tricuspid annular plane systolic excursion in patients with atrial fibrillation vs sinus rhythm., The American Journal of Cardiology, Vol.117, No.2, 226-232, 2016. (Summary) Echocardiography now plays a central guiding role in the management of patients with atrial fibrillation (AF). However, the current guidelines mention little about the presence AF during the assessment of echocardiographic variables in the clinical setting. AF itself may impact on tricuspid annular plane systolic excursion (TAPSE) as a right ventricular systolic function compared with sinus rhythm (SR). The aim of this study was to compare and assess the echocardiographic parameters including TAPSE in patients with AF and SR. From January 1, 2013, to September 30, 2014, patients with AF without any cardiovascular disease were retrospectively evaluated using echocardiography. Age-, gender-, and left ventricular ejection fraction-matched patients with SR were selected from our database on the basis of a comprehensive history, physical examination, and echocardiographic findings. During the study period, we identified 239 patients with AF (74 ± 9 years; 65% men) and without any cardiac disease who underwent echocardiography. We also included 281 patients in the SR group (74 ± 8 years; 67% men). In all study subjects, TAPSE in AF was smaller than in SR regardless of age (17 ± 3 vs 20 ± 3 mm, p <0.001). In the stepwise multiple regression model, TAPSE was strongly associated with the presence of AF (standardized β = -0.362, p <0.001) and stroke volume index (standardized β = 0.173, p <0.001) after adjustment for age, gender, heart rate, left ventricular ejection fraction, and tricuspid regurgitant grade. In conclusions, patients with AF had lower TAPSE than those with SR regardless of age. When we assess TAPSE in the clinical setting, we must pay attention to the presence of AF. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.amjcard.2015.10.035 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26651451 ● Summary page in Scopus @ Elsevier: 2-s2.0-84949257248 (DOI: 10.1016/j.amjcard.2015.10.035, PubMed: 26651451, Elsevier: Scopus)
233.	Akira Takashima, Shusuke Yagi, Koji Yamaguchi, Eri Takagi, Tamotsu Kanbara, Hirohisa Ogawa, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Tetsuya Kitagawa and Masataka Sata : Vegetation in the coronary sinus that concealed the presence of a coronary arteriovenous fistula in a patient with infectious endocarditis., International Journal of Cardiology, Vol.207, 266-268, 2016. (Keyword) Coronary sinus / Fistula / Infectious endocarditis / Vegetation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijcard.2016.01.057 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26808990 ● Summary page in Scopus @ Elsevier: 2-s2.0-84958019532 (DOI: 10.1016/j.ijcard.2016.01.057, PubMed: 26808990, Elsevier: Scopus)
234.	S Hayashi, Hirotsugu Yamada, Makoto Fukui, Hiro-O Ito and Masataka Sata : Correlation between arteriosclerosis and periodontal condition assessed by lactoferrin and [alpha]1-antitrypsin levels in gingival crevicular fluid., International Heart Journal, Vol.56, No.6, 639-643, 2015. (Summary) Patients with periodontal disease exhibit exacerbated atherosclerosis, aortic stiffness, or vascular endothelial dysfunction. However, in a recent scientific statement, the American Heart Association noted that neither has periodontal disease been proven to cause atherosclerotic vascular disease nor has the treatment of periodontal disease been proven to prevent atherosclerotic vascular disease. Therefore, the aim of the present study was to examine the correlation between periodontal condition and arteriosclerosis in patients with coronary artery disease (CAD), which is usually accompanied by systemic arteriosclerosis.We measured levels of gingival crevicular fluid lactoferrin (GCF-Lf) and 1-antitrypsin (GCF-AT) in 72 patients (67 ± 8 years, 56 men) with CAD. Furthermore, we evaluated the maximum intima-media thickness (max IMT) and plaque score of the carotid arteries as well as brachial-ankle pulse wave velocity (baPWV) and flow-mediated dilation (FMD) of the brachial artery, each of which is a parameter for determining arteriosclerosis status. The average level of GCF-Lf was 0.29 ± 0.36 µg/mL and that of GCF-AT was 0.31 ± 0.66 µg/mL, with significant correlation between the two (r = 0.701, P < 0.001). No significant difference in GCF-Lf and GCF-AT levels was observed between patients with single-, double-, and triple-vessel CAD. There were no significant correlations between the arteriosclerosis parameters (ie, max IMT, plaque score, baPWV, and FMD) and GCF-Lf or GCF-AT.No correlation between the GCF biomarkers and the severity of arteriosclerosis was detected. This result may suggest that worsening of the periodontal condition assessed by GCF biomarkers is not a major potential risk factor for arteriosclerosis. (Keyword) Periodontal disease / Coronary artery disease / Atherosclerosis (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.15-218 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26549390 ● Search Scopus @ Elsevier (PMID): 26549390 ● Search Scopus @ Elsevier (DOI): 10.1536/ihj.15-218 (DOI: 10.1536/ihj.15-218, PubMed: 26549390)
235.	Y Higashi, N Azuma, Y Takeishi, T Minamino, Y Kihara, K Node, Masataka Sata, Y Fukumoto, H Origasa, H Matsuo, H Naritomi, M Fujita and W Shimizu : Effect of a low-intensity pulsed ultrasound device, SX-1001, on clinical symptoms in buerger disease with limb ischemia., International Heart Journal, Vol.56, No.6, 632-638, 2015. (Summary) Buerger disease is a rare disease of unknown etiology and cannot be treated by bypass surgery or percutaneous re-endovascularization. Although the need for effective limb ischemia prevention strategies is increasingly being recognized, effective preventative strategies are insufficient. The aim of this study using a new pulsed ultrasound device, SX-1001, is to determine whether treatment using SX-1001 can mitigate rest pain and improve blood supply to ischemic legs in patients with Buerger disease. This study is a multicenter, double-blinded, parallel randomized clinical trial testing the efficacy and safety of SX-1001. Treatment using SX-1001 is expected to result in reduction of the visual analog scale score for pain in Buerger disease patients who have Fontaine stage III. A total of 44 patients from 20 hospitals in Japan will be enrolled. The primary endpoint of the trial is a change in rest pain intensity on the visual analog scale score from baseline to 24 weeks. This trial will be the first to show the safety and efficacy of low-intensity pulsed ultrasound using SX-1001 for clinical symptoms in patients with Buerger disease. Low-intensity pulsed ultrasound may be a new therapy for limb ischemia. Ethical approval has been obtained from each of the participating institutes. Study findings will be disseminated through peer-reviewed journals and at scientific conferences.This study is registered at UMIN Clinical Trial Registry (UMIN000014757). (Keyword) Adult / Double-Blind Method / Extremities / Female / Humans / Ischemia / Male / Middle Aged / Pain Management / Pain Measurement / Thromboangiitis Obliterans / Treatment Outcome / Ultrasonic Therapy / Ultrasonic Waves / Walking (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.15-191 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26549399 ● Summary page in Scopus @ Elsevier: 2-s2.0-84948967619 (DOI: 10.1536/ihj.15-191, PubMed: 26549399, Elsevier: Scopus)
236.	Mika Bando, Hirotsugu Yamada, Kenya Kusunose, Shuji Hayashi, Yuriko Takagawa, Yoshihito Saijo, Susumu Nishio, Kozue Ogasawara and Masataka Sata : Pulmonary embolism due to right atrial free-floating thrombus during echocardiographic examination: a case of a pulmonary saddle thrombus., Journal of Echocardiography, Vol.13, No.4, 145-147, 2015. (Summary) A 69-year-old female with polymyositis was referred to our hospital with a chief complaint of dyspnea. Transthoracic echocardiography showed right ventricular overloading. In addition to two-dimensional echocardiography, observation of the abnormal free-floating string-like mass by three-dimensional echocardiography provided superior visualization of the features of the mass which protruded into the right ventricle across the tricuspid valve during diastole. These findings enabled us to confirm the diagnosis of venous thrombus. The thrombus disappeared during the echocardiographic examination. Multidetector-row computed tomography showed a string-like thrombus across the bifurcation of the main pulmonary artery. Anticoagulation therapy was initiated with heparin and warfarin, and fondaparinux was started on the fourth day. Three-dimensional echocardiography was useful in characterizing the motion and extent of the thrombus. (Keyword) Anticoagulation / Echocardiography / Pulmonary embolism / Right atrial thrombus (Link to Publication Site) ● Publication site (DOI): 10.1007/s12574-015-0263-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26408320 ● Summary page in Scopus @ Elsevier: 2-s2.0-84949101634 (DOI: 10.1007/s12574-015-0263-3, PubMed: 26408320, Elsevier: Scopus)
237.	Y Kato, U Yokoyama, C Yanai, R Ishige, D Kurotaki, M Umemura, T Fujita, T Kubota, S Okumura, Masataka Sata, T Tamura and Y Ishikawa : Epac1 Deficiency Attenuated Vascular Smooth Muscle Cell Migration and Neointimal Formation., Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.35, No.12, 2617-2625, 2015. (Summary) OBJECTIVE: Vascular smooth muscle cell (SMC) migration causes neointima, which is related to vascular remodeling after mechanical injury and atherosclerosis development. We previously reported that an exchange protein activated by cAMP (Epac) 1 was upregulated in mouse arterial neointima and promoted SMC migration. In this study, we examined the molecular mechanisms of Epac1-induced SMC migration and the effect of Epac1 deficiency on vascular remodeling in vivo.APPROACH AND RESULTS: Platelet-derived growth factor-BB promoted a 2-fold increase in SMC migration in a primary culture of aortic SMCs obtained from Epac1+/+ mice (Epac1+/+-ASMCs), whereas there was only a 1.2-fold increase in Epac1-/--ASMCs. The degree of platelet-derived growth factor-BB-induced increase in intracellular Ca2+ was smaller in Fura2-labeled Epac1-/--ASMCs than in Epac1+/+-ASMCs. In Epac1+/+-ASMCs, an Epac-selective cAMP analog or platelet-derived growth factor-BB increased lamellipodia accompanied by cofilin dephosphorylation, which is induced by Ca2+ signaling, whereas these effects were rarely observed in Epac1-/--ASMCs. Furthermore, 4 weeks after femoral artery injury, prominent neointima were formed in Epac1+/+ mice, whereas neointima formation was significantly attenuated in Epac1-/- mice in which dephosphorylation of cofilin was inhibited. The chimeric mice generated by bone marrow cell transplantation from Epac1+/+ into Epac1-/- mice and vice versa demonstrated that the genetic background of vascular tissues, including SMCs rather than of bone marrow-derived cells affected Epac1-mediated neointima formation.CONCLUSIONS: These data suggest that Epac1 deficiency attenuates neointima formation through, at least in part, inhibition of SMC migration, in which a decrease in Ca2+ influx and a suppression of cofilin-mediated lamellipodia formation occur. (Keyword) arterial injury / intima-media thickness / migration / signal transduction / vascular smooth muscle (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.115.306534 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26427796 ● Summary page in Scopus @ Elsevier: 2-s2.0-84948111930 (DOI: 10.1161/ATVBAHA.115.306534, PubMed: 26427796, Elsevier: Scopus)
238.	Naoko Sawada, Hirotsugu Yamada, Kenya Kusunose, Shuji Hayashi, Takashi Iwase and Masataka Sata : 3D transthoracic echocardiography provides accurate cross-sectional area of the RV outflow tract., JACC. Cardiovascular Imaging, Vol.8, No.11, 1343-1345, 2015. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jcmg.2014.12.018 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25797126 ● Summary page in Scopus @ Elsevier: 2-s2.0-84947031165 (DOI: 10.1016/j.jcmg.2014.12.018, PubMed: 25797126, Elsevier: Scopus)
239.	Masaru Hatano, Hidehiro Yamada, Keiichi Fukuda, Koichiro Yoshioka, Masanori Funauchi, Masataka Kuwana, Masataka Sata, Mutsugu Taniguchi, Norifumi Nakanishi, Takefumi Saito, Saji Tsutomu and Shigetake Sasayama : Effects of the endothelin receptor antagonist bosentan on hemodynamics and exercise capacity in Japanese patients with mildly symptomatic pulmonary arterial hypertension, Heart and Vessels, Vol.30, No.6, 798-804, 2015. (Summary) Pulmonary arterial hypertension (PAH) trial has mostly enrolled patients with World Health Organization functional class (WHO FC) III or IV. However, PAH is rapidly progressive in nature even in patients with less severe forms at diagnosis. Following the recent studies in Western population, here we assessed the efficacy of bosentan in Japanese patients with WHO FCII PAH. In this open-label trial, bosentan 125 mg twice daily was administered for 12 weeks in 16 patients, and a hemodynamic evaluation was performed. Treatment was continued for a further 12 weeks, where the effect on exercise capacity was assessed in 13 patients. In 16 patients, mean pulmonary arterial pressure decreased from 40.4 ± 10.4 to 35.6 ± 12.6 mmHg (p = 0.018) and cardiac index increased from 2.54 ± 0.73 to 2.96 ± 0.82 L/min/m2 (p = 0.023). Thus, pulmonary vascular resistance decreased from 792 ± 565 to 598 ± 558 dyn·sec/cm5 (p = 0.006). In 13 patients followed up for 24 weeks, 6-min walking distance increased from baseline at Week 12 (p = 0.003) and Week 24 (p = 0.011). All patients were mildly symptomatic at baseline with dyspnea index (Borg scale) of 2.50 ± 1.58 and the specific activity scale (SAS) of 5.0 ± 1.4 METs. These values remained unchanged throughout the study. These results suggest that bosentan treatment was beneficial for Japanese patients with WHO FC II PAH and treatment should be started in the early stage of the disease. (Keyword) Bosentan / Endothelin receptor antagonist / Pulmonary arterial hypertension / Hemodynamics / World Health Organization functional class (Link to Publication Site) ● Publication site (DOI): 10.1007/s00380-014-0544-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25028167 ● Summary page in Scopus @ Elsevier: 2-s2.0-84947493138 (DOI: 10.1007/s00380-014-0544-1, PubMed: 25028167, Elsevier: Scopus)
240.	Shusuke Yagi, Ken-ichi Aihara, Daiju Fukuda, Akira Takashima, Mika Bando, Tomoya Hara, Sachiko Nishimoto, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Takeshi Tobiume, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Masashi Akaike and Masataka Sata : Reduced ratio of eicosapentaenoic acid and docosahexaenoic acid to arachidonic acid is associated with early onset of acute coronary syndrome., Nutrition Journal, Vol.14, No.1, 111, 2015. (Summary) BACKGROUND: The hospitalization rate for acute coronary syndrome (ACS) for people aged 50 has remained stable over the past decade. Increased serum levels of n-3 polyunsaturated fatty acids (PUFAs), such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are associated with a decreased incidence of cardiovascular events and mortality in older patients; however, it is currently unknown whether reduced serum levels of n-3 PUFAs is also a risk factor for ACS in patients aged 50 years.METHODS AND RESULTS: We retrospectively reviewed 102 (male/ female 73/29) Japanese ACS patients whose serum levels of EPA/arachidonic acid (AA) and DHA/AA were evaluated on admission. The EPA/AA ratio was the lowest in patients aged 50 compared to patients aged 51-74 and 75. Pearson correlation analysis showed that early ACS onset was associated with low EPA/AA and DHA/AA ratios, and multiple regression analysis determined that decreased ratios of EPA/AA and DHA/AA, and male sex, current smoker status, increased body mass index and triglyceride levels, independently correlated with early ACS onset. Conversely, low-density and high-density lipoproteins, glycated hemoglobin, and hypertension did not correlate with early ACS onset. Subgroup analyses of male patients revealed that decreased ratios of EPA/AA and DHA/AA independently correlated with early ACS onset.CONCLUSION: Decreased EPA/AA and DHA/AA ratios may be risk factors for early onset of ACS, suggesting that reduced EPA/AA and DHA/AA may represent targets for preventing ACS in Japanese young people. (Link to Publication Site) ● Publication site (DOI): 10.1186/s12937-015-0102-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26514181 ● Summary page in Scopus @ Elsevier: 2-s2.0-84945959581 (DOI: 10.1186/s12937-015-0102-4, PubMed: 26514181, Elsevier: Scopus)
241.	Michio Shimabukuro, T Saito, T Higa, K Nakamura, H Masuzaki, Masataka Sata and group Fukuoka diabetologists the : Risk stratification of coronary artery disease in asymptomatic diabetic subjects using multidetector computed tomography, Circulation Journal, Vol.79, No.11, 2422-2429, 2015. (Summary) BACKGROUND: Patients with type 2 diabetes mellitus (T2DM) show a greater risk for coronary artery disease (CAD), but the risk stratification in asymptomatic CAD patients has not been established. This study investigated the prevalence and severity for asymptomatic CAD and predictors in T2DM patients.METHODSANDRESULTS: In a multiclinic group, diabetic patients (320 men, 186 women) without known symptoms suggestive of CAD were recruited for multidetector computed tomography (MDCT). Patients were categorized according to severity of coronary atherosclerosis: Grade 1 (normal findings), Grade 2 (mild atherosclerosis without significant stenosis), Grade 3 (moderate stenosis/atherosclerosis, 50-74% stenosis), Grade 4 (moderate stenosis/atherosclerosis, 75-89% stenosis), Grade 5 (severe stenosis/atherosclerosis, 90% stenosis). The trend for severity grade of CAD was slightly higher in men than women (P=0.054). For critical lesions (combined Grades 3-5), the prevalence was almost equal (men 44% vs. women 37%; P=0.113). Multivariate models showed that in men, HbA1c7.4%, dyslipidemia, duration of diabetes, retinopathy, and other type of cardiovascular diseases were predictors of critical lesions and in women, duration of diabetes and retinopathy were predictors.CONCLUSIONS: The prevalence and severity of asymptomatic CAD are comparably high in men and women with T2DM. Risk stratification by using MDCT might be useful to predict asymptomatic coronary lesions requiring coronary revascularization. (Circ J 2015; 79: 2422-2429). (Keyword) Coronary atherosclerosis / Diabetes mellitus / Multidetector computed tomography / Sex difference (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-15-0325 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26399764 ● Search Scopus @ Elsevier (PMID): 26399764 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-15-0325 (DOI: 10.1253/circj.CJ-15-0325, PubMed: 26399764)
242.	S Bando, Daiju Fukuda, Takeshi Soeki, S Nishimoto, E Uematsu, Tomomi Matsuura, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Expression of NLRP3 in subcutaneous adipose tissue is associated with coronary atherosclerosis., Atherosclerosis, Vol.242, No.2, 407-414, 2015. (Summary) ObjectivesThe promotion of adipose tissue inflammation by lifestyle-related diseases such as obesity and diabetes accelerates atherogenesis; however, the underlying mechanisms remain incompletely understood. Nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome contributes to chronic inflammation in adipose tissue. Here, we investigated the link between NLRP3 expression in subcutaneous adipose tissue (SAT) and the severity of coronary atherosclerosis.Methods and resultsSAT was obtained from 72 patients who underwent heart device implantation and coronary angiography. Expression of NLRP3 inflammasome-related molecules (NLRP3, IL-1 and IL-18) in SAT were evaluated by quantitative RT-PCR. Laboratory markers related to lifestyle-related diseases were measured. Patients with obesity, dyslipidemia (P < 0.05, respectively), diabetes or hyperuricemia (P < 0.01, respectively) had significantly higher expression of NLRP3. Multivariate analysis demonstrated that body mass index and serum level of uric acid were predictors of NLRP3 expression in SAT. The expression of NLRP3 in SAT correlated negatively with serum adiponectin level (r = 0.23, P < 0.05). Patients with coronary artery disease showed higher NLRP3 expression than patients without significant stenosis (P < 0.01). Furthermore, the expression of NLRP3 in SAT correlated positively with the severity of coronary atherosclerosis as determined by Gensini score (r = 0.47, P < 0.0001) or SYNTAX score (r = 0.55, P < 0.0001). Multiple regression analysis revealed that the expression of NLRP3 in SAT remains as an independent predictors for the severity of coronary atherosclerosis.ConclusionsThe expression of NLRP3 in SAT, which is affected by lifestyle-related diseases, is associated with the severity of coronary atherosclerosis. Our results suggest that NLRP3 inflammasome in SAT may have a role in atherogenesis. (Keyword) Atherosclerosis / Adipose tissue / Inflammation / NLRP3 inflammasome / Lifestyle-related disease (Tokushima University Institutional Repository) ● Metadata: 109532 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2015.07.043 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26282945 ● Search Scopus @ Elsevier (PMID): 26282945 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2015.07.043 (Tokushima University Institutional Repository: 109532, DOI: 10.1016/j.atherosclerosis.2015.07.043, PubMed: 26282945)
243.	Tatsuo Motoki, Hirotsugu Kurobe, Yoichiro Hirata, Taisuke Nakayama, Hajime Kinoshita, Kevin A. Rocco, Hitoshi Sogabe, Takaki Hori, Masataka Sata and Tetsuya Kitagawa : PPAR-gamma agonist attenuates inflammation in aortic aneurysm patients., General Thoracic and Cardiovascular Surgery, Vol.63, No.10, 565-571, 2015. (Summary) Peroxisome proliferator-activated receptor (PPAR) -γ agonist, which is an anti-diabetes drug and reduces expression of tumor necrosis factor (TNF)-α, reported to have the effects for anti-inflammation in our body. In cardiovascular fields, this PPAR-γ agonist already reported to suppress progression of coronary atherosclerosis. Various cytokines, which is secreted from fat tissues around artery, promote atherosclerosis and/or aneurysmal changes in aorta/artery. Objective of our study is to clarify whether PPAR-γ agonist has anti-inflammatory effects in aorta of patients with aortic aneurysm (AA). The medical ethics committee in Tokushima University Hospital approved protocol for this study. Sixteen patients with AA (more than 5 cm in diameter, scheduled open surgery) were divided into two groups; one is PPAR-γ agonist administrating group [Formula: see text] n = 6, group P[Formula: see text], and another is the without group [Formula: see text] n = 10, group C[Formula: see text]. PPAR-γ agonist, whose dose was 15 mg/day, was administrated in the group P for more than 2 months before aneurysectomy and grafting (mean; 4.2 ± 3.4 months) (Supplemental Table 1). Biopsy specimens were obtained from abdominal subcutaneous fat, greater omentum, retroperitoneal periaortic fat and aneurysmal wall in surgical procedure. Blood examination also achieved before/after procedure. Harvested specimens were analyzed with histology (HE and EVG), immunohistochemistry (macrophage) and RT-PCR (adiponectin, MCP-1, TNF-α, CD68, matrix metalloprotease (MMP)-2, MMP-9). Macrophage infiltration in aortic wall and retroperitoneal periaortic fat among group P was significantly decreased compared to that among group C. Adiponectin expressions in both subcutaneous fat and retroperitoneal periaortic fat among the group P (adiponectin/β-actin) were significantly increased compared to those among the group C [subcutaneous fat; 16.8 ± 13.9 vs. 5.82 ± 2.94 (P = 0.04), retroperitoneal periaortic fat; 21.3 ± 24.1 vs. 2.12 ± 1.69 (P = 0.04)]. On the other hand, expressions of TNF-α, and MMP-9 in both aortic aneurysmal wall and retroperitoneal periaortic fat among group P were significantly decreased. [(Aortic aneurysmal wall; TNF-α; 0.45 ± 0.15 vs. 5.18 ± 3.49 (P = 0.02), MMP-9; 39.6 ± 69.0 vs. 721 ± 741 (P = 0.04)], [retroperitoneal periaortic fat; TNF-α; 1.14 ± 0.36 vs. 26.4 ± 25.0 (P = 0.048), MMP-9; 0.18 ± 0.21 vs. 50.0 ± 41.8 (P = 0.047)]. These data may indicate that PPAR-γ agonist become the way for preventing or delaying aortic aneurysm progression in patients. More studies will be needed to clarify this drug effects in detail. (Keyword) Aortic aneurysm / inflammation / Macrophage / PPAR-gamma agonist (Link to Publication Site) ● Publication site (DOI): 10.1007/s11748-015-0576-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26213347 ● Summary page in Scopus @ Elsevier: 2-s2.0-84943198660 (DOI: 10.1007/s11748-015-0576-1, PubMed: 26213347, Elsevier: Scopus)
244.	Hara Tomoya, Daiju Fukuda, Tanaka Kimie, Higashikuni Yasutomi, Hirata Yoichiro, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Rivaroxaban, a novel oral anticoagulant, attenuates atherosclerotic plaque progression and destabilization in ApoE-deficient mice., Atherosclerosis, Vol.242, No.2, 639-646, 2015. (Summary) OBJECTIVE: Activated factor X (FXa) plays a key role in the coagulation cascade, whereas accumulating evidence suggests that it also contributes to the pathophysiology of chronic inflammation on the vasculature. In this study, we assessed the hypothesis that rivaroxaban (Riv), a direct FXa inhibitor, inhibits atherogenesis by reducing macrophage activation.METHODS AND RESULTS: Expression levels of PAR-1 and PAR-2, receptors for FXa, increased in the aorta of apolipoprotein E-deficient (ApoE(-/-)) mice compared with wild-type mice (P < 0.01, P < 0.05, respectively). Administration of Riv (5 mg/kg/day) for 20 weeks to 8-week-old ApoE(-/-) mice reduced atherosclerotic lesion progression in the aortic arch as determined by en-face Sudan IV staining compared with the non-treated group (P < 0.05) without alteration of plasma lipid levels and blood pressure. Histological analyses demonstrated that Riv significantly decreased lipid deposition, collagen loss, macrophage accumulation and matrix metallopeptidase-9 (MMP-9) expression in atherosclerotic plaques in the aortic root. Quantitative RT-PCR analyses using abdominal aorta revealed that Riv significantly reduced mRNA expression of inflammatory molecules, such as MMP-9, tumor necrosis factor- (TNF-). In vitro experiments using mouse peritoneal macrophages or murine macrophage cell line RAW264.7 demonstrated that FXa increased mRNA expression of inflammatory molecules (e.g., interleukin (IL)-1 and TNF-), which was blocked in the presence of Riv.CONCLUSIONS: Riv attenuates atherosclerotic plaque progression and destabilization in ApoE(-/-) mice, at least in part by inhibiting pro-inflammatory activation of macrophages. These results indicate that Riv may be particularly beneficial for the management of atherosclerotic diseases, in addition to its antithrombotic activity. (Keyword) Activated factor X / atherosclerosis / Coagulation / inflammation / Macrophages / Rivaroxaban (Tokushima University Institutional Repository) ● Metadata: 109485 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2015.03.023 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25817329 ● Summary page in Scopus @ Elsevier: 2-s2.0-84941742835 (Tokushima University Institutional Repository: 109485, DOI: 10.1016/j.atherosclerosis.2015.03.023, PubMed: 25817329, Elsevier: Scopus)
245.	Susumu Nishio, Kenya Kusunose, Hirotsugu Yamada, Masami Yamao, Yukina Hirata, Kazuhiro Mori, Suguru Matsuoka and Masataka Sata : Echocardiographic screening for congenital heart disease in 8819 children: A report from local community events for children's healthcare., Journal of Cardiology, Vol.66, No.4, 315-319, 2015. (Summary) BACKGROUND: We had the opportunity to perform echocardiographic screening of children at local community events for children's healthcare sponsored by the prefectural government. The aim of this study was to assess the utility of echocardiographic screening by measuring the prevalence of congenital heart disease (CHD) and abnormal findings in children without history of diagnosed CHD.METHODS: Subjects consisted of 8819 infants and preschool children (1 month to 6 years) who underwent echocardiographic examination at public events from 2001 to 2013. Children with known CHD were excluded.RESULTS: We performed echocardiographic screening on 752 (range: 464-993) children at each event. At a total of 12 events, subjects consisted of 3175 infants less than one year (36%), 2292 one-year-olds (26%), 1058 two-year-olds (12%), 794 three-year-olds (9%), and other children up to age six years. We identified echocardiographic abnormalities in 137 children (15.5/1000 subjects), and 89 children (10.1/1000 subjects) were diagnosed with CHD. The prevalence of an echocardiographic abnormality did not change over the 12-year period (Kendall's tau=-0.272, p=0.19).CONCLUSIONS: CHD which could not be identified by prenatal echocardiography and neonatal auscultation could be detected in a substantial number of young children by echocardiographic screening. Echocardiographic screening may be useful for early diagnosis of CHD. However, our study is based on cross-sectional data without follow-up. Larger prospective studies are needed to verify the utility of echocardiographic screening with follow-up data in this cohort. (Keyword) Congenital heart disease / Echocardiography / Screening (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jjcc.2014.11.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25572021 ● Summary page in Scopus @ Elsevier: 2-s2.0-84939572949 (DOI: 10.1016/j.jjcc.2014.11.011, PubMed: 25572021, Elsevier: Scopus)
246.	Anna Tani, S Yamamoto, Masahiko Maegawa, Koutaro Kunimi, Sumika Matsui, Kaoru Keyama, Takeshi Katou, Hirokazu Uemura, Akira Kuwahara, Toshiya Matsuzaki, Toshiyuki Yasui, M Kamada, Takeshi Soeki, Masataka Sata and Minoru Irahara : Arterial stiffness is increased in young women with endometriosis., Journal of Obstetrics and Gynaecology, Vol.35, No.7, 711-715, 2015. (Summary) Endometriosis is a chronic gynaecological disorder that is accompanied by inflammation and oxidative stress. Atherosclerosis has a long subclinical progression in arteries of children and young adults decades before overt clinical manifestations of the disease. In this study, we determined arterial stiffness by measuring brachial-ankle pulse wave velocity (baPWV) in women with endometriosis to assess the presence of subclinical atherosclerosis. We also measured markers of inflammation and oxidative stress in women with endometriosis. baPWV in women with endometriosis aged over 30 years was significantly higher than that in women without endometriosis aged over 30 years (p < 0.05), but not in women aged less than 30. Serum high-sensitivity C-reactive protein level in women with endometriosis was significantly higher than that in controls (p < 0.05). Young women with endometriosis show significantly increased arterial stiffness, suggesting that women with endometriosis need to be cautious of the future onset of atherosclerosis. (Keyword) arterial stiffness / endometriosis / hs CRP / subclinical inflammation / young women (Link to Publication Site) ● Publication site (DOI): 10.3109/01443615.2014.992871 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25543526 ● Summary page in Scopus @ Elsevier: 2-s2.0-84944158077 (DOI: 10.3109/01443615.2014.992871, PubMed: 25543526, Elsevier: Scopus)
247.	Michio Shimabukuro, Yoshimasa Hasegawa, Moritake Higa, Rie Amano, Hirotsugu Yamada, Shunsaku Mizushima, Hiroaki Masuzaki and Masataka Sata : Subclinical carotid atherosclerosis burden in Japanese: comparison between Okinawa and Nagano residents., Journal of Atherosclerosis and Thrombosis, Vol.22, No.8, 854-868, 2015. (Summary) AIM: The prevalence of overweight and a change in atherosclerotic lipid profiles may be linked to region-specific differences in atherosclerotic diseases. We evaluated whether the lipid phenotype could be linked to region- and sex-specific differences in the degree of atherosclerosis.METHODS: Non-diabetic subjects included Okinawa (n=1674) and Nagano (n=1392) residents aged 30-75 years who underwent carotid ultrasonography for the measurement of maximum intima-media thickness (max IMT).RESULTS: Average max IMT was higher in Okinawa men and women, and the increase in max IMT with age was enhanced in men. Multiple regression analysis showed that in addition to age and systolic blood pressure, low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol were IMT determinants only in men for both Okinawa and Nagano. Meanwhile, HDL-cholesterol was a determinant for Okinawa men and women, but not for Nagano men and women.CONCLUSIONS: This is the first report to show region- and sex-specific differences in the determinants for max IMT in a Japanese population. The evaluation of the relationship between lipid profile patterns and region- and sex-specific differences in carotid atherosclerosis burden may be required. (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.26674 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26133316 ● Summary page in Scopus @ Elsevier: 2-s2.0-84940380486 (DOI: 10.5551/jat.26674, PubMed: 26133316, Elsevier: Scopus)
248.	Yukina Hirata, Hirotsugu Yamada, Kenya Kusunose, Takashi Iwase, Susumu Nishio, Shuji Hayashi, Mika Bando, Rie Amano, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Clinical Utility of Measuring Epicardial Adipose Tissue Thickness with Echocardiography Using a High-Frequency Linear Probe in Patients with Coronary Artery Disease., Journal of the American Society of Echocardiography, Vol.28, No.10, 1240-1246.e1, 2015. (Summary) The relationship between epicardial adipose tissue (EAT) and coronary artery disease (CAD) has recently attracted a great deal of attention in the medical community. The objective of this study was to determine whether measuring EAT thickness in the anterior interventricular groove (AIG) using echocardiography is feasible and whether this index can be a marker of CAD. A total of 311 patients (mean age, 67 ± 11 years; 208 men) who underwent coronary angiography between December 2011 and December 2013 were prospectively enrolled. EAT-AIG thickness and EAT thickness on the free wall of the right ventricle (RV) were measured in systole using a high-frequency linear probe. Seventy-one patients who underwent multidetector-row computed tomography were enrolled to validate the method for measuring EAT thickness using echocardiography. Subjects were divided into two groups, those with and without significant coronary stenosis, on the basis of findings on coronary angiography (≥ 75% luminal narrowing). EAT-AIG thickness measured using echocardiography was validated by computed tomography. EAT-AIG thickness was strongly correlated with EAT volume (r = 0.714, P < .001). The CAD group had thicker EAT-AIG than the non-CAD group (8.3 ± 3.0 vs 6.3 ± 2.5 mm, P < .001). EAT-RV thickness was greater in the CAD group than in the non-CAD group (5.0 ± 2.1 vs 4.4 ± 2.3 mm, P = .009) as well. The area under the curve on receiver operating characteristic curve analysis of EAT-AIG thickness for predicting CAD was 0.704, which was higher than the EAT-RV thickness. Measuring EAT thickness using echocardiography with a high-frequency linear probe was validated with computed tomography. EAT-AIG was thicker in the CAD group than in the non-CAD group, as was EAT-RV thickness. This noninvasive index may have potential as a diagnostic marker for predicting coronary atherosclerosis. (Tokushima University Institutional Repository) ● Metadata: 109714 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.echo.2015.07.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26275751 ● Summary page in Scopus @ Elsevier: 2-s2.0-84944180106 (Tokushima University Institutional Repository: 109714, DOI: 10.1016/j.echo.2015.07.006, PubMed: 26275751, Elsevier: Scopus)
249.	Hirofumi Tomiyama, Takahide Kohro, Yukihito Higashi, Bonpei Takase, Toru Suzuki, Tomoko Ishizu, Shinichiro Ueda, Tsutomu Yamazaki, Tomoo Furumoto, Kazuomi Kario, Teruo Inoue, Shinji Koba, Kentaro Watanabe, Yasuhiko Takemoto, Takuzo Hano, Masataka Sata, Yutaka Ishibashi, Koichi Node, Koji Maemura, Yusuke Ohya, Taiji Furukawa, Hiroshi Ito, Hisao Ikeda and Akira Yamashina : Reliability of measurement of endothelial function across multiple institutions and establishment of reference values in Japanese., Atherosclerosis, Vol.242, No.2, 433-442, 2015. (Summary) AIMS: For the standardization of flow-mediated vasodilatation (FMD) assessment as a clinical tool, validation of its reliability across multiple institutions and the establishment of normal/reference values based on reliable data from multiple institutions are needed.METHODS AND RESULTS: In Study 1, assessment of FMD (scan recording and analysis) using an ultrasonographic semi-automatic measuring system (sFMD) was conducted at 18 participating institutions (sFMD-INST) (n = 981). All of the brachial arterial scans were also analyzed at a core laboratory (sFMD-COLB). After 111 subjects with inadequate sFMD recordings were excluded (n = 880), the correlation between the sFMD-INST and sFMD-COLB improved from R = 0.725 to R = 0.838 (p < 0.001). In Study 2, based on good-quality sFMD data obtained from 6660 subjects without cardiovascular disease (CVD) and 729 subjects with CVD from 27 institutions, reference values of sFMD are proposed by the Framingham risk score (FRS)-based risk categories and according to gender and age. The receiver-operating characteristic curve analysis revealed a significant power of sFMD values in reference ranges to discriminate between subjects with and without CVD (e.g., area under curve = 0.64 in the FRS-low risk group).CONCLUSIONS: When the analysis was limited to cases with clear sFMD recordings, the reliability of the sFMD assessment (scan and its analysis) conducted in individual institutions appeared to be acceptable. Reference sFMD values (lower cuff occlusion) for the Japanese population are proposed based on reliable data derived from multiple institutions, and the reference values may identify patients without advanced vascular damage. (Keyword) Endothelial function / Reference value / Reliability / Standardization (Tokushima University Institutional Repository) ● Metadata: 115008 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2015.08.001 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26291496 ● Summary page in Scopus @ Elsevier: 2-s2.0-84939809758 (Tokushima University Institutional Repository: 115008, DOI: 10.1016/j.atherosclerosis.2015.08.001, PubMed: 26291496, Elsevier: Scopus)
250.	Shusuke Yagi, Ken-ichi Aihara, Masashi Akaike, Daiju Fukuda, HM Salim, Masayoshi Ishida, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Toshio Matsumoto and Masataka Sata : Predictive factors for efficacy of dipeptidyl peptidase-4 inhibitors in patients with type 2 diabetes mellitus., Diabetes & Metabolism Journal, Vol.39, No.4, 342-347, 2015. (Summary) BACKGROUND: Predictive factors for the efficacy of dipeptidyl peptidase-4 (DPP-4) inhibitors for lowering glycosylated hemoglobin (HbA1c) remain unclear in patients with type 2 diabetes mellitus. The aim of this study is therefore to clarify predictive factors of the efficacy of DPP-4 inhibitors for lowering HbA1c after 12 months of treatment.METHODS: A total of 191 consecutive type 2 diabetic patients (male sex 55%, mean age, 68.3±35.8 years), who had been treated with DPP-4 inhibitors for 12 months, were enrolled in this study and evaluated retrospectively.RESULTS: After 12 months of DPP-4 inhibitor treatment, random blood glucose level, and HbA1c level, decreased from 167±63 to 151±49 mg/dL (P<0.01), and from 7.5%±1.3% to 6.9%±0.9% (P<0.01) respectively, without severe side effects. Multiple regression analysis showed that predictors of DPP-4 inhibitor treatment efficacy in lowering HbA1c level after 12 months were a decrease in HbA1c level after 3 months of treatment, a high baseline HbA1c level, a low baseline body mass index, and the absence of coronary artery disease.CONCLUSION: Most suitable candidates for treatment with DPP-4 inhibitors are diabetics who are not obese and do not have coronary artery disease. In addition, long-term efficacy of DPP-4 inhibitors can be predicted by decrement of HbA1c after 3 months of treatment. (Keyword) Coronary artery disease / diabetes mellitus / Dipeptidyl-peptidase IV inhibitors / Obese / Predictive factors (Link to Publication Site) ● Publication site (DOI): 10.4093/dmj.2015.39.4.342 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26301197 ● Summary page in Scopus @ Elsevier: 2-s2.0-84939780057 (DOI: 10.4093/dmj.2015.39.4.342, PubMed: 26301197, Elsevier: Scopus)
251.	Masayasu Ikutomi, Makoto Sahara, Toshiaki Nakajima, Yoshiyasu Minami, Toshihiro Morita, Yasunobu Hirata, Issei Komuro, Fumitaka Nakamura and Masataka Sata : Diverse contribution of bone marrow-derived late-outgrowth endothelial progenitor cells to vascular repair under pulmonary arterial hypertension and arterial neointimal formation., Journal of Molecular and Cellular Cardiology, Vol.86, 121-135, 2015. (Summary) It is still controversial whether bone marrow (BM)-derived endothelial progenitor cells (EPCs) can contribute to vascular repair and prevent the progression of vascular diseases. We aimed to characterize BM-derived EPC subpopulations and to evaluate their therapeutic efficacies to repair injured vascular endothelium of systemic and pulmonary arteries. BM mononuclear cells of Fisher-344 rats were cultured under endothelial cell-conditions. Early EPCs appeared on days 3-6. Late-outgrowth and very late-outgrowth EPCs (LOCs and VLOCs) were defined as cells forming cobblestone colonies on days 9-14 and 17-21, respectively. Among EPC subpopulations, LOCs showed the highest angiogenic capability with enhanced proliferation potential and secretion of proangiogenic proteins. To investigate the therapeutic effects of these EPCs, Fisher-344 rats underwent wire-mediated endovascular injury in femoral artery (FA) and were concurrently injected intraperitoneally with 60mg/kg monocrotaline (MCT). Injured rats were then treated with six injections of one of three EPCs (1×10(6) per time). After 4weeks, transplanted LOCs, but not early EPCs or VLOCs, significantly attenuated neointimal lesion formation in injured FAs. Some of CD31(+) LOCs directly replaced the injured FA endothelium (replacement ratio: 11.7±7.0%). In contrast, any EPC treatment could neither replace MCT-injured endothelium of pulmonary arterioles nor prevent the progression of pulmonary arterial hypertension (PAH). LOCs modified protectively the expression profile of angiogenic and inflammatory genes in injured FAs, but not in MCT-injured lungs. BM-derived LOCs can contribute to vascular repair of injured systemic artery; however, even they cannot rescue injured pulmonary vasculature under MCT-induced PAH. (Keyword) Endothelial progenitor cell / Monocrotaline / Post-angioplasty restenosis / Pulmonary arterial hypertension / Vascular disease (Link to Publication Site) ● Publication site (DOI): 10.1016/j.yjmcc.2015.07.019 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26231083 ● Summary page in Scopus @ Elsevier: 2-s2.0-84939243774 (DOI: 10.1016/j.yjmcc.2015.07.019, PubMed: 26231083, Elsevier: Scopus)
252.	Kenya Kusunose, Hirotsugu Yamada, Junko Hotsuchi, Mika Bando, Susumu Nishio, Yukina Hirata, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki, Jun Kishi and Masataka Sata : Prediction of Future Overt Pulmonary Hypertension by 6-Min Walk Stress Echocardiography in Patients With Connective Tissue Disease., Journal of the American College of Cardiology, Vol.66, No.4, 376-384, 2015. (Summary) BACKGROUND: Early detection of pulmonary hypertension (PH) in connective tissue disease (CTD) is crucial to ensuring that patients receive timely treatment for this progressive disease. Exercise stress tests have been used to screen patients in an attempt to identify early-stage PH. Recent studies have described abnormal mean pulmonary artery pressure (mPAP)-cardiac output (Q) responses as having the potential to assess the disease state.OBJECTIVES: This study hypothesized that pulmonary circulation pressure-flow relationships obtained by 6-min walk (6MW) stress echocardiography would better delineate differential progression of PH and predict development of PH during follow-up.METHODS: We prospectively performed 6MW stress echocardiographic studies in 78 CTD patients (age 58 ± 12 years; 9% male) at baseline and follow-up. All patients underwent yearly echocardiographic follow-up studies for up to 5 years.RESULTS: During a median period of 32 months (range: 15 to 62 months), 16 patients reached the clinical endpoint of development of PH and none died during follow-up. PH was confirmed by right heart catheterization in all 16 patients (mPAP 25 mm Hg and pulmonary capillary wedge pressure 15 mm Hg). In a Cox proportional-hazards survival model, 6MW distance (hazard ratio [HR]: 0.99; p = 0.010), early diastolic tricuspid annulus motion velocity (HR: 0.79; p = 0.025), and mPAP/Q by 6MW stress (HR: 1.10; p = 0.005) were associated with development of PH. In sequential Cox models, a model on the basis of 6MW distance (chi-square, 6.6) was improved by mPAP/Q (chi-square: 14.4; p = 0.019). Using a receiver-operating characteristic curve, we found that the best cutoff value of mPAP/Q for predicting development of pulmonary hypertension was >3.3 mm Hg/l/min.CONCLUSIONS: The 6MW stress echocardiography noninvasively provides an incremental prognostic value of PH development in CTD. This is a single-center prospective cohort study. Larger multicenter studies are warranted to confirm this result. (Keyword) lupus erythematosus / mixed connective tissue disease / pulmonary circulation / systemic scleroderma (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jacc.2015.05.032 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26205595 ● Summary page in Scopus @ Elsevier: 2-s2.0-84937681606 (DOI: 10.1016/j.jacc.2015.05.032, PubMed: 26205595, Elsevier: Scopus)
253.	Mika Bando, Hirotsugu Yamada, Kenya Kusunose, Daiju Fukuda, Rie Amano, Rina Tamai, Yuta Torii, Yukina Hirata, Susumu Nishio, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Comparison of carotid plaque tissue characteristics in patients with acute coronary syndrome or stable angina pectoris: assessment by iPlaque, transcutaneous carotid ultrasonography with integrated backscatter analysis., Cardiovascular Ultrasound, Vol.13, No.1, 34, 2015. (Summary) BACKGROUND: The association of the tissue characteristics of carotid plaques with coronary artery disease has attracted interest. The present study compared the tissue characteristics of carotid plaques in patients with acute coronary syndrome (ACS) with those in patients with stable angina pectoris (SAP) using the iPlaque system, which is based on ultrasound integrated backscatter.METHODS AND RESULTS: Carotid ultrasound examinations were performed in 26 patients with ACS, and 38 age- and gender-matched patients with SAP. Neither plaque area nor maximal intima-media thickness differed significantly between the two groups. However, the average integrated backscatter value within the plaque was greater in the ACS patients than in the SAP patients. iPlaque analysis revealed that the percentage blue area (lipid pool) was greater in the ACS patients than in the SAP patients (43.4±11.2 vs 18.3±10.3 %, p<0.0001), and that the percentage green area (fibrosis) was lower in the ACS than in the SAP patients (7.5±7.5 % vs 20.7±11.7 %, p<0.0001).CONCLUSIONS: The lipid component of carotid plaques is greater in ACS patients than in SAP patients. Our iPlaque system provides a useful and feasible method for the tissue characterization of carotid plaques in the clinical setting. (Keyword) Carotid arteries / Plaque vulnerability / ultrasound / Acute coronary syndrome (ACS) (Tokushima University Institutional Repository) ● Metadata: 109520 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12947-015-0031-6 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26209244 ● Summary page in Scopus @ Elsevier: 2-s2.0-84937791819 (Tokushima University Institutional Repository: 109520, DOI: 10.1186/s12947-015-0031-6, PubMed: 26209244, Elsevier: Scopus)
254.	Hiromu Yamazaki, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki, Toshiyuki Niki, Yoshio Taketani, Atsunori Kitaoka, Kenya Kusunose, Takayuki Ise, Takeshi Tobiume, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada and Masataka Sata : Impact of indoxyl sulfate, a uremic toxin, on non-culprit coronary plaque composition assessed by integrated backscatter intravascular ultrasound., Circulation Journal, Vol.79, No.8, 1773-1779, 2015. (Summary) BACKGROUND: Uremic toxin has emerged as an important determinant of cardiovascular risk. The aim of this study was to examine the relationship between serum uremic toxin and coronary plaque composition on integrated backscatter intravascular ultrasound (IB-IVUS).MethodsandResults:IB-IVUS was performed in 47 patients with planned treatment for angina pectoris. Non-culprit intermediate plaque analyzed in this study had to be >5 mm apart from the intervention site. 3-D IB-IVUS analysis was performed to determine percent lipid volume (LV) and fibrous volume (FV). We also measured serum uremic toxins (indoxyl sulfate [IS], asymmetric dimethylarginine [ADMA], and p-cresol [PC]). Glomerular filtration rate correlated with IS (r=-0.329, P=0.04), but did not correlate with ADMA or PC. Percent LV correlated with IS (r=0.365, P=0.02), but did not correlate with ADMA or PC. Percent FV also correlated with IS (r=-0.356, P=0.03), but did not correlate with ADMA or PC. On multivariate regression, only IS was associated with percent LV (r=0.359, P=0.04) and percent FV (r=-0.305, P=0.04) independently of potentially confounding coronary risk factors.CONCLUSIONS: Among the uremic toxins, serum IS might be a novel useful biomarker to detect and monitor lipid-rich coronary plaque on IB imaging. (Circ J 2015; 79: 1773-1779). (Keyword) Coronary plaque / Indoxyl sulfate / Integrated backscatter intravascular ultrasound (Tokushima University Institutional Repository) ● Metadata: 109533 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-15-0019 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25971408 ● Summary page in Scopus @ Elsevier: 2-s2.0-84937904061 (Tokushima University Institutional Repository: 109533, DOI: 10.1253/circj.CJ-15-0019, PubMed: 25971408, Elsevier: Scopus)
255.	S Hayashi, Hirotsugu Yamada, Mika Bando, Y Saijo, S Nishio, Y Hirata, AL Klein and Masataka Sata : Optimal analysis of left atrial strain by speckle tracking echocardiography: P-wave versus R-wave trigger., Echocardiography, Vol.32, No.8, 1241-1249, 2015. (Summary) BACKGROUND: Left atrial (LA) strain analysis using speckle tracking echocardiography is useful for assessing LA function. However, there is no established procedure for this method. Most investigators have determined the electrocardiographic R-wave peak as the starting point for LA strain analysis. To test our hypothesis that P-wave onset should be used as the starting point, we measured LA strain using 2 different starting points and compared the strain values with the corresponding LA volume indices obtained by three-dimensional (3D) echocardiography.METHODS: We enrolled 78 subjects (61 ± 17 years, 25 males) with and without various cardiac diseases in this study and assessed global longitudinal LA strain by two-dimensional speckle tracking strain echocardiography using EchoPac software. We used either R-wave peak or P-wave onset as the starting point for determining LA strains during the reservoir (Rres, Pres), conduit (Rcon, Pcon), and booster pump (Rpump, Ppump) phases. We determined the maximum, minimum, and preatrial contraction LA volumes, and calculated the LA total, passive, and active emptying fractions using 3D echocardiography.RESULTS: The correlation between Pres and LA total emptying fraction was better than the correlation between Rres and LA total emptying fraction (r = 0.458 vs. 0.308, P = 0.026). Pcon and Ppump exhibited better correlation with the corresponding 3D echocardiographic parameters than Rcon (r = 0.560 vs. 0.479, P = 0.133) and Rpump (r = 0.577 vs. 0.345, P = 0.003), respectively.CONCLUSIONS: LA strain in any phase should be analyzed using P-wave onset as the starting point rather than R-wave peak. (Keyword) left atrium / strain / three-dimensional echocardiography / two-dimensional speckle tracking (Link to Publication Site) ● Publication site (DOI): 10.1111/echo.12834 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25363348 ● Summary page in Scopus @ Elsevier: 2-s2.0-84937512721 (DOI: 10.1111/echo.12834, PubMed: 25363348, Elsevier: Scopus)
256.	Tomoya Hara, Shusuke Yagi, Masashi Akaike and Masataka Sata : Transdermal patch of bisoprolol for the treatment of hypertension complicated with aortic dissection., International Journal of Cardiology, Vol.198, 220-221, 2015. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijcard.2015.06.112 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26173061 ● Summary page in Scopus @ Elsevier: 2-s2.0-84940416779 (DOI: 10.1016/j.ijcard.2015.06.112, PubMed: 26173061, Elsevier: Scopus)
257.	Hirotsugu Yamada and Masataka Sata : Does echocardiographic epicardial adipose tissue thickness become a useful biomarker?, Journal of Atherosclerosis and Thrombosis, Vol.22, No.6, 555-556, 2015. (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.ED015 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25891211 ● Summary page in Scopus @ Elsevier: 2-s2.0-84931043161 (DOI: 10.5551/jat.ED015, PubMed: 25891211, Elsevier: Scopus)
258.	Kimie Tanaka and Masataka Sata : Visualization of human coronary vasa vasorum in vivo., Circulation Journal, Vol.79, No.6, 1211-1212, 2015. (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-15-0356 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25877739 ● Summary page in Scopus @ Elsevier: 2-s2.0-84930074602 (DOI: 10.1253/circj.CJ-15-0356, PubMed: 25877739, Elsevier: Scopus)
259.	Kenya Kusunose, Junko Hotsuchi, Y Takagawa, S Nishio, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Serial imaging changes during treatment of immunoglobulin G4-related disease with multiple pseudotumors., Circulation, Vol.131, No.21, 1882-1883, 2015. (Keyword) Aged, 80 and over / Antibodies, Anti-Idiotypic / Arteries / Cardiomegaly / Coronary Aneurysm / Eyelid Diseases / Fluorodeoxyglucose F18 / Humans / Immunoglobulin G / Male / Paraproteinemias / Plasma Cells / Positron-Emission Tomography / Radiopharmaceuticals / Tomography, X-Ray Computed (Link to Publication Site) ● Publication site (DOI): 10.1161/CIRCULATIONAHA.115.015638 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26015466 ● Summary page in Scopus @ Elsevier: 2-s2.0-84936080389 (DOI: 10.1161/CIRCULATIONAHA.115.015638, PubMed: 26015466, Elsevier: Scopus)
260.	Shusuke Yagi, Ken-ichi Aihara, Daiju Fukuda, Akira Takashima, Tomoya Hara, Junko Hotsuchi, Takayuki Ise, Koji Yamaguchi, Takeshi Tobiume, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Masashi Akaike and Masataka Sata : Effects of docosahexaenoic acid on the endothelial function in patients with coronary artery disease., Journal of Atherosclerosis and Thrombosis, Vol.22, No.5, 447-454, 2015. (Summary) AIM: The consumption of n-3 polyunsaturated fatty acids (PUFA), including docosahexaenoic acid DHA), reduces the incidence of cardiovascular events, and reduced serum levels of n-3 PUFA may be associated with an increased risk of cardiovascular events. However, controversy remains regarding which components of PUFA are associated with the endothelial function in patients with coronary artery disease (CAD). We therefore examined the associations between the n-3 and n-6 PUFA levels and CAD.METHODS: We retrospectively reviewed 160 consecutive Japanese patients with CAD whose endothelial function was measured according to the percent change in flow-mediated dilation (FMD) and the serum levels of n-3 PUFA, including eicosapentaenoic acid (EPA) and DHA, and n-6 PUFA, including arachidonic acid (AA) and dihomo-gamma-linolenic acid (DHLA).RESULTS: A single regression analysis showed no relationships between the FMD and the serum levels of PUFA, including EPA, DHA, AA and DHLA. In contrast, a multiple regression analysis showed that the DHA level was a positive (P0.01) and age was a negative (P0.001) contributor to an increased FMD; however, sex, body mass index, systolic and diastolic blood pressure, current/past smoking and the levels of HbA1c, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, EPA, AA and DHLA did not significantly affect the outcome.CONCLUSIONS: The serum level of DHA is associated with the endothelial function evaluated according to the FMD in patients with CAD, thus suggesting that a low serum level of DHA may be a predictive biomarker for endothelial dysfunction. (Keyword) Flow-mediated dilation / n-3 polyunsaturated fatty acids / Docosahexaenoic acid (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.26914 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25342567 ● CiNii @ National Institute of Informatics (CRID): 1390282679408260352 ● Summary page in Scopus @ Elsevier: 2-s2.0-84929412906 (DOI: 10.5551/jat.26914, PubMed: 25342567, CiNii: 1390282679408260352, Elsevier: Scopus)
261.	Toshiyuki Niki, Takeshi Soeki, Koji Yamaguchi, Yoshio Taketani, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Elevated concentration of interferon-inducible protein of 10 kD (IP-10) is associated with coronary atherosclerosis., International Heart Journal, Vol.56, No.3, 269-272, 2015. (Summary) Several studies have shown that various chemokines are more highly expressed in atherosclerotic plaques than in normal vessel walls. In the present study, we investigated the relationship between coronary atherosclerosis and noteworthy chemokines, including interferon-inducible protein of 10 kD (IP-10); monocyte chemoattractant protein 1 (MCP-1); regulated on activation, normal T-cell expressed and secreted (RANTES); and high-sensitivity C-reactive protein (hsCRP), an established marker of atherosclerotic disease. We studied 28 patients who underwent coronary angiography because of suspected coronary artery disease (CAD). CAD was defined as stenosis of more than 50% of the vessel diameter on coronary angiograms. Blood samples were obtained both from the aorta and the coronary sinus (CS) just before coronary angiography. Relative to CAD (-) patients, those who were CAD (+) tended to have higher plasma concentrations of IP-10 in the aorta, as well as significantly higher transcoronary concentration gradients of circulating IP-10. There were no significant differences between the two groups in aortic plasma concentrations or transcoronary concentration gradients of MCP-1, RANTES, and hsCRP. Furthermore, both the aortic plasma concentrations and transcoronary concentration gradients of IP-10 correlated with the Gensini score (r = 0.58 and r = 0.63, respectively, P < 0.01), while the plasma MCP-1, RANTES, and serum hsCRP concentrations did not. This study suggests that IP-10 is a good surrogate marker of coronary atherosclerosis. (Keyword) Coronary artery disease / Coronary circulation / Chemokine (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.14-300 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25902883 ● Search Scopus @ Elsevier (PMID): 25902883 ● Search Scopus @ Elsevier (DOI): 10.1536/ihj.14-300 (DOI: 10.1536/ihj.14-300, PubMed: 25902883)
262.	Yoshiyasu Minami, Toshiaki Nakajima, Masayasu Ikutomi, Toshihiro Morita, Issei Komuro, Masataka Sata and Makoto Sahara : Angiogenic potential of early and late outgrowth endothelial progenitor cells is dependent on the time of emergence., International Journal of Cardiology, Vol.186, 305-314, 2015. (Summary) BACKGROUND: Recent studies have suggested that late-outgrowth endothelial progenitor cells (EPCs) derived from human peripheral blood mononuclear cells (hPBMNCs) might have higher angiogenic potential than classically-defined early-outgrowth EPCs (EOCs). However, it still remains unclear which of "so-called" EPC subpopulations defined in a variety of ways has the highest angiogenic potential.METHODS AND RESULTS: We classified hPBMNC-derived EPC subpopulations by the time of their emergence in culture. EOCs were defined as attached cells on culture days 3-7. Late-outgrowth EPCs, defined as the cell forming colonies with cobblestone appearance since day 10, were further classified as follows: "moderate"-outgrowth EPCs (MOCs) emerging on days 10-16, "late"-outgrowth EPCs (LOCs) on days 17-23, and "very late"-outgrowth EPCs (VOCs) on days 24-30. Flow cytometry analyses showed the clear differences of hematopoietic/endothelial markers between EOC (CD31+VE-cadherin-CD34-CD14+CD45+) and LOC (CD31+VE-cadherin+CD34+CD14-CD45-). We found that LOCs had the highest proliferation and tube formation capabilities in vitro along with the highest expression of angiogenic genes including KDR and eNOS. To investigate the in vivo therapeutic efficacies, each EPC subpopulation was intravenously transplanted into immunocompromised mice (total 4×105 cells) after unilateral hindlimb ischemia surgery. The LOC-treated mice exhibited significantly-enhanced blood flow recovery (flow ratios of ischemic/non-ischemic leg: 0.99±0.02 [LOC group] versus 0.67±0.07 to 0.78±0.09 [other groups]; P<0.05) and augmented capillary collateral formation in ischemic leg, which were attributable to their direct engraftment into host angiogenic vessels (approximately 10%) and paracrine effects.CONCLUSION: hPBMNC-derived late-outgrowth EPCs emerging on culture days 17-23 are superior to other EPC subpopulations with regard to therapeutic angiogenic potential. (Keyword) angiogenesis / Endothelial progenitor cell / Ischemic vascular disease / Regenerative medicine (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijcard.2015.03.166 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25838182 ● Summary page in Scopus @ Elsevier: 2-s2.0-84929190302 (DOI: 10.1016/j.ijcard.2015.03.166, PubMed: 25838182, Elsevier: Scopus)
263.	A Takashima, Michio Shimabukuro, M Tabata, Daiju Fukuda, E Uematsu, H Ishibashi-Ueda, S Takanashi and Masataka Sata : Histopathological heterogeneity of in-stent restenosis in four coronary endarterectomy specimens., Cardiovascular Pathology, Vol.24, No.3, 194-197, 2015. (Summary) Here, we histopathologically compare four patients undergoing coronary artery bypass with coronary endarterectomy and onlay patch grafting for in-stent restenosis (ISR) after the implantation of a bare-metal stent (BMS), sirolimus-eluting stent (SES), or paclitaxel-eluting stent (PES) in an everolimus-eluting stent (EES). Heterogeneity of ISR was noted histopathologically. In ISR for BMS, restenosis is likely caused by so-called neoatherosclerosis that occurred which altered the healing process of BMS implantation. Two ISR cases for SES showed a histopathological heterogeneity: one showed nodular calcified thrombus around stent strut protruding into the lumen, and the other showed concentric neointima composed of CD68-positive foam cell proliferation. In the ISR lesion for PES in EES, infiltrations with foam cells macrophages, particularly numerous eosinophilic cell infiltrations, suggest a peristent strut hypersensitivity reaction. We found a remarkable histopathological heterogeneity of ISR. The study using coronary endarterectomy specimens can give us pivotal information about the histopathological heterogeneity of ISR. (Keyword) Coronary artery bypass / Coronary endarterectomy / In-stent restenosis / Percutaneous coronary intervention (Link to Publication Site) ● Publication site (DOI): 10.1016/j.carpath.2014.11.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25483741 ● Summary page in Scopus @ Elsevier: 2-s2.0-84929093226 (DOI: 10.1016/j.carpath.2014.11.002, PubMed: 25483741, Elsevier: Scopus)
264.	S Hayashi, Hiroshi Yamada, S Nishio, Junko Hotsuchi, Mika Bando, Y Takagawa, Y Saijo, Y Hirata and Masataka Sata : Tricuspid annular motion velocity as a differentiation index of hypertrophic cardiomyopathy from hypertensive heart disease., Journal of Cardiology, Vol.65, No.6, 519-525, 2015. (Summary) BACKGROUND: Hypertensive heart disease (HHD) and hypertrophic cardiomyopathy (HCM) are the most frequently encountered entities presenting left ventricular hypertrophy in routine echocardiographic examination, and their differentiation is sometimes difficult. Abnormalities in right ventricular (RV) myocardium have been reported frequently in patients with HCM more than in those with HHD. We therefore hypothesized that tricuspid annular motion (TAM) velocity determined by pulsed tissue Doppler echocardiography can be used to detect RV dysfunction in HCM and discriminate these etiologies.METHODS: TAM velocities were compared among clinically stable patients with 60 HCM and 60 HHD patients as well as 60 age-matched healthy controls. Peak systolic, early diastolic (TAM-e'), and atrial systolic velocities were measured. RV myocardial performance index was measured by tissue Doppler method. To more accurately differentiate HCM from HHD, electrocardiographic findings and brain natriuretic peptide levels, which can both be examined simply and noninvasively, were investigated in addition to echocardiography.RESULTS: RV wall thickness of the HCM group was greater than the HHD group (p=0.092), while there was no significant difference in RV myocardial performance index between the HCM and HHD groups (p=0.606). TAM-e' was significantly lower in the HCM group than in HHD and control groups (p=0.001). To differentiate HCM from HHD, TAM-e' was a powerful predictor as per multivariate logistic regression analysis (hazard ratio, 0.665; p<0.001) of parameters other than those of left ventricular parameters, and the area under the receiver operating characteristic curve (AUC) was 0.686 and the best cut-off value was 8.0cm/s (62% sensitivity, 65% specificity). Multivariate logistic analysis revealed that electrocardiographic ST-T changes were the next most effective marker for differentiating HCM after TAM-e'. When TAM-e' and ST-T changes were combined, the AUC increased to 0.748.CONCLUSIONS: TAM-e' is a potentially useful index to differentiate HCM from HHD. (Keyword) Hypertensive heart disease / Hypertrophic cardiomyopathy / Left ventricular hypertrophy / Tissue Doppler echocardiography / Tricuspid annular motion (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jjcc.2014.08.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25199979 ● Summary page in Scopus @ Elsevier: 2-s2.0-84929404966 (DOI: 10.1016/j.jjcc.2014.08.005, PubMed: 25199979, Elsevier: Scopus)
265.	S Hayashi, Hirotsugu Yamada, S Nishio, Junko Hotsuchi, Mika Bando, Y Takagawa, Y Saijo, Y Hirata and Masataka Sata : Age-and gender-specific changes of tricuspid annular motion velocities in normal hearts., Journal of Cardiology, Vol.65, No.5, 397-402, 2015. (Summary) Mitral annular motion (MAM) and tricuspid annular motion (TAM) velocities obtained by pulsed tissue Doppler echocardiography have been used to evaluate left ventricular (LV) and right ventricular (RV) functions. Although TAM velocity has been clinically applied for evaluating various cardiac diseases, the effects of age and gender remain unclear. Therefore, we aimed to determine the effects of age and gender on TAM velocity in normal hearts. We randomly selected 265 subjects (mean age, 59 years; range, 20-89 years) without abnormal clinical, electrocardiographic, and echocardiographic findings from a pool of subjects who had undergone transthoracic echocardiography. They were classified into four age groups: 20-39, 40-59, 60-79, and >80 years. Pulsed wave Doppler was applied to obtain MAM velocity of the lateral side and TAM velocity of the RV free wall side. The peak systolic (s'), early diastolic (e'), and atrial systolic (a') velocities of MAM and TAM were measured in all subjects. While MAM-s' (r=-0.267, p<0.001) correlated with age, TAM-s' did not (p=0.755). TAM-s' in any age groups had no significant gender differences. TAM-e' (r=-0.447, p<0.001) and MAM-e' (r=-0.724, p<0.001) correlated with age, respectively. In those aged 40-59 years, both TAM-e' (p=0.002) and MAM-e' (p=0.048) in females were significantly higher than those in males. The gender differences diminished in the ≥60 years age groups. There was no age-associated decline in TAM-s', while TAM-e' varied with age and gender as did MAM-e'. Although the same criteria for the TAM-s' can be used for identifying abnormal RV systolic function regardless of age and gender, age and gender differences must be considered when one utilizes the TAM-e' for the diagnosis or management of cardiovascular disease. (Keyword) Tricuspid annular motion / Tissue Doppler echocardiography / Aging / Gender / Mitral annular motion (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jjcc.2014.06.013 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25062786 ● Summary page in Scopus @ Elsevier: 2-s2.0-84928929859 (DOI: 10.1016/j.jjcc.2014.06.013, PubMed: 25062786, Elsevier: Scopus)
266.	Hirotsugu Yamada and Masataka Sata : The role of pericardial fat: The good, the bad and the ugly., Journal of Cardiology, Vol.65, No.1, 2-4, 2015. (Keyword) Pericardial adipose tissue / Epicardial adipose tissue / Coronary artery disease (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jjcc.2014.07.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25149094 ● Summary page in Scopus @ Elsevier: 2-s2.0-84930182808 (DOI: 10.1016/j.jjcc.2014.07.004, PubMed: 25149094, Elsevier: Scopus)
267.	Takeshi Soeki, Koji Yamaguchi, Toshiyuki Niki, E Uematsu, S Bando, T Matsuura, Takayuki Ise, Kenya Kusunose, Junko Hotsuchi, Takeshi Tobiume, Shusuke Yagi, Daiju Fukuda, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Plasma microRNA-100 is associated with coronary plaque vulnerability., Circulation Journal, Vol.79, No.2, 413-418, 2015. (Summary) BACKGROUND: Although numerous studies have reported altered plasma levels of various microRNAs (miRNAs) in patients with cardiovascular disease, there are no data on the relationship between plasma miRNAs and vulnerable coronary plaque. In this study, we investigated whether plasma miRNAs might be a sensitive marker of coronary plaque vulnerability.MethodsandResults:Integrated backscatter intravascular ultrasound (IB-IVUS) was performed in 32 consecutive patients with angina pectoris who underwent percutaneous coronary intervention. Three-dimensional analysis of IB-IVUS was performed to determine the percentage of lipid volume (%LV) and fibrous volume (%FV). Circulating miRNAs were measured in EDTA-plasma simultaneously obtained from the aorta and the coronary sinus (CS). Muscle-enriched (miR-133a, miR-208a, miR-499), vascular-enriched (miR-92a, miR-100, miR-126, miR-127, miR-145), and myeloid cell-enriched miRNAs (miR-155, miR-223) were measured. Plasma miR-100 was higher in the CS than in the aorta, but there were no significant differences in the levels of other miRNAs between the aorta and CS. Plasma miR-100 in the aorta was positively correlated with %LV (r=0.48, P<0.01) and negatively correlated with %FV (r=-0.41, P<0.05). Importantly, transcoronary concentration gradient of circulating miR-100 was more strongly correlated with %LV (r=0.53, P<0.01) and %FV (r=-0.56, P<0.01).CONCLUSIONS: miR-100 might be released into the coronary circulation from vulnerable coronary plaques. This study provides insights into the role of miRNAs in coronary atherosclerotic disease. (Circ J 2015; 79: 413-418). (Keyword) Coronary artery disease / Coronary circulation / Intravascular ultrasound / MicroRNA (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-14-0958 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25519160 ● CiNii @ National Institute of Informatics (CRID): 1390001205108464000 ● Summary page in Scopus @ Elsevier: 2-s2.0-84928251309 (DOI: 10.1253/circj.CJ-14-0958, PubMed: 25519160, CiNii: 1390001205108464000, Elsevier: Scopus)
268.	S Kimura, Yuka Ueda, Takayuki Ise, Shusuke Yagi, Takashi Iwase, K Nishikawa, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Shinsuke Katoh, Masashi Akaike, Natsuo Yasui and Masataka Sata : Impact of supervised cardiac rehabilitation on urinary albumin excretion in patients with cardiovascular disease., International Heart Journal, Vol.56, No.1, 105-109, 2015. (Summary) Urinary albumin excretion is a predictor of cardiovascular death. Cardiac rehabilitation (CR) with exercise training (ET) has been shown to improve exercise capacity and prognosis in patients with cardiovascular disease (CVD). However, it remains unclear whether CR reduces urinary albumin excretion in CVD patients. We performed a retrospective, observational study using data obtained from 98 male CVD patients without macroalbuminuria and estimated glomerular filtration rate (eGFR) < 30 mL/minute/1.73 m(2) who participated in CR with ET during hospitalization. Twenty-three patients continued supervised ET for 6 months (supervised group) and 75 patients quit supervised ET (non-supervised group). The supervised ET program consisted of 60 minutes of supervised sessions 1-3 times a week and 30-60 minutes of home exercise at least twice a week. Urinary albumin/creatinine ratio (ACR) was significantly decreased in the supervised group at 6 months after enrollment (43 ± 71 mg/g to 17 ± 20 mg/g creatinine, P < 0.05) but not in the non-supervised group. eGFR was unchanged in the supervised group but was significantly decreased in the non-supervised group (72 ± 18 mL/minute/1.73 m(2) to 67 ± 17 mL/minute/1.73 m(2), P < 0.001). The results of multiple regression analysis showed that only supervised ET was an independent contributor to ACR. CR with supervised ET decreased urinary albumin excretion without deterioration of renal function. These findings suggest that continuation of a supervised ET program is associated with reduction in the development of CVD and reduction in cardiovascular morbidity and mortality in CVD patients. (Keyword) Cardiac rehabilitation / Renal function / Cardiovascular disease (Tokushima University Institutional Repository) ● Metadata: 109367 (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.14-161 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25742947 ● Search Scopus @ Elsevier (PMID): 25742947 ● Search Scopus @ Elsevier (DOI): 10.1536/ihj.14-161 (Tokushima University Institutional Repository: 109367, DOI: 10.1536/ihj.14-161, PubMed: 25742947)
269.	Shusuke Yagi, A Takashima, M Mitsugi, T Wada, Junko Hotsuchi, Ken-ichi Aihara, T Hara, Masayoshi Ishida, Daiju Fukuda, Takayuki Ise, Koji Yamaguchi, Takeshi Tobiume, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Masashi Akaike and Masataka Sata : Effect of combination tablets containing amlodipine 10 mg and irbesartan 100 mg on blood pressure and cardiovascular risk factors in patients with hypertension., Therapeutics and Clinical Risk Management, Vol.11, 83-88, 2015. (Summary) Background: Hypertension is one of the major risk factors for cardiovascular and cerebrovascular disease and mortality. Patients who receive insufficient doses of antihypertensive agents or who are poorly adherent to multidrug treatment regimens often fail to achieve adequate blood pressure (BP) control. The aim of this study was to determine the efficacy of an angiotensin II receptor blocker (ARB) and calcium channel blocker (CCB) combination tablet containing a regular dose of irbesartan (100 mg) and a high dose of amlodipine (10 mg) with regard to lowering BP and other risk factors for cardiovascular disease.Methods: We retrospectively evaluated data from 68 patients with essential hypertension whose treatment regimen was changed either from combination treatment with an independent ARB and a low-dose or regular-dose CCB or from a combination tablet of ARB and a low-dose or regular-dose CCB to a combination tablet containing amlodipine 10 mg and irbesartan 100 mg, because of incomplete BP control. Previous treatments did not include irbesartan as the ARB.Results: The combination tablet decreased systolic and diastolic BP. In addition, it significantly decreased serum uric acid, low-density lipoprotein cholesterol, and increased high-density lipoprotein cholesterol levels, independent of the BP-lowering effect. Treatment with the combination tablet did not affect serum triglycerides, plasma glucose, glycated hemoglobin, serum potassium or creatinine levels, or the urinary albumin excretion rate.Conclusion: The combination tablet containing amlodipine 10 mg and irbesartan 100 mg had a greater BP-lowering effect than an ARB and a low-dose or regular-dose CCB. In addition, the combination tablet had more favorable effects on serum uric acid, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol levels in patients with hypertension. (Keyword) blood pressure / combination tablet / uric acid / low-density lipoprotein cholesterol / high-density lipoprotein cholesterol (Link to Publication Site) ● Publication site (DOI): 10.2147/TCRM.S72299 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25624765 ● Summary page in Scopus @ Elsevier: 2-s2.0-84921260560 (DOI: 10.2147/TCRM.S72299, PubMed: 25624765, Elsevier: Scopus)
270.	Shusuke Yagi, T Hara, R Ueno, Ken-ichi Aihara, Daiju Fukuda, A Takashima, Junko Hotsuchi, Takayuki Ise, Koji Yamaguchi, Takeshi Tobiume, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Masashi Akaike and Masataka Sata : Serum concentration of eicosapentaenoic acid is associated with cognitive function in patients with coronary artery disease., Nutrition Journal, Vol.13, No.1, 112, 2014. (Summary) BACKGROUND: Recent studies have shown that intake of n-3 polyunsaturated fatty acids (PUFAs) is associated with reduced risk of cognitive impairment and coronary artery disease (CAD); however, it is currently unknown whether reduced serum n-3 PUFA is associated with cognitive impairment in patients with CAD.METHODS: We retrospectively evaluated cognitive function with the mini-mental state examination (MMSE), serum levels of PUFAs (including eicosapentaenoic acid [EPA], docosahexaenoic acid [DHA], dihomogammalinolenic acid [DGLA], and arachidonic acid [AA]), cardiovascular risk factors (hypertension, dyslipidemia, diabetes mellitus, cerebrovascular disease, and history of current/previous smoking), and parameters of cardiac function (left ventricular ejection fraction and brain natriuretic peptide levels) in 146 Japanese CAD patients. The associations between the MMSE scores and the other parameters were evaluated.RESULTS: Pearson correlation analysis showed that EPA (R =0.25, P <0.01), EPA/AA ratio (R =0.22, P =0.01), and left ventricular ejection fraction (R =0.15, P =0.04) were positively associated with MMSE score, and that age (R = -0.20, P <0.01) and brain natriuretic peptide levels (R = -0.28, P <0.01) were inversely associated with MMSE score. Multiple regression analysis showed that age (P <0.05) was negatively associated with MMSE score, while EPA (P <0.01) and EPA/AA ratio (P <0.05) were positively associated with MMSE score; however, sex; body mass index; left ventricular ejection fraction; levels of DHA, AA, and DGLA; DHA/AA ratio; brain natriuretic peptide; and presence of hypertension, dyslipidemia, diabetes mellitus, cerebrovascular disease, and history of current/previous smoking were statistically excluded.CONCLUSIONS: Serum EPA concentration is associated with cognitive function in patients with CAD, suggesting that a low serum EPA level is a risk factor for cognitive impairment independent of cardiac function, including left ventricular ejection fraction. This correlation potentially lends further support to a role of dietary n-3 PUFAs in preventing the cognitive decline in CAD patients. (Keyword) Aged / Arachidonic Acid / Cognition / Cognition Disorders / Coronary Disease / Eicosapentaenoic Acid / Fatty Acids, Omega-3 / Female / Humans / Japan / Male / Middle Aged / Retrospective Studies / Risk Factors / Stroke Volume (Link to Publication Site) ● Publication site (DOI): 10.1186/1475-2891-13-112 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25471307 ● Summary page in Scopus @ Elsevier: 2-s2.0-84926465688 (DOI: 10.1186/1475-2891-13-112, PubMed: 25471307, Elsevier: Scopus)
271.	Takeshi Soeki, Kunihiko Koshiba, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro, Kazuo Minakuchi, I Kishimoto, Kenji Kangawa and Masataka Sata : Effect of ghrelin on autonomic activity in healthy volunteers., Peptides, Vol.62, 1-5, 2014. (Summary) Ghrelin is a novel growth hormone (GH)-releasing peptide originally isolated from the stomach. Recently, we have shown that ghrelin suppresses cardiac sympathetic activity and prevents early left ventricular remodeling in rats with myocardial infarction. In the present study, we evaluated the effect of ghrelin on autonomic nerve activity in healthy human subjects. An intravenous bolus of human synthetic ghrelin (10g/kg) was administered to 10 healthy men (mean age, 33 years). Holter monitoring assessment was performed before and during 2h after the ghrelin therapy. The standard deviation of normal RR intervals (SDNN), square root of the mean of the sum of the squares of differences between adjacent RR intervals (rMSSD), high-frequency power (HF), and low-frequency power (LF) were analyzed. Blood samples were also obtained before and after the therapy. A single administration of ghrelin decreased both heart rate and blood pressure. Interestingly, ghrelin significantly decreased the LF and LF/HF ratio of heart rate variability and increased the SDNN, rMSSD, and HF. Ghrelin also elicited a marked increase in circulating GH, but not insulin-like growth factor-1. These data suggest that ghrelin might suppress cardiac sympathetic nerve activity and stimulate cardiac parasympathetic nerve activity. (Keyword) Ghrelin / Autonomic nerve activity / Heart rate variability / Electrocardiography / Hemodynamics (Link to Publication Site) ● Publication site (DOI): 10.1016/j.peptides.2014.09.015 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25265271 ● Search Scopus @ Elsevier (PMID): 25265271 ● Search Scopus @ Elsevier (DOI): 10.1016/j.peptides.2014.09.015 (DOI: 10.1016/j.peptides.2014.09.015, PubMed: 25265271)
272.	Masayoshi Ishida, Michio Shimabukuro, Shusuke Yagi, S Nishimoto, C Kozuka, Daiju Fukuda, Takeshi Soeki, H Masuzaki, M Tsutsui and Masataka Sata : MicroRNA-378 regulates adiponectin expression in adipose tissue: A new plausible mechanism., PLoS ONE, Vol.9, No.11, e111537, 2014. (Summary) AIMS: Mechanisms regulating adiponectin expression have not been fully clarified. MicroRNAs (miRNAs), small non-coding RNAs that regulate gene expression, are involved in biological processes, including obesity and insulin resistance. We evaluated whether the miRNA-378 pathway is involved in regulating adiponectin expression.METHODS AND RESULTS: First, we determined a putative target site for miRNA-378 in the 3 prime untranslated region (3'UTR) of the adiponectin gene by in silico analysis. The levels of adiponectin mRNA and protein were decreased in 3T3-L1 cells overexpressing the mimic of miRNA-378. Luminescence activity in HEK293T cells expressing a renilla-luciferase-adiponectin-3'UTR sequence was inhibited by overexpressing the mimic of miRNA-378, and the decrease was reversed by adding the inhibitor of miRNA-378. Moreover, we confirmed the inhibitory effects of the mimic were cancelled in a deleted mutant of the miR-378 3'-UTR binding site. Addition of tumor necrosis factor- (TNF) led a upregulation of miR-378 and downregulation of adiponectin at mRNA and protein levels in 3T3-L1 cells. Level of miR-378 was higher and mRNA level of adiponectin was lower in diabetic ob/ob mice than those of normal C57BL/6 mice and levels of miR378 and adiponectin were negatively well correlated (r=-0.624, p=0.004).CONCLUSIONS: We found that levels of miRNA-378 could modulate adiponectin expression via the 3'UTR sequence-binding site. Our findings warrant further investigations into the role of miRNAs in regulating the adiponectin expression. (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0111537 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25379946 ● Search Scopus @ Elsevier (PMID): 25379946 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0111537 (DOI: 10.1371/journal.pone.0111537, PubMed: 25379946)
273.	Koji Yamaguchi, Tetsuzo Wakatsuki, Takeshi Soeki, Toshiyuki Niki, Yoshio Taketani, Hiroyasu Oeduka, Kenya Kusunose, Takayuki Ise, Takashi Iwase, Hirotsugu Yamada and Masataka Sata : Effects of telmisartan on inflammatory cytokines and coronary plaque component as assessed on integrated backscatter intravascular ultrasound in hypertensive patients., Circulation Journal, Vol.78, No.1, 240-247, 2014. (Summary) Telmisartan has unique pleiotropic effects in addition to renin-angiotensin system (RAS)-inhibition effects. The aim of this study was to evaluate the effects of telmisartan on the coronary plaque component and local inflammatory cytokines. A total of 50 patients with hypertension were randomized to 2 groups: the telmisartan group (additional treatment with telmisartan 80mg/day, n=25) or the control group (additional treatment with other anti-hypertensive drugs except RAS blockers, n=25) for 6 months. Tissue characteristics of target coronary plaque were analyzed using integrated backscatter intravascular ultrasound (IB-IVUS) before and after treatment. Plasma levels of inflammatory cytokines sampled in the coronary sinus (CS) and peripheral vein were also measured. Significant increases in fibrous volume (51.2±10.4 to 58.3±7.7%, P=0.03) and reductions in lipid volume (38.4±12.4 to 32.8±9.7%, P=0.03) were observed on IB in the telmisartan group, while there were no significant changes in the plaque component in the control group. CS levels of inflammatory cytokines (matrix metalloproteinase [MMP]3, tumor necrosis factor-, high-sensitivity C-reactive protein and MMP9) were lower after than before treatment in the only telmisartan group (7.7±6.1 to 5.5±4.9ng/ml, 3.1±1.9 to 2.3±2.0pg/ml, 5.6±6.0 to 2.2±2.4mg/L, 36.1±39.3 to 19.9±27.5ng/ml, P=0.02, P=0.03, P=0.04, P=0.07, respectively). Decreased local inflammatory response and plaque stabilization on IB imaging were observed after 6 months of telmisartan treatment. These findings might be associated with local anti-inflammatory and anti-arteriosclerotic effects of telmisartan. (Keyword) Coronary plaque / Inflammatory cytokine / Integrated backscatter intravascular ultrasound / Telmisartan (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-13-0741 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24189463 ● CiNii @ National Institute of Informatics (CRID): 1390282680085613824 ● Summary page in Scopus @ Elsevier: 2-s2.0-84891099318 (DOI: 10.1253/circj.CJ-13-0741, PubMed: 24189463, CiNii: 1390282680085613824, Elsevier: Scopus)
274.	A Takashima, Takayuki Ise, Shusuke Yagi, Takashi Iwase, S Kimura, Yuka Ueda, K Nishikawa, A Ishii, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Shinsuke Katoh, Masashi Akaike and Masataka Sata : Cardiac rehabilitation reduces serum levels of oxidized low-density lipoprotein., Circulation Journal, Vol.78, No.11, 2682-2687, 2014. (Summary) BACKGROUND: Oxidized low-density lipoprotein (oxLDL) levels have been found to play an important role in the progression of atherosclerosis. However, methods for effectively reducing oxLDL levels have not been established. Comprehensive cardiac rehabilitation (CR) with exercise training prevents the progression of atherosclerosis, and might reduce oxLDL levels.MethodsandResults:We measured the serum levels of malondialdehyde-modified LDL (MDA-LDL), a marker of oxLDL, in 136 patients who were enrolled in a 6-month CR program. Peak oxygen consumption (VO2) and MDA-LDL levels were analyzed, before and 6 months after enrolment. In total, 67 patients completed the CR program (CR group) and 69 patients failed to complete the program (non-CR group). Peak VO2increased significantly in the CR group (P<0.01). The levels of MDA-LDL decreased significantly in the CR group (P<0.01) but not in the non-CR group. VO2(peak VO2after CR-peak VO2before CR) was negatively associated with MDA-LDL (MDA-LDL after CR-MDA-LDL before CR) (R(2)=0.11, P=0.01). Multiple regression analysis showed that continuing CR was an independent determining factor for lowering MDA-LDL levels.CONCLUSIONS: CR decreases oxLDL levels in patients with cardiovascular diseases. Moreover, CR may prevent cardiovascular events through an antioxidative effect. (Circ J 2014; 78: 2682-2687). (Keyword) Cardiac rehabilitation / Lipoproteins / Oxidative stress (Tokushima University Institutional Repository) ● Metadata: 109368 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-14-0532 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25241889 ● Search Scopus @ Elsevier (PMID): 25241889 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-14-0532 (Tokushima University Institutional Repository: 109368, DOI: 10.1253/circj.CJ-14-0532, PubMed: 25241889)
275.	田中君枝 and Masataka Sata : The treatment of atherosclerosis in the elderly, Cardioangiology, Vol.76, No.3, 289-295, 2014. (Keyword) atherosclerosis / inflammation / vasa vasorum / cholesterol / statin (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1523388080096837504 (CiNii: 1523388080096837504)
276.	Kenya Kusunose, N Tomita, S Nishio, Mika Bando, S Hayashi, Junko Hotsuchi, Takashi Iwase, Hirotsugu Yamada and Masataka Sata : Left main coronary artery compression syndrome with an incomplete atrioventricular septal defect presenting as angina induced by hyperthyroidism., Internal Medicine, Vol.53, No.18, 2083-2085, 2014. (Summary) We herein report the case of a 29-year-old woman who was diagnosed with incomplete atrioventricular septal defect and extrinsic compression of the left main coronary artery (LMCA) with chest pain due to postpartum thyroiditis. She exhibited chest pain with ST elevation, and coronary computed tomography showed that the LMCA was compressed between the dilated pulmonary artery and aorta. After her hyperthyroidism was treated, her chest pain resolved. Surgical repair of endocardiosis and coronary bypass grafting were performed. On the one-year follow-up visit, the dilation of the pulmonary artery and right heart was decreased. It is important to consider the possibility of compression of the LMCA in patients presenting with pulmonary hypertension and chest pain. (Keyword) left main compression syndrome / congenital heart disease / postpartum thyroiditis (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.53.2403 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25224192 ● CiNii @ National Institute of Informatics (CRID): 1390282679850242944 ● Summary page in Scopus @ Elsevier: 2-s2.0-84907454931 (DOI: 10.2169/internalmedicine.53.2403, PubMed: 25224192, CiNii: 1390282679850242944, Elsevier: Scopus)
277.	Takeshi Soeki, S Bando, E Uematsu, T Matsuura, Toshiyuki Niki, Takayuki Ise, Kenya Kusunose, Junko Hotsuchi, Yuka Ueda, N Tomita, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Pentraxin 3 is a local inflammatory marker in atrial fibrillation., Heart and Vessels, Vol.29, No.5, 653-658, 2014. (Summary) Increasing evidence indicates that inflammation contributes to the pathogenesis of atrial fibrillation (AF). Pentraxin 3 (PTX3) is produced abundantly in local inflammatory lesions while C-reactive protein (CRP) is produced mainly in the liver. In this study, we investigated whether a local level of PTX3 might be a sensitive marker for the local inflammation of AF. Blood from the periphery and left atrial appendage (LAA) was sampled from 23 patients with AF undergoing pulmonary vein isolation, and from 10 control subjects with Wolff-Parkinson-White syndrome. We measured peripheral and LAA plasma concentrations of CRP, interleukin-6 (IL-6), tumor necrosis factor- (TNF-), and PTX3. Plasma PTX3 concentrations in both locations were higher in patients with AF than in control subjects. PTX3 concentrations were significantly higher in the LAA than the periphery in patients with AF (3.7 ± 1.4 vs 3.3 ± 1.2 ng/ml, P < 0.01), but not in control subjects (2.4 ± 0.5 vs 2.4 ± 0.5 ng/ml, not significant). Patients and controls showed no significant differences in CRP, IL-6, or TNF- concentrations between the periphery and LAA. Interestingly, there was a significant positive correlation between LAA plasma concentrations of PTX3 and left atrial volume (r = 0.55, P < 0.01). These data demonstrate that Local PTX3 production in the left atrium might reflect the local inflammation of AF. (Keyword) Pentraxin 3 / Atrial fibrillation / inflammation (Link to Publication Site) ● Publication site (DOI): 10.1007/s00380-013-0400-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23979265 ● Summary page in Scopus @ Elsevier: 2-s2.0-84929517476 (DOI: 10.1007/s00380-013-0400-8, PubMed: 23979265, Elsevier: Scopus)
278.	S Nishio, Kenya Kusunose, Hirotsugu Yamada, Junko Hotsuchi, S Hayashi, Mika Bando, Y Saijo, Y Hirata, M Abe and Masataka Sata : Multimodality imaging of biatrial myxomas in an asymptomatic patient., Journal of Cardiology Cases, Vol.10, No.3, 85-87, 2014. (Summary) Myxomas are located in the left atrium in 7580% of cases and almost always present with signs and symptoms of a thromboembolic event. Biatrial myxomas are rare, and their incidence is generally less than 2.5% of all myxomas. We herein present a case of biatrial myxomas as an incidental finding by echocardiography where the patient underwent surgery. Echocardiography continues to be the initial imaging modality for intracardiac masses. Cardiac magnetic resonance provides superior tissue characterization, particularly important in differentiating a myxoma from a thrombus. Appropriate use of these non-invasive imaging modalities may lead to a correct diagnosis and good outcome. (Keyword) Myxoma / transesophageal echocardiography / Cardiac magnetic resonance imaging / Atrium (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jccase.2014.03.009 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.jccase.2014.03.009 (DOI: 10.1016/j.jccase.2014.03.009)
279.	T Hara, K Kishi-Tanaka, Takashi Iwase, Hirotsugu Yamada, Masashi Akaike and Masataka Sata : Utility of lower limb positive pressure test for diagnosis of diastolic heart failure: a case report., The Journal of Medical Investigation : JMI, Vol.61, No.3-4, 404-408, 2014. (Summary) A 70-year-old woman with dyspnea on exertion was admitted to our hospital. She had a history of apical hypertrophic cardiomyopathy (HCM) and repeated hospitalization for heart failure. Results of physical examination were normal except for leg edema. Echocardiography showed apical HCM with preserved LV systolic function (LVEF = 70%). Although dyspnea on exertion and leg edema improved rapidly with the use of diuretics, her symptoms soon worsened when daily activity was started again. In order to examine the effect of preload on hemodynamics, we performed a lower limb positive pressure test by compressing both legs using a household air leg massager. Echocardiography showed increases in mitral E velocity, E/A ratio and pulmonary venous D flow as well as decrease in stroke volume during the lower limb positive pressure test. Simultaneously-recorded pressure study also showed elevated LVEDP and increased v wave of pulmonary capillary wedge pressure. These results suggested that even a small increase in preload led to elevation of LVEDP and symptomatic worsening due to severe diastolic heart failure in the present case. The lower limb positive pressure test may be useful for assessing the effect of preload on hemodynamics in patients with diastolic heart failure. (Keyword) diastolic heart failure / lower limb positive pressure test / apical hypertrophic cardiomyopathy (Tokushima University Institutional Repository) ● Metadata: 109593 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.61.404 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25264062 ● CiNii @ National Institute of Informatics (CRID): 1390282679219954688 ● Summary page in Scopus @ Elsevier: 2-s2.0-84907518768 (Tokushima University Institutional Repository: 109593, DOI: 10.2152/jmi.61.404, PubMed: 25264062, CiNii: 1390282679219954688, Elsevier: Scopus)
280.	Michio Shimabukuro, C. Okawa, X. F. Lei, J. R. Kim-Kaneyama, Hirotsugu Yamada, Hirotsugu Kurobe, Daiju Fukuda, M. Sato, Tetsuya Kitagawa and Masataka Sata : Effects of ezetimibe on oxidized cholesterol components in epicardial fat and myocardium: a gas chromatography-mass spectrometry analysis, Atherosclerosis, Vol.235, No.2, 113, 2014. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2014.05.307 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2014.05.307 (DOI: 10.1016/j.atherosclerosis.2014.05.307)
281.	Ken Saito, S Takeda, Y Saito, M Kawamura, Y Yoshikawa, H Yano and Masataka Sata : Electrocardiographic and chronobiological features of paroxysmal AV block recorded by ambulatory electrocardiography., The Journal of Medical Investigation : JMI, Vol.61, No.3, 4, 380-387, 2014. (Summary) The goal of this study was to investigate the electrocardiographic and chronobio-logical features of paroxysmal atrioventricular (AV) block (PAVB) using data from ambulatory electrocardiography (AECG). The study population consisted of five men and six women aged from 47 to 82 years of age. Main presenting symptoms were pre-syncope in five patients (45.5%) and syncope in three patients (27.3%). Organic cardiovascular diseases were seen in eight patients (72.7%), and AV conduction disturbances were seen in six patients (54.5%), such as right bundle branch block, first to second degree AV block on standard 12-lead electrocardiography. Incidence of PAVB events were 1-329 (37.9 ± 98.0) episodes/patient/day, and the maximum pause during Holter recordings was 3.3-12.4 (6.39 ± 3.09) seconds. This maximum pause caused by intrinsic AV block was longer than that of vagally mediated AV block (8.4 ± 3.2 sec vs 4.7 ± 1.0 sec, p<0.05). In chronobiological analysis, episodes of PAVB exhibited a circadian rhythm characterized by a peak between 2:00 am and 4:00 am and a trough between 0:00 pm and 2:00 pm. AECG is a useful tool to detect the maximum pause occurring during sleep and provides critical data necessary to prevent the sudden cardiac death caused by PAVB. (Keyword) paraxysmal AV block / ambulatory electrocardiography / circadian rhythm / syncope / right bundle branch block (Tokushima University Institutional Repository) ● Metadata: 109588 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.61.380 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25264058 ● Summary page in Scopus @ Elsevier: 2-s2.0-84907500921 (Tokushima University Institutional Repository: 109588, DOI: 10.2152/jmi.61.380, PubMed: 25264058, Elsevier: Scopus)
282.	Shusuke Yagi, M Fujimura, Masashi Akaike, Ken-ichi Aihara, Takashi Iwase, M Tada, Yuka Ueda, Takayuki Ise, Koji Yamaguchi, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Increase in serum triglyceride was associated with coronary plaque vulnerability in a patient with rheumatoid arthritis., Journal of Cardiology Cases, Vol.10, No.2, 54-57, 2014. (Summary) Rates of morbidity and mortality from cardiovascular disease are high in patients with rheumatoid arthritis (RA); however, the mechanisms and biomarkers that reflect coronary plaque vulnerability have not yet been established. We present a case of acute coronary syndrome (ACS) presumably caused by exacerbation of chronic inflammation of RA, in which an abrupt increase in serum triglyceride was seen on the day of onset of ACS but not during effort angina. This case suggests that RA patients with an abrupt increase in triglyceride need intensive care including anti-platelet and statin therapy for the prevention of coronary plaque rupture.<Learning objective: Triglyceride might be a sensitive biomarker of activated macrophages and plaque vulnerability in patients with RA. RA patients with an abrupt increase in triglyceride might need intensive care including anti-platelet and statin therapy for the prevention of coronary plaque rupture.> (Keyword) Acute coronary syndrome / Triglyceride / Tumor necrosis factor- / Biomarker (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jccase.2014.04.009 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84905378195 (DOI: 10.1016/j.jccase.2014.04.009, Elsevier: Scopus)
283.	Shusuke Yagi, Ken-ichi Aihara, Takeshi Kondo, Itsuro Endo, Junko Hotsuchi, Takayuki Ise, Takashi Iwase, Masashi Akaike, Toshio Matsumoto and Masataka Sata : High serum parathyroid hormone and calcium are risk factors for hypertension in Japanese patients., Endocrine Journal, Vol.61, No.7, 727-733, 2014. (Summary) Excess parathyroid hormone (PTH), known as primary hyperparathyroidism (pHPT), results in hypercalcemia and bone loss. Recent studies have shown that PTH is associated with the occurrence of hypertension in Western countries; however, controversy remains regarding high serum levels of PTH and calcium as risk factors for hypertension in Japanese patients. We retrospectively enrolled 114 consecutive Japanese patients who visited our hospital for examination and treatment of hypercalcemia and/or hypertension with serum calcium levels ≥ 9.8 mg/dL. To estimate the prevalence of hypertension, the patients were categorized according to calcium levels into hypercalcemic (10.2-13.4 mg/dL) and normocalcemic (9.8-10.1 mg/dL) groups, which were further categorized into high PTH (50-440 pg/mL) and low PTH (8-49 pg/mL) groups. The prevalence of hypertension was higher in patients with hypercalcemia than in patients with normocalcemia in both the high and low PTH groups. The prevalence of hypertension was higher in patients with high serum PTH levels than in patients with low serum PTH levels in both the hypercalcemic and normocalcemic groups. Logistic multiple regression analysis determined that serum calcium (P < 0.05) and PTH (P < 0.01) levels were positive contributors to hypertension. In conclusion, high serum levels of PTH and calcium are risk factors for hypertension in Japanese patients. (Keyword) parathyroid hormone / calcium / hypertension (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.EJ14-0004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24849536 ● CiNii @ National Institute of Informatics (CRID): 1390001206300211712 ● Summary page in Scopus @ Elsevier: 2-s2.0-84905190698 (DOI: 10.1507/endocrj.EJ14-0004, PubMed: 24849536, CiNii: 1390001206300211712, Elsevier: Scopus)
284.	Masashi Akaike, Ken-ichi Aihara, Hiroaki Yanagawa, Takashi Iwase, Sumiko Yoshida, Sato Chiho, Saijo Tomoka, Hiroaki Mikasa, Kashiwada Yoshizaki, Yoshihisa Takaishi, Koichiro Tsuchiya, Toshiaki Tamaki, Toshio Matsumoto and Masataka Sata : Efficacy and safety of Citrus sudachi peel in obese adults:A randomized, double-blind, pilot study, Functional Foods in Health and Disease, Vol.4, No.6, 276-284, 2014. (Link to Publication Site) ● Publication site (DOI): 10.31989/ffhd.v4i7.5 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85054855286 (DOI: 10.31989/ffhd.v4i7.5, Elsevier: Scopus)
285.	Hirotsugu Yamada, Kenya Kusunose, S Nishio, Mika Bando, Junko Hotsuchi, S Hayashi, Takayuki Ise, Shusuke Yagi, Koji Yamaguchi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Pre-load stress echocardiography for predicting the prognosis in mild heart failure., JACC. Cardiovascular Imaging, Vol.7, No.7, 641-649, 2014. (Keyword) Doppler echocardiography / heart failure / leg-positive pressure / stress echocardiography / survival (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jcmg.2014.04.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24954460 ● Summary page in Scopus @ Elsevier: 2-s2.0-84904576445 (DOI: 10.1016/j.jcmg.2014.04.009, PubMed: 24954460, Elsevier: Scopus)
286.	S Bando, Takeshi Soeki, T Matsuura, Toshiyuki Niki, Takayuki Ise, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike, T Aiba, W Shimizu and Masataka Sata : Congenital long QT syndrome with compound mutations in the KCNH2 gene., Heart and Vessels, Vol.29, No.4, 554-559, 2014. (Summary) Congenital long QT syndrome is a genetic disorder encompassing a family of mutations that can lead to aberrant ventricular electrical activity. We report on two brothers with long QT syndrome caused by compound mutations in the KCNH2 gene inherited from parents who had no prolonged QT interval on electrocardiography. The proband had syncope, and his elder brother suffered from ventricular fibrillation. Genetic testing revealed that both brothers had multiple mutations in the KCNH2 gene, including a missense mutation of C1474T (exon 6) as well as a frameshift/nonsense mutation, resulting from the insertion of 25 nucleotides, which caused an altered amino acid sequence beginning at codon 302 and a premature termination codon (i.e., TAG) at codon 339 (exon 4). Family genetic screening found that their father had the same frameshift mutation, and their mother and sister had the same missense mutation, in the KCNH2 gene. However, these other family members were asymptomatic, with normal QT intervals on electrocardiography. These results suggest that compound mutations in the KCNH2 gene inherited independently from the parents made the phenotypes of their sons more severe. (Keyword) KCNH2 gene / Long QT syndrome / Compound mutation / Missense mutation / Frameshift mutation (Link to Publication Site) ● Publication site (DOI): 10.1007/s00380-013-0406-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24057343 ● Summary page in Scopus @ Elsevier: 2-s2.0-84904036858 (DOI: 10.1007/s00380-013-0406-2, PubMed: 24057343, Elsevier: Scopus)
287.	S Hayashi, Hirotsugu Yamada, Mika Bando, Junko Hotsuchi, Takayuki Ise, Koji Yamaguchi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Toshiaki Tamaki and Masataka Sata : Augmentation Index does not Reflect the Risk of Coronary Artery Disease in Elderly Patients., Circulation Journal, Vol.78, No.5, 1176-1182, 2014. (Summary) BACKGROUND: Augmentation index (AI) has been used as a clinical index of arterial stiffness and has been reported to be an independent predictor of cardiovascular events, but some investigators have reported that AI is not a useful marker to identify coronary artery disease (CAD) in elderly patients. The majority of CAD patients are elderly people, therefore the aim of this study was to examine whether AI is a useful marker to identify the risk of CAD.METHODS AND RESULTS: A total of 120 patients (69±10 years of age; 83 male) who underwent cardiac catheterization for suspected CAD were enrolled. Invasive central blood pressure (BP) was measured using a fluid-filled catheter. Non-invasive AI was calculated by the SphygmoCor (AtCor Medical) system at the end of catheterization. Subjects consisted of 99 patients with CAD and 21 patients without CAD. There was no significant difference in AI between the CAD and the non-CAD groups (24±10 vs. 24±14%). Non-invasive systolic central BP was lower than the invasive systolic central BP (115±18 vs. 130±23 mmHg, P<0.001) in all patients. Non-invasive diastolic central BP was greater than the invasive diastolic central BP (67±10 vs. 63±10 mmHg, P<0.001).CONCLUSIONS: In elderly patients, AI may not be a useful marker to identify CAD (Keyword) Arterial stiffness / Augmentation index / Central blood pressure / Coronary artery disease (Tokushima University Institutional Repository) ● Metadata: 106070 (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-13-1422 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24562676 ● CiNii @ National Institute of Informatics (CRID): 1390001205107150592 ● Summary page in Scopus @ Elsevier: 2-s2.0-84899659435 (Tokushima University Institutional Repository: 106070, DOI: 10.1253/circj.CJ-13-1422, PubMed: 24562676, CiNii: 1390001205107150592, Elsevier: Scopus)
288.	Y Kimura, M Komaki, K Iwasaki, Masataka Sata, Y Izumi and I Morita : Recruitment of bone marrow-derived cells to periodontal tissue defects., Frontiers in Cell and Developmental Biology, Vol.2, 19, 2014. (Summary) Bone marrow-derived cells (BMCs) are considered to be a major source of mesenchymal stem cells (MSCs) in adults and are known to be effective in periodontal tissue regeneration. However, whether endogenous BMCs are involved in periodontal tissue repair process is uncertain. We therefore created periodontal tissue defects in the buccal alveolar bone of mandibular first molars in bone marrow chimeric mice, and immunohistochemically examined the expression of stromal cell derived factor-1 (SDF-1) and the mobilization of BMCs. We found that SDF-1 expression was increased around the defects at as early as 1 week after injury and that BMCs were mobilized to the defects, while GFP+/CD45+ were rarely observed. Fluorescence-activated cell sorting (FACS) analysis demonstrated that the number of platelet-derived growth factor receptor (pdgfr) +/Sca-1+ (PS) cells in the bone marrow decreased after injury. Taken together, these results suggest that BMCs are mobilized to the periodontal tissue defects. Recruitment of BMCs, including a subset of MSCs could be a new target of periodontal treatment. (Keyword) bone marrow chimeric mice / periodontal defects / mesenchymal stem cells / recruitment / SDF-1 (Tokushima University Institutional Repository) ● Metadata: 114902 (Link to Publication Site) ● Publication site (DOI): 10.3389/fcell.2014.00019 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25364726 ● Search Scopus @ Elsevier (PMID): 25364726 ● Search Scopus @ Elsevier (DOI): 10.3389/fcell.2014.00019 (Tokushima University Institutional Repository: 114902, DOI: 10.3389/fcell.2014.00019, PubMed: 25364726)
289.	Kenya Kusunose, T Chono, Tomotsugu Tabata, Hirotsugu Yamada and Masataka Sata : Echocardiographic image tracker with a speckle adaptive noise reduction filter for the automatic measurement of the left atrial volume curve., European Heart Journal Cardiovascular Imaging, Vol.15, No.5, 509-514, 2014. (Summary) Aims: Since tracking accuracy in left atrial (LA) images decreases due to low image quality around the LA in the apical view, a practical tracking method for LA images has not yet been proposed. The aim of this study was to assess an accurate and high-speed LA volume tracking (LAVT) method for the automatic measurement of LA volume (LAV) curves. Methods and results: We used three approved protocols in this study: (i) LAV curves were measured by LAVT on computer-simulated images; (ii) in 20 healthy volunteers, we assessed the feasibility and accuracy of this method compared with expert's measurements; and (iii) echocardiography and multi-detector row computed tomography (MDCT) imaging were performed on the same day in 20 patients with suspected coronary artery disease. On computer-simulated images, mean absolute percentage LAVT error in one cardiac cycle was 3% in filtered images and 16% in original images. In 20 healthy volunteers, there are strong correlations between LAVT and the expert's LA measurements (LA maximum volume; R = 0.93, P < 0.001). In 400 LA images with 20 patients, an excellent correlation was obtained between LAVs using echocardiography and MDCT (R = 0.98, P < 0.001), with a small bias (14% of the mean) and narrow limits of agreement (+15% of the mean). The mean time required for the LAVT analysis was 1.8 min, for the MDCT analysis was 35.8 min, and for the manual echocardiographic analysis was 14.0 min. Conclusion: This LAVT method is fast, valid, accurate, and reproducible for determining LAV in both simulated images and the clinical setting. (Keyword) transesophageal echocardiography / Image tracking / Left atrium / Speckle / noise reduction (Link to Publication Site) ● Publication site (DOI): 10.1093/ehjci/jet196 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24165117 ● Summary page in Scopus @ Elsevier: 2-s2.0-84898856089 (DOI: 10.1093/ehjci/jet196, PubMed: 24165117, Elsevier: Scopus)
290.	Takayuki Ise, Takashi Iwase, S Masuda, Shusuke Yagi, Masashi Akaike, S Nishio, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Acute pulmonary thromboembolism from deep vein thrombosis induced by trauma to the popliteal vein with a tennis racket., Journal of Cardiology Cases, Vol.9, No.4, 162-164, 2014. (Summary) Acute pulmonary thromboembolism (PTE) is mainly caused by deep vein thrombosis (DVT) and sometimes leads to a fatal outcome. Few cases of sport-related lower extremity DVT, involving direct external trauma, have been reported. A 58-year-old man, without any risk factors for thromboembolism suffered acute PTE from DVT after playing tennis. A detailed history revealed that he had hit his popliteal vein with each swing of his tennis racket and the site of the trauma, at popliteal fossa, was exactly the same as the site of the DVT formation. Therefore, the cause of DVT was suspected to be the repeated trauma to the popliteal vein. The repeated external trauma to the popliteal vein may have caused vascular endothelial damage, leading to DVT. (Keyword) Acute pulmonary thromboembolism / Deep vein thrombosis / Trauma (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jccase.2014.01.001 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84897413698 (DOI: 10.1016/j.jccase.2014.01.001, Elsevier: Scopus)
291.	Ryo Tabata, Hirotsugu Yamada, 西尾進, 井口明子, 小幡史明, 中西嘉憲, 河南真吾, Shino Yuasa, Nobuhiko Shimizu, Harutaka Yamaguchi, Mitsuhiro Kohno, Masataka Sata, Kenji Tani, Hiroyashu Bando and Teruki Shin : 心エコー検査におけるリアルタイム遠隔診断支援システムの開発および運用経験, 月刊地域医学, Vol.28, No.3, 236-240, 2014. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1523106604839480448 (CiNii: 1523106604839480448)
292.	中山泰介, Hajime Kinoshita, Mikio Sugano, Hirotsugu Kurobe, Tamotsu Kanbara, Takashi Kitaichi, Hirotsugu Yamada, Masataka Sata, 藤田博, 曽我部仁史 and Tetsuya Kitagawa : ペースメーカーリード前尖穿通に伴う重症三尖弁閉鎖不全症に対する1手術例, Heart, Vol.46, No.3, 378-383, 2014. (Link to Publication Site) ● Publication site (DOI): 10.11281/shinzo.46.378 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.11281/shinzo.46.378 (DOI: 10.11281/shinzo.46.378)
293.	Shusuke Yagi, Kadota Muneyuki, Ken-ichi Aihara, Nishikawa Koji, Hara Tomoya, Takayuki Ise, Yuka Ueda, Takashi Iwase, Masashi Akaike, Michio Shimabukuro, Shinsuke Katoh and Masataka Sata : Association of lower limb muscle mass and energy expenditure with visceral fat mass in healthy men, Diabetology & Metabolic Syndrome, Vol.6, No.1, 27, 2014. (Summary) A high-calorie diet and physical inactivity, an imbalance between caloric intake and energy consumption, are major causes of metabolic syndrome (MetS), which manifests as accumulation of visceral fat and insulin resistance. However, the lifestyle-related factors associated with visceral fat mass in healthy men are not fully understood. We evaluated visceral fat area (VFA), skeletal muscle mass, caloric intake, and energy expenditure in 67 healthy male participants (mean age, 36.9 ± 8.8 years; body mass index 23.4 ± 2.5 kg/m2). Multiple regression analysis showed that the total skeletal muscle mass (P < 0.001) were negatively and age (P < 0.001) were positively associated with VFA. Lower limb muscle mass (P < 0.001) was strongly associated with VFA. However, total caloric intake, total energy expenditure, and energy expenditure during exercise were not associated with VFA. Skeletal muscle mass especially lower limb muscle mass negatively contributes to visceral fat mass in healthy men. Therefore, maintaining lower limb muscular fitness through daily activity may be a useful strategy for controlling visceral obesity and metabolic syndrome. (Link to Publication Site) ● Publication site (DOI): 10.1186/1758-5996-6-27 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24571923 ● Summary page in Scopus @ Elsevier: 2-s2.0-84896075201 (DOI: 10.1186/1758-5996-6-27, PubMed: 24571923, Elsevier: Scopus)
294.	N Sawada, A Jiang, F Takizawa, A Safdar, A Manika, Y Tesmenitsky, KT Kang, J Bischoff, H Kalwa, JL Sartoretto, Y Kamei, LE Benjamin, H Watada, Y Ogawa, Y Higashikuni, CW Kessinger, FA Jaffer, T Michel, Masataka Sata, K Croce, R Tanaka and Z Arany : Endothelial PGC-1α mediates vascular dysfunction in diabetes., Cell Metabolism, Vol.19, No.2, 246-258, 2014. (Summary) Endothelial dysfunction is a central hallmark of diabetes. The transcriptional coactivator PGC-1 is a powerful regulator of metabolism, but its role in endothelial cells remains poorly understood. We show here that endothelial PGC-1 expression is high in diabetic rodents and humans and that PGC-1 powerfully blocks endothelial migration in cell culture and vasculogenesis in vivo. Mechanistically, PGC-1 induces Notch signaling, blunts activation of Rac/Akt/eNOS signaling, and renders endothelial cells unresponsive to established angiogenic factors. Transgenic overexpression of PGC-1 in the endothelium mimics multiple diabetic phenotypes, including aberrant re-endothelialization after carotid injury, blunted wound healing, and reduced blood flow recovery after hindlimb ischemia. Conversely, deletion of endothelial PGC-1 rescues the blunted wound healing and recovery from hindlimb ischemia seen in type 1 and type 2 diabetes. Endothelial PGC-1 thus potently inhibits endothelial function and angiogenesis, and induction of endothelial PGC-1 contributes to multiple aspects of vascular dysfunction in diabetes. (Keyword) Animals / Cell Movement / Cells, Cultured / Diabetes Mellitus / Endothelial Cells / Gene Expression Regulation / Hindlimb / Humans / Mice / Mice, Knockout / Transcription Factors (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cmet.2013.12.014 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24506866 ● Summary page in Scopus @ Elsevier: 2-s2.0-84893480253 (DOI: 10.1016/j.cmet.2013.12.014, PubMed: 24506866, Elsevier: Scopus)
295.	M Sahara, M Ikutomi, T Morita, Y Minami, T Nakajima, Y Hirata, R Nagai and Masataka Sata : Deletion of Angiotensin-converting Enzyme 2 Promotes the Development of Atherosclerosis and Arterial Neointima Formation., Cardiovascular Research, Vol.101, No.2, 236-246, 2014. (Summary) AIMS: Angiotensin-converting enzyme 2 (ACE2) is known as a negative regulator of the renin-angiotensin system. We aimed to determine the roles of ACE2 on the development of vascular diseases.Methods and ResultsUsing two diversely different models of vascular diseases, hyperlipidemia-induced atherosclerosis in apolipoprotein E knockout (KO) mice and mechanical injury-induced arterial neointimal hyperplasia in C57Bl6 mice, we examined whether ACE2 deficiency could affect formation of the vascular lesions. ACE2 deficiency resulted in significantly larger vascular lesions in both aortic atherosclerotic plaques and arterial neointima formation, compared to ACE2+ control. These ACE2-deficient vascular lesions exhibited enhanced accumulation of macrophages into the lesions and proliferation of vascular smooth muscle cells (VSMCs), accompanied with increased angiotensin II (Ang-II) levels and enhanced expression of vascular inflammation-related genes, including vascular cell adhesion molecule (VCAM)-1, monocyte chemoattractant protein (MCP)-1 and matrix metalloproteinase (MMP)9 in aorta/artery tissues. Primary bone marrow macrophages and aortic VSMCs isolated from ACE2 KO mice also displayed enhanced proinflammatory responsiveness such as upregulated gene/protein expression of VCAM-1, MCP-1 and MMP9 to stimulation with tumor necrosis factor- and Ang-II. The similar phenotype was shown in human macrophages and aortic VSMCs that were transfected with ACE2-specific siRNA. In ACE2-deficient VSMCs, inhibition of c-Jun N-terminal kinase (JNK) by pharmacological blockade with SP600125 or genetic knockdown with JNK-specific siRNA significantly attenuated their proinflammatory phenotype.CONCLUSION: ACE2 deficiency promotes the development of vascular diseases associated with Ang-II-mediated vascular inflammation and activation of the JNK signaling, leading to the notion that ACE2 potentially confers protection against vascular diseases. (Keyword) angiotensin II / angiotensin-converting enzyme 2 remodeling / atherosclerosis / c-Jun N-terminal kinase / vascular disease (Link to Publication Site) ● Publication site (DOI): 10.1093/cvr/cvt245 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24193738 ● Summary page in Scopus @ Elsevier: 2-s2.0-84893040529 (DOI: 10.1093/cvr/cvt245, PubMed: 24193738, Elsevier: Scopus)
296.	Kazumi Takaishi, Shinji Kawahito, Hirotsugu Yamada, Takeshi Soeki, Masataka Sata and Hiroshi Kitahata : Increase in prominence of electrocardiographic J waves after a single dose of propofol in a patient with early ventricular repolarisation., Anaesthesia, Vol.69, No.2, 170-175, 2014. (Summary) J waves appear on an electrocardiogram as an elevation of the J point in the terminal portion of the QRS complex. J waves are often benign, but may be associated with malignant ventricular arrhythmias. In some cases, such problems appear to have been precipitated by propofol infusions. We observed a sudden increase in J waves and profound hypotension following a single intravenous dose of propofol in an 84-year-old woman with early repolarisation in the inferior ventricular wall. When early repolarisation (as shown by electrocardiographic J waves) is observed in the inferior ventricular wall pre-operatively, patients should be carefully monitored. Myocardial ischaemia and the use of drugs that might worsen J waves should be avoided. (Keyword) Aged, 80 and over / Anesthetics, Intravenous / Electrocardiography / Female / Humans / Hypotension / Intraoperative Complications / Monitoring, Intraoperative / Propofol / Ventricular Fibrillation (Link to Publication Site) ● Publication site (DOI): 10.1111/anae.12448 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24116860 ● Summary page in Scopus @ Elsevier: 2-s2.0-84892799834 (DOI: 10.1111/anae.12448, PubMed: 24116860, Elsevier: Scopus)
297.	Sachiko Matsumoto, Michio Shimabukuro, Daiju Fukuda, Takeshi Soeki, K Yamakawa, H Masuzaki and Masataka Sata : Azilsartan, an angiotensin II type 1 receptor blocker, restores endothelial function by reducing vascular inflammation and by increasing the phosphorylation ratio Ser1177/Thr497 of endothelial nitric oxide synthase in diabetic mice., Cardiovascular Diabetology, Vol.13, No.1, 30, 2014. (Summary) BACKGROUND: Azilsartan, an angiotensin II type 1 (AT1) receptor blocker (ARB), has a higher affinity for and slower dissociation from AT1 receptors and shows stronger inverse agonism compared to other ARBs. Possible benefits of azilsartan in diabetic vascular dysfunction have not been established.METHODS: We measured vascular reactivity of aortic rings in male KKAy diabetic mice treated with vehicle, 0.005% azilsartan, or 0.005% candesartan cilexetil for 3 weeks. Expression of markers of inflammation and oxidative stress was measured using semiquantitative RT-PCR in the vascular wall, perivascular fat, and skeletal muscle. Phosphorylation of eNOS at Ser1177 and Thr495 was measured using Western blotting, and the ratio of phosphorylation at Ser1177 to phosphorylation at Thr495 was used as a putative indicator of vascular eNOS activity.RESULTS: (1) Vascular endothelium-dependent relaxation with acetylcholine in KKAy mice was improved by azilsartan treatment compared to candesartan cilexetil; (2) the ratio of Ser1177/Thr495 phosphorylation of eNOS was impaired in KKAy and was effectively restored by azilsartan; (3) anomalies in the expression levels of MCP1, F4/80, Nox2, and Nox4 of the aortic wall and in the expression of TNFalpha in the perivascular fat were strongly attenuated by azilsartan compared to candesartan cilexetil.CONCLUSIONS: These results provide evidence that azilsartan prevents endothelial dysfunction in diabetic mice, more potently than does candesartan cilexetil. Azilsartan's higher affinity for and slower dissociation from AT1 receptors may underlie its efficacy in diabetic vascular dysfunction via a dual effect on uncoupled eNOS and on Nox. (Keyword) Angiotensin II Type 1 Receptor Blockers / Animals / Benzimidazoles / Diabetes Mellitus, Experimental / Endothelium, Vascular / Male / Mice / Mice, Inbred C57BL / Nitric Oxide Synthase Type III / Organ Culture Techniques / Oxadiazoles / Phosphorylation / Serine / Threonine / Vasculitis / Vasodilation (Link to Publication Site) ● Publication site (DOI): 10.1186/1475-2840-13-30 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24485356 ● Summary page in Scopus @ Elsevier: 2-s2.0-84893161576 (DOI: 10.1186/1475-2840-13-30, PubMed: 24485356, Elsevier: Scopus)
298.	R Tamai, T Hara, Hirotsugu Yamada, S Nishio, M Bando, J Hotchi, S Hayashi, Toshiyuki Niki, Tetsuya Kitagawa and Masataka Sata : Massive tricuspid regurgitation due to pacemaker-lead puncture of the tricuspid valve: successful diagnosis by 3-dimensional echocardiography., Journal of Medical Ultrasonics, Vol.41, No.1, 69-71, 2014. (Summary) An 83-year-old woman presented to our echocardiographic center with symptoms of right heart failure. A dual-chamber DDDR pacemaker had been implanted 9 years earlier. Two-dimensional echocardiography revealed right atrial and ventricular enlargement and massive tricuspid regurgitation with immobilization of the anterior leaflet of the tricuspid valve. Three-dimensional transesophageal echocardiography showed that the pacemaker lead had punctured the leaflet. These echocardiographic findings were confirmed during surgery. The pacemaker lead was transected and removed, and pericardial patch closure of the leaflet hole and tricuspid annuloplasty were performed. The mechanism of regurgitation was elucidated by real-time three-dimensional echocardiography, and surgical repair was straightforward. (Keyword) Pacemaker-lead puncture / Tricuspid regurgitation / 3-Dimensional echocardiography (Link to Publication Site) ● Publication site (DOI): 10.1007/s10396-013-0459-y (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84893154861 (DOI: 10.1007/s10396-013-0459-y, Elsevier: Scopus)
299.	Michio Shimabukuro, M Higa, R Kinjo, K Yamakawa, H Tanaka, C Kozuka, K Yabiku, SI Taira, Masataka Sata and H Masuzaki : Effects of the brown rice diet on visceral obesity and endothelial function: the BRAVO study., British Journal of Nutrition, Vol.111, No.2, 310-320, 2014. (Summary) Brown rice (BR) and white rice (WR) produce different glycaemic responses and their consumption may affect the dietary management of obesity. In the present study, the effects of BR and WR on abdominal fat distribution, metabolic parameters and endothelial function were evaluated in subjects with the metabolic syndrome in a randomised cross-over fashion. In study 1, acute postprandial metabolic parameters and flow- and nitroglycerine-mediated dilation (FMD and NMD) of the brachial artery were determined in male volunteers with or without the metabolic syndrome after ingestion of either BR or WR. The increases in glucose and insulin AUC were lower after ingestion of BR than after ingestion of WR (P= 0·041 and P= 0·045, respectively). FMD values were decreased 60 min after ingestion of WR (P= 0·037 v. baseline), but the decrease was protected after ingestion of BR. In study 2, a separate cohort of male volunteers (n 27) with the metabolic syndrome was randomised into two groups with different BR and WR consumption patterns. The values of weight-based parameters were decreased after consumption of BR for 8 weeks, but returned to baseline values after a WR consumption period. Insulin resistance and total cholesterol and LDL-cholesterol levels were reduced after consumption of BR. In conclusion, consumption of BR may be beneficial, partly owing to the lowering of glycaemic response, and may protect postprandial endothelial function in subjects with the metabolic syndrome. Long-term beneficial effects of BR on metabolic parameters and endothelial function were also observed. (Keyword) Glycaemic indices / Endothelial function / obesity (Link to Publication Site) ● Publication site (DOI): 10.1017/S0007114513002432 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23930929 ● Summary page in Scopus @ Elsevier: 2-s2.0-84896660266 (DOI: 10.1017/S0007114513002432, PubMed: 23930929, Elsevier: Scopus)
300.	Hayato Nose, Hideki Otsuka, Youichi Otomi, K Terazawa, Shoichiro Takao, Seiji Iwamoto, Takashi Iwase, Hirotsugu Yamada, Masataka Sata and Masafumi Harada : The physiological uptake pattern of (18)F-FDG in the left ventricular myocardium of patients without heart disease., The Journal of Medical Investigation : JMI, Vol.61, No.1, 2, 53-58, 2014. (Summary) Purpose: The purpose of this study was to evaluate the physiological uptake pattern of 18F-FDG in the left ventricular myocardium of patients under preparation for tumor FDG-PET. Patients and Methods: We enrolled 188 patients without cardiac disease. The accumulation patterns were classified as either none, diffuse, focal or focal on diffuse. When a focal uptake was only observed on the basal wall, then the patterns were classified as having either a ring, over half or spot uptake. Results: The frequencies of the myocardial FDG uptake patterns were as follows: none, n=52 (27.7%); diffuse, n=63 (33.5%); focal on diffuse, n=40 (21.3%) and focal, n=33 (17.6%). The age, blood glucose level, weight and dose of FDG did not differ significantly for each pattern. The focal and focal on diffuse patterns were seen in 73 patients, and 65 patients had a focal uptake only on the basal wall; ring uptake in 29 patients, over half in 20 and spot uptake in 16 patients. Conclusions: The physiological myocardial uptake showed several patterns. Focal uptake was often seen in patients with cardiac disease, but it did not always indicate an abnormal finding when the accumulation was only on the basal wall. (Keyword) F-FDG PET / heart / physiological myocardial uptake / fasting state (Tokushima University Institutional Repository) ● Metadata: 109517 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.61.53 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24705749 ● Search Scopus @ Elsevier (PMID): 24705749 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.61.53 (Tokushima University Institutional Repository: 109517, DOI: 10.2152/jmi.61.53, PubMed: 24705749)
301.	Hirotsugu Kurobe, Y Matsuoka, Y Hirata, N Sugasawa, MW Maxfield, Masataka Sata and Tetsuya Kitagawa : Azelnidipine suppresses the progression of aortic aneurysm in wild mice model through anti-inflammatory effects., Journal of Thoracic and Cardiovascular Surgery, Vol.146, No.6, 1501-1508, 2013. (Summary) BACKGROUND: Although systemic hypertension is closely associated with aortic aneurysm (AA) formation, there are many patients with AA without hypertension. In these patients, an inflammation-mediated progression of aneurysmal disease is likely responsible for AA growth and eventual rupture. Unfortunately, there remains no reproducible and durable small animal model of aortic aneurysmal disease, the development of which would enable the investigation of the pathophysiology of this vexing condition. The first aim was to establish a useful wild-type mouse model of AA with low mortality. The second aim was to use this model to assess the protective effect of azelnidipine, a new calcium channel blocker, against the progression of the AA independent of its antihypertensive effect.METHODS: Angiotensin II and -aminopropionitrile (a lysyl oxidase inhibitor) were administrated subcutaneously in 7-week-old C57BL/6J mice using an osmotic minipump for 4 weeks to generate a wild-type mouse model of AA. Concurrently, azelnidipine (a calcium channel blocker) or a placebo was administrated orally for 4 weeks. Mice were humanely killed and assessed at the end of the 4 weeks of pharmacologic manipulation.RESULTS: The combined infusion of angiotensin II and -aminopropionitrile induced degenerative aneurysm of the thoracic and/or abdominal aorta (11/12; 92%). The majority of aneurysms were located in the distal aortic arch and suprarenal abdominal aorta. Although there was no difference in systolic blood pressure between the control and azelnidipine-treated groups, azelnidipine significantly reduced the incidence of AA (2/11; 18%). Azelnidipine treatment reduced the pathologic findings normally associated with aneurysm formation within the aortic wall. Azelnidipine also reduced the number of macrophage antigen-3 (MAC-3)-positive cells in the periaortic adipose tissue and reduced the gene expression levels of tumor necrosis factor-alpha and matrix metalloproteinase-2 and -9 within the aortic wall.CONCLUSIONS: This study demonstrates that combined treatment with angiotensin II and -aminopropionitrile induces degenerative AAs in wild-type mice, and azelnidipine prevents aneurysm progression via its anti-inflammatory effect. (Keyword) Aminopropionitrile / Angiotensin II / Animals / Anti-Inflammatory Agents / Aorta, Abdominal / Aorta, Thoracic / Aortic Aneurysm, Abdominal / Aortic Aneurysm, Thoracic / Azetidinecarboxylic Acid / Blood Pressure / Calcium Channel Blockers / Dihydropyridines / Disease Models, Animal / Disease Progression / Inflammation Mediators / Macrophages / Male / Matrix Metalloproteinase 2 / Matrix Metalloproteinase 9 / Mice / Mice, Inbred C57BL / Sirtuin 1 / Time Factors / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jtcvs.2013.02.073 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23535154 ● Search Scopus @ Elsevier (PMID): 23535154 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jtcvs.2013.02.073 (DOI: 10.1016/j.jtcvs.2013.02.073, PubMed: 23535154)
302.	M Sumi, N Tateishi, H Shibata, T Ohki and Masataka Sata : Quercetin glucosides promote ischemia-induced angiogenesis, but do not promote tumor growth., Life Sciences, Vol.93, No.22, 814-819, 2013. (Summary) AIMS: Dietary flavonoid intake shows a significant inverse association with mortality from coronary heart disease, incidence of myocardial infarction and stroke. Quercetin is one of the most common flavonoids in our diet and has a several favorable biological activities. Quercetin glucosides, which are enzymatically trans-glycosylated isoquercitrin, have high water-solubility and bioavailability compared with quercetin. Here, we investigated the effects of quercetin glucosides on collateral development in a murine hindlimb ischemia model.MAIN METHODS: We induced hindlimb ischemia in 24- to 32-week-old male C3H/HeJ mice by resecting the right femoral artery. Then, 0.5% carboxymethyl cellulose (control) or quercetin glucosides (100 mg/kg/day) were administered daily by gavage. Blood flow was monitored weekly by laser Doppler imaging.KEY FINDINGS: Recovery of blood flow to the ischemic leg was significantly enhanced by quercetin glucosides (blood flow ratio at 4 weeks: control, 0.57±0.11; quercetin glucosides, 0.95±0.10, p<0.05). Furthermore, anti-CD31 immunostaining revealed that quercetin glucosides increased capillary density in the ischemic muscle (control, 200±24/mm2; quercetin glucosides, 364±41/mm2, p<0.01). Quercetin glucosides did not promote tumor growth. The beneficial effect of quercetin glucosides was abrogated in eNOS-deficient mice.SIGNIFICANCE: These results suggest that quercetin glucosides may have therapeutic potential to promote angiogenesis in ischemic tissue. (Keyword) NO / Quercetin glucosides / angiogenesis / collateral / flavonoids (Link to Publication Site) ● Publication site (DOI): 10.1016/j.lfs.2013.09.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24044885 ● Search Scopus @ Elsevier (PMID): 24044885 ● Search Scopus @ Elsevier (DOI): 10.1016/j.lfs.2013.09.005 (DOI: 10.1016/j.lfs.2013.09.005, PubMed: 24044885)
303.	Y Higashikuni, K Tanaka, M Kato, O Nureki, Y Hirata, R Nagai, I Komuro and Masataka Sata : Toll-Like Receptor-2 Mediates Adaptive Cardiac Hypertrophy in Response to Pressure Overload Through Interleukin-1 Upregulation via Nuclear Factor B Activation., Journal of the American Heart Association, Vol.2, No.6, e000267, 2013. (Summary) Background: Inflammation is induced in the heart during the development of cardiac hypertrophy. The initiating mechanisms and the role of inflammation in cardiac hypertrophy, however, remain unclear. Toll-like receptor2 (TLR2) recognizes endogenous molecules that induce noninfectious inflammation. Here, we examined the role of TLR2mediated inflammation in cardiac hypertrophy. Methods and Results: At 2 weeks after transverse aortic constriction, Tlr2/ mice showed reduced cardiac hypertrophy and fibrosis with greater left ventricular dilatation and impaired systolic function compared with wildtype mice, which indicated impaired cardiac adaptation in Tlr2/ mice. Bone marrow transplantation experiment revealed that TLR2 expressed in the heart, but not in bone marrowderived cells, is important for cardiac adaptive response to pressure overload. In vitro experiments demonstrated that TLR2 signaling can induce cardiomyocyte hypertrophy and fibroblast and vascular endothelial cell proliferation through nuclear factorB activation and interleukin1 upregulation. Systemic administration of a nuclear factorB inhibitor or antiinterleukin1 antibodies to wildtype mice resulted in impaired adaptive cardiac hypertrophy after transverse aortic constriction. We also found that heat shock protein 70, which was increased in murine plasma after transverse aortic constriction, can activate TLR2 signaling in vitro and in vivo. Systemic administration of antiheat shock protein 70 antibodies to wildtype mice impaired adaptive cardiac hypertrophy after transverse aortic constriction. Conclusions: Our results demonstrate that TLR2mediated inflammation induced by extracellularly released heat shock protein 70 is essential for adaptive cardiac hypertrophy in response to pressure overload. Thus, modulation of TLR2 signaling in the heart may provide a novel strategy for treating heart failure due to inadequate adaptation to hemodynamic stress. (Keyword) heart failure / hypertrophy / inflammation / interleukins / signal transduction (Link to Publication Site) ● Publication site (DOI): 10.1161/JAHA.113.000267 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24249711 ● Search Scopus @ Elsevier (PMID): 24249711 ● Search Scopus @ Elsevier (DOI): 10.1161/JAHA.113.000267 (DOI: 10.1161/JAHA.113.000267, PubMed: 24249711)
304.	Takeshi Soeki, Toshiyuki Niki, E. Uematsu, S. Bando, T. Matsuura, Kenya Kusunose, Takayuki Ise, Yuka Ueda, N. Tomita, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Daiju Fukuda, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike, Michio Shimabukuro, I. Kishimoto, Kenji Kangawa and Masataka Sata : Ghrelin protects the heart against ischemia-induced arrhythmias by preserving connexin-43 protein., Heart and Vessels, Vol.28, No.6, 795-801, 2013. (Summary) Vagal nerve stimulation has been postulated to confer an antifibrillatory effect. We studied whether ghrelin administration would exert an antiarrhythmic effect via modulation of autonomic nerve activity in rats after acute myocardial ischemia (MI). Male Sprague-Dawley rats were exposed to 30 min of ischemia following ligation of the left coronary artery. Animals were then randomized to receive either ghrelin (n = 26) or saline (n = 26) during the period of coronary ligation. Power spectral analysis of heart-rate variability revealed that the administration of ghrelin increased the high-frequency (HF) power and decreased the low-frequency (LF)/HF ratio. Ventricular tachyarrhythmias were less frequent in rats after MI who received ghrelin in comparison with rats that received saline. Immunoblotting and immunohistochemistry revealed that rats given saline alone during MI exhibited a marked reduction in phosphorylated connexin-43 within the left ventricle, whereas those that received ghrelin displayed only minor reductions in comparison with sham-operated rats. These effects of ghrelin were diminished by the coadministration of atropine or the blockade of vagal afferents. These data demonstrate that the beneficial effect of ghrelin might be mediated by modulation of cardiac autonomic nerve activity. (Keyword) Animals / Anti-Arrhythmia Agents / Atropine / Connexin 43 / Disease Models, Animal / Ghrelin / Heart Rate / Heart Ventricles / Male / Muscarinic Antagonists / Myocardial Ischemia / Phosphorylation / Rats / Rats, Sprague-Dawley / Tachycardia, Ventricular / Time Factors / Vagotomy / Vagus Nerve (Link to Publication Site) ● Publication site (DOI): 10.1007/s00380-013-0333-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23494606 ● Search Scopus @ Elsevier (PMID): 23494606 ● Search Scopus @ Elsevier (DOI): 10.1007/s00380-013-0333-2 (DOI: 10.1007/s00380-013-0333-2, PubMed: 23494606)
305.	Y Hirata, Hirotsugu Kurobe, M Higashida, Daiju Fukuda, Michio Shimabukuro, K Tanaka, Y Higashikuni, Tetsuya Kitagawa and Masataka Sata : HMGB1 plays a critical role in vascular inflammation and lesion formation via toll-like receptor 9., Atherosclerosis, Vol.231, No.2, 227-233, 2013. (Summary) OBJECTIVE: Endogenous ligands such as high-mobility group box 1 (HMGB1) and nucleic acids are released by dying cells and bind to Toll-like receptors (TLRs). As TLR9 is involved in both microbial and sterile inflammation by detecting both bacterial and endogenous DNA, we investigated its role in inflammation and lesion formation in a mouse model of vascular injury.METHODS AND RESULTS: C57BL/6 (WT) and TLR9 KO mice were subjected to wire-mediated vascular injury. Anti-HMGB1 antibody and purified HMGB1 protein were chronically delivered around the injured arteries by gelatin hydrogel, and neointima formation at 4 weeks after injury was evaluated. In addition, the same vascular injury was performed in bone-marrow chimeric mice (WT bone marrow into TLR KO mice; TLR9 KO bone marrow into WT mice). We also evaluated the production of inflammatory cytokines by mouse macrophages in response to HMGB1 and CpG-ODN. In wild-type mice after vascular injury, anti-HMGB1 antibody significantly reduced neointima formation and HMGB1 protein accelerated neointima hyperplasia. HMGB1 failed to accelerate lesion formation in TLR9 KO mice. The bone marrow transplantation study revealed that TLR9 in bone marrow-derived cells played a fundamental role in neointima formation. In vitro, HMGB1 and CpG-ODN synergistically induced the production of inflammatory cytokines by macrophages.CONCLUSIONS: HMGB1 serves as an endogenous mediator of inflammation and lesion formation via the TLR9 pathway in response to vascular injury. Blockade of HMGB1 and/or TLR9 may represent a novel approach to treating atherosclerosis. (Keyword) HMGB1 / Toll-like receptor / atherosclerosis / vascular remodeling / inflammation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2013.09.010 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24267232 ● Search Scopus @ Elsevier (PMID): 24267232 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2013.09.010 (DOI: 10.1016/j.atherosclerosis.2013.09.010, PubMed: 24267232)
306.	K Tanaka and Masataka Sata : Blockade of cytidine triphosphate synthase regulates smooth muscle cell and endothelial cell proliferation differentially., Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.33, No.10, 2286-2287, 2013. (Keyword) cyclopentenyl cytosine / cytidine triphosphate / drug-eluting stents / endothelial cells / muscle, smooth / neointima (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.113.302315 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24025545 ● Summary page in Scopus @ Elsevier: 2-s2.0-84885084036 (DOI: 10.1161/ATVBAHA.113.302315, PubMed: 24025545, Elsevier: Scopus)
307.	Taisuke Nakayama, Hirotsugu Kurobe, Noriko Sugasawa, Hajime Kinoshita, Mayuko Higashida, Yuki Matsuoka, Yasushi Yoshida, Yoichiro Hirata, Mie Sakata, Mark Maxfield, Yousuke Takahama, Masataka Sata, Toshiaki Tamaki, Tetsuya Kitagawa and Shuhei Tomita : Role of macrophage-derived Hypoxia-Inducible Factor (HIF)-1 as a mediator of vascular remodeling, Cardiovascular Research, Vol.99, No.4, 705-715, 2013. (Summary) Excessive vascular remodelling leads to progression of a wide range of vasculopathies, and the immune response to intimal injuries is crucial in this process. This vascular remodelling occurs in the hypoxic microenvironment and is closely related to the immune system. Macrophages play a key role in immunological-cell-mediated arterial remodelling. In this study, we clarified the role of macrophage-derived hypoxia-inducible factor (HIF-1α) in vascular remodelling. Wire-induced femoral arterial injury was inflicted in mice lacking the macrophage-specific HIF-1α gene and in their wild-type counterparts. The mutant mice showed both suppressed wire-induced neointimal thickening and decreased infiltration of inflammatory cells in the adventitia, compared with wild-type mice. Studies to clarify the mechanism of restrained vascular remodelling in the mutant mice revealed decreased production of pro-inflammatory cytokines by the activated macrophages and suppressed macrophage migration activity in the mutant mice. Gene expressions of the HIF-1α-deficient macrophages positively correlated with the phenotypic profile of M2 macrophages and negatively correlated with that of M1 macrophages. Our results show that HIF-1α in macrophages plays a crucial role in promoting vascular inflammation and remodelling. As decreasing HIF-1α activity in macrophages may prevent the progression of vascular remodelling, HIF-1α may be a possible therapeutic target in vascular diseases. (Keyword) Animals / Blood Vessels / Cell Movement / HMGB1 Protein / Hypoxia-Inducible Factor 1, alpha Subunit / Interleukin-6 / Macrophages / Mice / Mice, Inbred C57BL / Phenotype / Tumor Necrosis Factor-alpha (Tokushima University Institutional Repository) ● Metadata: 105898 (Link to Publication Site) ● Publication site (DOI): 10.1093/cvr/cvt146 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23752975 ● Search Scopus @ Elsevier (PMID): 23752975 ● Search Scopus @ Elsevier (DOI): 10.1093/cvr/cvt146 (Tokushima University Institutional Repository: 105898, DOI: 10.1093/cvr/cvt146, PubMed: 23752975)
308.	Michio Shimabukuro, Moritake Higa, Ken Yamakawa, Hiroaki Masuzaki and Masataka Sata : Miglitol, alpha-glycosidase inhibitor, reduces visceral fat accumulation and cardiovascular risk factors in subjects with the metabolic syndrome: A randomized comparable study., International Journal of Cardiology, Vol.167, No.5, 2108-2113, 2013. (Summary) BACKGROUND/OBJECTIVES: Visceral fat obesity plays an essential role in the clustering of cardiovascular risk factors. This study aimed to clarify the effects of miglitol, -glycosidase inhibitor, on body weight, fat distribution and cardiovascular risk factors in patients with the metabolic syndrome. METHODS AND RESULTS: One hundred and eleven drug naive patients with the metabolic syndrome were continuously recruited and randomly allocated to a group of life style modification (LSM) alone or a group of LSM with miglitol per os 50mg×3 (LSM+miglitol). After 12weeks of treatment, body weight (5.1%), body mass index (4.9%) and waist circumference were greatly reduced in miglitol group (n=42) than in LSM group (n=43). Plasma levels of insulin and glucose during an oral 75g glucose loading were decreased only in miglitol group. Visceral fat area, determined by abdominal computed tomography, was greatly reduced in miglitol group (baseline 188 vs 12weeks 161cm(2), p<0.0001) than in LSM group (184 vs 174cm(2), p<0.05). Subcutaneous fat area was reduced only in miglitol group (p<0.001). Systolic blood pressure was reduced in miglitol group (142 vs 133mm Hg, p<0.001), but not in control group (137 vs 134mm Hg). Serum levels of triglyceride, LDL-cholesterol, -GTP, and high-sensitive CRP were decreased and adiponectin was increased only in miglitol group. CONCLUSIONS: Our results indicated that miglitol showed an anti-obesity potential, which was achieved by reducing abdominal fat accumulation and/or enhanced insulin requirement, and then corrected both the metabolic and hemodynamic aberrations seen in patients with the metabolic syndrome (UMIN Clinical Trial Registry UMIN000007650). (Keyword) Endothelial function / insulin resistance / Post-prandial hyperglycemia / Visceral obesity (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijcard.2012.05.109 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22721642 ● Search Scopus @ Elsevier (PMID): 22721642 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ijcard.2012.05.109 (DOI: 10.1016/j.ijcard.2012.05.109, PubMed: 22721642)
309.	Shusuke Yagi, Masashi Akaike, Takayuki Ise, Yuka Ueda, Takashi Iwase and Masataka Sata : Renin-angiotensin-aldosterone system has a pivotal role in cognitive impairment., Hypertension Research, Vol.36, No.9, 753-758, 2013. (Summary) Because dementia is associated with both deterioration in the quality of life and poor prognosis, the prevention of cognitive impairment (CI) is a critical problem in public health promotion. Hypertension is a risk factor for the aggravation of CI, and the renin-angiotensin-aldosterone system (RAAS) is a key player in the increased incidence and development of hypertension. Therefore, the RAAS is considered to be a promoting factor for CI development. Conversely, recent studies have shown that lowering blood pressure with RAAS inhibitors decreases the incidence of CI, dementia and cardiovascular disease. Blood-brain barrier-penetrating RAAS inhibitors appear to have advantages in preventing cognitive decline because they can suppress the RAAS in the hippocampus, which has an important role in cognition. Thus, RAAS blockage is a notable strategy for preventing CI. (Keyword) Angiotensin-Converting Enzyme Inhibitors / Cognition / Cognition Disorders / Humans / Hypertension / Renin-Angiotensin System / Risk Factors (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2013.51 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23698805 ● Summary page in Scopus @ Elsevier: 2-s2.0-84883885656 (DOI: 10.1038/hr.2013.51, PubMed: 23698805, Elsevier: Scopus)
310.	M. Shimamura, H. Nakagami, Masataka Sata, M. Takaoka, J. Azuma, M. Osako Kiomy, H. Koriyama, H. Kurinami, K. Wakayama, T. Miyake and R. Morishita : Unique remodeling processes after vascular injury in intracranial arteries: analysis using a novel mouse model., Journal of Cerebral Blood Flow and Metabolism, Vol.33, No.8, 1153-1159, 2013. (Summary) The effectiveness of angioplasty and stenting in intracranial atherosclerotic diseases is controversial due to high rates of delayed restenosis and hemorrhage compared with extracranial arteries. However, the mechanisms underlying these differences are still unclear, because their pathophysiology is yet to be examined. To address this issue, we established a novel vascular injury model in the intracranial internal carotid arteries (IICAs) in mice, and analyzed the remodeling process in comparison to that of the femoral arteries (FAs). In IICAs, neointimal hyperplasia was observed from day 14 and grew until day 56. Although smooth muscle cells (SMCs) emerged in the neointima from day 28, SMCs in the injured media were continuously lost with eventual extinction of the media. Re-endothelialization was started from day 7 and completed on day 28. Accumulation of macrophages was continued in the adventitia until day 56. Compared with FAs, the following points are unique in IICAs: (1) delayed continuous formation of neointima; (2) accumulation of macrophages in the media on day 14; (3) continuous loss of SMCs in the media followed by extinction of the media itself; and (4) continuously growing adventitia. These pathophysiologic differences might be associated with unfavorable outcomes in percutaneous transluminal angioplasty and stenting in intracranial arteries. (Keyword) atherosclerosis / endothelium / inflammation / smooth muscle / vascular biology (Link to Publication Site) ● Publication site (DOI): 10.1038/jcbfm.2013.62 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23571280 ● Search Scopus @ Elsevier (PMID): 23571280 ● Search Scopus @ Elsevier (DOI): 10.1038/jcbfm.2013.62 (DOI: 10.1038/jcbfm.2013.62, PubMed: 23571280)
311.	Michio Shimabukuro, N. Higa, T. Tagawa, K. Yamakawa, Masataka Sata and S. Ueda : Defects of vascular nitric oxide bioavailability in subjects with impaired glucose tolerance: A potential link to insulin resistance., International Journal of Cardiology, Vol.167, No.1, 298-300, 2013. (Keyword) Adult / Aged / Biological Availability / Blood Glucose / Female / Glucose Intolerance / Humans / Insulin Resistance / Male / Middle Aged / Nitric Oxide (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijcard.2012.09.194 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23079092 ● Summary page in Scopus @ Elsevier: 2-s2.0-84878562297 (DOI: 10.1016/j.ijcard.2012.09.194, PubMed: 23079092, Elsevier: Scopus)
312.	Daiju Fukuda and Masataka Sata : Expanded roles of the renin-angiotensin system., Hypertension Research, Vol.36, No.7, 586-587, 2013. (Keyword) Angiotensin II Type 1 Receptor Blockers / Anti-Inflammatory Agents / Antihypertensive Agents / Antioxidants / Biphenyl Compounds / Female / Humans / Hypertension / Male / Tetrazoles (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2013.27 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23575385 ● Search Scopus @ Elsevier (PMID): 23575385 ● Search Scopus @ Elsevier (DOI): 10.1038/hr.2013.27 (DOI: 10.1038/hr.2013.27, PubMed: 23575385)
313.	Sumiko Yoshida, Ken-ichi Aihara, Yasumasa Ikeda, Yuka Sumitomo-Ueda, Ryoko Uemoto, Kazue Ishikawa, Takayuki Ise, Shusuke Yagi, Takashi Iwase, Yasuhiro Mouri, Matomo Sakari, Takahiro Matsumoto, Ken-ichi Takeyama, Masashi Akaike, Mitsuru Matsumoto, Masataka Sata, Kenneth Walsh, Shigeaki Kato and Toshio Matsumoto : Androgen receptor promotes sex-independent angiogenesis in response to ischemia and is required for activation of vascular endothelial growth factor receptor signaling., Circulation, Vol.128, No.1, 60-71, 2013. (Summary) These results document a physiological role of AR in sex-independent angiogenic potency and provide evidence of novel cross-talk between the androgen/AR signaling and VEGF/kinase insert domain protein receptor signaling pathways. (Link to Publication Site) ● Publication site (DOI): 10.1161/CIRCULATIONAHA.113.001533 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23723256 ● Search Scopus @ Elsevier (PMID): 23723256 ● Search Scopus @ Elsevier (DOI): 10.1161/CIRCULATIONAHA.113.001533 (DOI: 10.1161/CIRCULATIONAHA.113.001533, PubMed: 23723256)
314.	Hirotsugu Kurobe, Yoichiro Hirata, Yuki Matsuoka, Noriko Sugasawa, Mayuko Higashida, Taisuke Nakayama, W. Mark Maxfield, Yasushi Yoshida, Michio Shimabukuro, Tetsuya Kitagawa and Masataka Sata : Protective effects of selective mineralocorticoid receptor antagonist against aortic aneurysm progression in a novel murine model., The Journal of Surgical Research, Vol.185, No.1, 455-462, 2013. (Summary) BACKGROUND: The optimal medical management to delay the progression of aortic aneurysms has not been fully clarified, and the only standard treatment at present is antihypertensive therapy. Previous studies have shown beneficial effects of selective mineralocorticoid receptor (MR) antagonists on cardiovascular remodeling. The aim of the present study was to investigate the effect of a selective MR antagonist on aortic aneurysm progression.METHODS: Seven-week-old C57BL/6J male mice were administered with angiotensin II and -aminopropionitrile for 4 weeks. The mice received either vehicle or eplerenone, a selective MR antagonist (100 mg/kg daily) every day by gavage, starting at 7 weeks of age. The production of inflammatory cytokines in cultures of high mobility group box-1-stimulated macrophages with or without a MR antagonist was also analyzed using an enzyme-linked immunosorbent assay.RESULTS: Although no differences were found in the peak systolic blood pressure between the experimental groups, the mice in the eplerenone group showed a significant reduction in aneurysm development. On histologic analysis, coarse and stretched elastic fibers were markedly improved in the aortic wall in the eplerenone group. Real-time polymerase chain reaction of both aortic wall and perivascular adipose tissue demonstrated the expression of tumor necrosis factor-, interleukin-6, and matrix metalloproteinase-2 was significantly decreased in eplerenone group, and that of monocyte chemoattractant protein-1 in the aortic wall was also significantly decreased. Macrophage infiltration in the aortic wall and perivascular adipose tissue in the eplerenone group was also significantly decreased. The production of tumor necrosis factor- and interleukin-6 in macrophage culture, which was stimulated by high mobility group box-1 and CpG oligodeoxynucleotides, was also significantly decreased in the eplerenone group.CONCLUSIONS: Eprelenone suppressed aortic aneurysm progression through an anti-inflammatory effect. Thus, selective MR antagonists might be effective in preventing the progression of aortic aneurysms. (Keyword) Aortic aneurysm / MR antagonist / Preventive medicine (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jss.2013.05.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23731681 ● Search Scopus @ Elsevier (PMID): 23731681 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jss.2013.05.002 (DOI: 10.1016/j.jss.2013.05.002, PubMed: 23731681)
315.	Masataka Sata : Molecular mechanism of plaque destabilization (第77回日本循環器学会学術集会レポート① シンポジウム2), Journal of Clinical and Experimental Medicine, Vol.245, No.7, 615-617, 2013.
316.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, Daiju Fukuda, Masayoshi Ishida, Takayuki Ise, Toshiyuki Niki, Yuka Ueda, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Pharmacology of Aldosterone and the Effects of Mineralocorticoid Receptor Blockade on Cardiovascular Systems., Acta Cardiologica Sinica, Vol.29, No.3, 201-207, 2013. (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84878307366 (Elsevier: Scopus)
317.	Kenya Kusunose, Hirotsugu Yamada, S. Nishio, N. Tomita, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Interval from the Onset of Transmitral Flow to Annular Velocity Is a Marker of LV Filling Pressure., JACC. Cardiovascular Imaging, Vol.6, No.4, 528-530, 2013. (Keyword) Angina, Stable / Atrial Function, Left / Atrial Pressure / Cardiac Catheterization / Case-Control Studies / Echocardiography, Doppler, Color / Humans / Mitral Valve / Multivariate Analysis / Predictive Value of Tests / Prospective Studies / Time Factors / Ventricular Function, Left / Ventricular Pressure (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jcmg.2012.10.025 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23579016 ● Search Scopus @ Elsevier (PMID): 23579016 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jcmg.2012.10.025 (DOI: 10.1016/j.jcmg.2012.10.025, PubMed: 23579016)
318.	N Tomita, Hirotsugu Yamada, S Nishio, R Tamai, Kenya Kusunose, S Hayashi, Junko Hotsuchi and Masataka Sata : Patent foramen ovale diagnosed by real-time three-dimensional contrast transesophageal echocardiography: A case report., Journal of Cardiology Cases, Vol.7, No.4, e91-e92, 2013. (Summary) A 67-year-old man was admitted due to insensitiveness of right upper limb and dysarthria, and treated for suspected lacunar infarction or branch atherosclerotic disease. Carotid ultrasonography showed no abnormalities, and agitated contrast transesophageal echocardiography was performed to detect patent foramen ovale (PFO). Intravenously administered microbubbles did not appear in left atrium by 2-dimensional echocardiography, while contrasts were observed in left atrium using 3-dimensional echocardiography. Real-time 3-dimensional contrast transesophageal echocardiography may be the most useful method for the diagnosis of small PFO. (Keyword) Three-dimensional transesophageal echocardiography / Contrast echocardiography / Patent foramen ovale / Agitated saline bubble (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jccase.2012.10.011 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84876475886 (DOI: 10.1016/j.jccase.2012.10.011, Elsevier: Scopus)
319.	T. Hara and Masataka Sata : Spectacular migration of a central venous catheter into the pulmonary artery., Heart Asia, Vol.5, 42-43, 2013. (Link to Publication Site) ● Publication site (DOI): 10.1136/heartasia-2013-010287 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84879808095 (DOI: 10.1136/heartasia-2013-010287, Elsevier: Scopus)
320.	Michio Shimabukuro, Y. Hirata, M. Tabata, M. Dagvasumberel, H. Sato, Hirotsugu Kurobe, Daiju Fukuda, Takeshi Soeki, Tetsuya Kitagawa, S. Takanashi and Masataka Sata : Epicardial adipose tissue volume and adipocytokine imbalance are strongly linked to human coronary atherosclerosis., Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.33, No.5, 1077-1084, 2013. (Summary) The impact of epicardial adipose tissue (EAT) over abdominal or overall adiposity on coronary artery disease (CAD) is currently unknown. We compared the association among EAT volume (EATV), cytokine/adipocytokine profiles in EAT and subcutaneous fat, and atherogenic CAD. APPROACH AND RESULTS: Paired samples were obtained from EAT and subcutaneous adipose tissue during elective cardiac surgery for CAD (n=50) or non-CAD (n=50). EATV was the sum of cross-sectional EAT areas, and visceral and subcutaneous fat areas were determined at the umbilicus level on computed tomography scans. CD68(+), CD11c(+), and CD206(+) cells were counted using immunohistochemical staining. Cytokine/adipocytokine expression was evaluated using quantitative real-time polymerase chain reaction. Multivariate analysis indicated that male sex, age, diabetes mellitus, high triglycerides, and low high-density lipoprotein cholesterol, and EATV index (EATV/body surface area, cm(3)/m(2)) were significant CAD predictors (corrected R(2)=0.401; P<0.001); visceral fat area, hypertension, smoking, low-density lipoprotein cholesterol (140 mg/dL [3.63 mmol/L]) or statin use were not predictors. The EATV index positively correlated with the CD68(+) and CD11c(+) cell numbers and nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3), interleukin-1β, and interleukin-1R expression; and negatively correlated with adiponectin expression in EAT. A multivariate analysis model, including CD68(+) cells and interleukin-1β, and adiponectin expression in EAT strongly predicted CAD (corrected R(2)=0.756; P<0.001). EATV and macrophage and cytokine/adipocytokine signals in EAT strongly correlated with CAD. Our findings suggest that EATV and adipocytokine imbalance are strongly linked to human coronary atherosclerosis. (Keyword) Adipokines / Adipose Tissue / Aged / Antigens, CD / Antigens, CD11c / Antigens, Differentiation, Myelomonocytic / Cholesterol, HDL / Coronary Artery Disease / Female / Humans / Logistic Models / Male / Middle Aged / Pericardium (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.112.300829 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23471228 ● Search Scopus @ Elsevier (PMID): 23471228 ● Search Scopus @ Elsevier (DOI): 10.1161/ATVBAHA.112.300829 (DOI: 10.1161/ATVBAHA.112.300829, PubMed: 23471228)
321.	Takayuki Ise, K Fujioka, Takashi Iwase, J. Hotchi, Masashi Akaike and Masataka Sata : Ulcer-like projection caused by a penetrating branch to the bronchial artery., Journal of the American College of Cardiology, Vol.61, No.8, e147-147, 2013. (Keyword) Aged / Aorta, Thoracic / Back Pain / Bronchial Arteries / Female / Hematoma / Humans / Remission, Spontaneous / Rupture, Spontaneous / Tomography, X-Ray Computed (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jacc.2012.10.047 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23428223 ● Summary page in Scopus @ Elsevier: 2-s2.0-84874522803 (DOI: 10.1016/j.jacc.2012.10.047, PubMed: 23428223, Elsevier: Scopus)
322.	Tomoya Hara, Hirotsugu Yamada, Akira Takashima, Hiromu Yamasaki, Kozue Ogasawara, Sachiko Bando, Takayuki Ise, Toshiyuki Niki, Kenya Kusunose, Yuka Ueda, Noriko Tomita, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Hidehisa Horiguchi, Naomi Sakashita and Masataka Sata : Constrictive pericarditis with intrapericardial abscess., Circulation Journal, Vol.77, No.3, 786-788, 2013. (Keyword) Abscess / Aged / Autopsy / Fatal Outcome / Heart Diseases / Humans / Male / Methicillin-Resistant Staphylococcus aureus / Pericarditis, Constrictive / Pericardium / Staphylococcal Infections (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-12-1098 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23207988 ● Summary page in Scopus @ Elsevier: 2-s2.0-84874412877 (DOI: 10.1253/circj.CJ-12-1098, PubMed: 23207988, Elsevier: Scopus)
323.	N. Kawano, Koji Yamaguchi, Toshiyuki Niki, Yamamoto Takashi, Takashi Iwase, Yoshio Taketani, Takayuki Ise, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, K Kawano, A. Kakutani and Masataka Sata : Two cases of acute myocardial infarction during combined chemotherapy in young patients with testicular cancer., Journal of Cardiology Cases, Vol.7, No.6, e176-e180, 2013. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jccase.2013.02.009 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84877831795 (DOI: 10.1016/j.jccase.2013.02.009, Elsevier: Scopus)
324.	Michio Shimabukuro, Chisayo Kozuka, Shin-ichiro Taira, Kouichi Yabiku, Munkhbaatar Dagvasumberel, Masayoshi Ishida, Sachiko Matsumoto, Shusuke Yagi, Daiju Fukuda, Ken Yamakawa, Moritake Higa, Takeshi Soeki, Hisashi Yoshida, Hiroaki Masuzaki and Masataka Sata : Ectopic fat deposition and global cardiometabolic risk: New paradigm in cardiovascular medicine., The Journal of Medical Investigation : JMI, Vol.60, No.1, 2, 1-14, 2013. (Summary) The obesity epidemic is a global public health concern that increases the likelihood of morbidity and mortality of metabolic and cardiovascular disease (CVD) and threatens to reduce life expectancy around the world. The concept of the metabolic syndrome (MetS) takes into account that visceral fat plays an essential role in the development of metabolic and cardiovascular diseases. However, MetS cannot be used to assess global CVD risk but is at best one more modifiable CVD risk factor. Thus, global cardiometabolic risk (the global risk of cardiovascular disease resulting from traditional risk factors combined with the additional contribution of the metabolic syndrome and/or insulin resistance) should be considered individually. There is solid evidence supporting the notion that excess abdominal fat is predictive of insulin resistance and the presence of related metabolic abnormalities currently referred to as MetS. Despite the fact that abdominal obesity is a highly prevalent feature of MetS, the mechanisms by which abdominal obesity is causally related to MetS are not fully elucidated. Besides visceral fat accumulation, ectopic lipid deposition, especially in liver and skeletal muscle, has been implicated in the pathophysiology of diabetes, insulin resistance and obesity-related disorders. Also, ectopic fat deposition could be deteriorated in the heart components such as (1) circulatory and locally recruited fat, (2) intra- and extra-myocellular fat, (3) perivascular fat, and (4) pericardial fat. In this review, the contribution of ectopic lipid deposition to global cardiometabolic risk is reviewed and also discussed are potential underlying mechanisms including adipocytokine, insulin resistance and lipotoxicity. J. Med. Invest. 60: 1-14, February, 2013. (Keyword) obesity / insulin resistance / cardiovascular disease / diabetes mellitus (Tokushima University Institutional Repository) ● Metadata: 106036 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.60.1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23614905 ● Summary page in Scopus @ Elsevier: 2-s2.0-84876035311 (Tokushima University Institutional Repository: 106036, DOI: 10.2152/jmi.60.1, PubMed: 23614905, Elsevier: Scopus)
325.	高島啓, Takayuki Ise, Yuka Ueda, Takashi Iwase, Shusuke Yagi, 前田香代子, 西川幸治, 小笠原梢, Mika Bando, 坂東左知子, 冨田紀子, Toshiyuki Niki, 發知淳子, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Shinsuke Katoh, Masashi Akaike, Natsuo Yasui and Masataka Sata : Cardiac rehabilitation reduces level of oxidized LDL, 心臓リハビリテーション, Vol.18, No.1, 130-133, 2013. (Keyword) 酸化LDL / 心臓リハビリテーション / 心肺運動負荷試験 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520010381154583040 (CiNii: 1520010381154583040)
326.	Haruo Yamauchi, Noboru Motomura, Ung-il Chung, Masataka Sata, Daiya Takai, Aya Saito, Minoru Ono and Shinichi Takamoto : Growth-associated hyperphosphatemia in young recipients accelerates aortic allograft calcification in a rat model., Journal of Thoracic and Cardiovascular Surgery, Vol.145, No.2, 522-530, 2013. (Summary) OBJECTIVES: Cardiovascular allografts in the young have limited durability because of early graft calcification. The objective of this study was to examine the hypothesis that growth-associated hyperphosphatemia in youth accelerates aortic allograft calcification by osteogenic transformation of graft medial smooth muscle cells (SMCs). METHODS: The descending aortas of donor rats were subcutaneously transplanted into recipients. Syngeneic (Lewis-to-Lewis) transplantations between 3-week-old "young" (Y) rats and between 10-week-old "adult" (A) rats were combined with standard (ST, 0.9% phosphate) and low-phosphate (LP, 0.2%) diets, resulting in Y-ST, Y-LP, and A-ST groups. Allotransplantations (Brown-Norway-to-Lewis) involving these ages and diets were also made. The grafts and sera were retrieved from recipients after 14 days. Cultured rat aortic SMCs were used to analyze the effects of tumor necrosis factor-alpha (TNF-α) and phosphate on SMC calcification. RESULTS: In vivo, serum phosphate levels were higher in Y-ST (11.5 mg/dL) than those in Y-LP (8.9 mg/dL) and A-ST (8.5 mg/dL). Graft medial calcification appeared severe only in Y-ST. Allotransplants did not affect these outcomes. Graft medial cells showed phenotypic changes (contractile to synthetic) and osteogenic transformation (α-smooth muscle actin to Runx2 and osteocalcin), together with up-regulated proinflammatory TNF-α and sodium-phosphate cotransporter, Pit-1, despite ages and diets. In vitro, TNF-α induced phenotypic changes and osteogenic transformation of SMCs with Pit-1 up-regulation, but SMC calcification occurred only with high phosphate (4.5 mmol/L). CONCLUSIONS: Growth-associated hyperphosphatemia with inflammatory responses may be essential for accelerating allograft calcification in youth and could be a therapeutic target. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jtcvs.2012.03.010 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22513315 ● Search Scopus @ Elsevier (PMID): 22513315 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jtcvs.2012.03.010 (DOI: 10.1016/j.jtcvs.2012.03.010, PubMed: 22513315)
327.	T Hara, Koji Yamaguchi, Takashi Iwase, M Kadota, Mika Bando, K Ogasawara, S Bando, Takayuki Ise, Toshiyuki Niki, Yuka Ueda, N Tomita, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Eosinophilic Myocarditis due to Churg-Strauss syndrome with markedly elevated Eosinophil Cationic Protein., International Heart Journal, Vol.54, No.1, 51-53, 2013. (Summary) A 67-year-old woman with asthma visited our hospital with increasing dyspnea and new-onset paresthesia and purpura in her legs. Physical examination showed a wheeze, pretibial edema, and surrounding purpura. Chest X-rays showed cardiac decompensation and an electrocardiogram revealed a new ST-T change. Laboratory data showed leukocytosis, hypereosinophilia (10,450/μL), troponin T(+), elevated BNP, and markedly elevated eosinophil cationic protein (ECP) (> 150 ng/mL). Echocardiography revealed diffuse left ventricular hypokinesis (ejection fraction 30%) with increased wall thickness. Coronary angiography was normal. Cardiac magnetic resonance imaging implied diffuse myocardial edema and subendocardial late gadolinium enhancement. Skin biopsy of purpura showed superfi cial perivascular dermatitis with remarkable eosinophilic infiltrations. No evidence of drug allergies, parasitic infection, or myeloproliferative disorder was detected. Based on these findings, a diagnosis of eosinophilic myocarditis due to Churg-Strauss syndrome was considered. She was administered prednisolone at a dose of 1 mg/kg, cyclophosphamide, and diuretics. Several markers of eosinophilic myocarditis and heart failure gradually improved, including ECP. She was discharged 30 days later with no cardiac event. Eosinophilic myocarditis is characterized by predominantly eosinophilic infi ltration. Eosinophilic granule proteins, such as ECP and major basic protein, play important roles in the pathogenesis of eosinophilic myocarditis. We experienced a rare case of eosinophilic myocarditis due to Churg-Strauss syndrome. Markedly elevated ECP played an important role in the early diagnosis and subsequent reduction in ECP served as a marker of monitoring. In an asthmatic patient with dyspnea, hypereosinophilia, and vasculitis, Churg-Strauss syndrome with eosinophilic myocarditis should be considered. (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.54.51 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23428926 ● Search Scopus @ Elsevier (PMID): 23428926 ● Search Scopus @ Elsevier (DOI): 10.1536/ihj.54.51 (DOI: 10.1536/ihj.54.51, PubMed: 23428926)
328.	T. Hara, Tetsuzo Wakatsuki, Yoshio Taketani, Koji Yamaguchi, Takashi Iwase and Masataka Sata : A case of successful use of microsnare to hold and pull the retrograde guidewire for the intervention to peripheral chronic total occlusion., Cardiovascular Intervention and Therapeutics, Vol.28, No.3, 287-290, 2013. (Summary) A basket-shaped microsnare has various uses such as the pull through technique during coronary intervention to chronic total occlusion (CTO). A 79-year-old man underwent angioplasty for the femoral artery occlusion. We performed a controlled antegrade and retrograde tracking (CART) with dilatation of a balloon on the antegrade guidewire. The retrograde guidewire partly ran in the true lumen but could not pass through the CTO lesion because of inadequate CART. Eventually, we successfully gripped the top of the retrograde guidewire in the CTO lesion using the basket-shaped microsnare (Soutenir(®)). The microsnare may be useful for bidirectional approach in peripheral CTO lesions. (Keyword) Microsnare / Chronic total occlusions / Peripheral intervention (Link to Publication Site) ● Publication site (DOI): 10.1007/s12928-013-0158-z (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1522543655127492352 ● Search Scopus @ Elsevier (DOI): 10.1007/s12928-013-0158-z (DOI: 10.1007/s12928-013-0158-z, CiNii: 1522543655127492352)
329.	Z Tian, K Miyata, H Tazume, H Sakauguchi, T Kadomatsu, E Horio, O Takahashi, Y Komohara, K Araki, Y Hirata, M Tabata, S Takanashi, M Takeya, H Hao, Michio Shimabukuro, Masataka Sata, M Kawasuji and Y Oike : Perivascular adipose tissue-secreted angiopoietin-like protein2 (Angptl2) accelerates neointimal hyperplasia after endovascular injury., Journal of Molecular and Cellular Cardiology, Vol.57, 1-12, 2013. (Summary) Much attention is currently focused on the role of perivascular adipose tissue in development of cardiovascular disease (CVD). Some researchers view it as promoting CVD through secretion of cytokines and growth factors called adipokines, while recent reports reveal that perivascular adipose tissue can exert a protective effect on CVD development. Furthermore, adiponectin, an anti-inflammatory adipokine, reportedly suppresses neointimal hyperplasia after endovascular injury, whereas such vascular remodeling is enhanced by pro-inflammatory adipokines secreted by perivascular adipose, such as tumor necrosis factor- (TNF-). These findings suggest that extent of vascular remodeling, a pathological process associated with CVD development, depends on the balance between pro- and anti-inflammatory adipokines secreted from perivascular adipose tissue. We previously demonstrated that angiopoietin-like protein 2 (Angptl2), a pro-inflammatory factor secreted by adipose tissue, promotes adipose tissue inflammation and subsequent systemic insulin resistance in obesity. Here, we examined whether Angptl2 secreted by perivascular adipose tissue contributes to vascular remodeling after endovascular injury in studies of transgenic mice expressing Angptl2 in adipose tissue (aP2-Angptl2 transgenic mice) and Angptl2 knockout mice (Angptl2(-/-) mice). To assess the role of Angptl2 secreted by perivascular adipose tissue on vascular remodeling after endovascular injury, we performed adipose tissue transplantation experiments using these mice. Wild-type mice with perivascular adipose tissue derived from aP2-Angptl2 mice exhibited accelerated neointimal hyperplasia after endovascular injury compared to wild-type mice transplanted with wild-type tissue. Conversely, vascular inflammation and neointimal hyperplasia after endovascular injury were significantly attenuated in wild-type mice transplanted with Angptl2(-/-) mouse-derived perivascular adipose tissue compared to wild-type mice transplanted with wild-type tissue. RT-PCR analysis revealed that mouse Angptl2 expression in perivascular adipose tissue was significantly increased by aging, hypercholesterolemia, and endovascular injury, all risk factors for coronary heart disease (CHD). Immunohistochemical and RT-PCR analysis of tissues from patients with CHD and from non-CHD patients indicated that ANGPTL2 expression in epicardial adipose tissue was unchanged. Interestingly, that analysis also revealed a positive correlation in ANGPTL2 and ADIPONECTIN expression in epicardial adipose tissue of non-CHD patients, a correlation not seen in CHD patients. However, in epicardial adipose tissue from CHD patients, ANGPTL2 expression was positively correlated with that of TNF-, a correlation was not seen in non-CHD patients. These findings suggest that pro-inflammatory adipokines cooperatively accelerate CHD development and that maintaining a balance between pro- and anti-inflammatory adipokines likely protects non-CHD patients from developing CHD. Overall, our studies demonstrate that perivascular adipose tissue-secreted Angptl2 accelerates vascular inflammation and the subsequent CVD development. (Keyword) Adiponectin / Adipose Tissue / Adolescent / Adult / Aged / Aged, 80 and over / Angiopoietins / Animals / Child / Coronary Artery Disease / Coronary Vessels / Cytokines / Female / Femoral Artery / Gene Expression / Humans / Hypercholesterolemia / Hyperplasia / Male / Mice / Mice, Inbred C57BL / Mice, Transgenic / Middle Aged / Neointima / Transcriptional Activation / Vascular System Injuries (Link to Publication Site) ● Publication site (DOI): 10.1016/j.yjmcc.2013.01.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23333801 ● Search Scopus @ Elsevier (PMID): 23333801 ● Search Scopus @ Elsevier (DOI): 10.1016/j.yjmcc.2013.01.004 (DOI: 10.1016/j.yjmcc.2013.01.004, PubMed: 23333801)
330.	Hirata Yoichiro, Hirotsugu Kurobe, Nishio Chika, Tanaka Kimie, Daiju Fukuda, Uematsu Etsuko, Nishimoto Sachiko, Takeshi Soeki, Nagakatsu Harada, Hiroshi Sakaue, Tetsuya Kitagawa, Michio Shimabukuro, Yutaka Nakaya and Masataka Sata : Exendin-4, a glucagon-like peptide-1 receptor agonist, attenuates neointimal hyperplasia after vascular injury., European Journal of Pharmacology, Vol.699, No.1-3, 106-111, 2013. (Summary) Exendin-4 is a glucagon-like peptide-1 receptor agonist that has been used as a drug for treatment of type 2 diabetes. To investigate the effect of exendin-4 on the cardiovascular system, we investigated the impact of exendin-4 on neointimal hyperplasia of the femoral artery after vascular injury. We performed wire-mediated endovascular injury in C57BL/6 mice, followed by administration of exendin-4 24 nmol/kg/day via infusion pump. Four weeks after the injury, exendin-4 treatment significantly attenuated neointimal hyperplasia of the injured artery, although it did not affect glucose metabolism and lipid profile in wild-type mice. Immunofluorescence study revealed abundant expression of GLP-1 receptor on α-smooth muscle actin-positive cells in the injured vessel. Cell proliferation assay using rat aortic smooth muscle cells showed that exendin-4 reduced PDGF-BB induced smooth muscle cell proliferation through the cAMP/PKA pathway. Exendin-4 also inhibited TNFα production by peritoneal macrophages in response to inflammatory stimulus. Our findings indicate that a GLP-1 receptor agonist attenuated neointimal formation after vascular injury. GLP-1 receptor agonists or drugs that raise endogenous GLP-1 level might be effective in the treatment of vascular diseases. (Keyword) Exendin-4 / GLP-1 / endovascular injury / neointimal hyperplasia / diabetes mellitus (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2012.11.057 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23220706 ● Search Scopus @ Elsevier (PMID): 23220706 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2012.11.057 (DOI: 10.1016/j.ejphar.2012.11.057, PubMed: 23220706)
331.	Y. Fukuda, Takeshi Soeki and Masataka Sata : A novel doppler echocardiographic index integrating left and right ventricular function is superior to conventional indices for predicting adverse outcome of acute myocardial infarction., The Journal of Medical Investigation : JMI, Vol.60, No.1, 2, 97-105, 2013. (Summary) The ratio of peak diastolic early velocity (E) of left ventricular (LV) inflow to peak diastolic longitudinal velocity (e') of the mitral annulus (E/e') is thought to reflect LV filling pressure, and tricuspid annulus velocity at systole (s'-T) is thought to reflect right ventricular function. However, it has not been reported on significance of the combined use of E/e' and (s'-T) to predict outcome of acute myocardial infarction (AMI). Over 21 months, beginning in January 2007, we enrolled 65 AMI patients who were measured hemodynamic and echocardiographic parameters by Swan-Ganz (SG) catheterization just after reperfusion therapy and echocardiography immediately after reperfusion therapy. Cardiac index (CI) and pulmonary capillary wedge pressure (PCWP) via SG catheter were measured, and routine echocardiographic indices, including E, e', E/e', and (s'-T) were determined. In addition, we defined the functional integrated bi-myocardial tissue Doppler (FIT) index as (s'-T)÷E/e'. The relationships between CI, PCWP, and echocardiographic indices were investigated, including FIT index. Moreover, we investigated whether FIT index could predict adverse cardiac events. FIT index was significantly associated with not only CI but also PCWP. In the Cox proportional hazards model, FIT index<1.0 was a significant predictor for adverse outcome of AMI after adjustment for age, Killip class, history of previous coronary revascularization, location of culprit lesion, and LV ejection fraction. The novel index defined as (s'-T)÷E/e' could be quite useful predictor of prognosis in AMI. (Keyword) transesophageal echocardiography / tissue Doppler imaging / acute myocardial infarction / left ventricular filling pressure / right ventricular function (Tokushima University Institutional Repository) ● Metadata: 111304 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.60.97 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23614917 ● Summary page in Scopus @ Elsevier: 2-s2.0-84876044555 (Tokushima University Institutional Repository: 111304, DOI: 10.2152/jmi.60.97, PubMed: 23614917, Elsevier: Scopus)
332.	Hirata Yoichiro, Hirotsugu Kurobe, Uematsu Etsuko, Shusuke Yagi, Takeshi Soeki, Hirotsugu Yamada, Daiju Fukuda, Michio Shimabukuro, Nakayama Mizuho, Matsumoto Kunio, Sakai Yoshiki, Tetsuya Kitagawa and Masataka Sata : Beneficial effect of a synthetic prostacyclin agonist, ONO-1301, in rat autoimmune myocarditis model., European Journal of Pharmacology, Vol.699, No.1-3, 81-87, 2013. (Summary) Injury to the heart can result in cardiomyocyte hypertrophy, fibrosis, and cell death. Myocarditis sometimes progresses to dilated cardiomyopathy. We previously reported that ONO-1301, a synthetic prostacyclin agonist with thromboxane-synthase inhibitory activity, promotes production of hepatocyte growth factor (HGF) from various cell types and ameliorates ischemia-induced left ventricle dysfunction in the mouse, rat and pig. Here, we investigated the therapeutic efficacy of ONO-1301 in a rat model of myosin-induced experimental autoimmune myocarditis, in which the heart transits from an acute inflammatory phase to a chronic dilated cardiomyopathy phase. Four weeks after myosin injection to Lewis rats, ONO-1301 (6 mg/kg/day) was orally administered for 4 weeks (ONO-1301 group). Hemodynamic parameters and plasma brain natriuretic peptide (BNP) level were significantly improved by ONO-1301. Histological analysis revealed that capillary density in the myocardium was significantly increased by ONO-1301. ONO-1301 increased circulating endothelial progenitor cells (EPC) as determined by FACS analysis. These beneficial effects of ONO-1301 were partially abrogated by a neutralizing anti-HGF antibody (8 mg/kg/dose). These findings indicate beneficial effects of ONO-1301 in a rat experimental autoimmune myocarditis model. (Keyword) heart failure / HGF / dilated cardiomyopathy / experimental autoimmune myocarditis (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2012.11.045 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23219794 ● Search Scopus @ Elsevier (PMID): 23219794 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2012.11.045 (DOI: 10.1016/j.ejphar.2012.11.045, PubMed: 23219794)
333.	K. Yamakawa, Michio Shimabukuro, N. Higa, T. Asahi, K. Ohba, O. Arasaki, M. Higa, Y. Oshiro, H. Yoshida, T. Higa, T. Saito, S. Ueda, H. Masuzaki and Masataka Sata : Eicosapentaenoic acid supplementation changes fatty acid composition and corrects endothelial dysfunction in hyperlipidemic patients., Cardiology Research and Practice, Vol.2012, 754181, 2012. (Summary) We investigated the effects of purified eicosapentaenoic acid (EPA) on vascular endothelial function and free fatty acid composition in Japanese hyperlipidemic subjects. In subjects with hyperlipidemia (total cholesterol ≥220 mg/dL and/or triglycerides ≥150 mg/dL), lipid profile and forearm blood flow (FBF) during reactive hyperemia were determined before and 3 months after supplementation with 1800 mg/day EPA. Peak FBF during reactive hyperemia was lower in the hyperlipidemic group than the normolipidemic group. EPA supplementation did not change serum levels of total, HDL, or LDL cholesterol, apolipoproteins, remnant-like particle (RLP) cholesterol, RLP triglycerides, or malondialdehyde-modified LDL cholesterol. EPA supplementation did not change total free fatty acid levels in serum, but changed the fatty acid composition, with increased EPA and decreased linoleic acid, γ-linolenic acid, and dihomo-γ-linolenic acid. EPA supplementation recovered peak FBF after 3 months. Peak FBF recovery was correlated positively with EPA and EPA/arachidonic acid levels and correlated inversely with dihomo-γ-linolenic acid. EPA supplementation restores endothelium-dependent vasodilatation in hyperlipidemic patients despite having no effect on serum cholesterol and triglyceride patterns. These results suggest that EPA supplementation may improve vascular function at least partly via changes in fatty acid composition. (Link to Publication Site) ● Publication site (DOI): 10.1155/2012/754181 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23326753 ● Search Scopus @ Elsevier (PMID): 23326753 ● Search Scopus @ Elsevier (DOI): 10.1155/2012/754181 (DOI: 10.1155/2012/754181, PubMed: 23326753)
334.	羽星辰哉, Kenji Yagi, Yoshiteru Tada, Nobuhisa Matsushita, Yasuhisa Kanematsu, Mika Bando, Yuka Ueda, Hirotsugu Yamada, Junichiro Satomi, Kyoko Nishi, Masataka Sata and Shinji Nagahiro : A clinical study on severe neurogenic stress cardiomyopathy after subarachnoid hemorrhage, Shikoku Acta Medica, Vol.68, No.5, 6, 233-238, 2012. (Keyword) neurogenic stress cardiomyopathy / subarachnoid hemorrhage / sympathetic nerve (Tokushima University Institutional Repository) ● Metadata: 110362 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050845762395239424 (Tokushima University Institutional Repository: 110362, CiNii: 1050845762395239424)
335.	沖(松本) 美環 and Masataka Sata : 特集不安定プラークの病態と診断 n-3系多価不飽和脂肪酸とプラークの安定化作用, 月刊循環器 CIRCULATION, Vol.3, No.1, 84-90, 2012.
336.	Takeya Minami, Koichiro Kuwahara, Yasuaki Nakagawa, Minoru Takaoka, Hideyuki Kinoshita, Kazuhiro Nakao, Yoshihiro Kuwabara, Yuko Yamada, Chinatsu Yamada, Junko Shibata, Satoru Usami, Shinji Yasuno, Toshio Nishikimi, Kenji Ueshima, Masataka Sata, Hiroyasu Nakano, Takahiro Seno, Yutaka Kawahito, Kenji Sobue, Akinori Kimura, Ryozo Nagai and Kazuwa Nakao : Reciprocal expression of MRTF-A and myocardin is crucial for pathological vascular remodelling in mice., The EMBO Journal, Vol.31, No.23, 4428-4440, 2012. (Summary) Myocardin-related transcription factor (MRTF)-A is a Rho signalling-responsive co-activator of serum response factor (SRF). Here, we show that induction of MRTF-A expression is key to pathological vascular remodelling. MRTF-A expression was significantly higher in the wire-injured femoral arteries of wild-type mice and in the atherosclerotic aortic tissues of ApoE(-/-) mice than in healthy control tissues, whereas myocardin expression was significantly lower. Both neointima formation in wire-injured femoral arteries in MRTF-A knockout (Mkl1(-/-)) mice and atherosclerotic lesions in Mkl1(-/-); ApoE(-/-) mice were significantly attenuated. Expression of vinculin, matrix metallopeptidase 9 (MMP-9) and integrin β1, three SRF targets and key regulators of cell migration, in injured arteries was significantly weaker in Mkl1(-/-) mice than in wild-type mice. In cultured vascular smooth muscle cells (VSMCs), knocking down MRTF-A reduced expression of these genes and significantly impaired cell migration. Underlying the increased MRTF-A expression in dedifferentiated VSMCs was the downregulation of microRNA-1. Moreover, the MRTF-A inhibitor CCG1423 significantly reduced neointima formation following wire injury in mice. MRTF-A could thus be a novel therapeutic target for the treatment of vascular diseases. (Keyword) Animals / Atherosclerosis / COS Cells / Cell Movement / Cells, Cultured / Cercopithecus aethiops / Femoral Artery / Immunohistochemistry / Mice / Mice, Inbred C57BL / Mice, Knockout / Mice, Transgenic / Muscle, Smooth, Vascular / NIH 3T3 Cells / Neointima / Nuclear Proteins / RNA Interference / Serum Response Factor / Signal Transduction / Time Factors / Trans-Activators / Wound Healing (Link to Publication Site) ● Publication site (DOI): 10.1038/emboj.2012.296 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23103763 ● Search Scopus @ Elsevier (PMID): 23103763 ● Search Scopus @ Elsevier (DOI): 10.1038/emboj.2012.296 (DOI: 10.1038/emboj.2012.296, PubMed: 23103763)
337.	Takeshi Soeki and Masataka Sata : Role of epicardial adipose tissue in atrial fibrillation., Circulation Journal, Vol.76, No.12, 2738-2739, 2012. (Keyword) Adipose Tissue / Atrial Fibrillation / Coronary Artery Disease / Female / Humans / Male / Multidetector Computed Tomography / Pericardium (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-12-1283 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23095722 ● Search Scopus @ Elsevier (PMID): 23095722 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-12-1283 (DOI: 10.1253/circj.CJ-12-1283, PubMed: 23095722)
338.	Asuka Shiota, Michio Shimabukuro, Daiju Fukuda, Takeshi Soeki, Hiromi Sato, Etsuko Uematsu, Hirata Yoichiro, Hirotsugu Kurobe, Maeda Norikazu, Hiroshi Sakaue, Masuzaki Hiroaki, Shimomura Iichiro and Masataka Sata : Telmisartan ameliorates insulin sensitivity by activating the AMPK/SIRT1 pathway in skeletal muscle of obese db/db mice., Cardiovascular Diabetology, Vol.11, No.1, 139, 2012. (Summary) Telmisartan is a well-established angiotensin II type 1 receptor blocker that improves insulin sensitivity in animal models of obesity and insulin resistance, as well as in humans. Telmisartan has been reported to function as a partial agonist of the peroxisome proliferator-activated receptor (PPAR) γ, which is also targeted by the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase (SIRT1). Here, we investigated the pathways through which telmisartan acts on skeletal muscle, in vitro as well as in vivo. Nine-week-old male db/db mice were fed a 60% high-fat diet, with orally administrated either vehicle (carboxymethyl-cellulose, CMC), 5 mg/kg telmisartan, or 5 mg/kg telmisartan and 1 mg/kg GW9662, a selective irreversible antagonist of PPARγ, for 5 weeks. Effects of telmisartan on Sirt1 mRNA, AMPK phosphorylation, and NAD+/NADH ratio were determined in C2C12 cultured myocytes. Telmisartan treatment improved insulin sensitivity in obese db/db mice fed a high-fat diet and led to reduction in the size of hypertrophic pancreatic islets in these mice. Moreover, in vitro treatment with telmisartan led to increased expression of Sirt1 mRNA in C2C12 skeletal muscle cells; the increase in Sirt1 mRNA in telmisartan-treated C2C12 myoblasts occurred concomitantly with an increase in AMPK phosphorylation, an increase in NAD+/NADH ratio, and increases in the mRNA levels of PGC1α, FATP1, ACO, and GLUT4. Our results indicate that telmisartan acts through a PPARγ-independent pathway, but at least partially exerts its effects by acting directly on skeletal muscle AMPK/SIRT1 pathways. (Keyword) AMP-Activated Protein Kinases / Adipocytes / Administration, Oral / Angiotensin II Type 1 Receptor Blockers / Anilides / Animals / Benzimidazoles / Benzoates / Cell Line / Diabetes Mellitus / Diet, High-Fat / Disease Models, Animal / Dose-Response Relationship, Drug / Enzyme Activation / Fatty Acid Transport Proteins / Glucose Transporter Type 4 / Hypertrophy / Insulin / Islets of Langerhans / Male / Mice / Muscle Fibers, Skeletal / Muscle, Skeletal / NAD / Obesity / PPAR gamma / Phosphorylation / RNA, Messenger / Signal Transduction / Sirtuin 1 / Time Factors / Trans-Activators (Link to Publication Site) ● Publication site (DOI): 10.1186/1475-2840-11-139 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23137106 ● Search Scopus @ Elsevier (PMID): 23137106 ● Search Scopus @ Elsevier (DOI): 10.1186/1475-2840-11-139 (DOI: 10.1186/1475-2840-11-139, PubMed: 23137106)
339.	Masataka Sata : 異所性脂肪と動脈硬化, 動脈硬化予防, Vol.11, No.3, 42-47, 2012. (Keyword) atherosclerosis / angiogenesis / 心臓周囲脂肪 / 不安定プラーク / 心筋梗塞
340.	Daiju Fukuda and Masataka Sata : 動脈硬化とRAS, Angiotensin Research, Vol.9, No.4, 7-12, 2012.
341.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Takashi Iwase, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya, Masataka Sata, Masashi Akaike, Shigeaki Kato, Toshio Matsumoto and Toshiaki Tamaki : Heparin cofactor II, a serine protease inhibitor, promotes angiogenesis via activation of the AMP-activated protein kinase-endothelial nitric-oxide synthase signaling pathway, The Journal of Biological Chemistry, Vol.287, No.41, 34256-34263, 2012. (Summary) We previously clarified that heparin cofactor II (HCII), a serine proteinase inhibitor, exerts various protective actions on cardiovascular diseases in both experimental and clinical studies. In the present study, we aimed to clarify whether HCII participates in the regulation of angiogenesis. Male heterozygous HCII-deficient (HCII(+/-)) mice and male littermate wild-type (HCII(+/+)) mice at the age of 12-16 weeks were subjected to unilateral hindlimb ligation surgery. Laser speckle blood flow analysis showed that blood flow recovery in response to hindlimb ischemia was delayed in HCII(+/-) mice compared with that in HCII(+/+) mice. Capillary number, arteriole number, and endothelial nitric-oxide synthase (eNOS), AMP-activated protein kinase (AMPK), and liver kinase B1 (LKB1) phosphorylation in ischemic muscles were decreased in HCII(+/-) mice. Human purified HCII (h-HCII) administration almost restored blood flow recovery, capillary density, and arteriole number as well as phosphorylation levels of eNOS, AMPK, and LKB1 in ischemic muscles of HCII(+/-) mice. Although treatment with h-HCII increased phosphorylation levels of eNOS, AMPK, and LKB1 in human aortic endothelial cells (HAECs), the h-HCII-induced eNOS phosphorylation was abolished by compound C, an AMPK inhibitor, and by AMPK siRNA. In a similar fashion, tube formation, proliferation, and migration of HAECs were also promoted by h-HCII treatment and were abrogated by pretreatment with compound C. HCII potentiates the activation of vascular endothelial cells and the promotion of angiogenesis in response to hindlimb ischemia via an AMPK-eNOS signaling pathway. These findings suggest that HCII is a novel therapeutic target for treatment of patients with peripheral circulation insufficiency. (Keyword) Heparin cofactor II (HCII) / vascular endothelial cells / angiogenesis (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M112.353532 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22904320 ● Search Scopus @ Elsevier (PMID): 22904320 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M112.353532 (DOI: 10.1074/jbc.M112.353532, PubMed: 22904320)
342.	Shuji Hayashi, Hirotsugu Yamada, Susumu Nishio, Noriko Tomita, Junko Hotchi, Mika Bando, Maya Nakagawa, Rina Tamai, Daichi Hirota, Yukina Hirata and Masataka Sata : Double-chambered right ventricle presenting significant outflow tract obstruction only in the right decubitus position., Journal of Echocardiography, Vol.10, No.4, 146-147, 2012. (Keyword) double-chambered right ventricle / right mid-ventricular obstruction / postural change / doppler echocardiography / ventricular septal defect (Link to Publication Site) ● Publication site (DOI): 10.1007/s12574-012-0145-x (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1007/s12574-012-0145-x (DOI: 10.1007/s12574-012-0145-x)
343.	Masataka Sata : 虚血性心疾患と血管内皮機能, Heart, Vol.44, No.9, 1219-1222, 2012.
344.	Munkhbaatar Dagvasumberel, Michio Shimabukuro, Nishiuchi Takeshi, Junji Ueno, Shoichiro Takao, Daiju Fukuda, Hirata Yoichiro, Hirotsugu Kurobe, Takeshi Soeki, Takashi Iwase, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Shusuke Yagi, Tomita Noriko, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masafumi Harada, Tetsuya Kitagawa and Masataka Sata : Gender disparities in the association between epicardial adipose tissue volume and coronary atherosclerosis: A 3-dimensional cardiac computed tomography imaging study in Japanese subjects., Cardiovascular Diabetology, Vol.11, No.1, 106, 2012. (Summary) Growing evidence suggests that epicardial adipose tissue (EAT) may contribute to the development of coronary artery disease (CAD). In this study, we explored gender disparities in EAT volume (EATV) and its impact on coronary atherosclerosis. The study population consisted of 90 consecutive subjects (age: 63 ± 12 years; men: 47, women: 43) who underwent 256-slice multi-detector computed tomography (MDCT) coronary angiography. EATV was measured as the sum of cross-sectional epicardial fat area on CT images, from the lower surface of the left pulmonary artery origin to the apex. Subjects were segregated into the CAD group (coronary luminal narrowing > 50%) and non-CAD group. EATV/body surface area (BSA) was higher among men in the CAD group than in the non-CAD group (62 ± 13 vs. 33 ± 10 cm3/m2, p < 0.0001), but did not differ significantly among women in the 2 groups (49 ± 18 vs. 42 ± 9 cm3/m2, not significant). Multivariate logistic analysis showed that EATV/BSA was the single predictor for >50% coronary luminal narrowing in men (p < 0.0001). Predictors excluded were age, body mass index, hypertension, diabetes mellitus, and hyperlipidemia. Increased EATV is strongly associated with coronary atherosclerosis in men. (Keyword) Adipose Tissue / Age Factors / Aged / Asian Continental Ancestry Group / Body Surface Area / Chi-Square Distribution / Coronary Angiography / Coronary Artery Disease / Coronary Stenosis / Female / Health Status Disparities / Humans / Japan / Logistic Models / Male / Middle Aged / Multidetector Computed Tomography / Multivariate Analysis / Pericardium / Predictive Value of Tests / Risk Assessment / Risk Factors / Severity of Illness Index / Sex Factors (Link to Publication Site) ● Publication site (DOI): 10.1186/1475-2840-11-106 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22963346 ● Search Scopus @ Elsevier (PMID): 22963346 ● Search Scopus @ Elsevier (DOI): 10.1186/1475-2840-11-106 (DOI: 10.1186/1475-2840-11-106, PubMed: 22963346)
345.	Asuka Shiota, Michio Shimabukuro, Daiju Fukuda, Takeshi Soeki, Hiromi Sato, Etsuko Uematsu, Yoichiro Hirata, Hirotsugu Kurobe, Hiroshi Sakaue, Yutaka Nakaya, Hiroaki Masuzaki and Masataka Sata : Activation of AMPK-Sirt1 pathway by telmisartan in white adipose tissue: A possible link to anti-metabolic effects., European Journal of Pharmacology, Vol.692, No.1-3, 84-90, 2012. (Summary) Telmisartan exerts anti-metabolic effects beyond its angiotensin receptor blockade activities, but the mechanisms have hitherto remained elusive. We sought to elucidate the peroxisome proliferator-activated receptor-γ (PPAR-γ)-dependent and PPAR-γ-independent mechanisms underlying the anti-metabolic effects of telmisartan in white adipose tissue. Nine-week-old male C57BL/6 mice were fed with a 60% high-fat diet for 6 weeks, with 1mg/kg telmisartan or vehicle administrated orally during the last 3 weeks. 3T3-L1 adipocytes were cultured with telmisartan either with 2-chloro-5-nitro-N-phenylbenzamide (GW9662), a selective irreversible antagonist of PPAR-γ, or compound C, an ATP-competitive inhibitor of AMPK. Western blotting and semiquantitative RT-PCR analysis were used to assess adiponectin, Sirt1, and AMPK levels. Lipid accumulation was assessed by Oil red O staining. The activation of transcription factor PPAR-γ2 was evaluated by using a luciferase reporter assay for mPPAR-γ2 expression plasmid vector. Treatment with telmisartan increased serum adiponectin levels in high-fat diet-fed mice concomitantly with an upregulation of adiponectin mRNA in visceral adipose tissue. In vitro telmisartan treatment dose-dependently increased adiponectin mRNA in 3T3-L1 cells; the increase was inhibited by compound C, but not by GW9662. Telmisartan increased expression of Sirt1 mRNA and Sirt1 protein as well as the phosphorylation of AMPK in 3T3-L1 cells. Telmisartan can increase adiponectin production in white adipose tissue partly via a PPAR-γ2-independent mechanism. Precise understanding of this molecular mechanism will require further investigation. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2012.07.026 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22819702 ● Search Scopus @ Elsevier (PMID): 22819702 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2012.07.026 (DOI: 10.1016/j.ejphar.2012.07.026, PubMed: 22819702)
346.	Koji Yamaguchi and Masataka Sata : 高血圧症に対するRAAS抑制薬の有用性, Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.70, No.9, 1571-1576, 2012. (Keyword) angiotensin receptor blockers (ARBs) / angiotensin-converting enzyme (ACE) inhibitors / JSH2009 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1522262179735040128 ● Summary page in Scopus @ Elsevier: 2-s2.0-84871886724 (CiNii: 1522262179735040128, Elsevier: Scopus)
347.	Kenya Kusunose, Hirotsugu Yamada, Susumu Nishio, Noriko Tomita, Junko Hotchi, Mika Bando, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Index-beat Assessment of Left Ventricular Systolic and Diastolic Function during Atrial Fibrillation using Myocardial Strain and Strain Rate., Journal of the American Society of Echocardiography, Vol.25, No.9, 953-959, 2012. (Summary) Accurate assessment of left ventricular (LV) function in patients with atrial fibrillation (AF) remains difficult, mainly because of the beat-to-beat variability of many echocardiographic parameters. The aim of this study was to assess the hypothesis that LV function can be estimated from an index-beat echocardiographic assessment in patients with AF using myocardial strain and strain rate. A prospective study was conducted to assess 25 patients with AF (mean age, 66 ± 10 years). Peak systolic longitudinal strain (LS) and peak diastolic longitudinal strain rate (dSR) were measured using two different methods: (1) mean LS and dSR, the averages of instantaneous LS and dSR over 10 sec, and (2) index-beat LS and dSR, calculated when the ratio of the preceding (RR1) to the pre-preceding (RR2) interval was 1 (range, 0.96-1.04). These variables were compared with simultaneously measured LV pressure parameters using Millar catheters. There was a positive linear relationship between mean LS and index-beat LS at RR1/RR2 = 1 (r = 0.94, P < .001) and a positive linear relationship between mean dSR and index-beat dSR (r = 0.69, P < .001). Index-beat LS was correlated with the maximal positive derivative of LV pressure (peak +dP/dt) (r = -0.73, P < .001). Index-beat dSR was correlated with the time constant of isovolumic LV pressure decay (τ) (r = -0.63, P < .001). To investigate the independent predictors of τ, a stepwise multilinear regression analysis showed that index-beat dSR was the best predictor of τ. Index-beat parameters accurately reflect the mean values of parameters in patients with AF. These noninvasively obtained index-beat parameters are useful to assess surrogate LV function even in patients with AF. (Keyword) Aged / Atrial Fibrillation / Diastole / Echocardiography, Doppler / Female / Heart Rate / Hemodynamics / Humans / Male / Myocardial Contraction / Prospective Studies / Regression Analysis / Reproducibility of Results / Systole (Link to Publication Site) ● Publication site (DOI): 10.1016/j.echo.2012.06.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22763085 ● Search Scopus @ Elsevier (PMID): 22763085 ● Search Scopus @ Elsevier (DOI): 10.1016/j.echo.2012.06.009 (DOI: 10.1016/j.echo.2012.06.009, PubMed: 22763085)
348.	T. Hara, Takeshi Soeki, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Tetsuzo Wakatsuki and Masataka Sata : Bicuspid aortic valve endocarditis complicated by perivalvular abscess., The Journal of Medical Investigation : JMI, Vol.59, No.3,4, 261-265, 2012. (Summary) A 37-year-old man presenting with fever and chest pain was admitted to our hospital. Electrocardiogram showed sinus tachycardia and complete left bundle branch block. Transthoracic echocardiogram showed infective endocarditis in the bicuspid aortic valve, complicated by multiple hyperechoic vegetations and severe aortic regurgitation. Blood cultures were negative and intravenous empiric antibiotic therapy was begun. However, fever lasted for 7 days and follow-up echocardiography revealed a newly emerged perivalvular abscess. The patient eventually underwent an urgent aortic root replacement that confirmed the echocardiographic findings. Our case report emphasizes that all patients with suspected aortic valve endocarditis should undergo early and follow-up echocardiographic studies. (Keyword) bicuspid aortic valve / infectious endocarditis / perivalvular abscess / echocardiography (Tokushima University Institutional Repository) ● Metadata: 106030 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.59.261 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23037197 ● Search Scopus @ Elsevier (PMID): 23037197 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.59.261 (Tokushima University Institutional Repository: 106030, DOI: 10.2152/jmi.59.261, PubMed: 23037197)
349.	Mika Bando, Hirotsugu Yamada, 西尾進, 玉井利奈, 平田有紀奈, 弘田大智, 中川摩耶, 林修司, 冨田紀子, 發知淳子, 小笠原梢, 高島啓, 山崎宙, 坂東左知子, Takayuki Ise, Toshiyuki Niki, Yuka Ueda, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, Yasuhisa Kanematsu, Junichiro Satomi and Shinji Nagahiro : Effect of statin therapy on carotid artery plaque assessed by integrated backscatter color mapping : Development of imaging analytical software and its application on 3 cases, Shikoku Acta Medica, Vol.68, No.3-4, 147-152, 2012. (Summary) Background : The carotid plaque vulnerability is related to myocardial and cerebral infarction.We intended to develop an imaging system which enables to visualize tissue characteristics in thecarotid plaques based on ultrasound integrated backscatter(IB). And to test its clinical efficacy,effect of the statin therapy on the plaques was evaluated with our software. Methods and Results :Carotid ultrasound examination was performed and ultrasonographic RAW data of the plaqueswere obtained from8patients undergoing carotid artery endarterectomy. Tissue characteristicsin the plaques of resected examples were compared with preoperative ultrasonic images and thetissue IB values corresponding to the specimens were determined for developing our imaging system.Using this system, Color-coded maps of plaques in the three patients were constructed beforeand after lipid lowing therapy. We could demonstrate that lipid fraction in each plaque decreasedand fibrous or calcification fraction increased in the follow-up study. Conclusions : Changes inhistology of carotid plaques by statin could visualized with our imaging system. This techniquemay become a useful tool for the management of atherosclerosis. (Keyword) IBS (integrated backscatter) / carotid plaque / CEA (carotid endarterectomy) (Tokushima University Institutional Repository) ● Metadata: 102836 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050282812711314944 (Tokushima University Institutional Repository: 102836, CiNii: 1050282812711314944)
350.	Takeshi Soeki, Mitsuhiro Kitani, Kenya Kusunose, Shusuke Yagi, Yoshio Taketani, Kunihiko Koshiba, Tetsuzo Wakatsuki, Shunsuke Orino, Kazuhiro Kawano and Masataka Sata : Renoprotective and antioxidant effects of cilnidipine in hypertensive patients., Hypertension Research, Vol.35, No.11, 1058-1062, 2012. (Summary) Cilnidipine, an L/N-type calcium channel blocker (CCB), has been reported to have more beneficial effects on proteinuria progression in hypertensive patients than amlodipine, an L-type CCB. The N-type calcium channel blockade that inhibits renal sympathetic nerve activity might reduce glomerular hypertension by facilitating vasodilation of the efferent arterioles. However, the precise mechanism of the renoprotective effect of cilnidipine remains unknown. Because cilnidipine exerted significantly higher antioxidant activity than amlodipine in cultured human mesangial cells, we hypothesized that cilnidipine might exert a renoprotective effect by suppressing oxidative stress. A total of 35 hypertensive patients receiving a renin-angiotensin system inhibitor were randomly assigned to a cilnidipine (n=18; 10 mg per day cilnidipine titrated to 20 mg per day) or amlodipine (n=17; 5 mg per day amlodipine titrated to 10 mg per day) group; the target blood pressure (BP) was set at 130/85 mmHg. After 6 months of treatment, systolic and diastolic BPs were significantly reduced in both of the groups, without any significant difference between the groups. The urinary albumin, 8-hydroxy-2'-deoxyguanosine (OHdG) and liver-type fatty-acid-binding protein (L-FABP) to creatinine ratios significantly decreased in the cilnidipine group (P<0.05) compared with those in the amlodipine group. The reductions in urinary albumin, 8-OHdG and L-FABP were not correlated with the change in systolic BP. In conclusion, cilnidipine, but not amlodipine, ameliorated urinary albumin excretion and decreased urinary 8-OHdG and L-FABP in the hypertensive patients. Cilnidipine probably exerts a greater renoprotective effect through its antioxidative properties.Hypertension Research advance online publication, 5 July 2012; doi:10.1038/hr.2012.96. (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2012.96 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22763473 ● Search Scopus @ Elsevier (PMID): 22763473 ● Search Scopus @ Elsevier (DOI): 10.1038/hr.2012.96 (DOI: 10.1038/hr.2012.96, PubMed: 22763473)
351.	Hirofumi Tomiyama, Takahide Kohro, Yukihito Higashi, Bonpei Takase, Toru Suzuki, Tomoko Ishizu, Shinichiro Ueda, Tsutomu Yamazaki, Tomoo Furumoto, Kazuomi Kario, Teruo Inoue, Shinji Koba, Kentaro Watanabe, Yasuhiko Takemoto, Takuzo Hano, Masataka Sata, Yutaka Ishibashi, Koichi Node, Koji Maemura, Yusuke Ohya, Taiji Furukawa, Hiroshi Ito and Akira Yamashina : A multicenter study design to assess the clinical usefulness of semi-automatic measurement of flow-mediated vasodilatation of the brachial artery., International Heart Journal, Vol.53, No.3, 170-175, 2012. (Summary) Flow-mediated vasodilatation of the brachial artery (FMD) is a marker which is related to endothelial nitric oxide bioavailability. Commercially available ultrasound machines equipped with online computer-assisted semi-automatic analysis software to measure FMD have recently become available in Japan. These devices enable more convenient examination, enhanced reproducibility of FMD measurement, and a shortened examination time. Using such devices, in the present multicenter prospective study we propose to: 1) establish standardized FMD values and determine the annual rates of FMD change in healthy subjects; 2) confirm the predictive value of FMD for future cardiovascular events in Japanese subjects; 3) evaluate the potential usefulness of a multimarker strategy, including measurements of FMD, pulse-wave velocity (PWV), ankle-brachial pressure index, biochemical markers, and proteomic biomarkers obtained by mass spectroscopic analysis to assess the prognosis of subjects with coronary artery disease; and 4) clarify the usefulness of FMD measurement to predict the rate of progression of carotid atherosclerosis, arterial stiffness and microalbuminuria in subjects with hypertension or diabetes mellitus. In total, we estimate that approximately 4000 Japanese subjects in 3 different study groups will eventually be enrolled in this prospective observational investigation. We anticipate that the present study will provide important evidence for the usefulness of FMD measurement in the risk stratification for cardiovascular disease. (Keyword) Flow-mediated vasodilatation / Endothelium / Carotid atherosclerosis / Coronary artery disease / Hypertension (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.53.170 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22790685 ● CiNii @ National Institute of Informatics (CRID): 1390001205226555136 ● Search Scopus @ Elsevier (PMID): 22790685 ● Search Scopus @ Elsevier (DOI): 10.1536/ihj.53.170 (DOI: 10.1536/ihj.53.170, PubMed: 22790685, CiNii: 1390001205226555136)
352.	Yasuharu Watanabe, Tomoya Nakamura, Sho Ishikawa, Shiho Fujisaka, Isao Usui, Koichi Tsuneyama, Yoshinori Ichihara, Tsutomu Wada, Yoichiro Hirata, Takayoshi Suganami, Hirofumi Izaki, Shizuo Akira, Kensuke Miyake, Hiro-omi Kanayama, Michio Shimabukuro, Masataka Sata, Toshiyasu Sasaoka, Yoshihiro Ogawa, Kazuyuki Tobe, Kiyoshi Takatsu and Yoshinori Nagai : The Radioprotective 105/MD-1 complex contributes to diet-induced obesity and adipose tissue inflammation., Diabetes, Vol.61, No.5, 1199-1209, 2012. (Summary) Recent accumulating evidence suggests that innate immunity is associated with obesity-induced chronic inflammation and metabolic disorders. Here, we show that a Toll-like receptor (TLR) protein, radioprotective 105 (RP105)/myeloid differentiation protein (MD)-1 complex, contributes to high-fat diet (HFD)-induced obesity, adipose tissue inflammation, and insulin resistance. An HFD dramatically increased RP105 mRNA and protein expression in stromal vascular fraction of epididymal white adipose tissue (eWAT) in wild-type (WT) mice. RP105 mRNA expression also was significantly increased in the visceral adipose tissue of obese human subjects relative to nonobese subjects. The RP105/MD-1 complex was expressed by most adipose tissue macrophages (ATMs). An HFD increased RP105/MD-1 expression on the M1 subset of ATMs that accumulate in eWAT. Macrophages also acquired this characteristic in coculture with 3T3-L1 adipocytes. RP105 knockout (KO) and MD-1 KO mice had less HFD-induced adipose tissue inflammation, hepatic steatosis, and insulin resistance compared with wild-type (WT) and TLR4 KO mice. Finally, the saturated fatty acids, palmitic and stearic acids, are endogenous ligands for TLR4, but they did not activate RP105/MD-1. Thus, the RP105/MD-1 complex is a major mediator of adipose tissue inflammation independent of TLR4 signaling and may represent a novel therapeutic target for obesity-associated metabolic disorders. (Keyword) Adipocytes / Adipose Tissue / Animals / Antigens, CD / Antigens, Surface / Coculture Techniques / Dietary Fats / Epididymis / Fatty Liver / Gene Expression Regulation / Humans / inflammation / insulin resistance / Macrophages / Male / Membrane Glycoproteins / Mice / Mice, Inbred C57BL / knockout mice / obesity / Palmitic Acid / Stearic Acids / Toll-Like Receptor 4 (Link to Publication Site) ● Publication site (DOI): 10.2337/db11-1182 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22396206 ● Summary page in Scopus @ Elsevier: 2-s2.0-84860555433 (DOI: 10.2337/db11-1182, PubMed: 22396206, Elsevier: Scopus)
353.	Tamotsu Kanbara, Hirotsugu Kurobe, Takashi Kitaichi, Mikio Sugano, Nakayama Taisuke, Hajime Kinoshita, Takashi Iwase, Akaike Masafumi, Masahiro Abe, Masataka Sata, Toshio Matsumoto and Tetsuya Kitagawa : Autologous Peripheral Blood-Derived Mononuclear Cells Induced by Erythropoietin Improve Critical Ischemic Limbs., Annals of Vascular Diseases, Vol.5, No.1, 52-60, 2012. (Summary) Purpose: Efficient and secure collection of CD34+ cells are crucial for the angiogenic therapies. We have developed autologous peripheral blood-mononuclear cell (MNC) transplantation induced by erythropoietin (rhEPO) for critical ischemic limbs. Methods: Seven patients, including five with arteriosclerosis obliterans, one with Buerger's disease and one with progressive systemic sclerosis, underwent ten cell therapies. The first administration of rhEPO was performed two weeks before apheresis, and the second administration and blood donation were performed one week before apheresis to activate bone marrow. MNCs including CD34+ cells, isolated from peripheral blood by apheresis, were immediately injected intramuscularly into ischemic limbs. Results: The number of peripheral blood-CD34 + cells had significantly increased from 1.32 ± 0.83/microL, before the rhEPO induction, to 1.86 ± 0.94/microL, before the apheresis. The number of transplanted MNCs ranged between 0.5 × 10(9) and 16.5 × 10(9), and that of CD34+ cells, between 0.1 × 10(6) and 12.7 × 10(6), accounting for 0.02%-0.1% of MNCs. There were no serious complications. Finger ulcers with Buerger's disease were significantly improved one month after the transplantations, but the same or other ulcer(s) appeared 2-6 months later. Three patients had an improvement in rest pain, and one patient extended maximum pain-free walking distance. Conclusions: Erythropoietin-induced autologous peripheral blood-MNC transplantation is a useful and safe alternative for ischemic limbs. (Link to Publication Site) ● Publication site (DOI): 10.3400/avd.oa.11.00070 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23555486 ● Search Scopus @ Elsevier (PMID): 23555486 ● Search Scopus @ Elsevier (DOI): 10.3400/avd.oa.11.00070 (DOI: 10.3400/avd.oa.11.00070, PubMed: 23555486)
354.	Makoto Sahara, Masataka Sata, Toshihiro Morita, Yasunobu Hirata and Ryozo Nagai : Nicorandil attenuates monocrotaline-induced vascular endothelial damage and pulmonary arterial hypertension., PLoS ONE, Vol.7, No.3, e33367, 2012. (Summary) An antianginal K(ATP) channel opener nicorandil has various beneficial effects on cardiovascular systems; however, its effects on pulmonary vasculature under pulmonary arterial hypertension (PAH) have not yet been elucidated. Therefore, we attempted to determine whether nicorandil can attenuate monocrotaline (MCT)-induced PAH in rats. Sprague-Dawley rats injected intraperitoneally with 60 mg/kg MCT were randomized to receive either vehicle; nicorandil (5.0 mg·kg(-1)·day(-1)) alone; or nicorandil as well as either a K(ATP) channel blocker glibenclamide or a nitric oxide synthase (NOS) inhibitor N(ω)-nitro-L-arginine methyl ester (L-NAME), from immediately or 21 days after MCT injection. Four or five weeks later, right ventricular systolic pressure (RVSP) was measured, and lung tissue was harvested. Also, we evaluated the nicorandil-induced anti-apoptotic effects and activation status of several molecules in cell survival signaling pathway in vitro using human umbilical vein endothelial cells (HUVECs). Four weeks after MCT injection, RVSP was significantly increased in the vehicle-treated group (51.0±4.7 mm Hg), whereas it was attenuated by nicorandil treatment (33.2±3.9 mm Hg; P<0.01). Nicorandil protected pulmonary endothelium from the MCT-induced thromboemboli formation and induction of apoptosis, accompanied with both upregulation of endothelial NOS (eNOS) expression and downregulation of cleaved caspase-3 expression. Late treatment with nicorandil for the established PAH was also effective in suppressing the additional progression of PAH. These beneficial effects of nicorandil were blocked similarly by glibenclamide and l-NAME. Next, HUVECs were incubated in serum-free medium and then exhibited apoptotic morphology, while these changes were significantly attenuated by nicorandil administration. Nicorandil activated the phosphatidylinositol 3-kinase (PI3K)/Akt and extracellular signal-regulated kinase (ERK) pathways in HUVECs, accompanied with the upregulation of both eNOS and Bcl-2 expression. Nicorandil attenuated MCT-induced vascular endothelial damage and PAH through production of eNOS and anti-apoptotic factors, suggesting that nicorandil might have a promising therapeutic potential for PAH. (Keyword) Animals / Antihypertensive Agents / Apoptosis / Blotting, Western / Caspase 3 / Cells, Cultured / Drug Therapy, Combination / Endothelium, Vascular / Enzyme Inhibitors / Glyburide / Human Umbilical Vein Endothelial Cells / Humans / Hypertension, Pulmonary / Injections, Intraperitoneal / MAP Kinase Signaling System / Male / Monocrotaline / NG-Nitroarginine Methyl Ester / Nicorandil / Phosphatidylinositol 3-Kinases / Proto-Oncogene Proteins c-akt / Random Allocation / Rats / Rats, Sprague-Dawley / Signal Transduction / Ventricular Pressure (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0033367 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22479390 ● Search Scopus @ Elsevier (PMID): 22479390 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0033367 (DOI: 10.1371/journal.pone.0033367, PubMed: 22479390)
355.	Tomoya Hara, Koji Yamaguchi and Masataka Sata : Massive splenic infarction due to left ventricular apical thrombus in a patient with giant splenomegaly., Heart Asia, Vol.4, No.1, 53, 2012. (Link to Publication Site) ● Publication site (DOI): 10.1136/heartasia-2011-010070 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1136/heartasia-2011-010070 (DOI: 10.1136/heartasia-2011-010070)
356.	Michio Shimabukuro, H. Masuzaki and Masataka Sata : Intensive glucose lowering in cardiovascular risk management., --- unsolved questions ---, Circulation Journal, Vol.76, No.3, 593-595, 2012. (Keyword) Coronary Artery Disease / Cyclohexanes / Diabetes Mellitus / Female / Glycemic Index / Humans / Inositol / Male / Phenylalanine (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-12-0062 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22293455 ● Search Scopus @ Elsevier (PMID): 22293455 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-12-0062 (DOI: 10.1253/circj.CJ-12-0062, PubMed: 22293455)
357.	Higashikuni Yasutomi, Sainz Julie, Nakayama Kazuto, Takaoka Minoru, Enomoto Soichiro, Iwata Hiroshi, Tanaka Kimie, Sahara Makoto, Hirata Yasunobu, Nagai Ryozo and Masataka Sata : The ATP-binding cassette transporter ABCG2 protects against pressure overload-induced cardiac hypertrophy and heart failure by promoting angiogenesis and antioxidant response., Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.32, No.3, 654-661, 2012. (Summary) ATP-binding cassette transporter subfamily G member 2 (ABCG2), expressed in microvascular endothelial cells in the heart, has been suggested to regulate several tissue defense mechanisms. This study was performed to elucidate its role in pressure overload-induced cardiac hypertrophy. Pressure overload was induced in 8- to 12-week-old wild-type and Abcg2-/- mice by transverse aortic constriction (TAC). Abcg2-/- mice showed exaggerated cardiac hypertrophy and ventricular remodeling after TAC compared with wild-type mice. In the early phase after TAC, functional impairment in angiogenesis and antioxidant response in myocardium was found in Abcg2-/- mice. In vitro experiments demonstrated that ABCG2 regulates transport of glutathione, an important endogenous antioxidant, from microvascular endothelial cells. Besides, glutathione transported from microvascular endothelial cells in ABCG2-dependent manner ameliorated oxidative stress-induced cardiomyocyte hypertrophy. In vivo, glutathione levels in plasma and the heart were increased in wild-type mice but not in Abcg2-/- mice after TAC. Treatment with the superoxide dismutase mimetic ameliorated cardiac hypertrophy in Abcg2-/- mice after TAC to the same extent as that in wild-type mice, although cardiac dysfunction with impaired angiogenesis was observed in Abcg2-/- mice. ABCG2 protects against pressure overload-induced cardiac hypertrophy and heart failure by promoting angiogenesis and antioxidant response. (Keyword) ATP-Binding Cassette Transporters / Animals / Animals, Newborn / Antioxidants / Cells, Cultured / Disease Models, Animal / Endothelial Cells / Genotype / Glutathione / Heart Failure / Hindlimb / Humans / Hypertrophy, Left Ventricular / Ischemia / Male / Mice / Mice, Knockout / Muscle, Skeletal / Myocytes, Cardiac / Neoplasm Proteins / Neovascularization, Physiologic / Oxidative Stress / Phenotype / RNA Interference / Rats / Rats, Wistar / Time Factors / Transfection / Ventricular Function / Ventricular Remodeling (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.111.240341 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22116099 ● Summary page in Scopus @ Elsevier: 2-s2.0-84857511879 (DOI: 10.1161/ATVBAHA.111.240341, PubMed: 22116099, Elsevier: Scopus)
358.	久岡白陽花, Yuka Ueda, 前田香代子, 西川幸治, 坂東左知子, 林修司, 竹内秀和, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, 冨田紀子, Takashi Iwase, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Shinjiro Takata, Masashi Akaike, Natsuo Yasui and Masataka Sata : (若手優秀演題セッション)尿中アルブミン排泄量に及ぼす心臓リハビリテーションの効果, 心臓リハビリテーション, Vol.17, No.1, 159-161, 2012.
359.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Takayuki Ise, Yasumasa Ikeda, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : ロスバスタチンによる脂質低下作用非依存的な形態的および機能的頸動脈硬化改善作用, Progress in Medicine, Vol.32, No.2, 315-320, 2012.
360.	Yoichiro Hirata, Michio Shimabukuro, Etsuko Uematsu, Takeshi Soeki, Hirotsugu Yamada, Yoshiki Sakai, Mizuho Nakayama, Kunio Matsumoto, Takashi Igarashi and Masataka Sata : A synthetic prostacyclin agonist thrombozane synthase inhibitory activity, ONO-1301, protects myocardium from ischemia/reperfusion injury., European Journal of Pharmacology, Vol.674, No.2-3, 352-358, 2012. (Summary) ONO-1301, a synthetic prostacyclin agonist with thromboxane synthase inhibitory activity, promotes the production of hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) by various cell types. Here, we evaluated the therapeutic efficacy of ONO-1301 in rats with ischemia/reperfusion injury. Ligation of the left anterior descending arteries was performed in 10-week-old Wistar rats, and released 30 min later. A slow-release form of ONO-1301 was administered subcutaneously at 3h and 3 weeks after reperfusion injury. Hemodynamic parameters were significantly improved in the ONO-1301 group. Histological analysis revealed that ONO-1301 suppressed ischemic and fibrotic changes in the myocardium (ischemic area, control group: 58.6 ± 8.7% vs. ONO-1301 group: 44.4 ± 5.8%, fibrotic area, 33.5 ± 5.9% vs. 22.3 ± 6.2%, P<0.05, respectively), and enhanced neovascularization in the border zone. HGF expression was up-regulated by ONO-1301. Double-immunostaining revealed that myofibroblasts in the border zone of ischemic myocardium mainly expressed HGF. Our findings suggest that ONO-1301 might have therapeutic potential in treating ischemic heart disease. (Keyword) Animals / Delayed-Action Preparations / Enzyme Inhibitors / Epoprostenol / Fibrosis / Heart / Hepatocyte Growth Factor / Male / Myocardium / Neovascularization, Physiologic / Pyridines / Rats / Rats, Wistar / Reperfusion Injury / Thromboxane-A Synthase (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2011.10.038 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22094066 ● Search Scopus @ Elsevier (PMID): 22094066 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2011.10.038 (DOI: 10.1016/j.ejphar.2011.10.038, PubMed: 22094066)
361.	Yasutomi Higashikuni, Minoru Takaoka, Hiroshi Iwata, Kimie Tanaka, Yasunobu Hirata, Ryozo Nagai and Masataka Sata : Aliskiren in combination with valsartan exerts synergistic protective effects against ventricular remodeling after myocardial infarction in mice., Hypertension Research, Vol.35, No.1, 62-69, 2012. (Summary) The efficacy of aliskiren, a direct renin inhibitor, in ventricular remodeling after myocardial infarction (MI) compared with conventional renin-angiotensin system (RAS) inhibitors remains to be defined. This study was performed to examine the protective effects of aliskiren and its addition to valsartan, an angiotensin-II receptor blocker, against ventricular remodeling after MI. MI was induced in 8- to 12-week-old C57BL/6 mice by ligating the left anterior descending artery. At 3 days after MI, mice were divided into five groups and were treated with the following: (1) phosphate-buffered saline (PBS); (2) hydralazine (10 mg kg(-1) day(-1)); (3) valsartan (8 mg kg(-1) day(-1)); (4) aliskiren (25 mg kg(-1) day(-1)); and (5) combined aliskiren (25 mg kg(-1) day(-1)) and valsartan (8 mg kg(-1) day(-1)). With these doses of drugs, blood pressure-lowering effects compared with the PBS group were similar among the treated groups in sham-operated mice. At 28 days after MI, echocardiographic, hemodynamic and histological assessments demonstrated that monotherapy with valsartan or aliskiren alone significantly and similarly ameliorated ventricular remodeling after MI compared with the PBS and the hydralazine groups. Combination therapy of valsartan and aliskiren more greatly improved ventricular remodeling after MI with enhancement of angiogenesis and greater attenuation of tissue oxidative stress and inflammation. Our results indicate that aliskiren can be an alternative to conventional RAS inhibitors in the treatment of post-MI patients. Moreover, the dual therapy of valsartan and aliskiren may be more beneficial than either monotherapy. Further clinical trials will be warranted to sufficiently assess the safety and the efficacy of the use of aliskiren in post-MI patients. (Keyword) Amides / Angiotensin II Type 1 Receptor Blockers / Animals / Antihypertensive Agents / Blood Pressure / Drug Synergism / Fumarates / Heart / Lipid Peroxidation / Male / Mice / Myocardial Infarction / Myocardium / Renin-Angiotensin System / Tetrazoles / Valine / Ventricular Remodeling (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2011.136 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21833001 ● Search Scopus @ Elsevier (PMID): 21833001 ● Search Scopus @ Elsevier (DOI): 10.1038/hr.2011.136 (DOI: 10.1038/hr.2011.136, PubMed: 21833001)
362.	Masataka Sata : 特集 ω3系脂肪酸の魅力にせまる ω3系脂肪酸の多面的な作用心・血管系, 実験治療, Vol.78, 21-28, 2012.
363.	Hirotsugu Kurobe, Ken-ichi Aihara, Higashida Mayuko, Hirata Yoichiro, Nishiya Masako, Matsuoka Yuki, Tamotsu Kanbara, Nakayama Taisuke, Hajime Kinoshita, Mikio Sugano, Eiki Fujimoto, Kurobe Ayako, Sugawara Noriko, Takashi Kitaichi, Masashi Akaike, Masataka Sata, Toshio Matsumoto and Tetsuya Kitagawa : Ezetimibe monotherapy ameliorates vascular function in patients with hypercholesterolemia through decreasing oxidative stress., Journal of Atherosclerosis and Thrombosis, Vol.18, No.12, 1080-1089, 2011. (Summary) Ezetimibe, an inhibitor of cholesterol intestinal absorption, is a lipid lowering agent. However, anti-atherogenic effects of ezetimibe have not been fully elucidated. Therefore, the objective in this study was to clarify the vascular protective effects of ezetimibe in patients with hypercholesterolemia. Ezetimibe was administered to 20 patients with hypercholesterolemia (group E), and 20 age- and sex-matched patients with hypercholesterolemia were followed as controls (group C). Difference in metabolic profiles and cardiovascular surrogate markers before ezetimibe treatment and after 12 weeks of ezetimibe treatment were statistically evaluated. Ezetimibe treatment significantly reduced serum levels of low-density lipoprotein cholesterol (LDL-C) and malondialdehyde-modified low-density lipoprotein (MDA-LDL). In addition, the values of body mass index, body weight, waist circumference, plasma HbA1c and urinary albumin were significantly decreased in group E compared to those in group C. On the other hand, high-density lipoprotein cholesterol (HDL-C) and adiponectin levels were significantly increased in group E compared to those in group C. The values of brachial-ankle pulse wave velocity (ba-PWV), mean arterial blood pressure (m-ABP), and % of flow-mediated dilation (FMD) were significantly improved in group E. Furthermore, ultrasonic studies demonstrated amelioration of the vascular stiffness of common carotid arteries in group E but not in group C. These vascular protective effects of ezetimibe were statistically correlated with the decreased values of MDA-LDL and MDA-LDL-to-LDL-C ratio but not with those of LDL-C. Ezetimibe has a lipid lowering-independent vascular protective effect in patients with hypercholesterolemia through decreasing oxidative stress. (Keyword) Aged / Azetidines / Case-Control Studies / Endothelium, Vascular / Humans / Hypercholesterolemia / Lipids / Male / Middle Aged / oxidative stress (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.9548 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22027560 ● Search Scopus @ Elsevier (PMID): 22027560 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.9548 (DOI: 10.5551/jat.9548, PubMed: 22027560)
364.	寺島充康, 山岸正和, Masataka Sata and 七里守 : (座談会) DES時代の術後の管理-内皮機能の観点からイベント抑制を考える-, OPTIMAL THERAPY, Vol.4, No.1, 4-8, 2011.
365.	K. Kimura, K. Takenaka, A. Ebihara, K. Uno, H. Iwata, Masataka Sata, T. Kohro, H. Morita, Y. Yatomi and R. Nagai : Reproducibility and diagnostic accuracy of three-layer speckle tracking echocardiography in a swine chronic ischemia model., Echocardiography, Vol.28, No.10, 1148-1155, 2011. (Summary) The subendocardial myocardium normally has higher systolic strain than the subepicardial myocardium and can be damaged first in face of ischemia. We investigated the reproducibility and feasibility of novel three-layer speckle tracking system and compared the diagnostic accuracy with experienced visual interpretation. An ameroid constrictor was placed around the proximal left circumflex (LCX) coronary artery in 19 pigs. Four weeks later, subtotal stenosis was confirmed in all pigs by coronary angiogram. Two dead pigs and three pigs with pathological infarction were excluded. Transthoracic left ventricle (LV) short-axis echocardiograms were recorded at rest before and 4 weeks after the operation. LV posterior wall motion was scored by two experienced doctors and analyzed by the speckle tracking system (n = 14). Strain variables gave reasonable intra/interobserver reproducibility (mean absolute percentage errors = 13/19, intraclass correlation coefficients = 0.97/0.92). All strain variables and visual wall-motion scores changed significantly during stenosis (P < 0.05). Of all variables, endocardial strains, particularly the circumferential strain demonstrated the highest area under curve (AUC), showing better diagnostic accuracy than experienced visual interpretation (sensitivity 0.93 vs. 0.79, specificity 0.93 vs. 0.73, AUC 0.95 vs. 0.77, P < 0.05). Three-layer speckle tracking is a feasible and reproducible modality. In particular, endocardial speckle tracking provides incremental value in accurately identifying regional ischemia even in the rest echocardiography. (Keyword) Algorithms / Animals / Chronic Disease / Disease Models, Animal / Elastic Modulus / Elasticity Imaging Techniques / Feasibility Studies / Humans / Image Enhancement / Image Interpretation, Computer-Assisted / Imaging, Three-Dimensional / Male / Myocardial Ischemia / Reproducibility of Results / Sensitivity and Specificity / Swine (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1540-8175.2011.01517.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21967399 ● Search Scopus @ Elsevier (PMID): 21967399 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1540-8175.2011.01517.x (DOI: 10.1111/j.1540-8175.2011.01517.x, PubMed: 21967399)
366.	Koji Yamaguchi, Tetsuzo Wakatsuki, Toshiyuki Niki, Kenya Kusunose, Kunihiko Koshiba, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Noriko Tomita, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Local persistent hypercoagulability after sirolimus-eluting stent implantation in patients with stable angina., International Journal of Cardiology, Vol.153, No.3, 272-276, 2011. (Summary) Late stent thrombosis (LST) after sirolimus-eluting stent (SES) implantation has been demonstrated previously. Although incomplete neointimal coverage after SES implantation has been reported, local long-term hypercoagulability remains unknown. We evaluated the local persistent coagulative response in eighty-three consecutive patients with stable angina, treated with either SES (n=51) or BMS (n=32) implantation for isolated de novo left anterior descending (LAD) stenosis. We measured prothrombin fragment F1+2 (frF1+2) and D-dimer levels sampled in the coronary sinus (CS) and sinus of Valsalva (V). The transcardiac gradient (Δ) was defined as the CS level minus V level. The ΔfrF1 + 2 and ΔD-dimer were significantly greater in the SES group than in the BMS group (0.50 ± 0.35 vs -0.14 ± 0.15 nmol/l, p=0.009 and 0.24 ± 0.21 vs -0.05 ± 0.16 μg/ml, p=0.041, respectively). We selected the hypocoagulative [ΔfrF1 + 2<0.15 (mean value-SD) nmol/l, n=21] and hypercoagulative [ΔfrF1 + 2>0.85 (mean value+SD) nmol/l, n=14] groups out of the SES patients. Multivariate analysis was performed to identify independent predictors of local hypercoagulability. Total SES length was the only independent predictor of local hypercoagulability. There was a significant positive correlation between the ΔfrF1 + 2 and total stent length in the SES group (r=0.57, p<0.05). An increased local coagulative response was observed in the convalescent phase after SES implantation as compared to BMS. Careful long-term follow-up of patients after longer SES implantation is recommended in order to avoid LST. (Keyword) Aged / Angina, Stable / Cohort Studies / Coronary Thrombosis / Drug-Eluting Stents / Female / Humans / Male / Middle Aged / Sirolimus / Thrombophilia / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijcard.2010.08.014 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20826025 ● Search Scopus @ Elsevier (PMID): 20826025 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ijcard.2010.08.014 (DOI: 10.1016/j.ijcard.2010.08.014, PubMed: 20826025)
367.	東邦康智 and Masataka Sata : PDE5阻害薬の新しい臨床応用の可能性, Medicina, Vol.48, No.12, 1957-1960, 2011. (Keyword) テストステロン / 減少 / LOH症候群 / therapy / PDE5阻害薬 / 臨床 / application / 可能性
368.	原知也 and Masataka Sata : 心臓血管障害をどう診るか EDと内皮機能障害を中心に, Medicina, Vol.48, No.12, 1886-1888, 2011. (Keyword) 視点 / lifestyle-related disease / 心臓血管障害 / 内皮機能障害 / 中心
369.	Masataka Sata : 動脈硬化の病態における慢性炎症の役割, Folia Pharmacologica Japonica, Vol.138, No.5, 182-186, 2011. (Summary) 急性心筋梗塞の発症原因として，軽度な狭窄しかきたさない動脈硬化病変の破裂やびらんに起因する急性血栓性閉塞が注目されている．破綻した病変では，脂質コアの増大，被膜の菲薄化，平滑筋細胞数の減少，凝固能の亢進，コラーゲン含有量の減少，炎症細胞浸潤，タンパク分解酵素の発現亢進，プラーク内血管新生などが認められる．しかしプラーク脆弱化の機序，予防法などに関しては不明な点が多く，急性冠症候群の発症をバイオマーカーや画像診断で予知することは困難である．私たちは，臨床材料ならびに動物モデルを用いて，動脈硬化の進展と破綻の機序を研究している．ヒトの動脈硬化は，従来考えられていたよりかなり早期から始まり，各種生活習慣の悪化とともに急速に増悪し，突然イベントを誘発する．その病態においては，従来研究されてきた脂質の沈着や細胞増殖だけでなく，血管周囲のVasa Vasorum からの新生血管を介した細胞流入や微小出血が関与することがわかってきた．また，血管，特に冠動脈周囲には豊富に脂肪組織が存在し，血管の慢性炎症，動脈硬化に深く関与し，粥腫の進展と不安定化に重要な役割を担っていると考えられた．この一連の病態に，レニン-アンジオテンシン系は深く関与しており，その抑制は血管炎症，プロテアーゼ発現，内皮細胞アポトーシス，外膜血管新生を効果的に抑制し，プラークを安定化させた．本稿においては，生活習慣病によって動脈硬化が進展し破綻するまでの過程に関する最新の知見を解説する．特に，動脈硬化の病態における慢性炎症の役割とその新規制御因子として注目されているVasa Vasorumと血管周囲脂肪組織の役割を詳細に検討する． (Keyword) atherosclerosis / 病態 / 慢性炎症 / 役割 (Link to Publication Site) ● Publication site (DOI): 10.1254/fpj.138.182 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679252525568 ● Search Scopus @ Elsevier (DOI): 10.1254/fpj.138.182 (DOI: 10.1254/fpj.138.182, CiNii: 1390282679252525568)
370.	田中君枝 and Masataka Sata : 動脈硬化における血管新生・再生, Clinic All-Round, Vol.60, No.10, 2011-2014, 2011. (Keyword) 動脈硬化症 / 一次予防 / 二次予防 / atherosclerosis / angiogenesis / regeneration (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1521980705691835136 (CiNii: 1521980705691835136)
371.	Hiromu Yamazaki, Koji Yamaguchi, Takashi Iwase, Toshiyuki Niki, Kenya Kusunose, Noriko Tomita, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Yutaka Fukunaga, Hideki Nakanishi, Haruhiko Maruyama, Hiroyuki Matsuoka and Masataka Sata : A patient who developed toe necrosis due to poor blood circulation after an interdigital tick bite., Journal of Cardiology Cases, Vol.4, No.2, e106-e109, 2011. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jccase.2011.06.005 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.jccase.2011.06.005 (DOI: 10.1016/j.jccase.2011.06.005)
372.	Masataka Sata : スタチン製剤の新作用, The Journal of the Japan Medical Association, Vol.140, No.6, 1232, 2011. (Keyword) 脂質異常症 / 管理 / 動脈硬化性疾患 / prevention / スタチン / 製剤 / 作用
373.	Asuka Shiota, Yutaka Taketani, Yoichi Maekawa, Koji Yasutomo, Masataka Sata, Tohru Sakai, R. Mizuno, M. Isshiki, Hironori Yamamoto and Eiji Takeda : High phosphate diet reduces atherosclerosis formation in apolipoprotein E-deficient mice., Journal of Clinical Biochemistry and Nutrition, Vol.49, No.2, 109-114, 2011. (Summary) Although higher serum phosphate level is a risk factor for cardiovascular diseases in general population as well as chronic kidney disease patients, it has not been clarified whether higher phosphate can affect atherosclerotic plaque formation. In this study, we investigated the effect of prolonged-intake of different concentrations of phosphate on atherosclerosis formation using apolipoprotein E-deficient mice. Apolipoprotein E-deficient mice were fed with high fat diet including 0.6%, 1.2% or 1.8% phosphate. After 20-week treatment, atherosclerotic plaque formation in aorta in 1.8% phosphate diet group was unexpectedly less than that in the other groups. To elucidate mechanisms of suppression of plaque formation by high phosphate diet, we hypothesized that high phosphate diet may modify a profile of monocytes/macrophages suppressing plaque formation. We confirmed that elevated peripheral monocytes (CD11b+, F4/80+ cell numbers) in apolipoprotein E-deficient mice were decreased by feeding with 1.8% P diet. In addition, ex vivo study indicated that high dose of phosphate induced macrophage apoptosis. These observations suggest that excess phosphate intake decreased atherosclerosis formation, at least in part, by changing the profile of peripheral monocytes or inducing apoptosis of macrophages in apolipoprotein E-deficient mice. (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.10-150 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21980226 ● Search Scopus @ Elsevier (PMID): 21980226 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.10-150 (DOI: 10.3164/jcbn.10-150, PubMed: 21980226)
374.	Takeshi Soeki, Toshiyuki Niki, Kenya Kusunose, Sachiko Bando, Yoichiro Hirata, Noriko Tomita, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Elevated concentrations of pentraxin 3 are associated with coronary plaque vulnerability., Journal of Cardiology, Vol.58, No.2, 151-157, 2011. (Summary) Inflammation is a critical contributing factor to the development and progression of atherosclerosis. Pentraxin 3 (PTX3) is produced abundantly in atherosclerotic lesions while C-reactive protein (CRP) is mainly produced in the liver. In this study, we investigated whether plasma levels of PTX3 might be a sensitive marker both for the severity of coronary artery disease and vulnerable plaques. Next, we determined whether assays for inflammatory molecules can be used to monitor the therapeutic effects of telmisartan on stabilization of vulnerable atherosclerotic plaques. We measured PTX3 concentrations in the peripheral and coronary sinus plasma of 40 patients with angina pectoris (AP) and 20 control subjects. Next, in 28 patients with AP, we determined the correlation between levels of inflammatory molecules and the computed tomography (CT) density of plaques as a quantitative index of plaque vulnerability. There was no significant difference in peripheral plasma PTX3 concentrations between patients with AP and control subjects, while coronary sinus plasma PTX3 concentrations were significantly higher in AP patients than control subjects. The concentrations of PTX3 in coronary sinus and peripheral plasma correlated with Gensini scores as an index of severity of coronary atherosclerosis. Interestingly, there was a significantly negative correlation between plasma PTX3 concentrations and CT density (r=-0.67, p<0.01). On the other hand, CT density did not correlate with the peripheral plasma concentrations of monocyte chemoattractant protein-1 (MCP-1) or high-sensitivity CRP (hsCRP). Furthermore, telmisartan treatment for 6 months decreased plasma concentrations of PTX3 but not those of MCP-1 or hsCRP in 12 patients with essential hypertension. Multivariate regression analysis revealed that changes in PTX3 levels were independent of blood pressure changes. PTX3 is likely more specific than hsCRP as an indicator of coronary plaque vulnerability that could lead to plaque rupture. (Keyword) Aged / Angina Pectoris / Angiotensin II Type 1 Receptor Blockers / Benzimidazoles / Benzoates / Biological Markers / C-Reactive Protein / Coronary Artery Disease / Coronary Sinus / Disease Progression / Drug Monitoring / Female / Humans / Inflammation Mediators / Male / Middle Aged / Plaque, Atherosclerotic / Serum Amyloid P-Component / Severity of Illness Index / Tomography, Spiral Computed (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jjcc.2011.04.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21676590 ● Search Scopus @ Elsevier (PMID): 21676590 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jjcc.2011.04.005 (DOI: 10.1016/j.jjcc.2011.04.005, PubMed: 21676590)
375.	Shusuke Yagi and Masataka Sata : 鉱質コルチコイドの作用と機序, ICUとCCU, Vol.35, No.8, 605-611, 2011. (Keyword) ICU / CCU / steroid / 使用 / 鉱質コルチコイド / 作用 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1521699230403961728 (CiNii: 1521699230403961728)
376.	平田陽一郎, 高岡稔 and Masataka Sata : 動脈硬化と血管周囲脂肪組織, Cardiovascular Frontier, Vol.2, No.4, 14-18, 2011. (Keyword) atherosclerosis / research / Pa / RT / blood vessel / 周囲 / 脂肪組織
377.	Yoichiro Hirata, Minoru Tabata, Hirotsugu Kurobe, Tatsuo Motoki, Masashi Akaike, Chika Nishio, Mayuko Higashida, Hiroaki Mikasa, Yutaka Nakaya, Shuichiro Takanashi, Takashi Igarashi, Tetsuya Kitagawa and Masataka Sata : Coronary atherosclerosis is associated with macrophage polarization in epicardial adipose tissue., Journal of the American College of Cardiology, Vol.58, No.3, 248-255, 2011. (Summary) The purpose of this report was to assess the link between macrophage polarization in epicardial adipose tissue and atherosclerosis in patients with coronary artery disease (CAD). (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jacc.2011.01.048 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21737014 ● Search Scopus @ Elsevier (PMID): 21737014 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jacc.2011.01.048 (DOI: 10.1016/j.jacc.2011.01.048, PubMed: 21737014)
378.	Toshiyuki Niki, Tetsuzo Wakatsuki, Koji Yamaguchi, Kenya Kusunose, Kunihiko Koshiba, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Noriko Tomita, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Comparison of chronic-stage histopathological findings among 3 coronary stents implanted in the same patient., International Journal of Cardiology, Vol.150, No.1, e25-e27, 2011. (Summary) A 73-year-old woman suffering from anterior thoracic pain on exertion presented to our hospital. We performed coronary angiography and noted three stenotic legions in each coronary artery. For each angiographic finding, we implanted a bare metal stent (BMS), sirolimus-eluting stent (SES) and paclitaxel-eluting stent (PES) into the right coronary artery, left anterior descending and left circumflex coronary arteries, respectively. Nine months later, she died of lung disease, and we could compare the histopathological findings among the three coronary stents. In the drug-eluting stents, very thin intima, infiltration of inflammatory cells, and fibrin deposition were observed, while thick intima and no inflammatory findings were observed in the BMS. Fibrin deposition was more marked in the PES than in the SES. This report shows marked differences in the subsequent pathological course among three stents in the same patient. (Keyword) Aged / Coronary Stenosis / Drug-Eluting Stents / Female / Humans / Paclitaxel / Sirolimus / Stents (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijcard.2009.08.032 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19735952 ● Search Scopus @ Elsevier (PMID): 19735952 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ijcard.2009.08.032 (DOI: 10.1016/j.ijcard.2009.08.032, PubMed: 19735952)
379.	Masataka Sata : 心筋梗塞を起こし易い体質と対応策 -動脈硬化の病態におけるVasa VasorumとACE2-, 日本体質医学会雑誌, Vol.73, No.2, 137-144, 2011. (Keyword) 心筋梗塞 / 体質 / 対応策 / atherosclerosis / 病態 / Vasa / ACE2 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520291855549492096 (CiNii: 1520291855549492096)
380.	M Bando, Takeshi Soeki, Toshiyuki Niki, Kenya Kusunose, N Tomita, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Ventricular tachycardia in cardiac sarcoidosis controlled by radiofrequency catheter ablation., Internal Medicine, Vol.50, No.11, 1201-1206, 2011. (Summary) We report a case of a 78-year-old woman with cardiac sarcoidosis with a history of syncope and palpitation. Further assessment with echocardiography, gadolinium-enhanced cardiovascular magnetic resonance (CMR) and histology led to a diagnosis of cardiac sarcoidosis. As the patient suffered from ventricular tachycardia (VT) despite active corticosteroid therapy, an implantable cardioverter-defibrillator (ICD) was positioned. She was also administered a beta blocker, but an electrical storm appeared every several days requiring ICD therapy. The drug-refractory VT was finally controlled with a catheter ablation session, during which we could detect the VT focus in the right ventricular outflow tract next to the aneurysm by using an electroanatomic mapping system (CARTO). Referring to echocardiographic and CMR images proved very useful in detecting the aneurysm using the CARTO system. (Keyword) Adrenergic beta-Antagonists / Aged / Catheter Ablation / Comorbidity / Defibrillators, Implantable / Female / Humans / Magnetic Resonance Imaging / Sarcoidosis / Tachycardia, Ventricular / Treatment Failure / Treatment Outcome (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.50.4580 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21628935 ● Search Scopus @ Elsevier (PMID): 21628935 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.50.4580 (DOI: 10.2169/internalmedicine.50.4580, PubMed: 21628935)
381.	Kenya Kusunose, Hirotsugu Yamada, Noriko Tomita, Susumu Nishio, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Serial imaging changes during treatment of Takayasu arteritis with pulmonary artery stenosis., International Journal of Cardiology, Vol.148, No.3, 47-50, 2011. (Summary) Most cases of chronic stenosis or occlusive lesions of the pulmonary arteries are attributed to thromboembolism, and pulmonary arteritis is extremely rare as the primary cause of these entities. We report a case of pulmonary stenosis and occlusion caused by Takayasu arteritis. The patient was a 54-year-old woman who presented with dyspnea. Total occlusion of the left pulmonary artery and significant stenosis of the right pulmonary artery caused by Takayasu arteritis were confirmed by various imaging modalities including pulmonary angiography, (18)fluorodeoxyglucose-positron emission tomography, magnetic resonance imaging and real-time three-dimensional transesophageal echocardiography. After 6 weeks of steroid therapy, follow-up imaging studies showed that the stenotic lesion had resolved. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijcard.2009.02.036 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19299026 ● Search Scopus @ Elsevier (PMID): 19299026 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ijcard.2009.02.036 (DOI: 10.1016/j.ijcard.2009.02.036, PubMed: 19299026)
382.	Shusuke Yagi and Masataka Sata : アルドステロンと認知機能, 血圧, Vol.18, No.5, 8(440)-9(441), 2011.
383.	平田陽一郎 and Masataka Sata : RAS系阻害薬の使い方, Medical Practice, Vol.28, No.5, 839-843, 2011.
384.	H Tomiyama, Y Higashi, B Takase, K Node, Masataka Sata, T Inoue, Y Ishibashi, S Ueda, K Shimada and A Yamashina : Relationships among hyperuricemia, metabolic syndrome, and endothelial function., American Journal of Hypertension, Vol.24, No.7, 770-774, 2011. (Summary) We evaluated the relationship of the severity of hyperuricemia and the flow-mediated vasodilatation of the brachial artery (FMD) in patients with and without the metabolic syndrome (MetS). In a cross-sectional study, FMD was obtained in 2,732 Japanese healthy men (49 ± 8 years) who had no cardiovascular (CV) disease and were not on any medication for CV risk factors. MetS was defined according to Japanese criteria, and serum uric acid (UA) levels in the upper half of the fifth (highest) quintile range were defined as severe hyperuricemia, whereas those in the lower half of this quintile range were defined as mild hyperuricemia. Overall, the adjusted values of FMD were lower in the subjects with MetS (5.6 ± 0.1%; n = 413) than in those without MetS (6.2 ± 0.1%; n = 2,319) (P < 0.01). Among the subjects without MetS, the adjusted values of FMD were lower in both the subgroups with mild hyperuricemia and severe hyperuricemia than in the subgroup without hyperuricemia. On the contrary, among the subjects with MetS, the adjusted value of FMD was lower only in the subgroup with severe hyperuricemia (4.8 ± 0.3%) as compared with that in the group without hyperuricemia (5.7 ± 0.2%) (P < 0.05). In middle-aged healthy Japanese men without MetS, not only severe, but also mild hyperuricemia may be a significant independent risk factor for endothelial dysfunction in subjects without MetS, whereas only severe hyperuricemia (but not mild hyperuricemia) appeared to exacerbate endothelial dysfunction in similar subjects with MetS. (Keyword) Adult / Brachial Artery / Cross-Sectional Studies / Endothelium, Vascular / Humans / Hyperuricemia / Japan / Male / Metabolic Syndrome X / Middle Aged / Risk Factors / Severity of Illness Index / Uric Acid / Vasodilation (Link to Publication Site) ● Publication site (DOI): 10.1038/ajh.2011.55 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21490690 ● Search Scopus @ Elsevier (PMID): 21490690 ● Search Scopus @ Elsevier (DOI): 10.1038/ajh.2011.55 (DOI: 10.1038/ajh.2011.55, PubMed: 21490690)
385.	Shusuke Yagi, Masashi Akaike, Takashi Iwase, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Noriko Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Acute hemodynamic effects of adaptive servo ventilation in patients with pulmonary hypertension., International Journal of Cardiology, Vol.148, No.1, 125-127, 2011. (Keyword) Aged / Aged, 80 and over / Female / Hemodynamics / Humans / Hypertension, Pulmonary / Intermittent Positive-Pressure Ventilation / Male / Middle Aged / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijcard.2011.01.074 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21334081 ● Search Scopus @ Elsevier (PMID): 21334081 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ijcard.2011.01.074 (DOI: 10.1016/j.ijcard.2011.01.074, PubMed: 21334081)
386.	Yoichiro Hirata, Takeshi Soeki, Hirotsugu Yamada, Asuka Shiota, Michio Shimabukuro, Yoshiki Sakai, Mizuho Nakayama, Kunio Matsumoto, Takashi Igarashi and Masataka Sata : A synthetic prostacycline agonist, ONO-1301, ameliorates ventricular remodeling after acute myocardial infarction via up-regulation of HGF in rat., Biomedicine & Aging Pathology, Vol.1, No.2, 90-96, 2011. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biomag.2011.06.004 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.biomag.2011.06.004 (DOI: 10.1016/j.biomag.2011.06.004)
387.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, Takashi Iwase, Kazue Ishikawa, Sumiko Yoshida, Yuka Sumitomo-Ueda, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Noriko Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Effect of low-dose (1 mg/day) pitavastatin on left ventricular diastolic function and albuminuria in patients with hyperlipidemia., The American Journal of Cardiology, Vol.107, No.11, 1644-1649, 2011. (Summary) The aim of the present study was to evaluate the factors that modulate the protective action of statins on cardiorenal function, regardless of the lipid-lowering effect. To treat abnormal serum lipid profiles, low-dose pitavastatin (1.0 mg/day) was administered to 65 hyperlipidemic patients. The exclusion criteria included left ventricular ejection fraction <40% and apparent renal disease. Age- and gender-matched patients with hyperlipidemia (n = 40) served as the controls. After 12 to 16 weeks of pitavastatin treatment, pitavastatin had decreased low-density lipoprotein cholesterol (from 143.5 ± 31.4 to 98.2 ± 19.4 mg/dl, p <0.01), triglycerides (from 157.7 ± 57.2 to 140.5 ± 60.7 mg/dl, p <0.01), E/e' (from 10.8 ± 6.2 to 9.0 ± 4.5, p <0.05), a parameter of left ventricular diastolic function, and albuminuria (from 47.6 ± 55.9 to 28.5 ± 40.0 mg/g creatinine, p <0.01). Furthermore, pitavastatin decreased serum transforming growth factor-1 (from 709 ± 242 to 550 ± 299 pg/ml, p <0.01), urinary 8-hydroxy-2'-deoxyguanosine (from 6.6 ± 4.1 to 5.0 ± 3.1 g/g creatinine, p <0.01), an oxidative stress marker, and increased urinary nitrate and nitrite (from 22.5 ± 14.6 to 29.4 ± 27.6 nmol/g creatinine, p <0.05). No such changes were observed in the controls. Multiple regression analysis in the pitavastatin group revealed the effect of pitavastatin on cardiorenal function was associated with suppression of oxidative stress, but not on low-density lipoprotein cholesterol reduction. In conclusion, pitavastatin decreases E/e' and albuminuria, which is associated with suppression of oxidative stress. (Keyword) Aged / Albuminuria / Case-Control Studies / Cholesterol, LDL / Diastole / Female / Humans / Hydroxymethylglutaryl-CoA Reductase Inhibitors / Hyperlipidemias / Male / Middle Aged / Quinolines / Treatment Outcome / Triglycerides / Ventricular Function, Left (Link to Publication Site) ● Publication site (DOI): 10.1016/j.amjcard.2011.01.054 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21458773 ● Search Scopus @ Elsevier (PMID): 21458773 ● Search Scopus @ Elsevier (DOI): 10.1016/j.amjcard.2011.01.054 (DOI: 10.1016/j.amjcard.2011.01.054, PubMed: 21458773)
388.	Takahito Yagi, Michiko Sato, Yasumoto Nakazawa, Kimie Tanaka, Masataka Sata, Kenji Itoh, Yoshihide Takagi and Tetsuo Asakura : Preparation of double-raschel knitted silk vascular grafts and evaluation of short-term function in a rat abdominal aorta., Journal of Artificial Organs, Vol.14, No.2, 89-99, 2011. (Summary) Silk fibroin fiber has a long history of use in sutures because of its high strength and toughness. In the work reported in this paper, small-diameter vascular grafts 1.5 mm in diameter and 10 mm in length were prepared by coating a double-raschel knitted silk fiber graft with silk fibroin aqueous solution containing poly(ethylene glycol diglycidyl ether) as a cross-linking agent. The most important character of silk fibroin graft is remodeling, which is never observed for polyester fiber or expanded polytetrafluoroethylene grafts. The double-raschel knitted silk fiber graft with coating has sufficient physical strength and protects the ladder from the end in the implantation process. The coating also gives protection against leakage of blood from the graft, and elasticity to the graft. Eight weeks after implantation of the grafts in rat abdominal aorta, early formation of thrombosis was avoided. (Link to Publication Site) ● Publication site (DOI): 10.1007/s10047-011-0554-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21344164 ● Search Scopus @ Elsevier (PMID): 21344164 ● Search Scopus @ Elsevier (DOI): 10.1007/s10047-011-0554-z (DOI: 10.1007/s10047-011-0554-z, PubMed: 21344164)
389.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, Takashi Iwase, Yuka Sumitomo-Ueda, Sumiko Yoshida, Toshio Matsumoto and Masataka Sata : Bosentan improves systemic sclerosis-related peripheral circulation insufficiency., International Journal of Cardiology, Vol.147, No.3, 472-475, 2011. (Keyword) Adult / Aged / Blood Circulation / Female / Humans / Middle Aged / Pain Measurement / Raynaud Disease / Scleroderma, Systemic / Sulfonamides (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijcard.2011.01.025 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21296436 ● Search Scopus @ Elsevier (PMID): 21296436 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ijcard.2011.01.025 (DOI: 10.1016/j.ijcard.2011.01.025, PubMed: 21296436)
390.	M Ichioka, T Suganami, N Tsuda, I Shirakawa, Y Hirata, N Satoh-Asahara, Y Shimoda, M Tanaka, M Kim-Saijo, Y Miyamoto, Y Kamei, Masataka Sata and Y Ogawa : Increased expression of macrophage-inducible C-type lectin in adipose tissue of obese mice and humans., Diabetes, Vol.60, No.3, 819-826, 2011. (Summary) We have provided evidence that saturated fatty acids, which are released from adipocytes via macrophage-induced adipocyte lipolysis, serve as a naturally occurring ligand for the Toll-like receptor (TLR) 4 complex in macrophages, thereby aggravating obesity-induced adipose tissue inflammation. The aim of this study was to identify the molecule(s) activated in adipose tissue macrophages in obesity. We performed a cDNA microarray analysis of coculture of 3T3-L1 adipocytes and RAW264 macrophages. Cultured adipocytes and macrophages and the adipose tissue of obese mice and humans were used to examine mRNA and protein expression. We found that macrophage-inducible C-type lectin (Mincle; also called Clec4e and Clecsf9), a type II transmembrane C-type lectin, is induced selectively in macrophages during the interaction between adipocytes and macrophages. Treatment with palmitate, a major saturated fatty acid released from 3T3-L1 adipocytes, induced Mincle mRNA expression in macrophages at least partly through the TLR4/nuclear factor (NF)-κB pathway. Mincle mRNA expression was increased in parallel with macrophage markers in the adipose tissue of obese mice and humans. The obesity-induced increase in Mincle mRNA expression was markedly attenuated in C3H/HeJ mice with defective TLR4 signaling relative to control C3H/HeN mice. Notably, Mincle mRNA was expressed in bone-marrow cell (BMC)-derived proinflammatory M1 macrophages rather than in BMC-derived anti-inflammatory M2 macrophages in vitro. Our data suggest that Mincle is induced in adipose tissue macrophages in obesity at least partly through the saturated fatty acid/TLR4/NF-κB pathway, thereby suggesting its pathophysiologic role in obesity-induced adipose tissue inflammation. (Keyword) 3T3-L1 Cells / Adipose Tissue / Analysis of Variance / Animals / Blotting, Western / Cells, Cultured / Humans / Inflammation / Lectins, C-Type / Linear Models / Macrophages / Male / Membrane Proteins / Mice / NF-kappa B / Obesity / Palmitic Acid / RNA, Messenger / Reverse Transcriptase Polymerase Chain Reaction / Signal Transduction / Toll-Like Receptor 4 (Link to Publication Site) ● Publication site (DOI): 10.2337/db10-0864 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21282371 ● Search Scopus @ Elsevier (PMID): 21282371 ● Search Scopus @ Elsevier (DOI): 10.2337/db10-0864 (DOI: 10.2337/db10-0864, PubMed: 21282371)
391.	Kojiro Nagai, Kenya Kusunose, 西尾進, Yoshio Taketani, Hirotsugu Yamada, Masataka Sata, 近藤直樹, 岸史, Seiji Kishi, 荒岡利和, Motokazu Matsuura, Akira Mima, Hideharu Abe, Taichi Murakami, Masayuki Nakamura and Toshio Doi : Case of renal artery stenosis in an elderly patient after nephrectomy diagnosed by ultrasound sonography, showing improvement of blood pressure and renal dysfunction after renal artery stenting, Japanese Journal of Nephrology, Vol.53, No.1, 68-74, 2011. (Summary) Arteriosclerotic renal artery stenosis is one of the increasingly common diseases that affects many aged patients. There are various non-invasive methods to diagnose renal artery stenosis, such as contrast enhanced CT or MRI. However, these methods are not appropriate for patients with renal dysfunction. Ultrasound sonography is becoming one of the promising methods to diagnose artery stenosis because of photographic improvements. In this case, a 72-year-old woman was hospitalized 7 months after nephrectomy because of severe hypertension, heart failure and kidney dysfunction. The heart failure was quite uncontrollable in spite of massive administration of diuretics, and finally, hemodialysis was started to control her volume status. In consideration of her past history and abdominal bruit, we evaluated the renal artery stenosis by ultrasound sonography and confirmed the diagnosis by renal angiography. To improve hypertension control, we performed renal artery stenting, which resulted in an impressive improvement of her blood pressure and renal function. We recognized the importance of careful causal evaluation of renal dysfunction, even though it is difficult to apply invasive therapy to patients after nephrectomy. (Keyword) Aged / Female / Heart Failure / Humans / Hypertension / Nephrectomy / Renal Artery Obstruction / Renal Insufficiency / Stents / Treatment Outcome (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21370580 ● CiNii @ National Institute of Informatics (CRID): 1520009407114348800 ● Search Scopus @ Elsevier (PMID): 21370580 (PubMed: 21370580, CiNii: 1520009407114348800)
392.	K Tanaka, D Nagata, Y Hirata, Y Tabata, R Nagai and Masataka Sata : Augmented angiogenesis in adventitia promotes growth of atherosclerotic plaque in apolipoprotein E-deficient mice., Atherosclerosis, Vol.215, No.2, 366-373, 2011. (Summary) Accumulating evidence suggests that exaggerated formation of vasa vasorum (VV) plays an important role in the pathogenesis of atherosclerosis. However, it remains unclear whether augmented angiogenesis in the adventitia could promote hyperlipidemia-induced atherosclerotic lesion formation. First, we analyzed the time course of VV development in apolipoprotein E-deficient (ApoE-/-) mice. VV proliferation was observed only after atherosclerotic lesion formation. Next, we investigated whether forced perivascular angiogenesis could promote plaque progression. Basic fibroblast growth factor (bFGF) (100 μg/body) incorporated in acid gelatin hydrogel microspheres (AGHM) (bFGF+AGHM group, n=10), AGHM alone (AGHM group, n=7), or PBS (control group, n=8) was administered into the periaortic area of the retroperitoneal space in 10- to 11-week-old male ApoE-/- mice. At 13 weeks after the operation, lesions were significantly larger in the bFGF+AGHM group than in others (bFGF+AGHM: 3.4 ± 0.7 × 10(4)μm(2); AGHM: 0.1 ± 0.1 × 10(4)μm(2); control: 0 μm(2); p<0.0001), which was associated with increased neovascularization in the adventitia. The number of adventitial capillaries correlated with plaque size (r=0.69, p<0.0001). In the bFGF+AGHM group, an increase in the number of VV and accumulation of Mac3-positive macrophages were observed prior to atherosclerotic lesion formation. Our findings demonstrated that local administration of bFGF in the adventitia induced development of VV and accelerated plaque progression in ApoE-/- mice, supporting the notion that VV formation plays a crucial role in the pathogenesis of atherosclerosis. (Keyword) Animals / Apolipoproteins E / Atherosclerosis / Connective Tissue / Disease Progression / Fibroblast Growth Factor 2 / Male / Mice / Mice, Knockout / Neovascularization, Pathologic / Plaque, Atherosclerotic / Vasa Vasorum (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2011.01.016 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21306712 ● Search Scopus @ Elsevier (PMID): 21306712 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2011.01.016 (DOI: 10.1016/j.atherosclerosis.2011.01.016, PubMed: 21306712)
393.	平田陽一郎, Daiju Fukuda and Masataka Sata : 動脈硬化とレニン・アンジオテンシン系, Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.69, No.1, 55-59, 2011. (Keyword) atherosclerosis / Renin-angiotensin System / reactive oxygen species / 炎症 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1523106605801950464 ● Summary page in Scopus @ Elsevier: 2-s2.0-79952274758 (CiNii: 1523106605801950464, Elsevier: Scopus)
394.	Yoichiro Hirata, Hirotsugu Kurobe, Masashi Akaike, Fumio Chikugo, Takaki Hori, Yoshimi Bando, Chika Nishio, Mayuko Higashida, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : Enhanced inflammation in epicardial fat in patients with coronary artery disease., International Heart Journal, Vol.52, No.3, 139-142, 2011. (Summary) It has been hypothesized that epicardial fat, a local visceral fat depot with close proximity to coronary arteries, may serve as a source of inflammatory cytokines and cells in coronary atherosclerotic lesions. Here, we characterized infiltration of inflammatory cells and expression of adipocytokines in epicardial adipose tissue in patients with and without coronary artery disease (CAD). Pare samples were obtained from epicardial and subcutaneous adipose tissue during elective cardiac surgery (CAD, n = 8; non-CAD, n = 9). Inflammatory cell infiltration was investigated by immunohistochemical staining using antibodies against CD3, CD4, CD8 and CD68. Expression of adipocytokines was evaluated by real-time quantitative reverse transcription-polymerase chain reaction. Infiltration of macrophages and CD8-positive T cells in the epicardial adipose tissue in the CAD group was greater than that in the non-CAD group. In contrast, there was no significant difference between the two groups in the number of inflammatory cells in subcutaneous adipose tissue. No statistical difference could be found between the CAD group and the non-CAD group in the expression levels of adiponectin and inflammatory cytokines in epicardial adipose tissue. Our findings suggest that inflammatory cell infiltration is enhanced in epicardial adipose tissue, but not in subcutaneous fat, in patients with coronary artery disease. Chronic inflammation in epicardial fat may influence the pathogenesis of coronary atherosclerosis. (Keyword) Adipokines / Adipose Tissue / Aged / CD8-Positive T-Lymphocytes / Coronary Artery Disease / Female / Humans / Inflammation / Macrophages / Male / Middle Aged / Pericardium / Subcutaneous Tissue (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.52.139 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21646734 ● Search Scopus @ Elsevier (PMID): 21646734 ● Search Scopus @ Elsevier (DOI): 10.1536/ihj.52.139 (DOI: 10.1536/ihj.52.139, PubMed: 21646734)
395.	Kenya Kusunose, Tetsuzo Wakatsuki and Masataka Sata : Removal of pinched-off central venous catheter., Heart Asia, Vol.3, 32, 2011. (Link to Publication Site) ● Publication site (DOI): 10.1136/ha.2009.001321 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27325978 ● Search Scopus @ Elsevier (PMID): 27325978 ● Search Scopus @ Elsevier (DOI): 10.1136/ha.2009.001321 (DOI: 10.1136/ha.2009.001321, PubMed: 27325978)
396.	Koji Yamaguchi, Tetsuzo Wakatsuki, Toshiyuki Niki, Yoshio Taketani, H. Oezuka, Kenya Kusunose, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Observation of short-term atorvastatin-induced changes in coronary arterial plaque properties using integrated backscatter intravascular ultrasound in a patient., Journal of Cardiology Cases, Vol.3, No.3, e111-e114, 2011. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jccase.2011.03.007 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.jccase.2011.03.007 (DOI: 10.1016/j.jccase.2011.03.007)
397.	Shunji Hashizume, Masashi Akaike, Hiroyuki Azuma, Kazue Ishikawa, Sumiko Yoshida, Yuka Ueda, Shusuke Yagi, Yasumasa Ikeda, Takashi Iwase, Ken-ichi Aihara, Masahiro Abe, Masataka Sata and Toshio Matsumoto : Activation of peroxisome proliferator-activated receptor α in megakaryocytes reduces platelet-derived growth factor-BB in platelets., Journal of Atherosclerosis and Thrombosis, Vol.18, No.2, 138-147, 2011. (Summary) Platelet-derived growth factor (PDGF)-BB plays a crucial role in atherosclerosis and vascular remodeling by promoting the migration and proliferation of vascular smooth muscle cells. The objective of this study was to clarify the pleiotropic effect of peroxisome proliferator-activated receptor α (PPARα) activators on PDGF-BB expression in megakaryocytes and platelets. The expression of PPARα in a human erythroleukemia (HEL) cells was clearly detected by reverse transcriptase-PCR and immunofluorescence microscopy. The expression level of PPARα in HEL cells was unchanged regardless of differentiation into megakaryocytic cells by treatment with phorbol 12-myristate 13 acetate (TPA). The TPA-induced expression of PDGF-B mRNA and PDGF-BB protein levels in culture media was significantly decreased by treatment with PPARα activators, Wy14643 and fenofibric acid, in a dose-dependent manner. PDGF-BB expression induced by inflammatory cytokines, including interleukin-1β or interleukin-6, was also significantly suppressed by treatment with PPARα activators. Immunohistochemistry of human bone marrow showed the expression of PPARα in both the nucleus and cytoplasm of megakaryocytes. In addition, PDGF-BB levels in platelets were significantly decreased from 1,800±870 to 1,470±840 pg/10(5) platelets (mean±SD, p<0.05) by treatment with 300 mg fenofibrate once daily for 4 weeks in 13 patients with dyslipidemia. Activation of PPARα in megakaryocytes reduces PDGF-BB expression in platelets. PPARα activators may exert vasculo-protective action through suppression of PDGF-BB production in a megakaryocyte/platelet pathway. (Keyword) Adult / Blood Platelets / cell differentiation / Cell Line, Tumor / Dyslipidemias / Female / Fenofibrate / gene expression / Humans / immunohistochemistry / Lipids / Male / Megakaryocytes / Middle Aged / PPAR alpha / Platelet-Derived Growth Factor / Pyrimidines / RNA, Messenger / Tetradecanoylphorbol Acetate (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.5868 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21060209 ● Search Scopus @ Elsevier (PMID): 21060209 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.5868 (DOI: 10.5551/jat.5868, PubMed: 21060209)
398.	JR Kim-Kaneyama, N Takeda, A Sasaki, A Miyazaki, Masataka Sata, T Hirabayashi, M Shibanuma, G Yamada and K Nose : Hic-5 deficiency enhances mechanosensitive apoptosis and modulates vascular remodeling., Journal of Molecular and Cellular Cardiology, Vol.50, No.1, 77-86, 2011. (Summary) Forces associated with blood flow are crucial not only for blood vessel development but also for regulation of vascular pathology. Although there have been many studies characterizing the responses to mechanical stimuli, molecular mechanisms linking biological responses to mechanical forces remain unclear. Hic-5 (hydrogen peroxide-inducible clone-5) is a focal adhesion adaptor protein proposed as a candidate for a mediator of mechanotransduction. In the present study, we generated Hic-5-deficient mice by targeted mutation. Mice lacking Hic-5 are viable and fertile, and show no obvious histological abnormalities including vasculature. However, after wire injury of the femoral artery in Hic-5 deficient mice, histological recovery of arterial media was delayed due to enhanced apoptosis of vascular wall cells, whereas neointima formation was enhanced. Stretch-induced apoptosis was enhanced in cultured vascular smooth muscle cells (vascular SMCs) from Hic-5 deficient mice. Mechanical stress also induced the alteration of intracellular distribution of vinculin from focal adhesions to the whole cytoplasm in SMCs. Immunoelectron microscopic study of vascular SMCs from a wire-injured artery demonstrated that vinculin was dispersed in the nucleus and the cytoplasm in Hic-5-deficient mice whereas vinculin was localized mainly in the sub-plasma membrane region in wild type mice. Our findings indicate that Hic-5 may serve as a key regulator in mechanosensitive vascular remodeling. (Keyword) Animals / Apoptosis / Blotting, Southern / Blotting, Western / Cytoskeletal Proteins / DNA-Binding Proteins / Focal Adhesions / LIM Domain Proteins / Male / Mice / Mice, Inbred C57BL / Mice, Mutant Strains / Microscopy, Immunoelectron / Models, Biological / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Reactive Oxygen Species / Vinculin (Link to Publication Site) ● Publication site (DOI): 10.1016/j.yjmcc.2010.09.024 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20933520 ● Search Scopus @ Elsevier (PMID): 20933520 ● Search Scopus @ Elsevier (DOI): 10.1016/j.yjmcc.2010.09.024 (DOI: 10.1016/j.yjmcc.2010.09.024, PubMed: 20933520)
399.	Kenya Kusunose, Hirotsugu Yamada, Susumu Nishio, Yukio Mizuguchi, Masahito Choraku, Yasuhiro Maeda, Shinobu Hosokawa, Nobuo Yamazaki, Noriko Tomita, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Validation of longitudinal peak systolic strain by speckle tracking echocardiography with visual assessment and myocardial perfusion SPECT in patients with regional asynergy., Circulation Journal, Vol.75, No.1, 141-147, 2011. (Summary) Automated function imaging (AFI) is a recently developed method of calculating the longitudinal peak systolic strains (LS) of the regional left ventricular (LV) wall using speckle tracking echocardiography and displaying them on a single bull's-eye map. The feasibility of AFI in patients with regional LV wall motion abnormalities caused by myocardial infarction (MI) was evaluated by comparison with visual assessment and myocardial perfusion single-photon emission computed tomography (SPECT). Segmental LS was measured by AFI in 60 patients with MI (67 ± 11 years) and 58 controls (71 ± 9 years). Wall thickening (WT) was measured by SPECT in 20 patients with MI. There was a strong positive linear relationship between the wall motion score index by expert visual assessment and global LS. The receiver-operating characteristic analysis revealed the best cutoff value of 11% < LS to identify hypokinetic segments. The overall accuracy of wall motion scoring by LS in the 2,006 segments was 96.8% (κ = 0.90) compared with visual assessment. The correlation coefficient between LS and WT was R² = 0.65 in the 340 segments. Assessment of LV regional asynergy by AFI showed good agreement with visual and SPECT assessments. AFI is clinically useful for quantitative assessment of LV regional wall motion abnormalities. (Keyword) Aged / Aged, 80 and over / Algorithms / Case-Control Studies / Echocardiography, Doppler / Feasibility Studies / Humans / Image Interpretation, Computer-Assisted / Japan / Middle Aged / Myocardial Contraction / Myocardial Infarction / Myocardial Perfusion Imaging / Observer Variation / Predictive Value of Tests / Reproducibility of Results / Tomography, Emission-Computed, Single-Photon / Ventricular Dysfunction, Left / Ventricular Function, Left (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-10-0551 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21099120 ● Search Scopus @ Elsevier (PMID): 21099120 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-10-0551 (DOI: 10.1253/circj.CJ-10-0551, PubMed: 21099120)
400.	Y Nakazawa, M Sato, R Takahashi, D Aytemiz, C Takabayashi, T Tamura, S Enomoto, Masataka Sata and T Asakura : Development of small-diameter vascular grafts based on silk fibroin fibers from bombyx mori for vascular regeneration., Journal of Biomaterials Science. Polymer Edition, Vol.22, 195-206, 2011. (Summary) In the field of surgical revascularization, the need for functional small-diameter (1.5-4.0 mm in diameter) vascular grafts is increasing. Several synthetic biomaterials have been tested for this purpose, but in many cases they cause thrombosis. In this study, we report the development of small-diameter vascular grafts made from silk fibroin fibers from the domestic silkworm Bombyx mori or recombinant silk fibroin fibers from a transgenic silkworm. The vascular grafts were prepared by braiding, flattening and winding the silk fibers twice onto a cylindrical polymer tube followed by coating with an aqueous silk fibroin solution. The grafts, which are 1.5 mm in inner diameter and 10 mm in length, were implanted into rat abdominal aorta. An excellent patency (ca. 85%, n=27) at 12 months after grafting with wild-type silk fibers was obtained. Endothelial cells and smooth muscle cells migrated into the silk fibroin graft early after implantation, and became organized into an endothelium and a media-like smooth muscle layer. (Link to Publication Site) ● Publication site (DOI): 10.1163/092050609X12586381656530 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20557695 ● Search Scopus @ Elsevier (PMID): 20557695 ● Search Scopus @ Elsevier (DOI): 10.1163/092050609X12586381656530 (DOI: 10.1163/092050609X12586381656530, PubMed: 20557695)
401.	門田宗之, Yoshio Taketani, Tetsuzo Wakatsuki, Koji Yamaguchi, Kenya Kusunose, Toshiyuki Niki, 坂東左知子, 久岡白陽花, Yuka Ueda, 冨田紀子, 竹内秀和, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike, Masataka Sata, Kojiro Nagai and Toshio Doi : 繰り返す心不全と維持透析導入から離脱しえた腎動脈狭窄症の一例, Shikoku Acta Medica, Vol.66, No.5, 6, 175-180, 2010. (Tokushima University Institutional Repository) ● Metadata: 110339 (Tokushima University Institutional Repository: 110339)
402.	D Fukuda, S Enomoto, Y Hirata, R Nagai and Masataka Sata : The angiotensin receptor blocker, telmisartan, reduces and stabilizes atherosclerosis in ApoE and AT1aR double deficient mice., Biomedicine & Pharmacotherapy, Vol.64, No.10, 712-717, 2010. (Summary) The renin-angiotensin system (RAS) plays critical roles in the pathogenesis of atherosclerosis. Clinical studies demonstrate that pharmacological blockade of RAS with Angiotensin II type 1 receptor (AT1R) blockers (ARBs) is effective in the treatment of patients with cardiovascular diseases. Recent studies reported that telmisartan, an ARB, has a partial agonistic effect on peroxisome proliferator-activated receptor-gamma (PPAR-γ). The role of PPAR-γ-mediated signaling has been implicated in regulation of not only metabolic disorders but also atherosclerosis. Here, we investigated the effects of telmisartan, which is not related to AT1R blockade, using AT1aR and apolipoprotein E (ApoE) double-deficient (ApoE-/-AT1R-/-) mice in vivo. Both genetic ablation of AT1R in ApoE-deficient (ApoE-/-) mice and administration of telmisartan (10 mg/kg/day) to ApoE-/- mice for 20 weeks reduced the development of atherosclerosis (P<0.05, respectively). Telmisartan decreased lipid deposition (P<0.01) and increased collagen contents (P<0.05) in plaques in ApoE-/- mice. Administration of telmisartan to ApoE-/-AT1aR-/- mice also inhibited the progression of atherosclerosis in aorta (P<0.05) even in mice, which have no AT1aR genetically. Moreover, in these mice, telmisartan decreased macrophage accumulation and lipid deposition, and increased collagen contents in plaques in aortic root (P<0.05, respectively), indicating stabilization of plaques. Telmisartan-treated ApoE-/-AT1aR-/- mice showed lower body weight and higher plasma high-density lipoprotein levels compared with vehicle-treated mice (P<0.05, respectively). Telmisartan lowered systolic and diastolic blood pressure in ApoE-/-AT1aR-/- mice (P<0.01). These results suggest that telmisartan has protective effects on the development of atherosclerosis and metabolic disorders beyond AT1R blockade in ApoE-deficient mice. (Keyword) Angiotensin II Type 1 Receptor Blockers / Animals / Apolipoproteins E / Atherosclerosis / Benzimidazoles / Benzoates / Blood Pressure / Collagen / Lipids / Macrophages / Male / Mice / Mice, Inbred C57BL / Mice, Knockout / PPAR gamma / Receptor, Angiotensin, Type 1 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biopha.2010.09.014 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20970951 ● Search Scopus @ Elsevier (PMID): 20970951 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biopha.2010.09.014 (DOI: 10.1016/j.biopha.2010.09.014, PubMed: 20970951)
403.	Takayuki Ise, Ken-ichi Aihara, Yuka Ueda, Sumiko Yoshida, Yasumasa Ikeda, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Plasma heparin cofactor II activity is inversely associated with left atrial volume and diastolic dysfunction in humans with cardiovascular risk factors., Hypertension Research, Vol.34, No.2, 225-231, 2010. (Summary) Thrombin has a crucial role in cardiac remodeling through protease-activated receptor-1 activation in cardiac fibroblasts and cardiomyocytes. As heparin cofactor II (HCII) inhibits the action of tissue thrombin in the cardiovascular system, it is possible that HCII counteracts the development of cardiac remodeling. We investigated the relationships between plasma HCII activity and surrogate markers of cardiac geometry, including left atrial volume index (LAVI), relative wall thickness (RWT) and left ventricular mass index, and deceleration time (DcT) and the ratio of peak E velocity to early diastolic mitral annulus velocity (E/e' ratio) as surrogate markers of left ventricular diastolic dysfunction measured using echocardiography in 304 Japanese elderly individuals without systolic heart failure (169 men and 135 women; mean age: 65.4 ± 11.8 years). Mean plasma HCII activity in all participants was 95.8 ± 17.0% and there was no difference between the mean plasma HCII activities in males and females. Multiple regression analysis revealed that there were significant inverse relationships between plasma HCII activity and LAVI (coefficient: -0.2302, P<0.001), between HCII activity and RWT (coefficient: -0.0007, P<0.05), between HCII activity and DcT (coefficient: -0.5189, P<0.05) and between HCII activity and E/e' ratio (coefficient: -0.0558, P<0.01). Plasma HCII activity was independently and inversely associated with the development of cardiac remodeling, including cardiac concentric change, left atrial enlargement and left ventricular diastolic dysfunction. These findings suggest that cardiac tissue thrombin inactivation by HCII is a novel therapeutic target for cardiac remodeling and atherosclerosis. (Keyword) Aged / Cross-Sectional Studies / Female / Heparin Cofactor II / Humans / Male / Middle Aged / Risk Factors / Ventricular Dysfunction / Ventricular Remodeling (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2010.211 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21107326 ● Search Scopus @ Elsevier (PMID): 21107326 ● Search Scopus @ Elsevier (DOI): 10.1038/hr.2010.211 (DOI: 10.1038/hr.2010.211, PubMed: 21107326)
404.	Shusuke Yagi, Masashi Akaike, Takashi Iwase, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Sumiko Yoshida, Yuka Sumitomo-Ueda, Ken-ichi Aihara, Yoichiro Hirata, Munkhbaatar Dagvasumberel, Yoshio Taketani, Noriko Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Bosentan ameliorated exercise-induced pulmonary arterial hypertension complicated with systemic sclerosis., Internal Medicine, Vol.49, No.21, 2309-2312, 2010. (Summary) Pulmonary arterial hypertension (PAH) is a frequent complication in patients with systemic sclerosis. Bosentan is used in patients with symptomatic PAH; however, it has not been established whether or not bosentan ameliorates the progression of PAH in patients with no PAH-related symptoms. We present a case of systemic sclerosis with no PAH-related symptoms in which bosentan ameliorated exercise-induced PAH evaluated by 6-minute walk stress echocardiography, brachial flow-mediated dilation, and skin temperature of hands and feet. The results suggest that administration of bosentan in patients with early-stage PAH ameliorates pulmonary arterial vasodilatation through improvement of endothelial function. (Keyword) Exercise / Exercise Test / Female / Humans / Hypertension, Pulmonary / Middle Aged / Scleroderma, Systemic / Sulfonamides (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.49.3812 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21048365 ● CiNii @ National Institute of Informatics (CRID): 1390282679847104768 ● Search Scopus @ Elsevier (PMID): 21048365 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.49.3812 (DOI: 10.2169/internalmedicine.49.3812, PubMed: 21048365, CiNii: 1390282679847104768)
405.	H Iwata, I Manabe, K Fujiu, T Yamamoto, N Takeda, K Eguchi, A Furuya, M Kuro-o, Masataka Sata and R Nagai : Bone marrow-derived cells contribute to vascular inflammation but do not differentiate into smooth muscle cell lineages., Circulation, Vol.122, No.20, 2048-2057, 2010. (Summary) It has been proposed that bone marrow-derived cells infiltrate the neointima, where they differentiate into smooth muscle (SM) cells; however, technical limitations have hindered clear identification of the lineages of bone marrow-derived "SM cell-like" cells. Using a specific antibody against the definitive SM cell lineage marker SM myosin heavy chain (SM-MHC) and mouse lines in which reporter genes were driven by regulatory programs for either SM-MHC or SM α-actin, we demonstrated that although some bone marrow-derived cells express SM α-actin in the wire injury-induced neointima, those cells did not express SM-MHC, even 30 weeks after injury. Likewise, no SM-MHC(+) bone marrow-derived cells were found in vascular lesions in apolipoprotein E(-/-)mice or in a heart transplantation vasculopathy model. Instead, the majority of bone marrow-derived SM α-actin(+) cells were also CD115(+)CD11b(+)F4/80(+)Ly-6C(+), which is the surface phenotype of inflammatory monocytes. Moreover, adoptively transferred CD11b(+)Ly-6C(+) bone marrow cells expressed SM α-actin in the injured artery. Expression of inflammation-related genes was significantly higher in neointimal subregions rich in bone marrow-derived SM α-actin(+) cells than in other regions. It appears that bone marrow-derived SM α-actin(+) cells are of monocyte/macrophage lineage and are involved in vascular remodeling. It is very unlikely that these cells acquire the definitive SM cell lineage. (Keyword) Animals / Antigens, Differentiation / Apolipoproteins E / Bone Marrow Cells / Bone Marrow Transplantation / Cell Differentiation / Disease Models, Animal / Heart Transplantation / Humans / Inflammation / Mice / Mice, Knockout / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Transplantation, Homologous / Vasculitis (Link to Publication Site) ● Publication site (DOI): 10.1161/CIRCULATIONAHA.110.965202 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21041690 ● Search Scopus @ Elsevier (PMID): 21041690 ● Search Scopus @ Elsevier (DOI): 10.1161/CIRCULATIONAHA.110.965202 (DOI: 10.1161/CIRCULATIONAHA.110.965202, PubMed: 21041690)
406.	平田陽一郎, 高岡稔 and Masataka Sata : The role of periadventitial adipose tissue in vascular remodeling, The Cell, Vol.42, No.11, 459-463, 2010. (Keyword) 脂肪組織 / アディポネクチン / 動脈硬化 / 炎症 / 血管平滑筋細胞 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520291854881500672 (CiNii: 1520291854881500672)
407.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, Takashi Iwase, Sumiko Yoshida, Yuka Ueda, Yasumasa Ikeda, Kazue Ishikawa, Toshio Matsumoto and Masataka Sata : High plasma aldosterone concentration is a novel risk factor of cognitive impairment in patients with hypertension., Hypertension Research, Vol.34, No.1, 74-78, 2010. (Summary) Cognitive impairment leading to dementia is associated with high prevalence of hypertension, decreased quality of life and poor prognosis. Aldosterone is known as a risk factor for cardiovascular and cerebrovascular diseases. In addition, mineral corticoid receptors are abundantly expressed in the hippocampus, which plays a pivotal role in cognitive function; however, it has not been determined whether plasma aldosterone level is associated with cognitive impairment in patients with hypertension. We enrolled 68 patients with essential hypertension and assessed their cardiovascular risk factors, including blood pressure, hyperlipidemia, diabetes mellitus, obesity, smoking, history of cerebral infarction, renal function, parameters of inflammation, oxidative stress and nitric oxide bioavailability, a parameter of cerebral blood flow and carotid plaque by ultrasound examination, plasma renin activity and plasma aldosterone concentration (PAC). The mini-mental state examination (MMSE) was used to evaluate cognitive function. The relevance of cardiovascular risk factors and MMSE score was statistically evaluated. Multiple regression analysis showed that age (P<0.01), PAC (P<0.01) and history of cerebral infarction (P<0.05) were inversely and independently associated with MMSE score. Mineral corticoid receptor antagonists, including spironolactone and eplerenone, increased MMSE score in seven patients with hypertension, but not in the controls. In conclusion, increased PAC is associated with impaired cognitive function and mineral corticoid receptor blockade may protect against not only cardiovascular mortality, but also cognitive impairment in patients with hypertension.Hypertension Research advance online publication, 23 September 2010; doi:10.1038/hr.2010.179. (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2010.179 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20861841 ● Search Scopus @ Elsevier (PMID): 20861841 ● Search Scopus @ Elsevier (DOI): 10.1038/hr.2010.179 (DOI: 10.1038/hr.2010.179, PubMed: 20861841)
408.	Yasutomi Higashikuni, Julie Sainz, Kazuto Nakamura, Minoru Takaoka, Soichiro Enomoto, Hiroshi Iwata, Makoto Sahara, Kimie Tanaka, Nobutaka Koibuchi, Sumito Ito, Hiroyuki Kusuhara, Yuichi Sugiyama, Yasunobu Hirata, Ryozo Nagai and Masataka Sata : The ATP-Binding Cassette Transporter BCRP1/ABCG2 Plays a Pivotal Role in Cardiac Repair After Myocardial Infarction Via Modulation of Microvascular Endothelial Cell Survival and Function., Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.30, No.11, 2128-2135, 2010. (Summary) To clarify the impact of breast cancer resistance protein 1 (BCRP1)/ATP-binding cassette transporter subfamily G member 2 (ABCG2) expression on cardiac repair after myocardial infarction (MI). The ATP-binding cassette transporter BCRP1/ABCG2 is expressed in various organs, including the heart, and may regulate several tissue defense mechanisms. BCRP1/ABCG2 was mainly expressed in endothelial cells of microvessels in the heart. MI was induced in 8- to 12-week-old wild-type (WT) and Bcrp1/Abcg2 knockout (KO) mice by ligating the left anterior descending artery. At 28 days after MI, the survival rate was significantly lower in KO mice than in WT mice because of cardiac rupture. Echocardiographic, hemodynamic, and histological assessments showed that ventricular remodeling was more deteriorated in KO than in WT mice. Capillary, myofibroblast, and macrophage densities in the peri-infarction area at 5 days after MI were significantly reduced in KO compared with WT mice. In vitro experiments demonstrated that inhibition of BCRP1/ABCG2 resulted in accumulation of intracellular protoporphyrin IX and impaired survival of microvascular endothelial cells under oxidative stress. Moreover, BCRP1/ABCG2 inhibition impaired migration and tube formation of endothelial cells. BCRP1/ABCG2 plays a pivotal role in cardiac repair after MI via modulation of microvascular endothelial cell survival and function. (Keyword) ATP-Binding Cassette Transporters / Animals / Cell Survival / Endothelial Cells / Female / Mice / Mice, Knockout / Microvessels / Myocardial Infarction / Neoplasm Proteins / Recovery of Function / Wound Healing (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.110.211755 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20829509 ● Summary page in Scopus @ Elsevier: 2-s2.0-78149282951 (DOI: 10.1161/ATVBAHA.110.211755, PubMed: 20829509, Elsevier: Scopus)
409.	平田陽一郎, 高岡稔 and Masataka Sata : 異所性脂肪-血管周囲脂肪組織が血管リモデリングに与える影響-, Clinic All-Round, Vol.59, No.9, 1906-1910, 2010. (Keyword) 脂肪組織 / アディポネクチン / 動脈硬化 / 炎症 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1521417754711059200 (CiNii: 1521417754711059200)
410.	Masataka Sata : Early treatment of acute myocardial infarction: chain of survival, Shikoku Acta Medica, Vol.66, No.3, 4, 59-62, 2010. (Keyword) acute myocardial infarction / defibrillator / re-canalization / by-stander (Tokushima University Institutional Repository) ● Metadata: 110315 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050282812441808384 (Tokushima University Institutional Repository: 110315, CiNii: 1050282812441808384)
411.	Minoru Takaoka, Hiroshi Suzuki, Seiji Shioda, K Sekikawa, Yoshihiko Saito, Ryozo Nagai and Masataka Sata : Endovascular injury induces rapid phenotypic changes in perivascular adipose tissue., Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.30, No.8, 1576-1582, 2010. (Summary) Accumulating evidence suggests that adipose tissue not only stores energy but also secretes various bioactive substances called adipocytokines. Periadventitial fat is distributed ubiquitously around arteries throughout the body. It was reported that inflammatory changes in the periadventitial fat may have a direct role in the pathogenesis of vascular diseases accelerated by obesity. We investigated the effect of endovascular injury on the phenotype of perivascular fat. Endovascular injury significantly upregulated proinflammatory adipocytokines and downregulated adiponectin within periadventitial fat tissue in models of mouse femoral artery wire injury and rat iliac artery balloon injury. Genetic disruption of tumor necrosis factor (TNF)-alpha attenuated upregulation of proinflammatory adipocytokine expression, with reduced neointimal hyperplasia after vascular injury. Local delivery of TNF-alpha to the periadventitial area enhanced inflammatory adipocytokine expression, which was associated with augmented neointimal hyperplasia in TNF-alpha-deficient mice. Conditioned medium from a coculture of 3T3-L1 and RAW264 cells stimulated vascular smooth muscle cell proliferation. An anti-TNF-alpha neutralizing antibody in the coculture abrogated the stimulating effect of the conditioned medium. Our findings indicate that endovascular injury induces rapid and marked changes in perivascular adipose tissue, mainly mediated by TNF-alpha. It is suggested that the phenotypic changes in perivascular adipose tissue may have a role in the pathogenesis of neointimal hyperplasia after angioplasty. (Keyword) 3T3-L1 Cells / Adipokines / Adipose Tissue / Angioplasty, Balloon / Animals / Carotid Artery Injuries / Cell Proliferation / Chemokine CCL2 / Coculture Techniques / Culture Media, Conditioned / Disease Models, Animal / Hyperplasia / Inflammation Mediators / Interleukin-6 / Macrophages / Mice / Mice, Inbred C57BL / Mice, Knockout / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Phenotype / Rats / Rats, Wistar / Time Factors / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.110.207175 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20489168 ● Search Scopus @ Elsevier (PMID): 20489168 ● Search Scopus @ Elsevier (DOI): 10.1161/ATVBAHA.110.207175 (DOI: 10.1161/ATVBAHA.110.207175, PubMed: 20489168)
412.	Yuka Sumitomo-Ueda, Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Yasumasa Ikeda, Ryoko Uemoto, Shusuke Yagi, Takashi Iwase, Kazue Ishikawa, Yoichiro Hirata, Masashi Akaike, Masataka Sata, Shigeaki Kato and Toshio Matsumoto : Heparin cofactor II protects against angiotensin II-induced cardiac remodeling via attenuation of oxidative stress in mice., Hypertension, Vol.56, No.3, 430-436, 2010. (Summary) Heparin cofactor II (HCII), a serine protease inhibitor, inhibits tissue thrombin action after binding with dermatan sulfate proteoglycans in the extracellular matrix of the vascular system. We previously reported that heterozygous HCII-deficient (HCII(+/-)) humans and mice demonstrate acceleration of vascular remodeling, including atherosclerosis. However, the action of HCII on cardiac remodeling never has been determined. HCII(+/+) and HCII(+/-) mice at age 25 weeks were infused with angiotensin II (Ang II; 2.0 mg/kg/d) for 2 weeks by an osmotic mini-pump. Echocardiography revealed acceleration of cardiac concentric remodeling in HCII(+/-) mice and larger left atrial volume in HCII(+/-) mice than in HCII(+/+) mice. Histopathologic studies showed more prominent interstitial fibrosis in both the left atrium and left ventricle in HCII(+/-) mice than in HCII(+/+) mice. Daily urinary excretion of 8-hydroxy-2'-deoxyguanosine, a parameter of oxidative stress, and dihydroethidium-positive spots, indicating superoxide production in the myocardium, were markedly increased in Ang II-treated HCII(+/-) mice compared to those in HCII(+/+) mice. Cardiac gene expression levels of atrial natriuretic peptides and brain natriuretic peptides, members of the natriuretic peptide family, Nox 4, Rac-1, and p67(phox) as components of NAD(P)H oxidase, and transforming growth factor-beta1 and procollagen III were more augmented in HCII(+/-) mice than in HCII(+/+) mice. However, administration of human HCII protein attenuated all of those abnormalities in Ang II-treated HCII(+/-) mice. Moreover, human HCII protein supplementation almost abolished cardiac fibrosis in Ang II-treated HCII(+/+) mice. The results indicate that HCII has a protective role against Ang II-induced cardiac remodeling through suppression of the NAD(P)H oxidase-transforming growth factor-beta1 pathway. (Keyword) Analysis of Variance / Angiotensin II / Animals / Atrial Natriuretic Factor / Cardiomegaly / Echocardiography / Fibrosis / Heart Atria / Heparin Cofactor II / Mice / Mice, Transgenic / Myocardium / Natriuretic Peptide, Brain / Oxidative Stress / Transforming Growth Factor beta1 / Ventricular Remodeling (Link to Publication Site) ● Publication site (DOI): 10.1161/HYPERTENSIONAHA.110.152207 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20660821 ● Search Scopus @ Elsevier (PMID): 20660821 ● Search Scopus @ Elsevier (DOI): 10.1161/HYPERTENSIONAHA.110.152207 (DOI: 10.1161/HYPERTENSIONAHA.110.152207, PubMed: 20660821)
413.	Masataka Sata, M Sahara, T Morita, T Nakajima, Y Hirata and R Nagai : A phosphodiesterase-5 inhibitor vardenafil enhances angiogenesis through a protein kinase G-dependent hypoxia-inducible factor-1/vascular endothelial growth factor pathway., Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.30, No.7, 1315-1324, 2010. (Summary) We examined whether phosphodiesterase-5 (PDE5) inhibition can promote ischemia-induced angiogenesis. Unilateral hindlimb ischemia was generated by resecting right femoral artery in wild-type C3H/He mice, treated with either vehicle or a PDE5 inhibitor vardenafil (10 mg/kg per day). Four weeks after surgery, vardenafil significantly enhanced blood flow recovery and augmented capillary collateral formation in ischemic muscle (blood flow ratios of ischemic/nonischemic leg: 0.52+/-0.17 [vehicle] versus 0.92+/-0.09 [vardenafil], P<0.01). Vardenafil upregulated protein expression of vascular endothelial growth factor and hypoxia-inducible factor (HIF)-1 alpha in ischemic muscle and enhanced mobilization of Sca-1/Flk-1-positive endothelial progenitor cells (EPCs) in peripheral blood and bone marrow, contributing to neovascularization. Vardenafil also promoted capillary-like tube formation of human umbilical vein endothelial cells and increased the number of human blood mononuclear cell-derived EPCs in vitro. Furthermore, reporter assays showed that vardenafil and cGMP activated the transactivation activity of HIF-1 under hypoxia. These effects of vardenafil were markedly inhibited by genetic ablation of endothelial nitric oxide synthase, a soluble guanylate cyclase inhibitor, and a protein kinase G inhibitor, respectively. Our results suggest that PDE5 inhibition enhances ischemia-induced angiogenesis with mobilization of EPCs through a protein kinase G-dependent HIF-1/vascular endothelial growth factor pathway. PDE5 inhibition may have a therapeutic potential to treat ischemic cardiovascular diseases. (Keyword) Angiogenesis Inducing Agents / Animals / Capillaries / Cell Hypoxia / Cell Movement / Cells, Cultured / Collateral Circulation / Cyclic GMP / Cyclic GMP-Dependent Protein Kinases / Cyclic Nucleotide Phosphodiesterases, Type 5 / Disease Models, Animal / Endothelial Cells / Green Fluorescent Proteins / Hindlimb / Humans / Hypoxia-Inducible Factor 1, alpha Subunit / Imidazoles / Ischemia / Male / Mice / Mice, Inbred C3H / Mice, Inbred C57BL / Mice, Knockout / Mice, Transgenic / Muscle, Skeletal / Neovascularization, Physiologic / Nitric Oxide Synthase Type III / Phosphodiesterase 5 Inhibitors / Phosphodiesterase Inhibitors / Piperazines / RNA Interference / Recovery of Function / Regional Blood Flow / Signal Transduction / Stem Cells / Sulfones / Time Factors / Transfection / Triazines / Vascular Endothelial Growth Factor A (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.109.201327 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20413734 ● Search Scopus @ Elsevier (PMID): 20413734 ● Search Scopus @ Elsevier (DOI): 10.1161/ATVBAHA.109.201327 (DOI: 10.1161/ATVBAHA.109.201327, PubMed: 20413734)
414.	PH Huang, HY Tsai, CH Wang, YH Chen, JS Chen, FY Lin, CP Lin, TC Wu, Masataka Sata, JW Chen and SJ Lin : Moderate intake of red wine improves ischemia-induced neovascularization in diabetic mice-Roles of endothelial progenitor cells and nitric oxide., Atherosclerosis, Vol.212, No.2, 426-435, 2010. (Summary) Circulating endothelial progenitor cells (EPCs) play a significant role in postnatal neovascularization. Patients with diabetes have attenuated EPC functions and impaired angiogenic response after tissue ischemia. We investigated whether moderate red wine consumption can enhance blood flow recovery in response to tissue ischemia by enhancement of EPC functions in diabetic mice. Starting at 4 weeks after diabetes onset, red wine (4 ml/kg/day) or ethanol were administered to streptozotocin (STZ)-induced (type 1) diabetic mice and KKAy-Ta (type 2) mice. Unilateral hind limb ischemia surgery was conducted after 2 weeks of red wine or ethanol ingestion. Type 1 and type 2 diabetic mice given red wine, but not ethanol, had significantly increased collateral flow about 30% and augmented capillary density in ischemic tissues. These beneficial effects were markedly abolished by an eNOS inhibitor (L-NAME). Flow cytometry analysis showed impaired EPC-like cells (Sca-1+/Flk-1+) mobilization after ischemia surgery in diabetic mice, but augmented mobilization in red wine group (baseline vs. 2 days after operation: 0.88±0.06% vs. 1.73±0.29%, p=0.010). C-kit positive bone marrow cells isolated from diabetic mice given red wine had enhanced adhesion and migration compared to mice given vehicle. By in-vitro studies, incubation with red wine in high-glucose medium significantly reduced H2O2 production, and improved high glucose-suppressed EPC functions by nitric oxide-related mechanisms. Our findings demonstrate that red wine consumption enhances blood flow recovery after tissue ischemia in diabetic mice. These effects may partly derive from enhanced EPC functions by upregulation of eNOS activity. (Keyword) Animals / Bone Marrow Cells / Capillaries / Diabetes Mellitus, Experimental / Endothelial Cells / Ethanol / Flow Cytometry / Ischemia / Mice / NG-Nitroarginine Methyl Ester / Neovascularization, Physiologic / Nitric Oxide / Phosphorylation / Stem Cells / Streptozocin / Wine (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2010.06.034 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20637466 ● Search Scopus @ Elsevier (PMID): 20637466 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2010.06.034 (DOI: 10.1016/j.atherosclerosis.2010.06.034, PubMed: 20637466)
415.	Sumiko Yoshida, Ken-ichi Aihara, Hiroyuki Azuma, Ryoko Uemoto, Yuka Sumitomo-Ueda, Shusuke Yagi, Yasumasa Ikeda, Takashi Iwase, Susumu Nishio, Hiromi Kawano, Junko Miki, Hirotsugu Yamada, Yoichiro Hirata, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Dehydroepiandrosterone sulfate is inversely associated with sex-dependent diverse carotid atherosclerosis regardless of endothelial function., Atherosclerosis, Vol.212, No.1, 310-315, 2010. (Summary) BACKGROUND: Dehydroepiandrosterone sulfate (DHEAS) is thought to be associated with life expectancy and anti-aging. However, its biological significance in atherosclerosis remains controversial. Therefore, the aim of this study was to determine whether DHEAS is associated with development of carotid atherosclerosis in subjects with cardiovascular risk factors. SUBJECTS AND METHODS: A total of 419 Japanese individuals (208 males and 211 females) were recruited from Tokushima University Hospital, Japan. In all subjects, maximum intima-media thickness (max-IMT) in all carotid arteries, and mean-IMT and mean blood flow volume (BFV) in the common carotid arteries (CCA) were measured by ultrasonography; endothelial function was assessed by flow-mediated vasodilation of the brachial artery (%FMD). Serum DHEAS and classical cardiovascular risk factors were also evaluated. Statistical significance was determined by multiple regression analysis to elucidate independent determinants of max-IMT, mean-IMT, mean CCA-BFV, and %FMD. RESULTS: Serum DHEAS levels were higher in males than in females. Multiple regression analysis revealed that DHEAS was an independent negative factor for both max-IMT and mean-IMT in males but not in females. In contrast, DHEAS was the sole positive factor for mean CCA-BFV in females but not in males. In addition, there was no significant relationship between %FMD and DHEAS regardless of sex and other confounding factors. CONCLUSION: Although DHEAS is not involved in endothelial function, DHEAS is inversely associated with sex-dependent diverse carotid atherosclerosis such as increased max-IMT and mean-IMT in males and decreased CCA-BFV in females. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2010.05.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20627295 ● Search Scopus @ Elsevier (PMID): 20627295 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2010.05.011 (DOI: 10.1016/j.atherosclerosis.2010.05.011, PubMed: 20627295)
416.	Michiko Sato, Yasutomo Nakazawa, Rui Takahashi, Kimie Tanaka, Masataka Sata, Aytemiz Derya and Tetsuo Asakura : Small-diameter vascular grafts of Bombyx mori silk fibroin prepared by a combination of electrospinning and sponge coating., Materials Letters, Vol.64, No.16, 1786-1788, 2010. (Keyword) Small-diameter vascular graft / Silk fibroin / Electrospinning / PATENCY (Link to Publication Site) ● Publication site (DOI): 10.1016/j.matlet.2010.05.024 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1571698601428854400 ● Search Scopus @ Elsevier (DOI): 10.1016/j.matlet.2010.05.024 (DOI: 10.1016/j.matlet.2010.05.024, CiNii: 1571698601428854400)
417.	Kenya Kusunose, Hirotsugu Yamada, Takashi Iwase, Susumu Nishio, Noriko Tomita, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Shoichiro Takao, Masafumi Harada, Noriko Kagawa, Eiji Kudo and Masataka Sata : Images in cardiovascular medicine. Cardiac magnetic resonance imaging and 2-dimensional speckle tracking echocardiography in secondary cardiac amyloidosis., Circulation Journal, Vol.74, No.7, 1494-1496, 2010. (Keyword) Aged / Amyloidosis / Echocardiography / Heart Diseases / Humans / magnetic resonance imaging / Male / Mitral Valve / Regional Blood Flow (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-10-0141 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20501956 ● Search Scopus @ Elsevier (PMID): 20501956 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-10-0141 (DOI: 10.1253/circj.CJ-10-0141, PubMed: 20501956)
418.	Shusuke Yagi, Masashi Akaike, Mitsunori Fujimura, Takehiko Kimura, Takeshi Nishiuchi, Takashi Iwase, Ken-ichi Aihara, Sumiko Yoshida, Yuka Sumitomo-Ueda, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoichiro Hirata, Munkhbaatar Dagvasumberel, Yoshio Taketani, Noriko Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Congenital ventricular aneurysm as an unexpected complication of monomorphic premature ventricular contractions., Internal Medicine, Vol.49, No.10, 907-912, 2010. (Summary) Congenital ventricular diverticulum (CVD) in adults is a rare cardiac malformation, which includes fibrous type congenital ventricular aneurysm (CVA). CVA is often clinically asymptomatic and shows no abnormality in the electrocardiogram or chest X-ray. However, some cases of sudden death resulting from ventricular tachycardia, cardiac embolism or ventricular rupture have been reported. Therefore, physicians should perform further cardiac imaging studies to detect a CVA if ventricular arrhythmia originating from the left ventricle is observed. Here, we report two successfully followed cases of CVA which were diagnosed from premature ventricular contractions. (Keyword) congenital ventricular aneurysm / congenital ventricular diverticulum / ventricular arrythmia (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.49.3008 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20467175 ● CiNii @ National Institute of Informatics (CRID): 1390001204871212928 ● Search Scopus @ Elsevier (PMID): 20467175 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.49.3008 (DOI: 10.2169/internalmedicine.49.3008, PubMed: 20467175, CiNii: 1390001204871212928)
419.	H Iwata, Masataka Sata, T Morita, J Ando, D Sawaki, H Fujita, Y Hirata, S Takanashi, Y Hirata and R Nagai : Impact of primitive cells in intracoronary thrombi on lesion prognosis: Temporal analysis of cellular constituents of thrombotic material obtained from patients with acute coronary syndrome., Heart, Vol.96, No.10, 748-755, 2010. (Summary) Clinical evidence suggests that intracoronary thrombus formation is associated with a high incidence of late restenosis after successful coronary intervention in patients with myocardial infarction (MI). However, little is known about the mechanism by which intracoronary thrombi play pathological roles. We analysed the cellular constituents of 108 thrombi aspirated from coronary lesions with a thrombectomy device in 62 patients who underwent emergent coronary intervention for the treatment of acute (<24 h) or recent (24-72 h) ST-segment elevation MI (44 men, 18 women, aged 68.0+/-19.3 years). Immunohistological analysis of aspirated thrombotic materials revealed that the content of platelets, as determined by immunostaining for CD42a, had a negative correlation with the time after the onset of chest pain (correlation coefficient -0.683, p<0.01). Immunofluorescent staining for CD34 and breast cancer-resistant protein-1 (bcrp-1) detected primitive cells in intracoronary thrombi. Furthermore, the ratio of CD34-positive cells in intracoronary thrombi had a significant positive correlation with restenosis at follow-up coronary angiography (correlation coefficient 0.76, p=0.01). The findings of this study indicate that the early accumulation of primitive cells in platelet aggregates may play a role in neointimal growth after successful coronary intervention in patients with acute coronary syndrome. (Keyword) ATP-Binding Cassette Transporters / Acute Coronary Syndrome / Aged / Aged, 80 and over / Angioplasty, Balloon, Coronary / Antigens, CD34 / Coronary Restenosis / Coronary Thrombosis / Disease Progression / Female / Follow-Up Studies / Humans / Male / Middle Aged / Myocardial Infarction / Neoplasm Proteins / Platelet Aggregation / Prognosis / Stem Cells / Thrombectomy (Link to Publication Site) ● Publication site (DOI): 10.1136/hrt.2009.181040 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20448125 ● Search Scopus @ Elsevier (PMID): 20448125 ● Search Scopus @ Elsevier (DOI): 10.1136/hrt.2009.181040 (DOI: 10.1136/hrt.2009.181040, PubMed: 20448125)
420.	Masataka Sata : プラーク破綻の分子機構, Heart, Vol.42, No.4, 552-557, 2010. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679026259584 (CiNii: 1390282679026259584)
421.	Hirotsugu Yamada, Yuichiro Mishiro, Kenya Kusunose and Masataka Sata : Effects of additional administration of low-dose indapamide on patients with hypertension treated with angiotensin II receptor blocker., Journal of Cardiovascular Pharmacology and Therapeutics, Vol.15, No.2, 145-150, 2010. (Summary) BACKGROUND: Low-dose thiazide or thiazide-like diuretics have proven useful for the management of blood pressure in patients older than 65 years (elderly group). However, there are few reports about the antihypertensive effects of antihypertensive diuretic agents in patients younger than 65 years (middle-aged group). So, we evaluated the efficacy of low-dose indapamide on blood pressure. METHODS: Indapamide(1 mg) was given daily for 3 months and was then given every other day for 3 months to patients whose hypertension was poorly controlled with angiotensin II receptor blocker (ARB)-based treatment. RESULTS: After daily administration of indapamide, blood pressure was significantly decreased in both the middle-aged and elderly groups. Blood pressure was not significantly changed by every-other-day administration compared with that observed after daily administration in either group. The rate of attainment of the target blood pressure was 90.3% and 85.7% in the middle-aged and elderly groups, respectively. The serum uric acid levels were reduced after every-other-day administration compared to daily administration but tended to be higher than the levels at the baseline in both groups. CONCLUSIONS: The addition of low-dose indapamide is a useful strategy for the management of hypertension, as it reduced blood pressure without marked side effects. (Link to Publication Site) ● Publication site (DOI): 10.1177/1074248410361336 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20200326 ● Search Scopus @ Elsevier (PMID): 20200326 ● Search Scopus @ Elsevier (DOI): 10.1177/1074248410361336 (DOI: 10.1177/1074248410361336, PubMed: 20200326)
422.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, Kazue Ishikawa, Takashi Iwase, Yasumasa Ikeda, Takeshi Soeki, Sumiko Yoshida, Yuka Sumitomo-Ueda, Toshio Matsumoto and Masataka Sata : Endothelial nitric oxide synthase-independent protective action of statin against angiotensin II-induced atrial remodeling via reduced oxidant injury., Hypertension, Vol.55, No.4, 918-923, 2010. (Summary) Activation of the renin-angiotensin system exacerbates atrial remodeling, leading to atrial fibrillation and thrombosis, especially in a condition with decreased NO bioavailability. Recently, it has been reported that statins reduce the incidence of atrial fibrillation through attenuation of atrial remodeling; however, the mechanisms have not been completely elucidated. Therefore, we aimed to clarify the beneficial effect of statin on atrial remodeling in condition with reduced NO bioavailability. Endothelial NO synthase(-/-) mice were sham operated or infused with angiotensin II (Ang II) via an osmotic minipump for 2 weeks, and Ang II-infused mice were divided into 3 treatment groups: pitavastatin, Tempol (a free radical scavenger), or vehicle. Echocardiography and electrocardiography showed that Ang II infusion caused left atrial enlargement and a high incidence of atrial fibrillation, whereas pitavastatin and Tempol prevented these abnormalities. In histological analysis, Ang II-induced atrial interstitial fibrosis, perivascular fibrosis, and cardiomyocyte hypertrophy were all attenuated by pitavastatin and Tempol. Immunohistochemical staining showed that Ang II downregulated thrombomodulin and tissue factor pathway inhibitor and upregulated tissue factor and plasminogen activator inhibitor 1 in the left atrium and that pitavastatin and Tempol corrected the thrombogenic condition. Moreover, pitavastatin and Tempol reduced Ang II-induced atrial superoxide production and atrial transforming growth factor-beta1 expression and Smad 2/3 phosphorylation. Atrial rac1-GTPase activity, known to activate NADPH oxidase, was attenuated by pitavastatin but not by Tempol. In conclusion, pitavastatin exerts endothelial NO synthase-independent protective actions against Ang II-induced atrial remodeling and atrial fibrillation with enhanced thrombogenicity through suppression of oxidant injury. (Keyword) Analysis of Variance / Angiotensin II / Animals / Antioxidants / Atrial Fibrillation / Blood Pressure / Blotting, Western / Cardiomegaly / Cyclic N-Oxides / Echocardiography / Fibrosis / Heart Atria / Heart Rate / Hydroxymethylglutaryl-CoA Reductase Inhibitors / Male / Mice / Mice, Knockout / Myocytes, Cardiac / Nitric Oxide Synthase Type III / Oxidative Stress / Quinolines / Renin-Angiotensin System / Reverse Transcriptase Polymerase Chain Reaction / Signal Transduction / Smad2 Protein / Smad3 Protein / Spin Labels / Transforming Growth Factor beta1 (Link to Publication Site) ● Publication site (DOI): 10.1161/HYPERTENSIONAHA.109.146076 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20194307 ● Search Scopus @ Elsevier (PMID): 20194307 ● Search Scopus @ Elsevier (DOI): 10.1161/HYPERTENSIONAHA.109.146076 (DOI: 10.1161/HYPERTENSIONAHA.109.146076, PubMed: 20194307)
423.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, Takashi Iwase, Kazue Ishikawa, Sumiko Yoshida, Yuka Sumitomo-Ueda, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoichiro Hirata, Munkhbaatar Dagvasumberel, Yoshio Taketani, Noriko Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Ezetimibe ameliorates metabolic disorders and microalbuminuria in patients with hypercholesterolemia., Journal of Atherosclerosis and Thrombosis, Vol.17, No.2, 173-180, 2010. (Summary) AIM: Ezetimibe, an inhibitor of Niemann-Pick C1-like 1 protein, has been shown to reduce the intestinal absorption of cholesterol. We investigated whether it also has beneficial effects on metabolic disorder and/or renal insufficiency in patients with hypercholesterolemia. METHODS: Ezetimibe was administered to 38 Japanese patients with hypercholesterolemia to obtain appropriate low-density lipoprotein cholesterol (LDL-chol) levels. Age- and sex-matched patients with hypercholesterolemia (n=38) were the controls. We evaluated the effects of ezetimibe before and 4 to 8 weeks after ezetimibe treatment. RESULTS: Ezetimibe significantly decreased LDL-chol levels and metabolic syndrome-related factors, including body weight, waist circumference, blood pressure; homeostasis model assessment insulin resistance (HOMA-IR), and urinary albumin excretion, were significantly reduced. In addition, it decreased the level of high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor (TNF)-alpha, the urinary excretion of 8-hydroxy-2'-deoxyguanosine, a parameter of oxidative stress, and increased the urinary excretion of nitrate and nitrite (NOx). In the controls we observed no such changes. Excepting the decrease in the serum TNF-alpha level, the effects of ezetimibe were not correlated with decreased LDL-chol levels. CONCLUSION: Ezetimibe ameliorated the status of metabolic syndrome and microalbuminuria, reduced inflammation and oxidative stress, and increased nitric oxide bioavailability in a LDL-chol reduction-dependent and -independent manner. (Keyword) Aged / Albuminuria / Anticholesteremic Agents / Azetidines / C-Reactive Protein / Case-Control Studies / Cholesterol, LDL / Deoxyguanosine / Female / Humans / Hypercholesterolemia / Male / Metabolic Diseases / Metabolic Syndrome X / Middle Aged / Nitrates / Nitrites / Oxidative Stress / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.2378 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20150722 ● Search Scopus @ Elsevier (PMID): 20150722 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.2378 (DOI: 10.5551/jat.2378, PubMed: 20150722)
424.	PH Huang, YH Chen, HY Tsai, JS Chen, TC Wu, FY Lin, Masataka Sata, JW Chen and SJ Lin : Intake of Red Wine Increases the Number and Functional Capacity of Circulating Endothelial Progenitor Cells by Enhancing Nitric Oxide Bioavailability, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.30, No.4, 869-877, 2010. (Summary) Red wine (RW) consumption has been associated with a reduction of cardiovascular events, but limited data are available on potential mediating mechanisms. This study tested the hypothesis that intake of RW may promote the circulating endothelial progenitor cell (EPC) level and function through enhancement of nitric oxide bioavailability. Eighty healthy, young subjects were randomized and assigned to consume water (100 mL), RW (100 mL), beer (250 mL), or vodka (30 mL) daily for 3 weeks. Flow cytometry was used to quantify circulating EPC numbers, and in vitro assays were used to evaluate EPC functions. After RW ingestion, endothelial function determined by flow-mediated vasodilation was significantly enhanced; however, it remained unchanged after water, beer, or vodka intake. There were significantly increased numbers of circulating EPC (defined as KDR(+)CD133(+), CD34(+)CD133(+), CD34(+)KDR(+)) and EPC colony-forming units only in the RW group (all P<0.05). Only RW ingestion significantly enhanced plasma levels of nitric oxide and decreased asymmetrical dimethylarginine (both P<0.01). Incubation of EPC with RW (but not beer or ethanol) and resveratrol in vitro attenuated tumor necrosis factor-alpha-induced EPC senescence and improved tumor necrosis factor-alpha-suppressed EPC functions and tube formation. Incubation with nitric oxide donor sodium nitroprusside significantly ameliorated the inhibition of tumor necrosis factor-alpha on EPC proliferation, but incubation with endothelial nitric oxide synthase inhibitor l-NAME and PI3K inhibitor markedly attenuated the effect of RW on EPC proliferation. The intake of RW significantly enhanced circulating EPC levels and improved EPC functions by modifying nitric oxide bioavailability. These findings may help explain the beneficial effects of RW on the cardiovascular system. This study demonstrated that a moderate intake of RW can enhance circulating levels of EPC in healthy subjects by increasing nitric oxide availability. Direct incubation of EPC with RW and resveratrol can modify the functions of EPC, including attenuation of senescence and promotion of EPC adhesion, migration, and tube formation. These data suggest that RW ingestion may alter the biology of EPC, and these alterations may contribute to its unique cardiovascular-protective effect. (Keyword) Adult / Alcoholic Beverages / Antigens, CD / Antigens, CD34 / Arginine / Beer / Biological Availability / Biological Markers / Cell Adhesion / Cell Aging / Cell Movement / Cell Proliferation / Cells, Cultured / Endothelial Cells / Enzyme Inhibitors / Ethanol / Female / Flow Cytometry / Glycoproteins / Humans / Male / NG-Nitroarginine Methyl Ester / Nitric Oxide / Nitric Oxide Synthase Type III / Peptides / Phosphatidylinositol 3-Kinases / Phosphorylation / Prospective Studies / Proto-Oncogene Proteins c-akt / Stem Cells / Stilbenes / Tumor Necrosis Factor-alpha / Up-Regulation / Vascular Endothelial Growth Factor Receptor-2 / Vasodilation / Wine (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.109.200618 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20093623 ● Search Scopus @ Elsevier (PMID): 20093623 ● Search Scopus @ Elsevier (DOI): 10.1161/ATVBAHA.109.200618 (DOI: 10.1161/ATVBAHA.109.200618, PubMed: 20093623)
425.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, K Adachi, Y Sumitomo-Ueda, Shusuke Yagi, T Niki, Kenya Kusunose, N Tomita, Y Hirata, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, KI Aihara, Masafumi Harada, H Nishitani and Masataka Sata : Diagnostic utility of cardiac magnetic resonance for detection of cardiac involvement in female carriers of Duchenne muscular dystrophy., Heart Asia, Vol.2, 52-55, 2010. (Link to Publication Site) ● Publication site (DOI): 10.1136/ha.2010.002006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27325943 ● Search Scopus @ Elsevier (PMID): 27325943 ● Search Scopus @ Elsevier (DOI): 10.1136/ha.2010.002006 (DOI: 10.1136/ha.2010.002006, PubMed: 27325943)
426.	Tatsuo Motoki, Hirotsugu Kurobe, 平田陽一郎, 菅野幹雄, Homare Yoshida, Tamotsu Kanbara, Takashi Kitaichi, Masataka Sata and Tetsuya Kitagawa : ピオグリタゾン投与による腹部大動脈瘤ぬおける抗動脈硬化作用, Shikoku Acta Medica, Vol.66, No.3,4, 91-94, 2010. (Tokushima University Institutional Repository) ● Metadata: 110321 (Tokushima University Institutional Repository: 110321)
427.	Hajime Kinoshita, Tamotsu Kanbara, Hirotsugu Kurobe, Tatsuo Motoki, Mikio Sugano, Homare Yoshida, Takashi Kitaichi, Masataka Sata, Toshio Matsumoto and Tetsuya Kitagawa : Successful Implantations of Autologous Peripheral Blood-Derived Mononuclear Cells Pretreated by Erythropoietin and Blood Donation in a Patient with Buerger Disease and Intractable Finger Ulcers, Japanese Journal of Cardiovascular Surgery, Vol.39, No.1, 29-33, 2010. (Link to Publication Site) ● Publication site (DOI): 10.4326/jjcvs.39.29 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.4326/jjcvs.39.29 (DOI: 10.4326/jjcvs.39.29)
428.	Soichiro Enomoto, Makoto Sumi, Kan Kajimoto, Yasumoto Nakazawa, Rui Takahashi, Chiyuki Takabayashi, Tetsuo Asakura and Masataka Sata : Long-term Patency of Small-diameter Vascular Graft Made from Fibroin, a Silk-based Biodegradable Material., Journal of Vascular Surgery, Vol.51, No.1, 155-164, 2010. (Summary) There is an increasing need for vascular grafts in the field of surgical revascularization. However, smaller vascular grafts made from synthetic biomaterials, particularly those <5 mm in diameter, are associated with a high incidence of thrombosis. Fibroin is a biodegradable protein derived from silk. Silk fibroin from Bombyx mori provides an antithrombotic surface and serves as a scaffold for various cell types in tissue engineering. We evaluated the potential of fibroin to generate a vascular prosthesis for small arteries. A small vessel with three layers was woven from silk fibroin thread. These fibroin-based grafts (1.5 mm diameter, 10 mm length) were implanted into the abdominal aorta of 10- to 14-week-old male Sprague-Dawley rats by end-to-end anastomosis. Polytetrafluoroethylene (PTFE)-based grafts were used as the control. To investigate the origin of the cells in the neointima and media, bone marrow transplantation was performed from green fluorescent protein (GFP) rats to wild-type rats. The patency of fibroin grafts at 1 year after implantation was significantly higher than that of PTFE grafts (85.1% vs 30%, P < .01). Endothelial cells and smooth muscle cells (SMCs) migrated into the fibroin graft early after implantation and became organized into endothelial and medial layers, as determined by anti-CD31 and anti-alpha-smooth muscle actin immunostaining. The total number of SMCs increased 1.6-fold from 1 month to 3 months. Vasa vasorum also formed in the adventitia. Sirius red staining of the fibroin grafts revealed that the content of collagen significantly increased at 1 year after implantation, with a decrease in fibroin content. GFP-positive cells contributed to organization of a smooth muscle layer. Small-diameter fibroin-based vascular grafts have excellent long-term patency. Bone marrow-derived cells contribute to vascular remodeling after graft implantation. Fibroin might be a promising material to engineer vascular prostheses for small arteries. (Keyword) Absorbable Implants / Actins / Animals / Antigens, CD31 / Aorta, Abdominal / Aortography / Blood Vessel Prosthesis / Blood Vessel Prosthesis Implantation / Bone Marrow Cells / Bone Marrow Transplantation / Cell Movement / Collagen / Endothelial Cells / Fibroins / Green Fluorescent Proteins / Male / Materials Testing / Models, Animal / Myocytes, Smooth Muscle / Polytetrafluoroethylene / Prosthesis Design / Rats / Rats, Sprague-Dawley / Rats, Transgenic / Time Factors / Ultrasonography, Doppler, Color / Vascular Patency (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jvs.2009.09.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19954921 ● Search Scopus @ Elsevier (PMID): 19954921 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jvs.2009.09.005 (DOI: 10.1016/j.jvs.2009.09.005, PubMed: 19954921)
429.	Y Hirata, Takeshi Soeki, Masashi Akaike, Y Sakai, T Igarashi and Masataka Sata : Synthetic prostacycline agonist, ONO-1301, ameliorates left ventricular dysfunction and cardiac fibrosis in cardiomyopathic hamsters., Biomedicine & Pharmacotherapy, Vol.63, No.10, 781-786, 2009. (Summary) Impairment of cardiac function in cardiomyopathy has been postulated to be related to decreased blood flow and increased collagen synthesis. Administration of growth factors was reported to attenuate left ventricular (LV) remodeling and dysfunction in animal models of dilated cardiomyopathy. We previously reported that ONO-1301, a synthetic prostacyclin agonist with thromboxane-synthase inhibitory activity, promotes production of hepatocyte growth factor and vascular endothelial growth factor from various cell types and ameliorate ischemia-induced LV dysfunction in mice and pigs. We evaluated therapeutic efficacy of ONO-1301 in the Syrian hamster (TO-2), a model of genetically determined dilated cardiomyopathy. Either vehicle or a slow releasing form of ONO-1301 (ONO-1301-PLGA, 10mg/kg/3 weeks) was administered subcutaneously every 3 weeks to TO-2 hamsters from 24 to 32 weeks of age (n=12 for each group). Age-matched F1B hamsters were used as a control. Plasma concentration of HGF was elevated in ONO-1301-PLGA group (p<0.05). Echocardiographic study demonstrated that LV fractional shortening was significantly improved in the ONO-1301-PLGA group (25+/-4%, p<0.01) compared with that in the vehicle group (19+/-2%). Cardiac fibrosis was significantly reduced by ONO-1301-PLGA (p<0.05) as determined by Azan-Mallory staining. Capillary density of left ventricle was markedly reduced in TO-2 hamsters. ONO-1301-PLGA significantly increased capillary density in TO-2 group (p<0.05). ONO-1301 improved LV dysfunction and reduced cardiac fibrosis in the hamster model of dilated cardiomyopathy. ONO-1301 might hold a therapeutic potential in the treatment of dilated cardiomyopathy. (Keyword) Animals / Cardiomyopathy, Dilated / Cricetinae / Delayed-Action Preparations / Disease Models, Animal / Drug Carriers / Enzyme Inhibitors / Fibrosis / Lactic Acid / Male / Myocardium / Polyglycolic Acid / Pyridines / Thromboxane-A Synthase / Ventricular Dysfunction, Left (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biopha.2009.09.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19906506 ● Search Scopus @ Elsevier (PMID): 19906506 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biopha.2009.09.003 (DOI: 10.1016/j.biopha.2009.09.003, PubMed: 19906506)
430.	Kenya Kusunose, Hirotsugu Yamada, S Nishio, N Tomita, T Niki, K Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Y Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Clinical Utility of Single Beat E/e' Obtained by Simultaneous Recording of Flow and Tissue Doppler Velocities in Atrial Fibrillation with Preserved Systolic Function., JACC. Cardiovascular Imaging, Vol.2, No.10, 1147-1156, 2009. (Summary) We evaluated the usefulness of the ratio of the early diastolic transmitral flow velocity (E) to the mitral annular velocity (e') calculated from simultaneously recorded E and e' in atrial fibrillation (AF). The ratio of the E to the e' (E/e') has been reported as a useful index even in AF patients. However, E and e' were measured during different beats in the previous studies. Fifty-six AF patients with preserved systolic function (mean age 66 +/- 11 years) underwent routine echocardiographic study. The E/e' was calculated from the E and e' simultaneously recorded by the dual Doppler echocardiography. A single-beat E/e' was calculated from simultaneously recorded E and e' when the preceding RR interval/pre-preceding RR interval = 1. Brain natriuretic peptide (BNP) levels were also examined. Twenty-one patients underwent simultaneous pulmonary artery catheterization. The single-beat lateral E/e' correlated with pulmonary capillary wedge pressure (PCWP) (r = 0.74, p < 0.001). The single-beat lateral E/e' of >or=11 could predict elevated PCWP (>or=15 mm Hg) with a sensitivity of 90% and a specificity of 90%. The single-beat lateral E/e' also correlated well with the log BNP concentration. The single-beat lateral E/e' of >or=9.2 predicted a plasma BNP level of >or=200 pg/ml with 88% sensitivity and 84% specificity. The single-beat lateral E/e' correlated with plasma BNP level and PCWP in AF patients with preserved systolic function. In addition, the single-beat lateral E/e' (>or=11) was a good predictor of elevated PCWP (>or=15 mm Hg). Dual Doppler echocardiography offers an advantage of providing the single-beat lateral E/e' correctly even in AF patients, for the evaluation of left ventricular diastolic function. (Keyword) Adult / Aged / Aged, 80 and over / Atrial Fibrillation / Biological Markers / Catheterization, Swan-Ganz / Coronary Circulation / Diastole / Echocardiography, Doppler, Color / Echocardiography, Doppler, Pulsed / Female / Heart Rate / Humans / Linear Models / Male / Middle Aged / Mitral Valve / Natriuretic Peptide, Brain / Predictive Value of Tests / Pulmonary Wedge Pressure / Sensitivity and Specificity / Systole / Ventricular Function, Left (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jcmg.2009.05.013 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19833302 ● Search Scopus @ Elsevier (PMID): 19833302 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jcmg.2009.05.013 (DOI: 10.1016/j.jcmg.2009.05.013, PubMed: 19833302)
431.	M Takaoka, D Nagata, S Kihara, S Shimomura, Y Kimura, Y Tabata, Y Saito, R Nagai and Masataka Sata : Periadventitial adipose tissue plays a critical role in vascular remodeling., Circulation Research, Vol.105, No.9, 906-911, 2009. (Summary) Obesity is associated with a high incidence of cardiovascular complications. However, the molecular link between obesity and vascular disease is not fully understood. Most previous studies have focused on the association between cardiovascular disease and accumulation of visceral fat. Periadventitial fat is distributed ubiquitously around arteries throughout the body. Here, we investigated the impact of obesity on inflammation in the periadventitial adipose tissue and on lesion formation after vascular injury. High-fat, high-sucrose feeding induced inflammatory changes and decreased adiponectin expression in the periadventitial adipose tissue, which was associated with enhanced neointima formation after endovascular injury. Removal of periadventitial fat markedly enhanced neointima formation after injury, which was attenuated by transplantation of subcutaneous adipose tissue from mice fed on regular chow. Adiponectin-deficient mice showed markedly enhanced lesion formation, which was reversed by local delivery, but not systemic administration, of recombinant adiponectin to the periadventitial area. The conditioned medium from subcutaneous fat attenuated increased cell number of smooth muscle cells in response to platelet derived growth factor-BB. Our findings suggest that periadventitial fat may protect against neointimal formation after angioplasty under physiological conditions and that inflammatory changes in the periadventitial fat may have a direct role in the pathogenesis of vascular disease accelerated by obesity. (Keyword) AMP-Activated Protein Kinases / Adiponectin / Adipose Tissue / Animals / Cell Proliferation / Cells, Cultured / Connective Tissue / Culture Media, Conditioned / Disease Models, Animal / Femoral Artery / Green Fluorescent Proteins / Hyperplasia / Inflammation / Mice / Mice, Inbred C57BL / Mice, Knockout / Mice, Transgenic / Muscle, Smooth, Vascular / Obesity / Platelet-Derived Growth Factor / Rats / Recombinant Proteins / Tissue Culture Techniques / Transduction, Genetic / Tunica Intima / Vascular Diseases (Link to Publication Site) ● Publication site (DOI): 10.1161/CIRCRESAHA.109.199653 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19762682 ● Search Scopus @ Elsevier (PMID): 19762682 ● Search Scopus @ Elsevier (DOI): 10.1161/CIRCRESAHA.109.199653 (DOI: 10.1161/CIRCRESAHA.109.199653, PubMed: 19762682)
432.	HJ Kim, EK Yoo, JY Kim, YK Choi, HJ Lee, JK Kim, NH Jeoung, KU Lee, IS Park, BH Min, KG Park, CH Lee, BJ Aronow, Masataka Sata and IK Lee : Protective Role of Clusterin / Apolipoprotein J Against Neointimal Hyperplasia via Antiproliferative Effect on Vascular Smooth Muscle Cells and Cytoprotective Effect on Endothelial Cells., Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.29, No.10, 1558-1564, 2009. (Summary) Clusterin is induced in vascular smooth muscle cells (VSMCs) during atherosclerosis and injury-induced neointimal hyperplasia. However, its functional roles in VSMCs and endothelial cells remain controversial and elusive. This study was undertaken to clarify the role of clusterin in neointimal hyperplasia and elucidate its mechanism of action. Adenovirus-mediated overexpression of clusterin (Ad-Clu) repressed TNF-alpha-stimulated expression of MCP-1, fractalkine, ICAM-1, VCAM-1, and MMP-9, leading to inhibition of VSMC migration. Both Ad-Clu and secreted clusterin suppressed VSMC proliferation by inhibiting DNA synthesis, but not by inducing apoptosis. Ad-Clu upregulated p53 and p21(cip1/waf1) but downregulated cyclins D and E, leading to suppression of pRb phosphorylation and subsequent induction of G1 arrest in VSMCs. Clusterin deficiency augmented VSMC proliferation in vitro and accelerated neointimal hyperplasia in vivo, but concomitantly impaired reendothelialization in wire-injured murine femoral arteries. Moreover, Ad-Clu significantly reduced neointimal thickening in balloon-injured rat carotid arteries. Clusterin also diminished TNF-alpha-induced apoptosis of human umbilical vein endothelial cells and restored endothelial nitric oxide synthase expression suppressed by TNF-alpha. These results suggest that upregulation of clusterin during vascular injury may be a protective response against, rather than a causative response to, the development of neointimal hyperplasia. (Keyword) Animals / Cell Movement / Cell Proliferation / Clusterin / Cytoprotection / DNA / Endothelial Cells / G1 Phase / Hyperplasia / Male / Matrix Metalloproteinase 9 / Mice / Mice, Inbred C57BL / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / NF-kappa B / Phosphorylation / Rats / Rats, Sprague-Dawley / Retinoblastoma Protein / Tunica Intima (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.109.190058 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19696405 ● Search Scopus @ Elsevier (PMID): 19696405 ● Search Scopus @ Elsevier (DOI): 10.1161/ATVBAHA.109.190058 (DOI: 10.1161/ATVBAHA.109.190058, PubMed: 19696405)
433.	Po-Hsun Huang, Yung-Hsiang Chen, Chao-Hung Wang, Jia-Shiong Chen, Hsiao-Ya Tsai, Feng-Yen Lin, Wei-Yuh Lo, Tao-Cheng Wu, Masataka Sata, Jaw-Wen Chen and Shing-Jong Lin : Matrix Metalloproteinase-9 Is Essential for Ischemia-Induced Neovascularization by Modulating Bone Marrow-Derived Endothelial Progenitor Cells., Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.29, No.8, 1179-1184, 2009. (Summary) Both matrix metalloproteinases (MMPs) and endothelial progenitor cells (EPCs) have been implicated in the process of neovascularization. Here we show that the impaired neovascularization in mice lacking MMP-9 is related to a defect in EPC functions in vasculogenesis. Hindlimb ischemia surgery was conducted in MMP-9(-/-) mice and wild-type (MMP-9(+/+)) mice. Blood flow recovery was markedly impaired in MMP-9(-/-) mice when compared with that in wild-type mice as determined by laser Doppler imaging. Flow cytometry demonstrated that the number of EPC-like cells (Sca-1(+)/Flk-1(+)) in peripheral blood increased in wild-type mice after hindlimb ischemia surgery and exogenous vascular endothelial growth factor stimulation, but not in MMP-9(-/-) mice. Plasma levels and bone marrow concentrations of soluble Kit-ligand (sKitL) were significantly elevated in wild-type mice in response to tissue ischemia, but not in MMP-9(-/-) mice. C-kit positive bone marrow cells of MMP-9(-/-) mice have attenuated adhesion and migration than those isolated from wild-type mice. In in vitro studies, incubation with selective MMP-9 inhibitor suppressed the colony formation, migration, and tube formation capacities of EPC. Transplantation of bone marrow cells from wild-type mice restored collateral flow formation in MMP-9(-/-) mice. These findings suggest that MMP-9 deficiency impairs ischemia-induced neovascularization, and these effects may occur through a reduction in releasing the stem cell-active cytokine, and EPC mobilization, migration, and vasculogenesis functions. (Keyword) Animals / Aorta / Bone Marrow Cells / Cell Movement / Disease Models, Animal / Endothelial Cells / Flow Cytometry / Hindlimb / Humans / Ischemia / Matrix Metalloproteinase 9 / Mice / Neovascularization, Pathologic / Stem Cells (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.109.189175 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19461050 ● Search Scopus @ Elsevier (PMID): 19461050 ● Search Scopus @ Elsevier (DOI): 10.1161/ATVBAHA.109.189175 (DOI: 10.1161/ATVBAHA.109.189175, PubMed: 19461050)
434.	T Tokudome, I Kishimoto, K Yamahara, T Osaki, N Minamino, T Horio, K Sawai, Y Kawano, M Miyazato, Masataka Sata, M Kohno, K Nakao and K Kangawa : Impaired Recovery of Blood Flow Following Hind-Limb Ischemia in Mice Lacking Guanylyl Cyclase-A, a Receptor for Atrial and Brain Natriuretic Peptides., Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.29, No.10, 1516-1521, 2009. (Summary) Atrial and brain natriuretic peptides (ANP and BNP, respectively) function via guanylyl cyclase (GC)-A, resulting in diuresis, natriuresis, and blood vessel dilation. Here, we investigated the role of endogenous ANP/BNP-GC-A signaling on reparative vascular remodeling using a hind-limb ischemia model. In GC-A-deficient mice (GC-A-KO), hind-limb ischemia resulted in autoamputation or severe ulcers in 60% of mice (6/10) during the 28-day observation period. In wild-type (WT) mice, partial amputation or mild ulcers were detected in only 20% of mice (2/10). Laser Doppler perfusion imaging revealed that the recovery of blood flow in the ischemic limb was significantly inhibited in GC-A-KO mice compared with WT mice. Immunostainings with anti-PECAM-1 antibody demonstrated that, in GC-A-KO, the capillary density of the ischemic tissue was significantly diminished compared to WT. Furthermore, bone marrow transplantation showed the predominant role of GC-A on local ischemic tissue rather than on vascular progenitor cells mobilized from bone marrow during vascular remodeling. In cultured human endothelial cells, ANP treatment significantly stimulated mRNA expressions of vascular endothelial growth factor and endothelial nitric oxide synthase via Erk1/2-dependent mechanism. These results suggest that endogenous ANP and BNP play important roles in reparative vascular remodeling in ischemic tissue. (Keyword) Animals / Atrial Natriuretic Factor / Blood Vessels / Cell Adhesion Molecules / Cells, Cultured / Extracellular Signal-Regulated MAP Kinases / Hindlimb / Humans / Ischemia / Male / Mice / Microfilament Proteins / Natriuretic Peptide, Brain / Nitric Oxide Synthase Type III / Phosphoproteins / RNA, Messenger / Receptors, Atrial Natriuretic Factor / Regeneration / Regional Blood Flow / Vascular Endothelial Growth Factor A (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.109.187526 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19628785 ● Search Scopus @ Elsevier (PMID): 19628785 ● Search Scopus @ Elsevier (DOI): 10.1161/ATVBAHA.109.187526 (DOI: 10.1161/ATVBAHA.109.187526, PubMed: 19628785)
435.	H Iwata, K Nakamura, M Sumi, M Ninomiya, Y Sakai, Y Hirata, Masashi Akaike, T Igarasi, S Takamoto, R Nagai and Masataka Sata : Local delivery of synthetic prostacycline agonist augments collateral growth and improves cardiac function in a swine chronic cardiac ischemia model., Life Sciences, Vol.85, No.5-6, 255-261, 2009. (Summary) It was reported that administration of angiogenic growth factors can augment collateral growth in ischemic tissues. It is assumed that angiogenic effects of cell transplantation may be mainly mediated by secretion of angiogenic cytokines. We tested feasibility of clinical use of ONO-1301, a synthetic small molecule that stimulates secretion of growth factors from various cell types, to treat patients with chronic myocardial ischemia. Effects of ONO-1301 on fibroblasts and endothelial cells were evaluated in vitro. We examined the efficacy of local delivery of ONO-1301 in models of rat hindlimb ischemia and swine chronic ischemic myocardium. ONO-1301 stimulated hepatocyte growth factor secretion from human fibroblasts. ONO-1301 promoted vascular-like tube formation by endothelial cells in vitro. Direct injection of a slow-release form of ONO-1301 (SR-ONO) to rat hindlimb ischemic muscle enhanced perfusion recovery. In a swine cardiac ischemia model, direct injection of SR-ONO into the ischemic myocardium significantly augmented collateral formation (SR-ONO vs. control; 1.7+/-0.2 vs. 1.0+/-0.2 Rentrop score), with improved local ventricular wall motion, reduced enlargement of left ventricular diastolic volume (49.5+/-1.9 mL vs. 59.7+/-4.2 mL) and increased cardiac index (4.2+/-0.1 vs. 3.4+/-0.2 L/min/m(2)). Histological analysis revealed that SR-ONO suppressed fibrosis in ischemic tissue (collagen volume fraction; 7.5+/-1.1% vs. 12.8+/-2.2%) and enhanced neovascularization (capillary density, 275.6 vs. 159.3/mm(2); arterioles 36.6 vs. 25.5 /mm(2)). Local delivery of SR-ONO might be effective for therapeutic angiogenesis and propose that local administration of slow-release of synthetic small molecules represents new strategy for therapeutic angiogenesis. (Keyword) Animals / Cells, Cultured / Collateral Circulation / Delayed-Action Preparations / Disease Models, Animal / Endothelium, Vascular / Fibroblasts / Hepatocyte Growth Factor / Hindlimb / Laser-Doppler Flowmetry / Male / Microcirculation / Myocardial Ischemia / Neovascularization, Pathologic / Prostaglandins I / Pyridines / Rats / Rats, Sprague-Dawley / Swine (Link to Publication Site) ● Publication site (DOI): 10.1016/j.lfs.2009.06.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19527738 ● Search Scopus @ Elsevier (PMID): 19527738 ● Search Scopus @ Elsevier (DOI): 10.1016/j.lfs.2009.06.002 (DOI: 10.1016/j.lfs.2009.06.002, PubMed: 19527738)
436.	Daiju Fukuda, Soichiro Enomoto, Ibuki Shirakawa, Ryozo Nagai and Masataka Sata : Fluvastatin accelerates re-endothelialization impaired by local sirolimus treatment., European Journal of Pharmacology, Vol.612, No.1-3, 87-92, 2009. (Summary) Sirolimus-eluting stent reduces restenosis after percutaneous coronary intervention. However, accumulating evidence suggests that sirolimus potentially affects re-endothelialization, leading to late thrombosis. Statins have protective effects on endothelium. Recently, statins are reported to increase the number of circulating endothelial progenitor cells (EPCs) and accelerate re-endothelialization after vascular injury. Here, we tested the hypothesis that fluvastatin has beneficial effect on re-endothelialization after local sirolimus treatment. We performed wire-mediated vascular injury to both sides of femoral arteries of wild-type mice and bone marrow chimeric mice. Either sirolimus (100 microg) or DMSO was administered locally to the perivascular area of the injured arteries. All mice received either fluvastatin (5 mg/kg/day) or vehicle by gavage starting at one week before the surgery until sacrifice. At 4 weeks after the surgery, re-endothelialization of the sirolimus-treated artery was significantly less than that of DMSO-treated one in the vehicle-treated mice as determined by the percentage of CD31-positive area (P<0.05). Systemic administration of fluvastatin accelerated the re-endothelialization in the sirolimus-treated artery to the similar degree of that in the DMSO-treated artery (P=NS). Contribution of bone marrow-derived cells to re-endothelialization was seldom observed in bone marrow chimeric mice regardless of fluvastatin administration. Fluvastatin significantly ameliorated proliferation (2.5-folds) and migration activities (2.3-folds) of mature endothelial cells impaired by sirolimus treatment (P<0.05, respectively). Fluvastatin increased endothelial nitric oxide synthase expression and decreased plasminogen activator inhibitor-1 expression in mature endothelial cell in the presence of sirolimus (P<0.05, respectively). Our findings suggest that fluvastatin has protective effects against impaired re-endothelialization after sirolimus treatment. (Keyword) Animals / Antigens, CD31 / Bone Marrow Transplantation / Cells, Cultured / Endothelium, Vascular / Fatty Acids, Monounsaturated / Female / Femoral Artery / Fluorescein-5-isothiocyanate / Fluorescent Dyes / Humans / Immunohistochemistry / Immunosuppressive Agents / Indoles / Male / Mice / Mice, Inbred C57BL / Mice, Transgenic / Random Allocation / Sirolimus / Time Factors / Tunica Intima / Tunica Media (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2009.04.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19371739 ● Search Scopus @ Elsevier (PMID): 19371739 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2009.04.006 (DOI: 10.1016/j.ejphar.2009.04.006, PubMed: 19371739)
437.	Kazuyuki Hanajiri, Hiroshi Mitsui, Toshiyuki Maruyama, Naoaki Hashimoto, Masataka Sata and Masao Omata : Echographic detection of diethylnitrosamine-induced liver tumors in rats and the effect of the intratumoral injection of an inhibitor of c-Jun N-terminal kinase., Journal of Gastroenterology and Hepatology, Vol.24, No.5, 866-871, 2009. (Summary) There have so far been few reports describing echographic studies of chemically-induced carcinogenesis in rodent livers. Using echography, we observed diethylnitrosamine-induced liver tumors in rats and examined the effect of an intratumoral injection of an inhibitor of c-Jun N-terminal kinase. Male Wistar rats were given 100 ppm of diethylnitrosamine for 6 weeks and their liver nodules were examined by echography weekly. The size of the nodules was measured and they were examined histologically. The effect of SP600125, an inhibitor of c-Jun N-terminal kinase, on the growth of rat hepatoma cell line McA-RH7777 was tested in vitro. Thereafter, SP600125 was injected into the liver nodules under echographic guidance in vivo and the changes in the proliferating cell nuclear antigen expression and size of the nodules were examined. The four distinct lobes of rat livers were clearly observed by transabdominal echography. The nodules in the livers were first detected 6 weeks after the treatment began, when they were as small as 1.6 mm in diameter. The nodules thereafter became more malignant histologically as they grew larger than 4 mm. SP600125 decreased the expression of proliferating cell nuclear antigen and the growth of McA-RH7777 cells. After SP600125 was injected in vivo, the proliferating cell nuclear antigen level and the growth rate of the rat liver nodules all significantly decreased. Our results indicate that echography is quite useful for follow-up studies of liver carcinogenesis in rats, and c-Jun N-terminal kinase might be another therapeutic target in liver neoplasms. (Keyword) Animals / Anthracenes / Antineoplastic Agents / Cell Line, Tumor / Cell Proliferation / Diethylnitrosamine / Dose-Response Relationship, Drug / Injections, Intralesional / JNK Mitogen-Activated Protein Kinases / Liver / Liver Neoplasms / Male / Proliferating Cell Nuclear Antigen / Protein Kinase Inhibitors / Rats / Rats, Wistar / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1440-1746.2008.05722.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19220657 ● Search Scopus @ Elsevier (PMID): 19220657 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1440-1746.2008.05722.x (DOI: 10.1111/j.1440-1746.2008.05722.x, PubMed: 19220657)
438.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Hirotsugu Kurobe, Nobuyuki Takamori, Yasumasa Ikeda, Yuka Sumitomo, Sumiko Yoshida, Shusuke Yagi, Takashi Iwase, Kazue Ishikawa, Masataka Sata, Tetsuya Kitagawa and Toshio Matsumoto : Heparin cofactor II is an independent protective factor against peripheral arterial disease in elderly subjects with cardiovascular risk factors., Journal of Atherosclerosis and Thrombosis, Vol.16, No.2, 127-134, 2009. (Summary) AIM: Heparin cofactor II (HCII) specifically inactivates thrombin action at the injured vascular wall. We have reported that HCII is a protective factor against coronary in-stent restenosis and carotid atherosclerosis; however, it is unclear whether there is any correlation between plasma HCII levels and the development of peripheral arterial disease (PAD). METHODS: Plasma HCII activity and the ankle brachial pressure index (ABI) were determined in 494 elderly subjects with cardiovascular risk factors. PAD was diagnosed by ABI below 0.9, and 62 subjects were diagnosed with PAD. The relationship between factors that affect cardiovascular events and the prevalence of PAD was statistically evaluated. RESULTS: Mean HCII activity in PAD subjects was significantly lower than in non-PAD subjects (87.5+/-19.7% v.s. 94.6+/-17.8%, p=0.009). Multivariate logistic regression analysis showed that age (odds ratio [OR]: 1.062, p=0.0016), current smoking (OR 3.028, p=0.002) and diabetes mellitus (OR 2.656, p=0.008) were independent and progressive determinants of PAD. In contrast, HCII was an independent inhibitory factor of PAD (OR: 0.982, p=0.048). CONCLUSIONS: Plasma HCII activity is inversely related to the prevalence of PAD. HCII may function as the sole protective factor against PAD in elderly people with cardiovascular risk factors. (Keyword) Aged / Aged, 80 and over / Cardiovascular Diseases / Female / Heparin Cofactor II / Humans / Male / Middle Aged / Peripheral Vascular Diseases / Prevalence / Protective Agents / Risk Factors (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.E695 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19403987 ● Search Scopus @ Elsevier (PMID): 19403987 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.E695 (DOI: 10.5551/jat.E695, PubMed: 19403987)
439.	D Fukuda, S Enomoto, R Nagai and Masataka Sata : Inhibition of renin-angiotensin system attenuates periadventitial inflammation and reduces atherosclerotic lesion formation., Biomedicine & Pharmacotherapy, Vol.63, No.10, 754-761, 2009. (Summary) Recent evidence indicates that renin-angiotensin system (RAS) plays an important role in the pathogenesis of atherosclerosis. It was reported that inhibition of RAS with angiotensin II type 1 receptor blockers (ARBs) or angiotensin converting enzyme inhibitors (ACEIs) is effective in prevention of atherosclerosis. Here, we investigated the effects of an ARB or/and an ACEI on atherosclerosis development and periadventitial inflammation in apolipoprotein E (ApoE)-deficient mice. RT-PCR revealed that major RAS components were expressed in periaortic tissue. Ang II infusion significantly increased accumulation of bone marrow derived cells into both neointima (p<0.05) and periaortic tissue (p<0.01). Male ApoE- deficient mice were treated with either vehicle, TA606A (10mg/kg/day, ARB), imidapril (3mg/kg/day, ACEI) or TA606A plus imidapril (TA606A 10mg/kg/day+imidapril 3mg/kg/day, ARB+ACEI) for 24 weeks starting at 12 weeks of age. ARB, ACEI, and ARB+ACEI significantly reduced atherosclerotic lesion formation in aorta compared with vehicle (p<0.05), with reduced expression of monocyte chemoattractant protein-1 in periaortic tissues (p<0.01). Neither blood pressure nor heart rate was changed by the treatments at these lower doses. Imidapril significantly reduced lipid deposition in atheroma and plasminogen activator inhibitor-1 expression in periadventitial tissue (p<0.05, respectively). Imidapril and combination therapy significantly attenuated macrophage infiltration into the atherosclerotic plaque (p<0.05, respectively). All treatments reduced macrophage accumulation in the periadventitial tissue 12 weeks after treatment (p<0.05, respectively). These results suggest that inhibition of renin-angiotensin system attenuates periadventitial inflammation and reduces atherosclerotic lesion formation. (Keyword) Angiotensin II Type 1 Receptor Blockers / Angiotensin-Converting Enzyme Inhibitors / Animals / Aorta / Apolipoproteins E / Atherosclerosis / Chemokine CCL2 / Connective Tissue / Gene Expression Regulation / Imidazoles / Imidazolidines / Inflammation / Male / Mice / Mice, Knockout / Pyridines / Renin-Angiotensin System / Tetrazoles (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biopha.2009.02.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19304450 ● Search Scopus @ Elsevier (PMID): 19304450 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biopha.2009.02.006 (DOI: 10.1016/j.biopha.2009.02.006, PubMed: 19304450)
440.	D Nagata, A Kiyosue, M Takahashi, H Satonaka, K Tanaka, Masataka Sata, T Nagano, R Nagai and Y Hirata : A new constitutively active mutant of AMP-activated protein kinase inhibits anoxia-induced apoptosis of vascular endothelial cell., Hypertension Research, Vol.32, No.2, 133-139, 2009. (Summary) The inhibition of apoptotic changes in vascular endothelial cells is important for preventing vascular damage from hypoxia. AMP-activated protein kinase (AMPK) has recently been identified as playing a role in vascular protection. Although the chemical reagent 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) has been used to stimulate AMPK activity, AICAR has been associated with several nonspecific reactions. We therefore constructed a new constitutively active mutant of AMPK alpha 1 (NcaAMPK), which lacks the autoinhibitory domain in AMPK alpha 1 and in which threonine 172 has been replaced with aspartate. We investigated whether NcaAMPK has an anti-apoptotic effect in vascular endothelial cells under anoxic conditions. NcaAMPK, or green fluorescent protein (GFP) as a control, was overexpressed in human umbilical vein endothelial cells (HUVECs). After HUVECs were incubated for 40 h under normoxic or anoxic conditions, we examined cell viability, caspase 3/7 activity, and expression and phosphorylation levels of apoptosis-related proteins. Cell viabilities under anoxic conditions were improved in NcaAMPK-overexpressing cells. Anoxia increased caspase 3/7 activity, but NcaAMPK reduced this increase significantly. NcaAMPK overexpression increased protein kinase B/Akt Ser473 and endothelial nitric oxide synthase Ser1177 phosphorylation, but pretreatment with the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) did not decrease the viability of NcaAMPK-overexpressing HUVECs. Furthermore, co-expression of a dominant-negative Akt reduced the improvement in cell viability and the suppression of poly (ADP-ribose) polymerase cleavage by NcaAMPK under anoxic conditions. In conclusion, NcaAMPK inhibited anoxia-induced apoptosis in vascular endothelial cells through Akt activation, suggesting that activation of AMPK might protect against ischemic vascular injury. (Keyword) Adenoviridae / Aminoimidazole Carboxamide / Anoxia / Apoptosis / Blotting, Western / Caspase 3 / Caspase 7 / Cell Death / Cross-Linking Reagents / Cyclic AMP-Dependent Protein Kinases / DNA Primers / Endothelial Cells / Endothelium, Vascular / Enzyme Inhibitors / Genetic Vectors / Humans / Mutation / NG-Nitroarginine Methyl Ester / Nitric Oxide Synthase Type III / Oncogene Protein v-akt / Poly(ADP-ribose) Polymerases / Proto-Oncogene Proteins c-bcl-2 / Ribonucleotides / Tetrazolium Salts (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2008.25 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19262472 ● Search Scopus @ Elsevier (PMID): 19262472 ● Search Scopus @ Elsevier (DOI): 10.1038/hr.2008.25 (DOI: 10.1038/hr.2008.25, PubMed: 19262472)
441.	Y Ono, Yutaka Nakaya, S Bando, Takeshi Soeki, Susumu Ito and Masataka Sata : Telmisartan Decreases Plasma Levels of Asymmetrical Dimethyl-L-Arginine and Improves Lipid and Glucose Metabolism and Vascular Function, International Heart Journal, Vol.50, No.1, 73-83, 2009. (Summary) Telmisartan is an angiotensin II receptor blocker (ARB) and also an activator of peroxisome proliferator-activated receptor-gamma (PPAR-gamma). We investigated whether telmisartan improves vascular endothelial function in patients with essential hypertension with the production of endothelial nitric oxide synthase (eNOS) through PPAR-gamma.Telmisartan was administered to 15 patients with essential hypertension. To assess vascular function, asymmetric dimethylarginine (ADMA), an eNOS inhibitor synthesized by endothelial cells, and the pulse-wave velocity (PWV) were measured. The serum levels of lipid, glucose, and glycohemoglobin (HbA1c) were also evaluated before and after treatment. Telmisartan therapy significantly decreased the blood pressure and total- and LDL-cholesterol levels. HbA1c was also significantly improved but not in fasting plasma glucose. The serum levels of ADMA were significantly decreased (0.48 +/- 0.08 to 0.42 +/- 0.05 nmol/mL; P = 0.01). PWV values were significantly decreased by telmisartan from 1,822.5 +/- 352.3 to 1,661.5 +/- 299.8 cm/second (P = 0.04*). Telmisartan decreased PWV presumably via the activation of PPAR-gamma, suggesting that this agent improves vascular endothelial function via its pleiotropic effects, a mechanism that is different from its hypotensive effects. (Keyword) Administration, Oral / Aged / Angiotensin II Type 1 Receptor Blockers / Arginine / Benzimidazoles / Benzoates / Blood Glucose / Blood Pressure / Cholesterol, LDL / Dose-Response Relationship, Drug / Endothelium, Vascular / Female / Humans / Hypertension / Male / Nitric Oxide Synthase Type III / PPAR gamma / Treatment Outcome (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.50.73 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19246848 ● Search Scopus @ Elsevier (PMID): 19246848 ● Search Scopus @ Elsevier (DOI): 10.1536/ihj.50.73 (DOI: 10.1536/ihj.50.73, PubMed: 19246848)
442.	Kentaro Meguro, Haruko Iida, Haruhito Takano, Toshihiro Morita, Masataka Sata, Ryozo Nagai and Toshiaki Nakajima : Function and Role of Voltage-Gated Sodium Channel (NaV1.7) Expressed in Aortic Smooth Muscle Cells., American Journal of Physiology, Heart and Circulatory Physiology, Vol.296, No.1, H211-219, 2009. (Summary) Voltage-gated Na(+) channel currents (I(Na)) are expressed in several types of smooth muscle cells. The purpose of this study was to evaluate the expression of I(Na), its functional role, pathophysiology in cultured human (hASMCs) and rabbit aortic smooth muscle cells (rASMCs), and its association with vascular intimal hyperplasia. In whole cell voltage clamp, I(Na) was observed at potential positive to -40 mV, was blocked by tetrodotoxin (TTX), and replacing extracellular Na(+) with N-methyl-d-glucamine in cultured hASMCs. In contrast to native aorta, cultured hASMCs strongly expressed SCN9A encoding Na(V)1.7, as determined by quantitative RT-PCR. I(Na) was abolished by the treatment with SCN9A small-interfering (si)RNA (P < 0.01). TTX and SCN9A siRNA significantly inhibited cell migration (P < 0.01, respectively) and horseradish peroxidase uptake (P < 0.01, respectively). TTX also significantly reduced the secretion of matrix metalloproteinase-2 6 and 12 h after the treatment (P < 0.01 and P < 0.05, respectively). However, neither TTX nor siRNA had any effect on cell proliferation. L-type Ca(2+) channel current was recorded, and I(Na) was not observed in freshly isolated rASMCs, whereas TTX-sensitive I(Na) was recorded in cultured rASMCs. Quantitative RT-PCR and immunostaining for Na(V)1.7 revealed the prominent expression of SCN9A in cultured rASMCs and aorta 48 h after balloon injury but not in native aorta. In conclusion, these studies show that I(Na) is expressed in cultured and diseased conditions but not in normal aorta. The Na(V)1.7 plays an important role in cell migration, endocytosis, and secretion. Na(V)1.7 is also expressed in aorta after balloon injury, suggesting a potential role for Na(V)1.7 in the progression of intimal hyperplasia. (Keyword) Animals / Aorta, Thoracic / Balloon Dilation / Cell Movement / Endocytosis / Humans / immunohistochemistry / Male / Matrix Metalloproteinase 8 / Myocytes, Smooth Muscle / RNA / Rabbits / Rats / Reverse Transcriptase Polymerase Chain Reaction / Sodium Channel Blockers / Sodium Channels / Tetrodotoxin (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpheart.00960.2008 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18978189 ● Search Scopus @ Elsevier (PMID): 18978189 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpheart.00960.2008 (DOI: 10.1152/ajpheart.00960.2008, PubMed: 18978189)
443.	S Enomoto, Masataka Sata, D Fukuda, K Nakamura and R Nagai : Rosuvastatin prevents endothelial cell death and reduces atherosclerotic lesion formation in ApoE-deficient mice., Biomedicine & Pharmacotherapy, Vol.63, No.1, 19-26, 2009. (Summary) Accumulating evidence suggests that statins have beneficial effects which are independent of their lipid-lowering actions, on vascular cells. Here, we investigated whether the HMG-CoA reductase inhibitor rosuvastatin can inhibit atherosclerotic lesion development with favorable effects on endothelial cells in ApoE-deficient mice. Rosuvastatin rapidly phosphorylated Akt and endothelial nitric oxide synthase (eNOS) in human endothelial cells. Endothelial cell death induced by serum starvation was significantly inhibited by rosuvastatin (percent cell death; 45.9+/-2.4% vs. 37.3+/-1.1%, p<0.05). Eight-week-old ApoE-deficient mice were orally administered vehicle or rosuvastatin at a dose of 20mg/kg/day for 24 weeks. There was no significant difference in cholesterol profile. Rosuvastatin preserved endothelial lining at the aortic root (CD31-positive luminal side; 63.8+/-2.8% vs. 81.7+/-3.9%, p<0.05). En face Sudan IV staining of aorta revealed that rosuvastatin significantly decreased the atherosclerotic area (21.9+/-2.9% vs. 11.9+/-1.9%, p<0.05). Lipid deposition at the atherosclerotic area was also suppressed by rosuvastatin with more stabilized morphologic features as determined by oil red O staining (3.4+/-0.4% vs. 1.7+/-0.4%, p<0.05). Our findings indicate that rosuvastatin protects endothelial cells from death with phosphorylation of Akt and eNOS. These effects may contribute, at least in part, to the anti-atherosclerotic effects of rosuvastatin. (Keyword) Animals / Apolipoproteins E / Atherosclerosis / Cell Death / Cells, Cultured / Endothelial Cells / Female / Fluorobenzenes / Gene Expression Regulation / Humans / Hydroxymethylglutaryl-CoA Reductase Inhibitors / Mice / Mice, Knockout / Nitric Oxide Synthase Type III / Proto-Oncogene Proteins c-akt / Pyrimidines / Sulfonamides (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biopha.2007.11.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18162361 ● Search Scopus @ Elsevier (PMID): 18162361 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biopha.2007.11.002 (DOI: 10.1016/j.biopha.2007.11.002, PubMed: 18162361)
444.	T Inoue, H Matsuoka, Y Higashi, S Ueda, Masataka Sata, K Shimada, Y Ishibashi and K Node : Flow-Mediated Vasodilation as a Diagnostic Modality for Vascular Failure., Hypertension Research, Vol.31, No.12, 2105-2113, 2008. (Summary) Vascular endothelial dysfunction represents an initial step of "vascular failure," which we have recently proposed as a comprehensive syndrome of failed vascular functions that extends from risk factors to established atherosclerotic disease. The early detection of vascular failure is essential in order to appropriately intervene and prevent its progression. Many efforts have been made to assess vascular endothelial function, and one of the most promising methods is the measurement of endothelium-dependent flow-mediated vasodilation (FMD) using high-frequency ultrasonographic imaging and transient occlusion of the brachial artery. The reactive hyperemia caused by the transient brachial arterial occlusion induces the release of local nitric oxide, resulting in vasodilation that can be quantified as an index of vasomotor function. The noninvasive nature of this technique allows repeated measurements over time to study the effectiveness of various interventions that may affect vascular health. Although there are technical and interpretive limitations of this technique, FMD-guided therapeutic approaches for vascular failure should contribute to the improvement of cardiovascular mortality and morbidity. (Keyword) Atherosclerosis / Biological Markers / Brachial Artery / Endothelium, Vascular / Humans / Nitric Oxide / Regional Blood Flow / Vasodilation (Link to Publication Site) ● Publication site (DOI): 10.1291/hypres.31.2105 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19139600 ● Search Scopus @ Elsevier (PMID): 19139600 ● Search Scopus @ Elsevier (DOI): 10.1291/hypres.31.2105 (DOI: 10.1291/hypres.31.2105, PubMed: 19139600)
445.	Kenya Kusunose, Hirotsugu Yamada, Takashi Todoroki, Susumu Nishio, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Tetsuya Kitagawa and Masataka Sata : Platypnea-orthodeoxia syndrome associated with patent foramen ovale and aortic ectasia., Echocardiography, Vol.26, No.1, 114-117, 2008. (Summary) A 59-year-old man was admitted for dyspnea on exertion and edema. The patient did not have any pulmonary diseases that could cause dyspnea. Transesophageal echocardiography on the tilting bed with contrast infusion revealed a right-to-left shunt through the patent foramen ovale. Therefore, he was diagosed as platypnea-orthodeoxia syndrome due to the patent foramen ovale. Surgical closure was done and all of his symptoms had improved. (Keyword) Aortic Diseases / Dyspnea / transesophageal echocardiography / Edema, Cardiac / Foramen Ovale, Patent / Humans / Male / Middle Aged / syndrome / Treatment Outcome (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1540-8175.2008.00780.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19017323 ● Search Scopus @ Elsevier (PMID): 19017323 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1540-8175.2008.00780.x (DOI: 10.1111/j.1540-8175.2008.00780.x, PubMed: 19017323)
446.	K Nakamura, N Koibuchi, H Nishimatsu, Y Higashikuni, Y Hirata, K Kugiyama, R Nagai and Masataka Sata : Candesartan ameliorates cardiac dysfunction observed in ACE2-deficient mice., Hypertension Research, Vol.31, No.10, 1953-1961, 2008. (Summary) The renin-angiotensin (Ang) system plays a critical role in the regulation of blood pressure, body fluid, electrolyte homeostasis, and organ remodeling under physiological and pathological conditions. The carboxypeptidase ACE2 is a homologue of angiotensin-converting enzyme (ACE). It has been reported that ACE2-deficient mice develop cardiac dysfunction with increased plasma levels of Ang II. However, the molecular mechanism by which genetic disruption of ACE2 results in heart dysfunction is not fully understood. Here, we generated mice with targeted disruption of the Ace2 gene and compared the cardiovascular function of ACE2(-/y) mice with that of their wild-type littermates. ACE2-deficient mice were viable and fertile and lacked any gross structural abnormalities. Echocardiographic study detected no functional difference between ACE2(-/y) and wild-type mice at 12 weeks of age. Twenty-four-week-old ACE2(-/y) mice displayed significantly enlarged hearts with impaired systolic and diastolic function. The Ang II level was elevated in the plasma and heart of ACE2(-/y) mice. Pharmacological blockade of Ang II type 1 receptor (AT1) with candesartan attenuated the development of cardiac dysfunction in ACE2(-/y) mice. These results suggest that enhanced stimulation of AT1 may play a role in the development of cardiac dysfunction observed in ACE2-deficient mice. (Keyword) Age Factors / Angiotensin II / Angiotensin II Type 1 Receptor Blockers / Animals / Benzimidazoles / Cardiomegaly / Disease Models, Animal / Echocardiography / Female / Hypertension / Male / Mice / Mice, Inbred C57BL / Mice, Mutant Strains / Myocardium / Peptidyl-Dipeptidase A / Proto-Oncogene Proteins / Receptor, Angiotensin, Type 1 / Receptors, G-Protein-Coupled / Tetrazoles (Link to Publication Site) ● Publication site (DOI): 10.1291/hypres.31.1953 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19015603 ● Search Scopus @ Elsevier (PMID): 19015603 ● Search Scopus @ Elsevier (DOI): 10.1291/hypres.31.1953 (DOI: 10.1291/hypres.31.1953, PubMed: 19015603)
447.	JR Kim-Kaneyama, N Wachi, Masataka Sata, S Enomoto, K Fukabori, K Koh, M Shibanuma and K Nose : Hic-5, an adaptor protein expressed in vascular smooth muscle cells, modulates the arterial response to injury in vivo., Biochemical and Biophysical Research Communications, Vol.376, No.4, 682-687, 2008. (Summary) Focal adhesion components are targets for biochemical and mechanical stimuli that evoke crucial injury. Hic-5 (hydrogen peroxide-inducible clone 5) is a multidomain adaptor protein which is implicated in the regulation of integrin signaling in focal adhesion. The aim of this research was to test the hypothesis that Hic-5, a focal adhesion LIM protein expressed in smooth muscle cells, is involved in dynamic processes by pathological stimuli in the vessel wall. Here, we describe the analysis of the function of Hic-5 using a mouse model of vascular injury that may mimic balloon angioplasty. At 4 days after vascular injury, marked down-regulation of the Hic-5 expression was observed in the smooth muscle layer, and local delivery of the Hic-5 using adenovirus vectors repressed injury-induced neointimal expansion. In addition, Hic-5 reduced cells migration into three-dimensional collagen gels, and the forced expression of Hic-5 in cells embedded in the collagen gel matrix repressed the expression of uPA that participates in smooth muscle cell migration. These results suggest that Hic-5 modulates cellular responses to pathological stimuli in the vessel wall. (Keyword) Adenoviridae / Angioplasty, Balloon / Animals / Carotid Artery Injuries / Cell Movement / Cell Proliferation / Collagen / Cytoskeletal Proteins / DNA-Binding Proteins / Disease Models, Animal / Focal Adhesions / Gels / Humans / Hyperplasia / LIM Domain Proteins / Mice / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Rats / Transduction, Genetic / Tunica Intima / Urokinase-Type Plasminogen Activator (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2008.09.051 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18812162 ● Search Scopus @ Elsevier (PMID): 18812162 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2008.09.051 (DOI: 10.1016/j.bbrc.2008.09.051, PubMed: 18812162)
448.	K Wakayama, M Shimamura, Masataka Sata, N Koibuchi, N Sato, T Ogihara and R Morishita : A model of cerebrovascular injury in rats., Journal of Neuroscience Methods, Vol.175, No.2, 187-195, 2008. (Summary) Although the pathophysiology of post-angioplasty restenosis has been extensively studied in extracranial arteries using transluminal vascular injury model in rodents, it is still not well known in the intracranial arteries, which have quite different structures from extracranial arteries. Here, we examined whether 1-min placement of modified intraluminal suture could induce an injury in the internal carotid artery (ICA) in rats and observed temporal profile of histological change after the injury. HE staining showed that the injured intracranial ICA was dilated, while the media was markedly thinned at 1 day after injury. The internal elastic lamina was not observed, and the media contained few cells. At 1 week after injury, a thin layer of neointimal hyperplasia was observed on the luminal side of the internal elastic lamina. Neointimal hyperplasia developed until at least 4 weeks after injury. Morphometric analysis demonstrated that the healing process of the injury was related to arterial remodeling. Immunohistochemical staining for alpha-smooth muscle actin and electron microscopic analysis showed that the neointima was composed of smooth muscle cells. Re-endothelialization was observed from 1 to 4 weeks after injury by immunohistochemical staining for von Willebrand's factor and electron microscopic analysis. Vascular endothelial growth factor was expressed in neointima on days 7 and 14. Interestingly, superoxide anion was not increased in injured arteries on day 3, when the infiltration of macrophages was intensive, but increased on day 7, when infiltrating macrophages almost disappeared. These findings might shed new light on pathophysiology of post-angioplasty restenosis in intracranial arteries. (Keyword) Actins / Animals / Antigens, CD / Antigens, Differentiation, Myelomonocytic / Arteries / Basement Membrane / Cerebrovascular Disorders / Disease Models, Animal / Endothelium, Vascular / Gene Expression Regulation / Male / Microscopy, Electron, Transmission / Rats / Rats, Wistar / Time Factors / Vascular Endothelial Growth Factor A / von Willebrand Factor (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jneumeth.2008.08.018 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18786566 ● Search Scopus @ Elsevier (PMID): 18786566 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jneumeth.2008.08.018 (DOI: 10.1016/j.jneumeth.2008.08.018, PubMed: 18786566)
449.	U Yokoyama, S Minamisawa, H Quan, T Akaike, M Jin, K Otsu, C Ulucan, X Wang, E Baljinnyam, M Takaoka, Masataka Sata and Y Ishikawa : Epac1 is upregulated during neointima formation and promotes vascular smooth muscle cell migration., American Journal of Physiology, Heart and Circulatory Physiology, Vol.295, No.4, H1547-1555, 2008. (Summary) Vascular remodeling after mechanoinjury largely depends on the migration of smooth muscle cells, an initial key step to wound healing. However, the role of the second messenger system, in particular, the cAMP signal, in regulating such remodeling remains controversial. Exchange protein activated by cAMP (Epac) has been identified as a new target molecule of the cAMP signal, which is independent from PKA. We thus examined whether Epac plays a distinct role from PKA in vascular remodeling. To examine the role of Epac and PKA in migration, we used primary culture smooth muscle cells from both the fetal and adult rat aorta. A cAMP analog selective to PKA, 8-(4-parachlorophenylthio)-cAMP (pCPT-cAMP), decreased cell migration, whereas an Epac-selective analog, 8-pCPT-2'-O-Me-cAMP, enhanced migration. Adenovirus-mediated gene transfer of PKA decreased cell migration, whereas that of Epac1 significantly enhanced cell migration. Striking morphological differences were observed between pCPT-cAMP- and 8-pCPT-2'-O-Me-cAMP-treated aortic smooth muscle cells. Furthermore, overexpression of Epac1 enhanced the development of neointimal formation in fetal rat aortic tissues in organ culture. When the mouse femoral artery was injured mechanically in vivo, we found that the expression of Epac1 was upregulated in vascular smooth muscle cells, whereas that of PKA was downregulated with the progress of neointimal thickening. Our findings suggest that Epac1, in opposition to PKA, increases vascular smooth muscle cell migration. Epac may thus play an important role in advancing vascular remodeling and restenosis upon vascular injury. (Keyword) Animals / Aorta / Cell Movement / Cell Shape / Cells, Cultured / Cyclic AMP / Cyclic AMP-Dependent Protein Kinases / Disease Models, Animal / Female / Femoral Artery / Gestational Age / Guanine Nucleotide Exchange Factors / Male / Mice / Mice, Inbred ICR / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Pregnancy / Protein Kinase Inhibitors / Rats / Rats, Wistar / Signal Transduction / Thionucleotides / Time Factors / Transduction, Genetic / Tunica Intima / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpheart.01317.2007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18689492 ● Search Scopus @ Elsevier (PMID): 18689492 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpheart.01317.2007 (DOI: 10.1152/ajpheart.01317.2007, PubMed: 18689492)
450.	Y Hirata, A Kiyosue, M Takahashi, H Satonaka, D Nagata, Masataka Sata, E Suzuki and R Nagai : Progression of Renal Dysfunction in Patients with Cardiovascular Disease., Current Cardiology Reviews, Vol.4, No.3, 198-202, 2008. (Summary) It has been established that patients with chronic kidney disease (CKD) suffer from frequent cardiovascular events. On the other hand, recent studies suggest that renal damage tends to worsen in patients with cardiovascular diseases (CVD). Although the mechanisms for the cardiorenal association are unclear, the presence of arteriosclerotic risk factors common to both CVD and CKD is important. In arteriosclerosis, vascular derangement progresses not only in the heart but also in the kidney. In addition, heart failure, cardiac catheterization and hesitation of medical treatments due to renal dysfunction may explain the progression of renal damage. Therefore, the goal of treatments is a total control of arteriosclerotic risk factors. Medication should be selected among agents with protective effects on both heart and kidney. It is important to always consider the presence of CKD for the treatment of the cardiovascular disease and strictly control the risk factors. (Link to Publication Site) ● Publication site (DOI): 10.2174/157340308785160543 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19936196 ● Search Scopus @ Elsevier (PMID): 19936196 ● Search Scopus @ Elsevier (DOI): 10.2174/157340308785160543 (DOI: 10.2174/157340308785160543, PubMed: 19936196)
451.	S Imaizumi, S Miura, K Nakamura, Y Kiya, Y Uehara, B Zhang, Y Matsuo, H Urata, M Ideishi, K.A. Rye, Masataka Sata and K Saku : Antiarrhythmogenic effect of reconstituted high-density lipoprotein against ischemia/reperfusion in rats, Journal of the American College of Cardiology, Vol.51, No.16, 1604-1612, 2008. (Summary) This study analyzed the antiarrhythmogenic effect of reconstituted high-density lipoprotein (rHDL) against ischemia/reperfusion in vivo. Recent studies have suggested that a reduction in the plasma HDL level may contribute to cardiac sudden death. Although there are currently only a few therapeutic strategies for increasing HDL, an exciting new therapeutic option, rHDL, has recently been developed to prevent coronary artery disease. To analyze the suppression of reperfusion arrhythmia by rHDL (apolipoprotein A-I with 1-palmitoyl-2-oleoyl-phosphatidyl-choline), 92 male Wistar rats were divided into 10 groups: rats that had been pre-treated with or without rHDL, apolipoprotein A-I, or 1-palmitoyl-2-oleoyl-phosphatidyl-choline in the presence or absence of inhibitors of Akt protein kinase, nitric oxide (NO), or extracellular-signal-regulated kinase (ERK) administered intravenously before left coronary artery occlusion. We also used human coronary artery endothelial cells and adenosine triphosphate-binding cassette transporter (ABC) A1-, ABCG1-, or scavenger receptor class B, type I-transfected ldlA7 cells systems. The duration of ventricular tachycardia or ventricular fibrillation after reperfusion in rHDL-pre-treated rats was much shorter than that in untreated rats. Apolipoprotein A-I or 1-palmitoyl-2-oleoyl-phosphatidyl-choline alone had no effect. The effect of rHDL was blocked by inhibitors of Akt, NO, and ERK. Plasma NO concentration in the rHDL group was significantly higher. In addition, rHDL activated phospho(p)-Akt, p-ERK, and p-endothelial NO synthesis in endothelial cells. The rHDL activated p-ERK in ABCA1- or ABCG1-transfected but not scavenger receptor class B, type I-transfected ldlA7 cells. The rHDL-induced NO production, probably mediated by ABCA1 or ABCG1 through an Akt/ERK/NO pathway in endothelial cells, may suppress reperfusion-induced arrhythmias. The HDL-based therapy may hold the promise of reducing the incidence of such arrhythmias after ischemia/reperfusion. (Keyword) Animals / Anti-Arrhythmia Agents / Apolipoprotein A-I / Cholesterol, HDL / Endothelium / Extracellular Signal-Regulated MAP Kinases / Male / Myocardial Ischemia / Myocardial Reperfusion / Nitric Oxide / Proto-Oncogene Proteins c-akt / Rats / Rats, Wistar / Signal Transduction / Tachycardia, Ventricular (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jacc.2007.12.040 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18420105 ● Search Scopus @ Elsevier (PMID): 18420105 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jacc.2007.12.040 (DOI: 10.1016/j.jacc.2007.12.040, PubMed: 18420105)
452.	K Kumano, S Masuda, Masataka Sata, T Saito, S.Y. Lee, M Sakata-Yanagimoto, T Tomita, T Iwatsubo, H Natsugari, M Kurokawa, S Ogawa and S Chiba : Both Notch1 and Notch2 contribute to the regulation of melanocyte homeostasis, Pigment Cell & Melanoma Research, Vol.21, No.1, 70-78, 2008. (Summary) Notch signaling affects a variety of mammalian stem cells, but there has been limited evidence that a specific Notch molecule regulates adult stem cells. Recently, it was reported that the reduced Notch signaling initiated at the embryonic stage results in a gradual hair graying phenotype after birth. Here we demonstrate that the oral administration of a gamma-secretase inhibitor (GSI) to wild-type adult C57/Bl6 mice led to a gradual increase in gray spots, which remained unchanged for at least 20 weeks after discontinuing the GSI. In GSI-treated mice, there was a severe decrease in unpigmented melanocytes in the bulge/subbulge region where melanocyte stem cells are located. While we confirmed that Notch1+/-Notch2+/- double heterozygous mice with a C57/Bl6 background were born with a normal hair color phenotype and gradually turned gray after the second hair cycle, in the c-kit mutant Wv background, Notch1+/- and Notch2+/- mice had larger white spots on the first appearance of hair than did the Wv/+ mice, which did not change throughout life. Notch1+/-Notch2+/-Wv/+ mice had white hair virtually all over the body at the first appearance of hair and the depigmentation continued to progress thereafter. Using a neural crest organ culture system, GSI blocked the generation of pigmented melanocytes when added to the culture during the period of melanoblast proliferation, but not during the period of differentiation. These observations imply roles of Notch signaling in both development of melanocyte during embryogenesis and maintenance of melanocyte stem cells in adulthood, while the degree of requirement is distinct in these settings: the latter is more sensitive than the former to the reduced Notch signaling. Furthermore, Notch1 and Notch2 cooperates with c-kit signaling during embryogenesis, and they cooperate with each other to regulate melanocyte homeostasis after birth. (Keyword) Amyloid Precursor Protein Secretases / Animals / Cell Differentiation / Cell Proliferation / Embryo Culture Techniques / Enzyme Inhibitors / Gene Expression Regulation, Developmental / Genotype / Hair Color / Hair Follicle / Homeostasis / Melanocytes / Mice / Mice, Inbred C57BL / Mice, Mutant Strains / Mice, Transgenic / Mutation / Neural Crest / Organ Culture Techniques / Phenotype / Proto-Oncogene Proteins c-kit / Receptor, Notch1 / Receptor, Notch2 / Signal Transduction / Stem Cells / Time Factors / Vibrissae (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1755-148X.2007.00423.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18353145 ● Summary page in Scopus @ Elsevier: 2-s2.0-41049101021 (DOI: 10.1111/j.1755-148X.2007.00423.x, PubMed: 18353145, Elsevier: Scopus)
453.	M Shimazaki, K Nakamura, I Kii, T Kashima, N Amizuka, M Li, K Fukuda, T Nishiyama, S Kitajima, Y Saga, M Fukayama, Masataka Sata and A Kudo : Periostin is essential for cardiac healing after acute myocardial infarction, The Journal of Experimental Medicine, Vol.205, No.2, 295-303, 2008. (Summary) Acute myocardial infarction (AMI) is a common and lethal heart disease, and the recruitment of fibroblastic cells to the infarct region is essential for the cardiac healing process. Although stiffness of the extracellular matrix in the infarct myocardium is associated with cardiac healing, the molecular mechanism of cardiac healing is not fully understood. We show that periostin, which is a matricellular protein, is important for the cardiac healing process after AMI. The expression of periostin protein was abundant in the infarct border of human and mouse hearts with AMI. We generated periostin(-/-) mice and found no morphologically abnormal cardiomyocyte phenotypes; however, after AMI, cardiac healing was impaired in these mice, resulting in cardiac rupture as a consequence of reduced myocardial stiffness caused by a reduced number of alpha smooth muscle actin-positive cells, impaired collagen fibril formation, and decreased phosphorylation of FAK. These phenotypes were rescued by gene transfer of a spliced form of periostin. Moreover, the inhibition of FAK or alphav-integrin, which blocked the periostin-promoted cell migration, revealed that alphav-integrin, FAK, and Akt are involved in periostin signaling. Our novel findings show the effects of periostin on recruitment of activated fibroblasts through FAK-integrin signaling and on their collagen fibril formation specific to healing after AMI. (Keyword) Animals / Cell Adhesion Molecules / Cicatrix / Collagen / Fibroblasts / Focal Adhesion Kinase 1 / Heart Ventricles / Humans / Male / Mice / Mice, Knockout / Myocardial Infarction / RNA, Messenger / Transforming Growth Factor beta / Wound Healing (Link to Publication Site) ● Publication site (DOI): 10.1084/jem.20071297 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18208976 ● Search Scopus @ Elsevier (PMID): 18208976 ● Search Scopus @ Elsevier (DOI): 10.1084/jem.20071297 (DOI: 10.1084/jem.20071297, PubMed: 18208976)
454.	M Matsumoto, Masataka Sata, D Fukuda, K Tanaka, M Soma, Y Hirata and R Nagai : Orally administered eicosapentaenoic acid reduces and stabilizes atherosclerotic lesions in ApoE-deficient mice, Atherosclerosis, Vol.197, No.2, 524-533, 2008. (Summary) Accumulating evidence demonstrates that dietary intake of n-3 polyunsaturated fatty acids (PUFAs) is associated with reduced incidence of cardiovascular events. However, the molecular mechanisms by which n-3 PUFAs prevent atherosclerosis are not fully understood. Here, we examined the effect of eicosapentaenoic acid (EPA), a major n-3 PUFA, on the pathogenesis of atherosclerosis in ApoE-deficient mice. Five-week-old ApoE-deficient male mice were fed on western-type diet supplemented with 5% (w/w) EPA (EPA group, n=7) or not (control group, n=5) for 13 weeks. An analysis of the fatty acid composition of liver homogenates revealed a marked increase of the n-3 PUFA content in the EPA group (n-3/n-6 ratio: 0.20+/-0.01 vs. 2.5+/-0.2, p<0.01). En face Sudan IV staining of the aorta and oil red O-staining of the aortic sinus revealed that EPA significantly suppressed the development of atherosclerotic lesions. We also observed anti-atherosclerotic effects of EPA in LDL-receptor-deficient mice. The lesions of the EPA group contained more collagen (19.6+/-2.4% vs. 32.9+/-3.9%, p<0.05) and smooth muscle cells (1.3+/-0.2% vs. 3.6+/-0.8%, p<0.05) and less macrophages (32.7+/-4.1% vs. 14.7+/-2.0%, p<0.05). Pretreatment with EPA attenuated the up-regulation of VCAM-1, ICAM-1 and MCP-1 in HUVECs as well as the expression of MMP-2 and MMP-9 in macrophage-like cells induced by TNF-alpha. The anti-inflammatory effects of EPA were abrogated when the expression of peroxisome proliferator-activated receptor alpha (PPARalpha) was suppressed. EPA may potentially reduce and stabilize atherosclerotic lesions through its anti-inflammatory effects. (Keyword) Animals / Aorta / Apolipoproteins E / Atherosclerosis / Cells, Cultured / Chemokine CCL2 / Dietary Fats, Unsaturated / Disease Models, Animal / Eicosapentaenoic Acid / Endothelial Cells / Endothelium, Vascular / Humans / Inflammation / Intercellular Adhesion Molecule-1 / Low Density Lipoprotein Receptor-Related Protein-1 / Male / Mice / Mice, Knockout / Umbilical Veins / Vascular Cell Adhesion Molecule-1 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2007.07.023 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17765904 ● Search Scopus @ Elsevier (PMID): 17765904 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2007.07.023 (DOI: 10.1016/j.atherosclerosis.2007.07.023, PubMed: 17765904)
455.	P-H Huang, Masataka Sata, H Nishimatsu, M Sumi, Y Hirata and R Nagai : Pioglitazone ameliorates endothelial dysfunction and restores ischemia-induced angiogenesis in diabetic mice, Biomedicine & Pharmacotherapy, Vol.62, No.1, 46-52, 2008. (Summary) Angiogenesis, the formation of new blood vessels, is a physiological response to tissue ischemia. Clinical evidence suggests that diabetic patients have endothelial dysfunction and impaired angiogenesis in response to ischemia. Here, we investigated the impact of diabetes on ischemia-induced collateral growth, and tested the hypothesis that peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist augments collateral flow to ischemic tissue. We conducted unilateral hindlimb ischemia surgery in KKAy mice. Blood flow recovery was markedly impaired in diabetic mice compared with that in wild-type mice as determined by laser Doppler imaging. Treatment of KKAy mice with pioglitazone partially restored the blood flow recovery. Anti-CD31 immunostaining revealed that pioglitazone also significantly improved the capillary density in ischemic limb muscle. Endothelial NO synthase (eNOS) activity was ameliorated in diabetic mice treated with pioglitazone as determined by vasorelaxation in response to acetylcholine. Pioglitazone normalized vascular endothelial growth factor (VEGF) protein levels, which was decreased in ischemic muscle of KKAy mice, and up-regulated eNOS phosphorylation at Ser-1177 and Akt phosphorylation at Ser-473 in ischemic muscle. Pioglitazone had no beneficial effects on blood flow recovery in diabetic mice treated with N(G)-nitro-l-arginine methyl ester (L-NAME). Our findings demonstrate that pioglitazone significantly ameliorates endothelial dysfunction and enhances blood flow recovery after tissue ischemia in diabetic mice. Activation of eNOS appears to be essential for pioglitazone to promote angiogenesis in ischemic tissue. (Keyword) Animals / Diabetes Mellitus, Type 2 / Disease Models, Animal / Endothelium, Vascular / Hypoglycemic Agents / Ischemia / Laser-Doppler Flowmetry / Male / Mice / Mice, Inbred C57BL / Neovascularization, Physiologic / Nitric Oxide Synthase Type III / PPAR gamma / Phosphorylation / Thiazolidinediones / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biopha.2007.06.014 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17692499 ● Search Scopus @ Elsevier (PMID): 17692499 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biopha.2007.06.014 (DOI: 10.1016/j.biopha.2007.06.014, PubMed: 17692499)
456.	K Tanaka, Masataka Sata, T Natoti, J-R Kim-Kaneyama, K Nose, M Shibanuma, H Hirata and R Nagai : Circulating progenitor cells contribute to neointimal formation in non-irradiated chimeric mice, The FASEB journal, Vol.22, No.2, 428-436, 2008. (Summary) Recent evidence suggests that bone marrow-derived cells may contribute to repair and lesion formation following vascular injury. In most studies, bone marrow-derived cells were tracked by transplanting exogenous cells into bone marrow that had been compromised by irradiation. It remains to be determined whether endogenous circulating progenitors actually contribute to arterial remodeling under physiological conditions. Here, we established a parabiotic model in which two mice were conjoined subcutaneously without any vascular anastomosis. When wild-type mice were joined with transgenic mice that expressed green fluorescent protein (GFP) in all tissues, GFP-positive cells were detected not only in the peripheral blood but also in the bone marrow of the wild-type mice. The femoral arteries of the wild-type mice were mechanically injured by insertion of a large wire. At 4 wk, there was neointima hyperplasia that mainly consisted of alpha-smooth muscle actin-positive cells. GFP-positive cells were readily detected in the neointima (14.8+/-4.5%) and media (31.1+/-8.8%) of the injured artery. Some GFP-positive cells expressed alpha-smooth muscle actin or an endothelial cell marker. These results indicate that circulating progenitors contribute to re-endothelialization and neointimal formation after mechanical vascular injury even in nonirradiated mice. (Keyword) Actins / Animals / Bone Marrow Transplantation / Cell Movement / Genes, Reporter / Hyperplasia / Male / Mice / Mice, Inbred C57BL / Mice, Transgenic / Microscopy, Immunoelectron / Parabiosis / Stem Cells (Link to Publication Site) ● Publication site (DOI): 10.1096/fj.06-6884com (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17848623 ● Search Scopus @ Elsevier (PMID): 17848623 ● Search Scopus @ Elsevier (DOI): 10.1096/fj.06-6884com (DOI: 10.1096/fj.06-6884com, PubMed: 17848623)
457.	D Fukuda, Masataka Sata, N Ishizaka and R Nagai : Critical role of bone marrow angiotensin II type 1 receptor in the pathogenesis of atherosclerosis in apolipoprotein E deficient mice, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.28, No.1, 90-96, 2008. (Summary) It is suggested that the angiotensin II (Ang II)-Ang II type 1 receptor (AT1R) pathway plays a pivotal role in the pathogenesis of atherosclerosis. Recently, bone marrow (BM) cells were reported to express AT1R. Here, we investigated the role of AT1R in BM in the pathogenesis of atherosclerosis. Genetic ablation or pharmacological blockade of AT1R led to a significant reduction and stabilization of atherosclerotic lesions in ApoE-/- mice. To elucidate the role of AT1R in BM, we generated several BM chimeric mice. Ang II promoted atherosclerosis progression in the BM chimeric mice that had AT1aR in BM, regardless of the absence of AT1aR in the recipient vasculature (P<0.05). BM chimeric mice whose BM AT1aR was disrupted showed significantly less atherosclerotic lesions in aorta (P<0.05) and more stable plaque with reduced accumulation of BM-derived cells compared with BM chimeric mice that had AT1aR-positive BM. Most of the BM-derived cells in atheroma were positive for a macrophage marker and expressed matrix metalloproteinase (MMP)-9 and monocyte chemoattractant protein-1. Our findings suggest that AT1R in BM plays an important role in the pathogenesis of atherosclerosis. (Keyword) Angiotensin II / Animals / Apolipoproteins E / Atherosclerosis / Bone Marrow Transplantation / Disease Models, Animal / Male / Mice / Mice, Knockout / Receptor, Angiotensin, Type 1 / Transplantation Chimera (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.107.152363 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17962627 ● Search Scopus @ Elsevier (PMID): 17962627 ● Search Scopus @ Elsevier (DOI): 10.1161/ATVBAHA.107.152363 (DOI: 10.1161/ATVBAHA.107.152363, PubMed: 17962627)
458.	M Shimamura, N Sato, Masataka Sata, H Kurinami, D Takeuchi, K Wakayama, T Hayashi, H Iida and R Morishita : Delayed post-ischemic treatment with fluvastatin improved cognitive impairment after stroke in rats, Stroke, Vol.38, No.12, 3251-3258, 2007. (Summary) Recent clinical evidences indicate that statins may have beneficial effects on the functional recovery after ischemic stroke. However, the effect of delayed postischemic treatment with statins is still unclear. In the present study, we evaluated the effects of fluvastatin in the chronic stage of cerebral infarction in a rat model. Rats exposed to permanent middle cerebral artery occlusion were treated for 3 months with fluvastatin beginning from 7 days after stroke. MRI, behavioral analysis, and immunohistochemistry were performed. Two months of treatment with fluvastatin showed the significant recovery in spatial learning without the decrease in serum total cholesterol level and worsening of infarction. Microangiography showed a significant increase in capillary density in the peri-infarct region in fluvastatin-treated rats after 3 months of treatment. Consistently, BrdU/CD31-positive cells were significantly increased in fluvastatin-treated rats after 7 days of treatment. MAP1B-positive neurites were also increased in the peri-infarct region in fluvastatin-treated rats. In addition, rats treated with fluvastatin showed the reduction of superoxide anion after 7 days of treatment and the reduction of A beta deposits in the thalamic nuclei after 3 months of treatment. Thus, delayed postischemic administration of fluvastatin had beneficial effects on the recovery of cognitive function without affecting the infarction size after ischemic stroke. Pleiotropic effects of fluvastatin, such as angiogenesis, neuritogenesis, and inhibition of superoxide production and A beta deposition, might be associated with a favorable outcome. (Keyword) Animals / Anticholesteremic Agents / Cognition / Disease Models, Animal / Fatty Acids, Monounsaturated / Humans / Immunohistochemistry / Indoles / Infarction, Middle Cerebral Artery / Ischemia / Magnetic Resonance Imaging / Neovascularization, Pathologic / Rats / Rats, Wistar / Stroke / Superoxides / Treatment Outcome (Link to Publication Site) ● Publication site (DOI): 10.1161/STROKEAHA.107.485045 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17975105 ● Search Scopus @ Elsevier (PMID): 17975105 ● Search Scopus @ Elsevier (DOI): 10.1161/STROKEAHA.107.485045 (DOI: 10.1161/STROKEAHA.107.485045, PubMed: 17975105)
459.	T Yamada, T Kondo, Y Numaguchi, M Tsuzuki, T Matsubara, I Manabe, Masataka Sata, R Nagai and T Murohara : Angiotensin II receptor blocker inhibits neointimal hyperplasia through regulation of smooth muscle-like progenitor cells, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.27, No.11, 2363-2369, 2007. (Summary) Angiotensin II (ATII) type 1 receptor (AT1R) blocker (ARB) has been shown to inhibit neointimal formation. Bone marrow-derived mononuclear cells (BM-MNCs) give rise to smooth muscle (SM)-like cells at injured arterial wall and contribute to neointimal formation. However, role of the renin-angiotensin system in the homing process of SM-like cells during neointimal formation is unknown. When human BM-MNCs and peripheral blood MNCs (PB-MNCs) were cultured under treatment with PDGF-BB and bFGF, these cells gave rise to SM-like cells with expression of alphaSMA, SMemb, and SM1 proteins. RT-PCR showed the expression of AT1R, ATII type 2 receptor (AT2R), alphaSMA, and SMemb mRNAs. ATII accelerated the differentiation of SM-like cells, which was inhibited by an ARB CV11974 (P<0.05). We then examined the effects of ATII, CV11974, and AT2R antagonist PD123319 on neointimal formation and BM-derived SM-like cell incorporation at injured arteries in vivo. BM from green fluorescence protein (GFP)-transgenic mice was transplanted to irradiated WT mice. GFP-BM chimera mice were subjected to wire injury on the left femoral artery. ATII (100 ng/kg/min) stimulated whereas CV11974 (1 mg/kg/d) inhibited neointimal formation. Number of GFP+ alphaSMA+ cells at neointima correlated with the intima/media ratio (r=0.69, P<0.05). BM-derived SM-like progenitor cells contributed to the neointimal formation after arterial injury. ATII accelerated whereas ARB suppressed this process. These are new aspects of the ARB-mediated inhibition of atherosclerotic disease progression. (Keyword) Angiotensin II / Angiotensin II Type 1 Receptor Blockers / Animals / Bone Marrow Cells / Cell Differentiation / Cells, Cultured / Disease Models, Animal / Femoral Artery / Humans / Imidazoles / Mice / Mice, Transgenic / Myocytes, Smooth Muscle / Peripheral Vascular Diseases / Pyridines (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.107.147124 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17717297 ● Search Scopus @ Elsevier (PMID): 17717297 ● Search Scopus @ Elsevier (DOI): 10.1161/ATVBAHA.107.147124 (DOI: 10.1161/ATVBAHA.107.147124, PubMed: 17717297)
460.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Yasumasa Ikeda, Masataka Sata, Nobuyuki Takamori, Shusuke Yagi, Takashi Iwase, Yuka Sumitomo, Hirotaka Kawano, Takashi Yamada, Toru Fukuda, Takahiro Matsumoto, Keisuke Sekine, Takashi Sato, Yuko Nakamichi, Yoko Yamamoto, Kimihiro Yoshimura, Tomoyuki Watanabe, Takashi Nakamura, Akimasa Oomizu, Minoru Tsukada, Hideki Hayashi, Toshiki Sudo, Shigeaki Kato and Toshio Matsumoto : Strain-dependent embryonic lethality and exaggerated vascular remodeling in heparin cofactor II-deficient mice, The Journal of Clinical Investigation, Vol.117, No.6, 1514-1526, 2007. (Summary) Heparin cofactor II (HCII) specifically inhibits thrombin action at sites of injured arterial wall, and patients with HCII deficiency exhibit advanced atherosclerosis. However, the in vivo effects and the molecular mechanism underlying the action of HCII during vascular remodeling remain elusive. To clarify the role of HCII in vascular remodeling, we generated HCII-deficient mice by gene targeting. In contrast to a previous report, HCII(-/-) mice were embryonically lethal. In HCII(+/-) mice, prominent intimal hyperplasia with increased cellular proliferation was observed after tube cuff and wire vascular injury. The number of protease-activated receptor-1-positive (PAR-1-positive) cells was increased in the thickened vascular wall of HCII(+/-) mice, suggesting enhanced thrombin action in this region. Cuff injury also increased the expression levels of inflammatory cytokines and chemokines in the vascular wall of HCII(+/-) mice. The intimal hyperplasia in HCII(+/-) mice with vascular injury was abrogated by human HCII supplementation. Furthermore, HCII deficiency caused acceleration of aortic plaque formation with increased PAR-1 expression and oxidative stress in apoE-KO mice. These results demonstrate that HCII protects against thrombin-induced remodeling of an injured vascular wall by inhibiting thrombin action and suggest that HCII is potentially therapeutic against atherosclerosis without causing coagulatory disturbance. (Keyword) Animals / Base Sequence / Blood Vessels / DNA Primers / Embryo Loss / Female / Gene Targeting / Genes, Lethal / Genotype / Heparin Cofactor II / Heterozygote / Homozygote / Male / Mice / Mice, Inbred C57BL / knockout mice / Pregnancy (Link to Publication Site) ● Publication site (DOI): 10.1172/JCI27095 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17549254 ● Search Scopus @ Elsevier (PMID): 17549254 ● Search Scopus @ Elsevier (DOI): 10.1172/JCI27095 (DOI: 10.1172/JCI27095, PubMed: 17549254)
461.	K Nakamura, Masataka Sata, H Iwata, Y Sakai, Y Hirata, K Kugiyama and R Nagai : A synthetic small molecule, ONO-1301, enhances endgenous growth factor expression and augments angiogenesis in ischemic heart, Clinical Science, Vol.112, No.12, 607-616, 2007. (Summary) It has been shown previously that administration of angiogenic growth factors as genes or proteins can augment collateral growth in ischaemic tissues. In the present study, we have investigated the effect of ONO-1301, a synthetic prostacyclin agonist with thromboxane-synthase-inhibitory activity, on expression of endogenous growth factors and angiogenesis. ONO-1301 induced secretion of HGF (hepatocyte growth factor) and VEGF (vascular endothelial growth factor) from cultured normal human dermal fibroblasts in a dose-dependent manner. Dibutyryl cAMP, an analogue of cAMP, and forskolin, an adenylate cyclase activator, mimicked the effect of ONO-1301. Conversely, Rp-cAMP (adenosine 3',5'-cyclic monophosphorothioate), an inhibitor of cAMP, partially inhibited the effect of ONO-1301, suggesting that cAMP mediated the effect of ONO-1301 in up-regulating the expression of HGF and VEGF, at least in part. ONO-1301 promoted tube-like formation by HUVECs (human umbilical vein endothelial cells) when co-cultured with fibroblasts, and the angiogenic effect of ONO-1301 was abrogated by administration of a neutralizing antibody against HGF or VEGF. To generate a slow-releasing form of ONO-1301, ONO-1301 was mixed with poly(DL-lactic-co-glycolic acid). The slow-releasing form of ONO-1301 was injected directly into the ischaemic myocardium of mice immediately after ligation of the left anterior descending artery. The slow-releasing form of ONO-1301 up-regulated HGF and VEGF expression and increased capillary density in the border zone (342.7+/-29.7 capillaries/mm(2) in controls compared with 557.2+/-26.7 capillaries/mm(2) in treated animals; P<0.01) at 7 days. The slow-releasing form of ONO-1301 ameliorated left ventricular enlargement after 28 days and improved survival rate. In conclusion, our results indicate that ONO-1301 up-regulated endogenous growth factors and promoted angiogenesis in response to acute ischaemia. Therefore ONO-1301 might have a therapeutic potential in treating ischaemic diseases. (Keyword) Animals / Dilatation, Pathologic / Dose-Response Relationship, Drug / Enzyme Inhibitors / Epoprostenol / Fibroblasts / Hepatocyte Growth Factor / Humans / Intercellular Signaling Peptides and Proteins / Male / Mice / Mice, Inbred Strains / Myocardial Ischemia / Myocardium / Neovascularization, Pathologic / Pyridines / Thromboxane-A Synthase / Up-Regulation / Vascular Endothelial Growth Factor A / Ventricular Dysfunction, Left (Link to Publication Site) ● Publication site (DOI): 10.1042/CS20060301 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17263691 ● Search Scopus @ Elsevier (PMID): 17263691 ● Search Scopus @ Elsevier (DOI): 10.1042/CS20060301 (DOI: 10.1042/CS20060301, PubMed: 17263691)
462.	M Shimamura, N Sato, Masataka Sata, K Wakayama, T Ogihara and R Morishita : Expression of hepatocyte growth factor and c-Met after spinal cord injury in rats, Brain Research, Vol.1151, 188-194, 2007. (Summary) Since hepatocyte growth factor (HGF) plays a pivotal role in the development of the central nervous system and pathological conditions, we examined the long-term changes in the mRNA and protein expression of HGF and its receptor c-Met after spinal cord injury (SCI) in rats. HGF mRNA was significantly increased from 7 days after SCI in the injured segment, and the peak was at 7 days after SCI as assessed by real-time RT-PCR. Importantly, c-met mRNA expression was up-regulated from 1 day after SCI, and reached a peak at 14 days after SCI. Although up-regulation of HGF and c-met mRNA expression in the injured segment gradually decreased, the increased expression level persisted until 56 days after SCI. Consistent with HGF mRNA expression, HGF protein level was significantly increased mainly in the injured region, which persisted until 56 days after SCI. Immunohistochemistry showed that most of GFAP-positive reactive astrocytes expressed HGF and c-Met both on 14 days and 56 days after SCI. Staining with the mitotic indicator, bromodeoxyuridine (BrdU), revealed that a small number of BrdU-incorporated cells were co-localized with HGF/GFAP-positive or c-Met/GFAP-positive cells both on 14 and 56 days. These data suggest that HGF and c-Met were up-regulated mainly in the reactive astrocytes around the injured region in the subacute to chronic stage of spinal cord injury. Since HGF plays a critical role in neurotrophic activity, activation of the HGF/c-Met signaling system might be involved in the process of post-traumatic regeneration. (Keyword) Analysis of Variance / Animals / Bromodeoxyuridine / Cell Count / Disease Models, Animal / Female / Gene Expression Regulation / Glial Fibrillary Acidic Protein / Hepatocyte Growth Factor / Proto-Oncogene Proteins c-met / RNA, Messenger / Rats / Rats, Inbred F344 / Reverse Transcriptase Polymerase Chain Reaction / Spinal Cord Injuries / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1016/j.brainres.2007.03.022 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17425951 ● Search Scopus @ Elsevier (PMID): 17425951 ● Search Scopus @ Elsevier (DOI): 10.1016/j.brainres.2007.03.022 (DOI: 10.1016/j.brainres.2007.03.022, PubMed: 17425951)
463.	I Kojima, T Tanaka, R Inagi, H Kato, T Yamashita, A Sakiyama, O Ohneda, N Takeda, Masataka Sata, T Miyata, T Fujita and M Nangaku : Protective role of HIF-2α against ischemic damage and oxidative stress in the kidney, Journal of the American Society of Nephrology, Vol.18, No.4, 1218-1226, 2007. (Summary) Central to cellular responses to hypoxic environment is the hypoxia-inducible factor (HIF) transcriptional control system. A role for HIF-2alpha was investigated in a model of renal ischemia-reperfusion injury (IRI) associated with oxidative stress using HIF-2alpha knockdown mice. In these mice, HIF-2alpha expression was approximately one half that of wild-type mice, whereas HIF-1alpha expression was equivalent. HIF-2alpha knockdown mice were more susceptible to renal IRI, as indicated by elevated blood urea nitrogen levels and semiquantitative histologic analysis. Immunostaining with markers of oxidative stress showed enhanced oxidative stress in the kidney of HIF-2alpha knockdown mice, which was associated with peritubular capillary loss. Real-time quantitative PCR analysis showed decreased expression of antioxidative stress genes in the HIF-2alpha knockdown kidneys. Studies that used small interference RNA confirmed regulation of the antioxidative stress genes in cultured endothelial cells. Although HIF-2alpha knockdown mice were anemic, serum erythropoietin levels were not significantly increased, reflecting inappropriate response to anemia as a result of HIF-2alpha knockdown. Experiments that used hemodiluted mice with renal ischemia demonstrated that anemia of this degree did not affect susceptibility to ischemia. Knockdown of HIF-2alpha in inflammatory cells by bone marrow transplantation experiments demonstrated that HIF-2alpha in inflammatory cells did not contribute to susceptibility to renal IRI. Restoration of HIF-2alpha in endothelium by intercrossing with Tie1-Cre mice ameliorated renal injury by IRI, demonstrating a specific role of endothelial HIF-2alpha. These results suggest that HIF-2alpha in the endothelium has a protective role against ischemia of the kidney via amelioration of oxidative stress. (Keyword) Animals / Basic Helix-Loop-Helix Transcription Factors / Ischemia / Kidney / Male / Mice / Mice, Inbred C57BL / Oxidative Stress / Reperfusion Injury (Link to Publication Site) ● Publication site (DOI): 10.1681/ASN.2006060639 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17344427 ● Search Scopus @ Elsevier (PMID): 17344427 ● Search Scopus @ Elsevier (DOI): 10.1681/ASN.2006060639 (DOI: 10.1681/ASN.2006060639, PubMed: 17344427)
464.	T Suzuki, T Nishi, T Nagino, K Sasaki, K Aizawa, N Kada, D Sawaki, Y Munemasa, T Matsumura, S Muto, Masataka Sata, K Miyagawa, M Horikoshi and R Nagai : Functional interaction between the transcription factor Kruppel-like factor 5 and poly(ADP-ribose) polymerase-1 in cardiovascular apoptosis, The Journal of Biological Chemistry, Vol.282, No.13, 9895-9901, 2007. (Summary) Krüppel-like factor 5 (KLF5) is a transcription factor important in regulation of the cardiovascular response to external stress. KLF5 regulates pathological cell growth, and its acetylation is important for this effect. Its mechanisms of action, however, are still unclear. Analysis in KLF5-deficient mice showed that KLF5 confers apoptotic resistance in vascular lesions. Mechanistic analysis further showed that it specifically interacts with poly(ADP-ribose) polymerase-1 (PARP-1), a nuclear enzyme important in DNA repair and apoptosis. KLF5 interacted with a proteolytic fragment of PARP-1, and acetylation of KLF5 under apoptotic conditions increased their affinity. Moreover, KLF5 wild-type (but not a non-acetylatable point mutant) inhibited apoptosis as induced by the PARP-1 fragment. Collectively, we have found that KLF5 regulates apoptosis and targets PARP-1, and further, for acetylation to regulate these effects. Our findings thus implicate functional interaction between the transcription factor KLF5 and PARP-1 in cardiovascular apoptosis. (Keyword) 3T3 Cells / Acetylation / Animals / Apoptosis / Cardiovascular System / Cell Line / HeLa Cells / Humans / Kruppel-Like Transcription Factors / Male / Mice / Mice, Knockout / Point Mutation / Poly(ADP-ribose) Polymerases (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M608098200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17283079 ● Search Scopus @ Elsevier (PMID): 17283079 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M608098200 (DOI: 10.1074/jbc.M608098200, PubMed: 17283079)
465.	M Sumi, Masataka Sata, S.I. Miura, K.A. Rye, N Toya, Y Kanaoka, K Yanaga, T Ohki, K Saku and R Nagai : Reconstituted high-density lipoprotein stimulates differentiation of endothelial progenitor cells and enhances ischemia-induced angiogenesis, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.27, No.4, 813-818, 2007. (Summary) Plasma high-density lipoprotein (HDL) levels have an inverse correlation with incidence of ischemic heart disease as well as other atherosclerosis-related ischemic conditions. However, the molecular mechanism by which HDL prevents ischemic disease is not fully understood. Here, we investigated the effect of HDL on differentiation of endothelial progenitor cells and angiogenesis in murine ischemic hindlimb model. Intravenous injection of reconstituted HDL (rHDL) significantly augmented blood flow recovery and increased capillary density in the ischemic leg. rHDL increased the number of bone marrow-derived cells incorporated into the newly formed capillaries in ischemic muscle. rHDL induced phosphorylation of Akt in human peripheral mononuclear cells. rHDL (50 to 100 microg apolipoprotein A-I/mL) promoted differentiation of peripheral mononuclear cells to endothelial progenitor cells in a dose-dependent manner. The effect of rHDL on endothelial progenitor cells differentiation was abrogated by coadministration of LY294002, an inhibitor of phosphatidylinositol 3-kinase. rHDL failed to promote angiogenesis in endothelial NO-deficient mice. rHDL directly stimulates endothelial progenitor cell differentiation via phosphatidylinositol 3-kinase/Akt pathway and enhances ischemia-induced angiogenesis. rHDL may be useful in the treatment of patients with ischemic cardiovascular diseases. (Keyword) Animals / Bone Marrow / Cell Differentiation / Cells, Cultured / Chimera / Collateral Circulation / Endothelial Cells / Hindlimb / Humans / Ischemia / Lipoproteins, HDL / Male / Mice / Mice, Inbred Strains / Mice, Knockout / Neovascularization, Physiologic / Nitric Oxide Synthase Type III / Phosphatidylinositol 3-Kinases / Proto-Oncogene Proteins c-akt / Regional Blood Flow / Signal Transduction / Stem Cells (Link to Publication Site) ● Publication site (DOI): 10.1161/01.ATV.0000259299.38843.64 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17272742 ● Search Scopus @ Elsevier (PMID): 17272742 ● Search Scopus @ Elsevier (DOI): 10.1161/01.ATV.0000259299.38843.64 (DOI: 10.1161/01.ATV.0000259299.38843.64, PubMed: 17272742)
466.	T Inoue, Masataka Sata, Y Hikichi, R Sohma, D Fukuda, T Uchida, M Shimizu, H Komoda and K Node : Mobilization of CD34-Positive bone marrow-derived cells after coronary stent implantation: impact on restenosis, Circulation, Vol.115, No.5, 553-561, 2007. (Summary) Recently, accumulating evidence has indicated that bone marrow-derived stem cells are capable of differentiating into vascular cells. It has been hypothesized that the inflammatory response after vascular injury triggers the mobilization of endothelial and smooth muscle progenitor cells from bone marrow. We measured circulating CD34-positive mononuclear cells, activation of integrin Mac-1 on the surface of neutrophils, and plasma granulocyte-colony stimulating factor levels in 40 patients undergoing coronary stenting. After bare-metal stenting, CD34-positive cells increased, reaching a maximum on day 7 after stenting. The maximum change compared with baseline before stenting was more striking in patients with restenosis than without restenosis (332+/-108% versus 148+/-49%; P<0.05). In contrast, CD34-positive cells decreased after sirolimus-eluting stenting (72+/-21% on day 7). The change in CD34-positive cells on day 7 relative to baseline was closely correlated with that in activated Mac-1 at 48 hours (R=0.52, P<0.01) and that in granulocyte-colony stimulating factor levels at 24 hours (R=0.42, P<0.05). Cell culture assay on day 7 showed that mononuclear cells differentiated into CD31-positive endothelium-like cells after bare-metal stenting. In patients with restenosis, mononuclear cells differentiating into alpha-smooth muscle actin-positive smooth muscle-like cells also were observed. Implantation of sirolimus-eluting stents suppressed both types of differentiation. Stent implantation may induce differentiation of bone marrow cells into endothelial or smooth muscle cells. Endothelial cells may participate in reendothelialization, a protective reaction against vascular injury, whereas smooth muscle cells may participate in neointimal thickening and restenosis. Sirolimus-eluting stents appear to inhibit the mobilization and differentiation of bone marrow cells. (Keyword) Aged / Antigens, CD34 / Bone Marrow Cells / Cell Movement / Coronary Artery Disease / Coronary Restenosis / Female / Heart Catheterization / Humans / Male / Middle Aged / Stents / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1161/CIRCULATIONAHA.106.621714 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17261663 ● Search Scopus @ Elsevier (PMID): 17261663 ● Search Scopus @ Elsevier (DOI): 10.1161/CIRCULATIONAHA.106.621714 (DOI: 10.1161/CIRCULATIONAHA.106.621714, PubMed: 17261663)
467.	M Sahara, Masataka Sata, T Morita, K Nakamura, Y Hirata and R Nagai : Diverse contribution of bone marrow-derived cells to vascular remodeling associated with pulmonary arterial hypertension and arterial neointimal formation, Circulation, Vol.115, No.4, 509-517, 2007. (Summary) Recent evidence suggests that bone marrow (BM)-derived cells may differentiate into vascular cells that participate in arterial repair and/or lesion formation. However, it remains uncertain whether BM-derived cells also can participate in vascular remodeling associated with pulmonary arterial hypertension. The BM of Sprague-Dawley rats was reconstituted with that of green fluorescent protein-transgenic rats. The BM-chimeric rats were injected intraperitoneally with 60 mg/kg monocrotaline after unilateral subpneumonectomy, and they concurrently underwent wire-mediated endovascular injury in femoral artery. After 28 days, they had elevated right ventricular systolic pressure (58.8+/-5.4 versus 20.4+/-2.4 mm Hg in sham-control; P<0.01). The pulmonary arterioles were markedly thickened, with an infiltration of green fluorescent protein-positive macrophages into the perivascular areas. The endothelium of pulmonary arterioles contained only a few green fluorescent protein-positive cells, and green fluorescent protein-positive cells were seldom detected as smooth muscle cells in the lesions of thickened pulmonary arterioles. In contrast, BM-derived smooth muscle-like cells could be readily detected in the thickened neointima and media of the wire-injured femoral artery. Moreover, intravenous injection of 1x10(8) BM cells from young rats had no beneficial effects on pulmonary hypertension, pulmonary arterial remodeling, or survival in the aged rats treated with monocrotaline plus unilateral subpneumonectomy. No injected BM cell was identified as an endothelial cell or a smooth muscle cell. These results suggest that BM-derived cells can participate in arterial neointimal formation after mechanical injury, whereas they do not contribute substantially to pulmonary arterial remodeling associated with monocrotaline-induced pulmonary arterial hypertension in the pneumonectomized rats. (Keyword) Animals / Animals, Genetically Modified / Arterioles / Bone Marrow Cells / Bone Marrow Transplantation / Capillaries / Cell Differentiation / Disease Models, Animal / Femoral Artery / Green Fluorescent Proteins / Hypertension, Pulmonary / Male / Monocrotaline / Pneumonectomy / Pulmonary Artery / Pulmonary Embolism / Rats / Rats, Sprague-Dawley / Thrombosis / Tunica Intima / Ventricular Dysfunction, Right (Link to Publication Site) ● Publication site (DOI): 10.1161/CIRCULATIONAHA.106.655837 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17242277 ● Search Scopus @ Elsevier (PMID): 17242277 ● Search Scopus @ Elsevier (DOI): 10.1161/CIRCULATIONAHA.106.655837 (DOI: 10.1161/CIRCULATIONAHA.106.655837, PubMed: 17242277)
468.	I Shirakawa, Masataka Sata, A Saiura, Y Kaneda, H Yashiro, Y Hirata, M Makuuchi and R Nagai : Atorvastatin attenuates transplant-associated coronary arteriosclerosis in a murine model of cardiac transplantation, Biomedicine & Pharmacotherapy, Vol.61, No.2-3, 154-159, 2007. (Summary) Accelerated coronary arteriosclerosis remains a major problem for the long-term survival of cardiac transplant recipients. However, the pathogenesis of transplant vasculopathy is poorly understood and there is no effective therapy. HMG-CoA reductase inhibitors, or statins, are widely prescribed to lower plasma cholesterol level. Accumulating evidence indicates that statins have various effects on vascular cells which are independent of their lipid-lowering effect. We investigated whether orally administered atorvastatin, one of the most potent statins, inhibits the development of intima hyperplasia in a mouse model of cardiac transplantation. Cardiac allografts from DBA mice were transplanted heterotopically into B10.D2 mice. Mice were administered either vehicle or atorvastatin everyday by gavage. Morphometrical analysis revealed that atorvastatin significantly reduced the development of coronary arteriosclerosis on the cardiac allografts harvested at one month. Immunohistochemical analysis revealed that atorvastatin attenuated infiltration of inflammatory cells with reduced expression of TGF-beta and adhesion molecules. These results suggest that atorvastatin may be effective in preventing transplant-associated arteriosclerosis along with other immunosuppressive agents. (Keyword) Animals / Anticholesteremic Agents / Coronary Artery Disease / Gene Expression Regulation / Heart Transplantation / Heptanoic Acids / Hyperplasia / Immunohistochemistry / Mice / Mice, Inbred DBA / Pyrroles / Transforming Growth Factor beta / Tunica Intima / Vascular Diseases (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biopha.2006.09.017 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17258886 ● Search Scopus @ Elsevier (PMID): 17258886 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biopha.2006.09.017 (DOI: 10.1016/j.biopha.2006.09.017, PubMed: 17258886)
469.	A Sumi, Masataka Sata, A Hashimoto, T Imaizumi, K Yanaga, T Ohki, T Mori and R Nagai : OPC-28326, a selective femoral arterial vasodilator, augments ischemia induced angiogenesis, Biomedicine & Pharmacotherapy, Vol.61, No.4, 209-215, 2007. (Summary) OPC-28326, 4-(N-methyl-2-phenylethylamino)-1-(3,5-dimethyl-4-propionyl-aminobenzoyl) piperidine hydrochloride monohydrate, is a newly developed selective peripheral vasodilator and increases blood flow to lower extremities with alpha2-adrenergic antagonist property. Here, we investigated the effect of OPC-28326 on ischemia-induced angiogenesis. OPC-28326 enhanced tube formation by human aortic endothelial cells (HAECs). Moreover, OPC-28326 enhanced the number of microvessels sprouting from aortic rings embedded in collagen gel. OPC-28326 markedly induced phosphorylation of endothelial nitric oxide synthase (eNOS) in HAECs via phosphatidylinositol-3 kinase PI3K/Akt (PI3K/Akt) pathway. Next, the angiogenic effect of OPC-28326 was evaluated in a mouse hindlimb ischemia model. Blood flow recovery to the ischemic leg was significantly enhanced by OPC-28326. Furthermore, anti-CD31 immunostaining revealed that OPC-28326 increased capillary density in the ischemic muscle. However, OPC-28326 failed to promote blood flow recovery in ischemic hindlimb in eNOS-deficient mice. These results suggest that OPC-28326 promotes angiogenesis, which was associated with activation of eNOS via PI3K/Akt pathway. OPC-28326 might be promising to treat patients with ischemic vascular diseases. (Keyword) Aniline Compounds / Animals / Aorta / Blotting, Western / Cells, Cultured / Dose-Response Relationship, Drug / Endothelial Cells / Endothelium, Vascular / Hindlimb / Humans / Ischemia / Laser-Doppler Flowmetry / Mice / Mice, Inbred C3H / Mice, Inbred C57BL / Neovascularization, Physiologic / Nitric Oxide Synthase Type III / Phosphorylation / Piperidines / Rats / Regional Blood Flow / Vasodilator Agents (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biopha.2006.12.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17223008 ● Search Scopus @ Elsevier (PMID): 17223008 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biopha.2006.12.004 (DOI: 10.1016/j.biopha.2006.12.004, PubMed: 17223008)
470.	K Wakayama, M Shimamura, Masataka Sata, N Sato, K Kawakami, H Fukuda, T Tomimatsu, T Ogihara and R Morishita : Quantitative measurement of neurological deficit after mild (30 min) transient middle cerebral artery occlusion in rats, Brain Research, Vol.1130, No.1, 181-187, 2007. (Summary) Although 30-min transient middle cerebral artery occlusion (30-min tMCAo) causes reproducible subcortical infarction in rats, it is difficult to evaluate the resulting neurological deficit using common behavioral tests such as the rota-rod test, adhesive-removal test, or narrow beam test. Establishment of a method of quantitative evaluation would help to develop a novel therapeutic approach to treat cerebral infarction. To solve this problem, we examined whether the neurological deficit could be detected by the Montoya staircase test or methamphetamine-induced rotation, which are commonly used in a Parkinson disease model induced by intrastriatal injection of 6-hydroxydopamine (6-OHDA). From 10 to 14 days after tMCAo, the Montoya staircase test showed significant clumsiness in forelimb tasks contralateral to the lesion side, whereas sham-operated rats showed no significant clumsiness in both forelimbs. The number of ipsilateral rotations induced by methamphetamine was also increased in tMCAo-rats at 21 days after tMCAo. Although Pearson's correlations coefficient showed that the results of these tests were correlated with the infarction volume, there was no significant correlation between the results of these two tests. These findings imply that the neurological deficit detected by both tests might reflect the severity of ischemic injury, but each test might evaluate different aspects of neurological deficit. Thus, the Montoya staircase test and methamphetamine-induced rotation are useful to evaluate neurological deficit in the chronic stage of subcortical infarction induced by 30-min tMCAo. (Keyword) Animals / Behavioral Research / Brain Damage, Chronic / Brain Ischemia / Disease Models, Animal / Endpoint Determination / Infarction, Middle Cerebral Artery / Male / Methamphetamine / Motor Skills / Movement Disorders / Rats / Rats, Wistar / Rotation / Severity of Illness Index (Link to Publication Site) ● Publication site (DOI): 10.1016/j.brainres.2006.10.088 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17173875 ● Search Scopus @ Elsevier (PMID): 17173875 ● Search Scopus @ Elsevier (DOI): 10.1016/j.brainres.2006.10.088 (DOI: 10.1016/j.brainres.2006.10.088, PubMed: 17173875)
471.	M Sumi, Masataka Sata, N Toya, K Yanaga, T Ohki and R Nagai : Transplantation of adipose stromal cells, but not mature adipocytes, augments ischemia-induced angiogenesis, Life Sciences, Vol.80, No.6, 559-565, 2007. (Summary) Therapeutic angiogenesis has emerged as a promising therapy to treat patients with ischemic diseases. Transplantation of bone marrow cells (BMCs) is reported to augment collateral development in ischemic organs either by differentiating into vascular cells or by secreting angiogenic cytokines. Recent evidence suggests that adipose tissues secrete a number of humoral factors and contain pluripotent stem cells. Here, we evaluated the therapeutic potential of adipose tissue-derived cells to promote angiogenesis in a mouse model of hind limb ischemia. Stromal vascular fraction cells (SVFs) were isolated from inguinal adipose tissue. Endothelial-like cells or smooth muscle-like cells could be obtained from the culture of SVFs in the presence of growth factors. Freshly isolated BMCs, SVFs, or mature adipocytes were transplanted into the ischemic hind limb of mice. SVFs significantly augmented collateral development as determined by the restoration of blood perfusion and capillary density of the ischemic muscle. Angiogenic effects of SVFs were as potent as those of BMCs. Mature adipocytes showed no proangiogenic effects. The ischemic muscle contained endothelial cells or smooth muscle cells that derived from the transplanted SVFs and BMCs. These results suggest that SVFs might be used to promote angiogenesis in ischemic tissues. (Keyword) Adipocytes / Adipose Tissue / Animals / Cell Differentiation / Green Fluorescent Proteins / Ischemia / Lower Extremity / Mice / Mice, Inbred C57BL / Mice, Transgenic / Neovascularization, Physiologic / Regional Blood Flow / Stromal Cells (Link to Publication Site) ● Publication site (DOI): 10.1016/j.lfs.2006.10.020 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17157325 ● CiNii @ National Institute of Informatics (CRID): 1570572701515935232 ● Search Scopus @ Elsevier (PMID): 17157325 ● Search Scopus @ Elsevier (DOI): 10.1016/j.lfs.2006.10.020 (DOI: 10.1016/j.lfs.2006.10.020, PubMed: 17157325, CiNii: 1570572701515935232)
472.	M Abe, Masataka Sata, E Suzuki, R Takeda, M Takahashi, H Nishimatsu, D Nagata, K Kangawa, H Matsuo, R Nagai and Y Hirata : Effects of adrenomedullin on acute ischemia-induced collateral development and mobilization of bone marrow-derived cells, Clinical Science, Vol.111, No.6, 381-387, 2006. (Summary) Adrenomedullin exerts not only vasodilatory effects, but also angiogenic effects. In the present study, we investigated the effects of adrenomedullin on collateral formation and circulating bone-marrow-derived cells after acute tissue ischaemia. Bone marrow of 8-10-week-old female C57BL/6J mice was replaced with that from GFP (green fluorescent protein) transgenic mice (GFP mice). At 8 weeks after transplantation, hindlimb ischaemia was induced by resecting the right femoral artery and a plasmid expressing human adrenomedullin (50 mug) was injected into the ischaemic muscle, followed by in vivo electroporation on a weekly basis. Overexpression of adrenomedullin significantly enhanced the blood flow recovery compared with controls (blood flow ratio, 1.0+/-0.2 compared with 0.6+/-0.3 respectively, at week 4; P<0.05) and increased capillary density in the ischaemic leg as determined by anti-CD31 immunostaining of the ischaemic muscle (567+/-40 compared with 338+/-65 capillaries/mm(2) respectively, at week 5; P<0.05). There were more GFP-positive cells in the thigh muscle of the mice injected with adrenomedullin than in that of the control mice (29.6+/-4.5 compared with 16.5+/-3.3 capillaries/mm(2) respectively, at week 5; P<0.05). We repeated the same experiments using LacZ-knock-in mice instead of GFP mice, and obtained similar results. These findings suggest that adrenomedullin may augment ischaemia-induced collateral formation with some effects on circulating bone-marrow-derived cells. (Keyword) Adrenomedullin / Animals / Bone Marrow Transplantation / Collateral Circulation / Female / Flow Cytometry / Green Fluorescent Proteins / Hematopoietic Stem Cell Mobilization / Hematopoietic Stem Cells / Hindlimb / Ischemia / Mice / Mice, Inbred C57BL / Mice, Transgenic / Muscle, Skeletal / Vasodilator Agents (Link to Publication Site) ● Publication site (DOI): 10.1042/CS20060137 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16922679 ● Search Scopus @ Elsevier (PMID): 16922679 ● Search Scopus @ Elsevier (DOI): 10.1042/CS20060137 (DOI: 10.1042/CS20060137, PubMed: 16922679)
473.	K Hanajiri, T Maruyama, Y Kaneko, H Mitsui, S Watanabe, Masataka Sata, R Nagai, T Kashima, J Shibahara, M Omata and Y Matsumoto : Microbubble-induced increase in ablation of liver tumors by high-intensity focused ultrasound, Hepatology Research, Vol.36, No.4, 308-314, 2006. (Summary) We studied the possibility of using high-intensity focused ultrasound (HIFU) together with a microbubble agent to treat hepatocellular carcinoma. Development of liver tumors in rats was induced by administration of Dimethylnitrosamin (100ppm). Rats with liver tumors were anesthetized, underwent laparotomy, and were given the microbubble agent Levovist or saline intravenously. After the injection, the liver was exposed to HIFU for 30s (2.18MHz, 600W/cm(2), 40mm in diameter). Immediately after HIFU exposure, ultrasound images of the HIFU area were evaluated. Then the liver was excised and the volume of coagulated tissue was measured. The mean volumes of hyperechoic areas after HIFU were as follows (mm(3), Levovist versus saline: 355.3+/-180.7 versus 47.4+/-35.6, P<0.001, n=13). The volumes of liver tissue coagulated by HIFU were as follows (mm(3), Levovist versus saline: 275.3+/-120.0 versus 60.1+/-23.6, P<0.001, n=13). On microscopic examination of areas exposed to HIFU, implosion cysts were seen, and many cancer cells were found to have been destroyed completely (loss of cell membranes or nuclei). In conclusion, the microbubble agent Levovist can increase the volume of tissue coagulated by HIFU. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.hepres.2006.08.013 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16990046 ● Search Scopus @ Elsevier (PMID): 16990046 ● Search Scopus @ Elsevier (DOI): 10.1016/j.hepres.2006.08.013 (DOI: 10.1016/j.hepres.2006.08.013, PubMed: 16990046)
474.	M Yoshioka, S Yuasa, K Matsumura, K Kimura, T Shiomi, N Kimura, C Shukunami, Y Okada, M Mukai, H Shin, R Yozu, Masataka Sata, S Ogawa, Y Hiraki and K Fukuda : Chondromodulin-I maintains cardiac valvular function by preventing angiogenesis, Nature Medicine, Vol.12, No.10, 1151-1159, 2006. (Summary) The avascularity of cardiac valves is abrogated in several valvular heart diseases (VHDs). This study investigated the molecular mechanisms underlying valvular avascularity and its correlation with VHD. Chondromodulin-I, an antiangiogenic factor isolated from cartilage, is abundantly expressed in cardiac valves. Gene targeting of chondromodulin-I resulted in enhanced Vegf-A expression, angiogenesis, lipid deposition and calcification in the cardiac valves of aged mice. Echocardiography showed aortic valve thickening, calcification and turbulent flow, indicative of early changes in aortic stenosis. Conditioned medium obtained from cultured valvular interstitial cells strongly inhibited tube formation and mobilization of endothelial cells and induced their apoptosis; these effects were partially inhibited by chondromodulin-I small interfering RNA. In human VHD, including cases associated with infective endocarditis, rheumatic heart disease and atherosclerosis, VEGF-A expression, neovascularization and calcification were observed in areas of chondromodulin-I downregulation. These findings provide evidence that chondromodulin-I has a pivotal role in maintaining valvular normal function by preventing angiogenesis that may lead to VHD. (Keyword) Aged / Angiogenesis Inhibitors / Animals / Aorta / Culture Media, Conditioned / Echocardiography / Heart Valve Diseases / Humans / Intercellular Signaling Peptides and Proteins / Male / Membrane Proteins / Mice / Mice, Inbred ICR / Mice, Transgenic / Middle Aged / Mitral Valve / Neovascularization, Pathologic / Rats / Rats, Wistar (Link to Publication Site) ● Publication site (DOI): 10.1038/nm1476 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16980969 ● Search Scopus @ Elsevier (PMID): 16980969 ● Search Scopus @ Elsevier (DOI): 10.1038/nm1476 (DOI: 10.1038/nm1476, PubMed: 16980969)
475.	K Ohtani, K Egashira, Y Ihara, K Nakano, K Funakoshi, G Zhao, Masataka Sata and K Sunagawa : Angiotensin II Type 1 Receptor Blockade Attenuates In-Stent Restenosis by Inhibiting Inflammation and Progenitor Cells, Hypertension, Vol.48, No.4, 664-670, 2006. (Summary) The precise mechanism by which angiotensin II type 1 receptor blocker reduces in-stent restenosis in clinical trials is unclear. We, therefore, investigated the mechanism of in-stent neointima formation. Male cynomolgus monkeys and rabbits were fed a high-cholesterol diet and were allocated to untreated control and type 1 receptor blocker groups. Five days after grouping, multilink stents were implanted in the iliac artery. The type 1 receptor blocker reduced the development of in-stent neointima formation by approximately 30% in rabbits and monkeys. To investigate potential mechanisms, we examined the expression of renin-angiotensin system markers, all of which increased in monocytes and smooth muscle-like cells in the neointima and media within 7 days. The type 1 receptor blocker attenuated increased oxidative stress, the enhanced expression of markers of the rennin-angiotensin system and monocyte chemoattractant protein-1, and macrophage infiltration. The effects of type 1 receptor blocker on the differentiation of peripheral blood mononuclear cells into vascular progenitor cells were also examined. Treatment with type 1 receptor blocker suppressed the enhanced differentiation to smooth muscle progenitor cells induced by stenting. The type 1 receptor blocker attenuated in-stent neointima formation by inhibiting redox-sensitive inflammatory changes and by reducing recruitment of the progenitor cells. These potential actions of type 1 receptor blocker on inflammation and progenitor cells constitute a novel mechanism of suppression of in-stent restenosis by type 1 receptor blocker. (Keyword) Angiotensin II Type 1 Receptor Blockers / Animals / Apoptosis / Biological Markers / Blood Pressure / Blood Vessels / Cell Differentiation / Constriction, Pathologic / Iliac Artery / Imidazoles / Inflammation / Inflammation Mediators / Isoenzymes / Macaca fascicularis / Male / Monocytes / Myocytes, Smooth Muscle / NADPH Oxidase / Oxidative Stress / Rabbits / Recurrence / Renin-Angiotensin System / Stem Cells / Stents / Tetrazoles / Tunica Intima / Valine (Link to Publication Site) ● Publication site (DOI): 10.1161/01.HYP.0000237974.74488.30 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16940231 ● Search Scopus @ Elsevier (PMID): 16940231 ● Search Scopus @ Elsevier (DOI): 10.1161/01.HYP.0000237974.74488.30 (DOI: 10.1161/01.HYP.0000237974.74488.30, PubMed: 16940231)
476.	K Tateishi, M Ohta, B Guleng, F Kanai, Y Tanaka, Y Asaoka, A Jazag, J Imamura, T Imamura, H Ijichi, T Ikenoue, T Kawakami, Y Fukushima, M Washida, Masataka Sata, M Miyagishi, K Taira, H Yoshida, T Kawabe and M Omata : TRAIL-induced cell death cooperates with IFN-gammma activation in the graft-versus-tumor effect against colon tumors, International Journal of Cancer, Vol.118, No.9, 2237-2246, 2006. (Summary) The graft-versus-tumor (GVT) effect that occurs following allogeneic bone marrow transplantation (BMT) and donor lymphocyte infusion (DLI) is currently being subjected to intensive investigation because of clinical evidence for GVT efficacy against leukemia. In this report, we investigate the efficacy and molecular mechanisms of GVT against solid tumors, using a modification of the mouse parent-to-F1 BMT model. Mouse Colon26 cells in which tumor necrosis factor related apoptosis-inducing ligand (TRAIL) receptor expression was stably knocked down were transplanted to investigate the role of the TRAIL-TRAIL receptor system in the GVT effect. In addition, Fas ligand-(FasL) deficient mice on a C57BL6 (B6) background were used as donors, to determine the significance of the Fas-FasL system for the antitumor effect. The group that received B6 DLI followed by preconditioning with 950 rad irradiation underwent tumor reduction associated with the induction of IFN-gamma, TRAIL and tumor-cell apoptosis. In vitro cultured Colon26 cells were resistant to TRAIL but susceptible to the combination of IFN-gamma and TRAIL in a TRAIL-dose-dependent manner. The infusion of lymphocytes from FasL-defective donors reduced the tumor progression, although efficacy was decreased in the TRAIL receptor knockdown tumors but not in wild-type ones, compared with infusion of B6-derived lymphocytes. The findings indicate that GVT activity against subcutaneous colon tumors is efficiently induced by preconditioning with irradiation and allogeneic DLI, and that TRAIL and IFN-gamma act cooperatively in the antitumor effect. (Keyword) Animals / Apoptosis / Apoptosis Regulatory Proteins / Bone Marrow Transplantation / Colonic Neoplasms / Dose-Response Relationship, Drug / Down-Regulation / Fas Ligand Protein / Female / Graft vs Tumor Effect / Interferon-gamma / Lymphocyte Transfusion / Male / Membrane Glycoproteins / Mice / Mice, Inbred BALB C / Mice, Inbred C57BL / Receptors, TNF-Related Apoptosis-Inducing Ligand / Receptors, Tumor Necrosis Factor / TNF-Related Apoptosis-Inducing Ligand / Transplantation, Homologous / Tumor Cells, Cultured / Tumor Necrosis Factor-alpha / Tumor Necrosis Factors (Link to Publication Site) ● Publication site (DOI): 10.1002/ijc.21658 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16331624 ● Search Scopus @ Elsevier (PMID): 16331624 ● Search Scopus @ Elsevier (DOI): 10.1002/ijc.21658 (DOI: 10.1002/ijc.21658, PubMed: 16331624)
477.	Tetsufumi Yamamoto, Masataka Sata, Daiju Fukuda and Shinichi Takamoto : The angiotensin II type 1 receptor blocker candesartan attenuates graft vasculopathy, The Journal of Surgical Research, Vol.132, No.1, 62-68, 2006. (Summary) Transplant arteriosclerosis remains the major cause of graft failure after cardiac transplantation, although recent progress in immunosuppressive therapy has dramatically improved short-term survival of recipient. We investigated the effects of the angiotensin II type 1 receptor (AT(1)R) blocker candesartan on the development of transplant arteriosclerosis in a murine model of cardiac transplantation. Hearts from DBA/2 (H-2(d)) mice were heterotopically transplanted into B10.D2 (H-2(d)) mice. Recipients were treated with oral administration of candesartan (1 mg/kg per day) or vehicle. Allografts were analyzed at 14 or 30 days after transplantation. Candesartan significantly reduced the development of coronary arteriosclerosis (intima/media ratio: 0.86 +/- 0.09 versus 0.57 +/- 0.10, P < 0.05), without affecting the degree of parenchymal rejection at 30 days. There was no significant difference in the expression of adhesion molecules and cytokines at 14 days. Candesartan significantly reduced the number of peripheral mononuclear cells that differentiated into smooth muscle-like cells in the presence of basic fibroblast growth factor and platelet-derived growth factor BB (27.1 +/- 3.1 versus 17.3 +/- 1.8 cells/HPF, P < 0.05). Angiotensin II may play a role in the pathogenesis of transplant arteriosclerosis. Blockade of AT(1)R might be effective as a prophylactic therapy for transplant arteriosclerosis along with conventional immunosuppressive drugs. (Keyword) Angiotensin II Type 1 Receptor Blockers / Animals / Arteriosclerosis / Benzimidazoles / Female / Graft Rejection / Heart Transplantation / Interleukin-6 / Male / Mice / Mice, Inbred DBA / Mice, Inbred Strains / Postoperative Complications / Tetrazoles / Transplantation Chimera / Tunica Intima / Vascular Diseases (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jss.2005.07.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16140337 ● Summary page in Scopus @ Elsevier: 2-s2.0-33645999083 (DOI: 10.1016/j.jss.2005.07.011, PubMed: 16140337, Elsevier: Scopus)
478.	S Nishimura, S Nagai, Masataka Sata, M Katoh, H Yamashita, Y Saeki, R Nagai and S Sugiura : Expression of green fluorescent protein impairs the force-generating ability of isolated rat ventricular cardiomyocytes, Molecular and Cellular Biochemistry, Vol.286, No.1-2, 59-65, 2006. (Summary) Green fluorescent protein (GFP) is widely used as a biologically inert expression marker for studying the effects of transgene expression in heart tissue, but its influence on the contractile function of cardiomyocytes has not yet been fully evaluated. We measured the contractile function of isolated rat ventricular myocytes before and after infection with a recombinant adenovirus expressing GFP (Adv-GFP). Myocytes infected with a non-transgene-containing adenovirus (Adv-Null) or uninfected myocytes (UI) served as controls. Using a carbon-fiber-based force-length measurement system for single cardiomyocytes, we evaluated the contractile function over a wide range of loading conditions including the shortening fraction (%FS) and maximal shortening velocity (Vmax) under the unloaded condition, and isometric force. At 24 hours after infection, nearly 80% of the Adv-GFP-infected myocytes expressed GFP. We found that the %FS and Vmax did not differ among the three groups, however, the isometric force showed a mild, but significant, decrease only in Adv-GFP myocytes (Adv-GFP: 29.1 +/- 4.0 mN/mm2; Adv-Null: 42.8 +/- 6.2 mN/mm2; UI: 47.1 +/- 4.8 mN/mm2; p = 0.03). An evaluation of the contractile function of isolated cardiomyocytes under high load conditions revealed impaired isometric contractility by GFP expression. Adv-GFP expression may not be an ideal control for specific gene expression experiments in myocardial tissue. (Keyword) Adenoviridae / Animals / Calcium / Cell Shape / Cell Size / Cell Survival / Female / Gene Expression / Genetic Vectors / Green Fluorescent Proteins / Heart Ventricles / Myocytes, Cardiac / Rats / Rats, Wistar / Transfection (Link to Publication Site) ● Publication site (DOI): 10.1007/s11010-005-9090-6 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16532258 ● Search Scopus @ Elsevier (PMID): 16532258 ● Search Scopus @ Elsevier (DOI): 10.1007/s11010-005-9090-6 (DOI: 10.1007/s11010-005-9090-6, PubMed: 16532258)
479.	Shintaro Yamazaki, Kenji Miki, Tadatoshi Takayama, Kiyoshi Hasegawa, Masataka Sata, Yutaka Midorikawa, Hiroyuki Aburatani and Masatoshi Makuuchi : Hepatic gene induction in murine bone marrow after hepatectomy, Journal of Hepatology, Vol.44, No.2, 325-333, 2006. (Summary) Bone marrow cells are highly plastic and differentiate into various cell types, including hepatocytes. To explore the mechanisms underlying these processes, we focused on the initial responses of bone marrow to hepatectomy, using a mouse model. To evaluate hepatic differentiation in bone marrow cells we measured hepatocyte-related gene expression in mice undergoing partial hepatectomy with or without pretreatment for 1 week with 2-acetyl aminofluorene (AAF). Hepatectomy induced several genes related to early hepatic differentiation in bone marrow. Expression of these genes was enhanced by the administration of AAF, whereas genes specific for mature hepatocytes were not detected. We characterised the bone marrow cell population expressing hepatocyte differentiation genes. alpha-fetoprotein mRNA was induced in Lin- and either CD34+, c-kit+, Sca-1+, CD49f+ or CD45+ cells. The genes upregulated in the liver after AAF treatment and hepatectomy were identified using oligonucleotide microarrays. These included genes associated with the acute phase response. Dexamethasone inhibited the expression of early hepatic differentiation genes in the bone marrow of AAF/PHx mice. Early hepatic differentiation genes were induced in bone marrow in response to hepatectomy, especially when regeneration of the remnant liver was suppressed. Circulating signals generated in the AAF/PHx liver might activate this differentiation. (Keyword) 2-Acetylaminofluorene / Animals / Bone Marrow / Bone Marrow Cells / cell differentiation / Cell Proliferation / Disease Models, Animal / Flow Cytometry / Gene Expression Regulation / Hepatectomy / Hepatocyte Nuclear Factors / Liver Regeneration / Male / Mice / Mice, Inbred C57BL / Microarray Analysis / RNA, Messenger / Reverse Transcriptase Polymerase Chain Reaction / Transcriptional Activation / alpha-Fetoproteins (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jhep.2005.07.025 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16226826 ● Summary page in Scopus @ Elsevier: 2-s2.0-30344442784 (DOI: 10.1016/j.jhep.2005.07.025, PubMed: 16226826, Elsevier: Scopus)
480.	Ryo Takeda, Hiroaki Nishimatsu, Etsu Suzuki, Hiroshi Satonaka, Daisuke Nagata, Shigeyoshi Oba, Masataka Sata, Masao Takahashi, Yuji Yamamato, Yasuo Terauchi, Takashi Kadowaki, Kenji Kangawa, Tadaichi Kitamura, Ryozo Nagai and Yasunobu Hirata : Ghrelin improves renal function in mice with ischemic acute renal failure, Journal of the American Society of Nephrology, Vol.17, No.1, 113-121, 2006. (Summary) Growth hormone and IGF-1 have been suggested to have tissue-protective effects. Ghrelin is a stomach-derived growth hormone secretagogue. The effects of ghrelin on ischemia/reperfusion-induced renal failure in mice were examined. Ischemic acute renal failure was induced by bilateral renal artery clamping for 45 min and reperfusion for 24 h. Ghrelin (100 microg/kg mouse) or vehicle was injected subcutaneously six times before surgery and three times after surgery every 8 h. Twenty-four hours after reperfusion, the right kidney was isolated and perfused. Acetylcholine (ACh)- and adrenomedullin-induced endothelium-dependent vasorelaxation of renal vessels significantly improved in ghrelin-pretreated mice (%Delta renal perfusion pressure by 10(-7) M ACh -63.5 +/- 3.7 versus -41.2 +/- 5.5%; P < 0.05). This change was associated with significant increases of nitric oxide release in the kidneys of ghrelin-treated mice (10(-7) M ACh 35.5 +/- 5.8 versus 16.9 +/- 3.5 fmol/g kidney per min; P < 0.05). Serum concentration of urea nitrogen (53 +/- 7 versus 87 +/- 15 mg/dl; P < 0.05) and renal injury score were significantly lower in the ghrelin group (2.5 +/- 0.8 versus 5.3 +/- 1.5; P < 0.01). Tubular apoptotic index was significantly lower in the ghrelin group (5 +/- 5 versus 28 +/- 4; P < 0.05). Furthermore, the survival rate after the 60-min ischemic period was higher in the ghrelin group (80 versus 20%; P < 0.05). Ghrelin treatment significantly increased the serum level of IGF-1. However, such renal protective effects of ghrelin on ischemia/reperfusion injury were not observed in insulin receptor substrate-2 knockout mice. These results suggest that ghrelin may protect the kidneys from ischemia/reperfusion injury and that this effect is related to an improvement of endothelial function through an IGF-1-mediated pathway. (Keyword) Acute Kidney Injury / Animals / apoptosis / Endothelium, Vascular / Ghrelin / Insulin Receptor Substrate Proteins / Insulin-Like Growth Factor I / Intracellular Signaling Peptides and Proteins / Kidney / Male / Mice / Mice, Inbred BALB C / nitric oxide / Peptide Hormones / Phosphatidylinositol 3-Kinases / Phosphoproteins / Reperfusion Injury / Survival Rate (Link to Publication Site) ● Publication site (DOI): 10.1681/ASN.2004080626 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16306169 ● Summary page in Scopus @ Elsevier: 2-s2.0-33645450266 (DOI: 10.1681/ASN.2004080626, PubMed: 16306169, Elsevier: Scopus)
481.	M Ohta, K Tateishi, F Kanai, H Watanabe, S Kondo, B Guleng, Y Tanaka, Y Asaoka, A Jazag, J Imamura, H Ijichi, T Ikenoue, Masataka Sata, M Miyagishi, K Taira, M Tada, T Kawabe and M Omata : p53-Independent Negative Regulation of p21/Cyclin-Dependent Kinase-Interacting Protein 1 by the Sonic Hedgehog-Glioma-Associated Oncogene 1 Pathway in Gastric Carcinoma Cells, Cancer Research, Vol.65, No.23, 10822-10829, 2005. (Summary) The activation of Hedgehog (Hh) signaling has been implicated in the growth of various tumor types, including gastric carcinoma. However, the precise mechanisms of Hh activation and suppression of tumor growth by the blockade of Hh signaling in gastric carcinoma cells remain unknown. The aim of this study was to elucidate the mechanism of abnormal Hh signaling and the key molecules contributing to dysregulated growth of gastric carcinoma. The Sonic hedgehog (Shh) ligand and its receptor Patched were expressed in all five gastric carcinoma cell lines examined (MKN1, MKN7, MKN45, MKN74, and AGS cells). The blockade of Hh signaling with anti-Shh antibody inhibited the growth of all five gastric carcinoma cell lines. Shh was overexpressed (mean, 12.8-fold) in 8 of 14 (57.0%) cancerous tissue samples from patients with gastric carcinoma as compared with expression in the surrounding noncancerous tissues. The disruption of glioma-associated oncogene 1 (Gli1) by small interfering RNA induced an increase in p21/cyclin-dependent kinase-interacting protein 1 (CIP1), interfered with the G1-S transition, and suppressed cell proliferation. The stimulation or inhibition of Hh signaling did not affect p53 activity and the induction of p21/CIP1 expression and the G1 arrest by inhibition of Hh signaling were not affected by the p53 status. These findings suggest that the overexpression of Shh contributes to constitutive Hh activation and that this signaling pathway negatively regulates p21/CIP1 through a Gli1-dependent and p53-independent mechanism in gastric carcinoma cells. (Keyword) Adult / Aged / Aged, 80 and over / Cell Cycle / Cell Line, Tumor / Cyclin-Dependent Kinase Inhibitor p21 / Female / Hedgehog Proteins / Humans / Male / Middle Aged / RNA Interference / RNA, Messenger / RNA, Small Interfering / Signal Transduction / Stomach Neoplasms / Trans-Activators / Transcription Factors / Transfection / Tumor Suppressor Protein p53 / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1158/0008-5472.CAN-05-0777 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16322228 ● Search Scopus @ Elsevier (PMID): 16322228 ● Search Scopus @ Elsevier (DOI): 10.1158/0008-5472.CAN-05-0777 (DOI: 10.1158/0008-5472.CAN-05-0777, PubMed: 16322228)
482.	K Saito, N Ishizaka, M Hara, G Matsuzaki, Masataka Sata, I Mori, M Ohno and R Nagai : Lipid accumulation and transforming growth factor-β upregulation in the kidneys of rats administered angiotensin II, Hypertension, Vol.46, No.5, 1180-1185, 2005. (Summary) Abnormal lipid metabolism may play a role in progressive renal failure. We studied whether lipid accumulation occurs and whether lipid deposits are colocalized with transforming growth factor-beta1 (TGF-beta1) in the kidney of angiotensin II-infused animals. Oil red O staining showed marked lipid deposition in the tubular epithelial and vascular wall cells of angiotensin II-treated but not in norepinephrine-treated rats. Histological analyses showed that increased amounts of superoxide and intense TGF-beta1 mRNA expression were present in lipid-positive tubular epithelial cells in angiotensin II-infused animals. Protein expression of sterol regulatory element-binding protein 1 (SREBP-1) and mRNA expression of fatty acid synthase in the kidney were &3 times and 1.5 times, respectively, higher in angiotensin II-treated rats than in controls. Treatment of angiotensin II-infused animals with an iron chelator, deferoxamine, attenuated the angiotensin II-induced increases in renal expression of SREBP-1 and fatty acid synthase and normalized the lipid content in the renal cortical tissues. Abnormal lipid metabolism may be associated with upregulation of TGF-beta1 expression and aberrant iron homeostasis in the kidneys of angiotensin II-infused animals. (Keyword) Angiotensin II / Animals / Deferoxamine / Fatty Acid Synthetase Complex / Gene Expression Regulation / In Situ Hybridization / Iron / Iron Chelating Agents / Kidney / Lipid Metabolism / Lipids / Male / Plasminogen Activator Inhibitor 1 / RNA, Messenger / Rats / Rats, Sprague-Dawley / Staining and Labeling / Sterol Regulatory Element Binding Protein 1 / Superoxides / Tissue Distribution / Transforming Growth Factor beta / Transforming Growth Factor beta1 / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1161/01.HYP.0000184653.75036.d5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16203876 ● Search Scopus @ Elsevier (PMID): 16203876 ● Search Scopus @ Elsevier (DOI): 10.1161/01.HYP.0000184653.75036.d5 (DOI: 10.1161/01.HYP.0000184653.75036.d5, PubMed: 16203876)
483.	K Tanaka, Masataka Sata, D Fukuda, Y Suematsu, N Motomura, S Takamoto, Y Hirata and R Nagai : Age-associated Aortic Stenosis in Apolipoprotein E-deficient Mice, Journal of the American College of Cardiology, Vol.46, No.1, 134-141, 2005. (Summary) The present study was designed to assess aortic valve morphology and function in mice of advanced age. We also evaluated the potential contribution of bone-marrow-derived cells to the pathogenesis of aortic stenosis. Age-associated valvular degeneration is characterized by lipid accumulation, collagen deposition, and calcification containing smooth muscle-like cells and osteoblast-like cells. Cellular and molecular factors that mediate these changes remain unknown. We extensively examined the aortic valves of senile wild-type and apolipoprotein E (ApoE)-/- mice with echocardiography. The aortic valves were analyzed by immunohistochemistry and electron microscopy. The bone marrow of wild-type and ApoE-/- mice was reconstituted with that of green fluorescent protein (GFP) or beta-galactosidase (LacZ) mice, which expressed GFP or LacZ ubiquitously. Transaortic flow velocity was correlated with age in wild-type and ApoE-/- mice. The aortic valves of old ApoE-/- mice showed sclerosis that resembled the pathology of human aortic stenosis. A significant number of GFP-positive cells (10.7 +/- 4.1%) in the sclerotic valves of ApoE-/- mice expressed alpha-smooth muscle actin, whereas most of the GFP-positive cells were identified as endothelial cells or macrophages in wild-type mice. There were bone-marrow-derived cells that were positive for osteoblast-related proteins near the sites of ectopic calcification. The sclerotic valves displayed frequent apoptotic cell death and chemokine expression. Senile ApoE-deficient mice display aortic valve sclerosis that is similar to that observed in humans. The sclerotic valves displayed frequent apoptotic cell death and chemokine expression. Smooth muscle-like cells observed in degenerative valves might derive, at least in part, from bone marrow. (Keyword) Age Factors / Animals / Aortic Valve / Aortic Valve Stenosis / Apolipoproteins E / Apoptosis / Bone Marrow Cells / Chemokine CCL2 / Chemokine CXCL12 / Chemokines, CXC / Female / Male / Mice / Mice, Inbred C57BL / Platelet-Derived Growth Factor / Vascular Endothelial Growth Factor A (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jacc.2005.03.058 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15992647 ● Search Scopus @ Elsevier (PMID): 15992647 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jacc.2005.03.058 (DOI: 10.1016/j.jacc.2005.03.058, PubMed: 15992647)
484.	B Guleng, K Tateishi, M Ohta, F Kanai, A Jazag, H Ichijo, Y Tanaka, M Washida, K Morikane, Y Fukushima, T Yamori, T Tsuruo, T Kawabe, M Miyagishi, K Taira, Masataka Sata and M Omata : Blockade of the stromal cell-derived factor-1/CXCR4 axis attenuates in vivo tumor growth by inhibiting angiogenesis in a vascular endothelial growth factor-independent manner, Cancer Research, Vol.65, No.13, 5864-5871, 2005. (Summary) The interaction between the chemokine receptor CXCR4 and its specific ligand, stromal cell-derived factor-1 (SDF-1/CXCL12), mediates several cellular functions. In cancer, SDF-1-positive or CXCR4-positive cells of various lineages are detected within tumor tissues. Recent intensive research has indicated the possibility that blocking CXCR4 could reduce the metastatic potential of cancer cells. Here, we show that the inhibition of the SDF-1/CXCR4 axis decreases the growth of s.c. gastrointestinal tumors through the suppression of tumor neoangiogenesis. The neutralization of CXCR4 suppressed the growth in vivo of tumors derived from mouse Colon38 and PancO2 cells, whereas it did not affect the growth of Colon38 and PancO2 cells in vitro. This attenuation of tumor growth was found to be independent of the expression of CXCR4 by the cancer cells themselves, because CXCR4 knocked-down Colon38 cells grew similarly to control cells. Furthermore, CD31-positive tumor capillaries were reduced to 45% (P < 0.001) and intratumor blood flows were decreased to 65% (P < 0.01) by blockade of CXCR4. The vascular endothelial growth factor (VEGF) concentration in the tumors was not affected by the neutralization of CXCR4. Taken together with the detection of CXCR4-positive endothelial cells in the tumor tissues, the findings suggest that the antiangiogenic effects of the blockade of CXCR4 are related to a reduction of the establishment of tumor endothelium independently of VEGF inhibition. Our data indicate that the SDF-1/CXCR4 pathway might be a general target for anticancer strategies and that blocking this system could be cooperatively effective in combination with other antiangiogenic therapies, such as blockade of VEGF. (Keyword) Animals / Cell Growth Processes / Chemokine CXCL12 / Chemokines, CXC / Colonic Neoplasms / Endothelial Cells / Mice / Mice, Inbred BALB C / Mice, Inbred C57BL / Mice, Nude / Mice, Transgenic / Neovascularization, Pathologic / Pancreatic Neoplasms / Plasmids / RNA Interference / Receptors, CXCR4 / Vascular Endothelial Growth Factor A (Link to Publication Site) ● Publication site (DOI): 10.1158/0008-5472.CAN-04-3833 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15994964 ● Search Scopus @ Elsevier (PMID): 15994964 ● Search Scopus @ Elsevier (DOI): 10.1158/0008-5472.CAN-04-3833 (DOI: 10.1158/0008-5472.CAN-04-3833, PubMed: 15994964)
485.	M Ohta, K Tateishi, F Kanai, S Ueha, B Guleng, M Washida, Y Tanaka, H Ijichi, T Ikenoue, Masataka Sata, T Sudo, S Siina, T Kawabe, K Matsushima and M Omata : Reduced p38 mitogen-activated protein kinase in donor grafts accelerates acute intestinal graft-versus-host disease in mice, European Journal of Immunology, Vol.35, No.7, 2210-2221, 2005. (Summary) The gastrointestinal tract is a major target of graft-versus-host disease (GVHD), which constitutes a life-threatening complication of bone marrow transplantation. GVHD is mainly caused by the activation of donor-derived lymphocytes, in which cytokine cascades play essential roles. Since p38 MAPK (p38) has been identified as a regulator of cytokine reactions and proposed as a molecular target for anti-inflammatory therapy, we investigated the contribution of p38 to the severity of murine intestinal GVHD. Unexpectedly, p38alpha(+/-) donor graft induced more acute GVHD-related mortality and more severe gut injury. The survival of p38alpha(+/-) donor-derived intestinal intraepithelial lymphocytes (IEL) was prolonged in vitro and in vivo, and TNF-alpha expression in the p38alpha(+/-) donor-derived IEL was also increased compared with wild-type cells. In contrast, the p38alpha(+/-) grafted mice resulted in decreased expansion of donor lymphocytes in mesenteric lymph nodes, and the up-regulation of IL-12p40 and IL-18 was diminished. These findings suggest that p38 has dichotomous effects for inflammatory response in vivo; not only regulates inflammatory cytokine expression and lymphocyte expansion, but also has distinct regulatory functions for IEL in intestinal GVHD. In conclusion, the inhibition of p38 may not be a suitable anti-inflammatory strategy for GVHD due to the associated intestinal injury. (Keyword) Acute Disease / Animals / Apoptosis / Bone Marrow Transplantation / Colonic Diseases / Cytokines / Graft vs Host Disease / Green Fluorescent Proteins / Immunophenotyping / Kinetics / Lymphocytes / Mice / Mice, Inbred C57BL / Mice, Transgenic / Mitogen-Activated Protein Kinase 14 / Severity of Illness Index (Link to Publication Site) ● Publication site (DOI): 10.1002/eji.200425897 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15971269 ● Search Scopus @ Elsevier (PMID): 15971269 ● Search Scopus @ Elsevier (DOI): 10.1002/eji.200425897 (DOI: 10.1002/eji.200425897, PubMed: 15971269)
486.	M Sahara, Masataka Sata, Y Natsuzaki, K Tanaka, T Morita, Y Hirata, H Okano and R Nagai : Comparison of various bone marrow fractions in the ability to participate in vascular remodeling after mechanical injury, Stem Cells, Vol.23, No.7, 874-878, 2005. (Summary) In contrast to conventional assumption, recent reports propose the possibility that hematopoietic stem cells (HSCs) may have broader potential to differentiate into various cell types. Here, we tested the pluripotency of HSCs by comparing vascular lesions induced by mechanical injury after bone marrow reconstitution with total bone marrow (TBM) cells, c-Kit+ Sca-1+ Lin- (KSL) cells, or a single HSC cell (Tip-SP CD34-KSL cell, CD34- c-Kit+ Sca-1+ Lin- cell with the strongest dye-efflux activity) harboring green fluorescent protein (GFP). The lesions contained a significant number of GFP-positive cells in the TBM and KSL groups, whereas GFP-positive cells were rarely detected in the HSC group. These results suggest that transdifferentiation of a highly purified HSC seems to be a rare event, if it occurs at all, whereas bone marrow cells including the KSL fraction can give rise to vascular cells that substantially contribute to repair or lesion formation after mechanical injury. (Keyword) Animals / Antigens, CD34 / Blood Vessels / Bone Marrow Cells / Cell Differentiation / Cell Transplantation / Endothelium, Vascular / Green Fluorescent Proteins / Hematopoietic Stem Cell Transplantation / Mice / Mice, Inbred C57BL / Mice, Transgenic / Microscopy, Fluorescence / Stem Cell Transplantation / Stem Cells / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1634/stemcells.2005-0012 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15941860 ● Search Scopus @ Elsevier (PMID): 15941860 ● Search Scopus @ Elsevier (DOI): 10.1634/stemcells.2005-0012 (DOI: 10.1634/stemcells.2005-0012, PubMed: 15941860)
487.	H Iwata, Masataka Sata and R Nagai : Complete aspiration of thrombi from an occluded coronary artery., Heart, Vol.91, No.4, 530, 2005. (Keyword) Adult / Coronary Angiography / Coronary Thrombosis / Humans / Male / Suction / Thrombectomy (Link to Publication Site) ● Publication site (DOI): 10.1136/hrt.2004.044644 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15772221 ● Search Scopus @ Elsevier (PMID): 15772221 ● Search Scopus @ Elsevier (DOI): 10.1136/hrt.2004.044644 (DOI: 10.1136/hrt.2004.044644, PubMed: 15772221)
488.	T Kitamura, Masataka Sata, N Motomura and S Takamoto : Seeding of recipient bone marrow cells reduces neointimal hyperplasia of deendothelialized rat aortic allograft, International Heart Journal, Vol.46, No.2, 303-312, 2005. (Summary) Transplant vasculopathy is a leading cause of graft failure and a major contributor to the lack of success with small caliber vascular allografts. In this study we evaluate techniques of bone marrow cell seeding on small caliber vessels and assess the impact of this tactic on neointimal hyperplasia in de-endothelialized rat aortic allografts. In a preliminary study, bone marrow cells from Lewis rats were seeded onto the chemically de-endothelialized luminal surface of the abdominal aorta of WKY rats - with or without fibrin glue. In the allograft transplantation model, de-endothelialized fresh aortic allografts of WKY rats were orthotopically transplanted into Lewis recipients either directly (n = 6) or after recipient bone marrow cell seeding (n = 6). Histological evaluation was performed at 28 days. Bone marrow cells were able to adhere to the de-endothelialized aortic wall owing to the use of fibrin glue, but were unable to do so without fibrin glue. In the de-endothelialized allograft transplantation model, recipient bone marrow seeding led to a significant reduction of the ratio of intimal to medial area (0.40 +/- 0.08 versus 0.79 +/- 0.08, P = 0.0077). Some of the seeded cells remained in the intima for 4 weeks and some infiltrated the media, expressing CD31 or alpha-SMA. The results suggest that recipient bone marrow cell seeding on de-endothelialized aortic allograft is feasible with the use of fibrin glue and that this technique reduces neointimal hyperplasia of the graft. (Keyword) Actins / Animals / Antigens, CD31 / Aorta / Bone Marrow Cells / Bone Marrow Transplantation / Endothelium, Vascular / Fibrin Tissue Adhesive / Hyperplasia / Male / Rats / Rats, Inbred Lew / Rats, Inbred WKY / Transplantation, Homologous (Link to Publication Site) ● Publication site (DOI): 10.1536/ihj.46.303 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15876813 ● Search Scopus @ Elsevier (PMID): 15876813 ● Search Scopus @ Elsevier (DOI): 10.1536/ihj.46.303 (DOI: 10.1536/ihj.46.303, PubMed: 15876813)
489.	JR Kim-Kaneyama, W Suzuki, K Ichikawa, T Ohki, Y Kohno, Masataka Sata, K Nose and M Shibanuma : Uni-axial stretching regulates intracellular localization of Hic-5 expressed in smooth-muscle cells in vivo, Journal of Cell Science, Vol.118, No.Pt 5, 937-949, 2005. (Summary) Hic-5 is a focal adhesion protein belonging to the paxillin LIM family that shuttles in and out of the nucleus. In the present study, we examined the expression of Hic-5 among mouse tissues by immunohistochemistry and found its expression only in smooth-muscle cells in several tissues. This result is consistent with a previous report on adult human tissues and contradicts the relatively ubiquitous expression of paxillin, the protein most homologous to Hic-5. One factor characterizing smooth-muscle cells in vivo is a continuous exposure to mechanical stretching in the organs. To study the involvement of Hic-5 in cellular responses to mechanical stress, we exposed mouse embryo fibroblasts to a uni-axial cyclic stretching and found that Hic-5 was relocalized from focal adhesions to stress fibers through its C-terminal LIM domains during the stress. In sharp contrast to this, paxillin did not change its focal-adhesion-based localization. Of the factors tested, which included interacting partners of Hic-5, only CRP2 (an only-LIM protein expressed in vascular smooth-muscle cells) and GIT1 were, like Hic-5, localized to stress fibers during the cyclic stretching. Interestingly, Hic-5 showed a suppressive effect on the contractile capability of cells embedded in three-dimensional collagen gels, and the effect was further augmented when CRP2 co-localized with Hic-5 to fiber structures of those cells. These results suggested that Hic-5 was a mediator of tensional force, translocating directly from focal adhesions to actin stress fibers upon mechanical stress and regulating the contractile capability of cells in the stress fibers. (Keyword) Actinin / Amino Acid Motifs / Animals / Antibodies, Monoclonal / CCAAT-Enhancer-Binding Protein-beta / COS Cells / Cell Adhesion / Cell Cycle Proteins / Cell Nucleus / Cells, Cultured / Collagen / Cytoskeletal Proteins / Cytoskeleton / DNA-Binding Proteins / Fibroblasts / Focal Adhesions / GTPase-Activating Proteins / Immunoblotting / Immunohistochemistry / Immunoprecipitation / LIM Domain Proteins / Mice / Mice, Inbred ICR / Microscopy, Electron / Microscopy, Fluorescence / Muscle Contraction / Muscle, Smooth / Paxillin / Phosphoproteins / Plasmids / Protein Structure, Tertiary / Protein Transport / Time Factors / Tissue Distribution / Transfection (Link to Publication Site) ● Publication site (DOI): 10.1242/jcs.01683 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15713747 ● Search Scopus @ Elsevier (PMID): 15713747 ● Search Scopus @ Elsevier (DOI): 10.1242/jcs.01683 (DOI: 10.1242/jcs.01683, PubMed: 15713747)
490.	D Fukuda, Masataka Sata, K Tanaka and R Nagai : Potent inhibitory effect of sirolimus on circulating vascular progenitor cells, Circulation, Vol.111, No.7, 926-931, 2005. (Summary) Neointimal hyperplasia is the major cause of in-stent restenosis (ISR). The sirolimus-eluting stent (SES) has emerged as a promising therapy to prevent ISR; however, the exact mechanism by which locally delivered sirolimus, an immunosuppressive agent, prevents ISR remains unknown. Recent evidence suggests that circulating progenitor cells may contribute to neointimal formation. Mononuclear cells (MNCs) were isolated from peripheral blood of healthy human volunteers. Smooth muscle (SM)-like cells outgrew from the culture of MNCs (1x10(6)) in the presence of platelet-derived growth factor-BB and basic fibroblast growth factor, whereas endothelial cell-like cells were obtained in the presence of vascular endothelial growth factor. Sirolimus potently inhibited SM-like cell outgrowth. The number of SM-like cells was significantly reduced at a concentration as low as 0.1 ng/mL (15.9+/-5.8% of control, P<0.001). Sirolimus also exerted an inhibitory effect on endothelial cell-like cells that originated from MNCs. Wire-mediated vascular injury was induced in femoral arteries of bone marrow chimeric mice. Either vehicle or sirolimus was administered locally to the perivascular area of the injured arteries. Sirolimus significantly reduced neointima hyperplasia at 4 weeks (intima/media ratio 2.0+/-0.3 versus 1.0+/-0.2, P<0.05) with a decreased number of bone marrow-derived SM-like cells and hematopoietic cells in the lesion. Reendothelialization was retarded in the arteries treated with sirolimus. The potent inhibitory effects of sirolimus on circulating smooth muscle progenitor cells may mediate the clinical efficacy of SES, at least in part. Sirolimus potentially may affect reendothelialization after stent implantation. (Keyword) Animals / Blood Cells / Bone Marrow Transplantation / Cell Culture Techniques / Cell Differentiation / Cells, Cultured / Endothelium, Vascular / Femoral Artery / Graft Occlusion, Vascular / Growth Substances / Humans / Immunosuppressive Agents / Lac Operon / Leukocytes, Mononuclear / Mice / Mice, Transgenic / Myocytes, Smooth Muscle / Sirolimus / Stem Cells / Stents (Link to Publication Site) ● Publication site (DOI): 10.1161/01.CIR.0000155612.47040.17 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15710768 ● Search Scopus @ Elsevier (PMID): 15710768 ● Search Scopus @ Elsevier (DOI): 10.1161/01.CIR.0000155612.47040.17 (DOI: 10.1161/01.CIR.0000155612.47040.17, PubMed: 15710768)
491.	Y Hirata, Masataka Sata, N Motomura, M Takanashi, Y Suematsu, M Ono and S Takamoto : Human umbilical cord blood cells improve cardiac function after myocardial infarction, Biochemical and Biophysical Research Communications, Vol.327, No.2, 609-614, 2005. (Summary) Human umbilical cord blood (UCB) contains an abundance of immature stem/progenitor cells and has been clinically used as an alternative to bone marrow transplantation. In addition, cord blood can be obtained non-invasively, in contrast to invasive bone marrow aspiration. We investigated the potential of human UCB CD34(+) cells to improve cardiac function following myocardial infarction. Myocardial infarction was induced in Wistar rats by ligation of the left coronary artery. Either 2x10(5) human UCB CD34(+) cells or equivalent cell-free medium was injected into the injured myocardium of the rats following induction of myocardial infarction. CD34(+) cell transplantation significantly improved ventricular function as compared to the control group. Immunofluorescence staining for human CD34, CD45, and PECAM-1 revealed surviving cells in the myocardium. Our findings suggest that transplanted human cells survived and improved cardiac function following myocardial infarction. These results may show the usefulness of UCB CD34(+) cells for myocardial infarction. (Keyword) Animals / Antigens, CD34 / Cell Survival / Fetal Blood / Humans / Male / Myocardial Infarction / Myocardium / Neovascularization, Physiologic / Rats / Rats, Wistar / Stem Cell Transplantation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2004.12.044 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15629157 ● Search Scopus @ Elsevier (PMID): 15629157 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2004.12.044 (DOI: 10.1016/j.bbrc.2004.12.044, PubMed: 15629157)
492.	Y Higashikuni, Masataka Sata and R Nagai : Reversible left ventricular hypertrophy after Tako-Tsubo-like cardiomyopathy., Acta Cardiologica, Vol.60, No.1, 77-79, 2005. (Summary) Tako-tsubo-like cardiomyopathy is a newly-recognized enigmatic disease characterized by transient left ventricular dysfunction of a broad area of the apex with a hyperkinetic area around the cardiac base. There is ST-segment elevation with no coronary stenosis. The exact mechanism for this entity remains unknown. Here, we report a case of tako-tsubo-like cardiomyopathy that showed a marked left ventricular hypertrophy (LVH) when the wall motion returned to normal. LVH was normalized at 10 months. The cause of LVH remains unknown. (Keyword) Aged / Aspirin / Benzimidazoles / Cardiomyopathy, Dilated / Chest Pain / Drug Therapy, Combination / Electrocardiography / Female / Follow-Up Studies / Humans / Hypertrophy, Left Ventricular / Magnetic Resonance Imaging / Myocardial Ischemia / Nifedipine / Risk Assessment / Severity of Illness Index / Tetrazoles / Ventricular Dysfunction, Left (Link to Publication Site) ● Publication site (DOI): 10.2143/AC.60.1.2005056 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15779859 ● Search Scopus @ Elsevier (PMID): 15779859 ● Search Scopus @ Elsevier (DOI): 10.2143/AC.60.1.2005056 (DOI: 10.2143/AC.60.1.2005056, PubMed: 15779859)
493.	T Natori, Masataka Sata, R Nagai and M Makuuchi : Cimetidine inhibits angiogenesis and suppresses tumor growth, Biomedicine & Pharmacotherapy, Vol.59, No.1-2, 56-60, 2005. (Summary) Cimetidine, a histamine type-2 receptor antagonist, has been reported to improve survival of patients with cancers. However, the exact mechanisms by which cimetidine suppresses development of cancers remain to be elucidated. Solid tumors require neovascularization for their growth. Here, we investigated the effects of cimetidine on tumor growth and angiogenesis. Syngeneic colon cancer cells, CMT93 cells, were inoculated into the subcutaneous space of C57BL/6 mice. Mice were treated with either saline or cimetidine. Tumor size was measured everyday and angiogenesis was evaluated histologically. Cimetidine markedly suppressed tumor growth with reduced neovascularization in the tumor. Cimetidine had no effect on proliferation of CMT93 cells in vitro. Vascular endothelial growth factor production by cancer cells was not affected by cimetidine, while vascular-like tube formation by endothelial cells in vitro was significantly impaired in the presence of cimetidine. Our findings suggest that cimetidine suppresses tumor growth, at least in part, by inhibiting tumor-associated angiogenesis. (Keyword) Angiogenesis Inhibitors / Animals / Antineoplastic Agents / Cell Line, Tumor / Cimetidine / Drug Screening Assays, Antitumor / Growth Inhibitors / Male / Mice / Mice, Inbred C57BL / Neovascularization, Pathologic (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biopha.2004.05.018 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15740937 ● Search Scopus @ Elsevier (PMID): 15740937 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biopha.2004.05.018 (DOI: 10.1016/j.biopha.2004.05.018, PubMed: 15740937)
494.	K Saito, N Ishizaka, T Aizawa, Masataka Sata, N Iso-o, E Noiri, I Mori, M Ohno and R Nagai : Iron chelation and a free radical scavenger suppress angiotensin II-induced upregulation of TGF-1 in the heart, American Journal of Physiology, Heart and Circulatory Physiology, Vol.288, No.4, H1836-H1843, 2005. (Summary) Long-term administration of angiotensin II causes myocardial loss and cardiac fibrosis. We previously found iron deposition in the heart of the angiotensin II-infused rat, which may promote angiotensin II-induced cardiac damage. In the present study, we have investigated whether an iron chelator (deferoxamine) and a free radical scavenger (T-0970) affect the angiotensin II-induced upregulation of transforming growth factor-beta1 (TGF-beta1). Angiotensin II infusion for 7 days caused a robust increase in TGF-beta1 mRNA expression in vascular smooth muscle cells, myofibroblast-like cells, and migrated monocytes/macrophages. T-0970 and deferoxamine suppressed the upregulation of TGF-beta1 mRNA and reduced the extent of cardiac fibrosis in the heart of rats treated with angiotensin II. These agents blocked the angiotensin II-induced upregulation of heme oxygenase-1, a potent oxidative and cellular stress-responsive gene, but they did not significantly affect systolic blood pressure or plasma levels of aldosterone. In addition, T-0970 and deferoxamine suppressed the angiotensin II-induced upregulation of monocyte chemoattractant protein-1 in the heart. These results collectively suggest that iron and the iron-mediated generation of reactive oxygen species may contribute to angiotensin II-induced upregulation of profibrotic and proinflammatory genes, such as TGF-beta1 and monocyte chemoattractant protein-1. (Keyword) Aldosterone / Angiotensin II / Animals / Chemokine CCL2 / Deferoxamine / Enzyme Inhibitors / Ferritins / Fibrosis / Free Radical Scavengers / Gene Expression / Heme Oxygenase (Decyclizing) / Heme Oxygenase-1 / Iron / Iron Chelating Agents / Male / Myocardium / Oxidative Stress / Phenylurea Compounds / Protoporphyrins / Pyridines / RNA, Messenger / Rats / Rats, Sprague-Dawley / Transforming Growth Factor beta / Transforming Growth Factor beta1 / Up-Regulation / Vasoconstrictor Agents (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpheart.00679.2004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15550525 ● Search Scopus @ Elsevier (PMID): 15550525 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpheart.00679.2004 (DOI: 10.1152/ajpheart.00679.2004, PubMed: 15550525)
495.	N Ishizaka, K Saito, E Noiri, Masataka Sata, H Ikeda, A Ohno, J Ando, I Mori, M Ohno and R Nagai : Administration of angiotensin II induces iron deposition and upregulation of TGF-β1 mRNA in the rat liver, American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, Vol.288, No.4, R1063-R1070, 2005. (Summary) We previously found that ANG II infusion into rats causes iron deposition in the kidney and heart, which may have a role in the regulation of profibrotic gene expression and tissue fibrosis. In the present study, we have investigated whether ANG II can also induce iron accumulation in the liver. Prussian blue staining detected frequent iron deposition in the interstitium of the liver of rats treated with pressor dose ANG II for 7 days, whereas iron deposition was absent in the livers of control rats. Immunohistochemical and histological analyses showed that some iron-positive nonparenchymal cells were positive for ferritin and heme oxygenase-1 (HO-1) protein and TGF-beta1 mRNA and were judged to be monocytes/macrophages. It was shown that ANG II infusion caused about a fourfold increase in ferritin and HO-1 protein expression by Western blot analysis and about a twofold increase in TGF-beta1 mRNA expression by Northern blot analysis, which were both suppressed by treating ANG II-infused rats with losartan and deferoxamine. In addition, mild interstitial fibrosis was observed in the liver of rats that had been treated with pressor dose ANG II for 7 days or with nonpressor dose ANG II for 30 days, the latter of which also caused loss of hepatocytes and intrahepatic hemorrhage in the liver. Taken together, our data suggest that ANG II infusion induces aberrant iron homeostasis in the liver, which may have a role in the ANG II-induced upregulation of profibrotic gene expression in the liver. (Keyword) Angiotensin II / Animals / Antihypertensive Agents / Blotting, Northern / Blotting, Western / Ferritins / Heme Oxygenase (Decyclizing) / Homeostasis / Infusions, Intravenous / Iron / Iron Chelating Agents / Liver / Male / RNA, Messenger / Rats / Rats, Sprague-Dawley / Transforming Growth Factor beta / Transforming Growth Factor beta1 / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpregu.00281.2004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15604307 ● Search Scopus @ Elsevier (PMID): 15604307 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpregu.00281.2004 (DOI: 10.1152/ajpregu.00281.2004, PubMed: 15604307)
496.	Tetsufumi Yamamoto, Masataka Sata, Daiju Fukuda and Shinichi Takamoto : The angiotensin II type 1 receptor blocker valsartan attenuates graft vasculopathy, Basic Research in Cardiology, Vol.100, No.1, 84-91, 2005. (Summary) Transplant arteriosclerosis remains the major cause of graft failure after cardiac transplantation. Here, we investigated the effects of the angiotensin II type 1 receptor blocker valsartan on the development of transplant arteriosclerosis in a murine model of cardiac transplantation. Hearts from DBA/2 (H-2(d)) mice were heterotopically transplanted into B10.D2 (H-2(d)) mice. Recipients were treated with oral administration of valsartan (10 mg/kg/day) or vehicle. Morphometrical analysis of the cardiac allografts harvested at 30 days revealed that valsartan significantly reduced the development of coronary atherosclerosis (intima/media ratio: 0.39 +/- 0.05 vs. 0.66 +/- 0.08, P < 0.01). At two weeks after transplantation, there was no significant difference between the two groups in expression of adhesion molecules and cytokines. Valsartan significantly reduced the number of peripheral mononuclear cells that differentiated into smooth muscle-like cells in the presence of basic fibroblast growth factor and platelet-derived growth factor BB (18.0 +/- 1.5 vs. 30.3 +/- 4.4 cells/HPF, P = 0.01). These results suggest that angiotensin II plays a role in the pathogenesis of transplant arteriosclerosis and that blockade of angiotensin II type 1 receptor might be effective as a prophylactic therapy for transplant arteriosclerosis along with conventional immunosuppressive drugs. (Keyword) Angiotensin II Type 1 Receptor Blockers / Animals / Coronary Artery Disease / Coronary Vessels / Heart Transplantation / Male / Mice / Mice, Inbred DBA / Tetrazoles / Valine (Link to Publication Site) ● Publication site (DOI): 10.1007/s00395-004-0489-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15490202 ● Search Scopus @ Elsevier (PMID): 15490202 ● Search Scopus @ Elsevier (DOI): 10.1007/s00395-004-0489-0 (DOI: 10.1007/s00395-004-0489-0, PubMed: 15490202)
497.	N Kobayashi, T Yasu, H Ueba, Masataka Sata, S Hashimoto, M Kuroki, M Saito and M Kawakami : Mechanical stress promotes the expression of smooth muscle-like properties in marrow stromal cells, Experimental Hematology, Vol.32, No.12, 1238-1245, 2004. (Summary) It is poorly understood what kind of factors are involved in lineage commitment and maturation of mesenchymal stem cells. The present study investigates whether mechanical stress promotes expression of smooth muscle cell (SMC)-specific cytoskeletal protein in marrow stromal cells. Fibroblast-like stromal cells expressing STRO-1 antigen were isolated from rat bone marrow by density gradient separation. After preincubation for 7, 14, or 21 days in static condition, cells were exposed to one of three types of fluid flow-induced mechanical forces (flow dominant, pressure dominant, or combined) for 36 hours. The expression of SMC-specific cytoskeletal protein [alpha smooth muscle actin (alphaSMA) and smooth muscle myosin heavy chain (SMMHC)] was evaluated by immunofluorescence staining and Western blotting. The proportion of SMMHC-positive cells was increased with longer preincubation periods (p < 0.01 vs 7-day incubation) and by any types of mechanical stimulation (p < 0.01 vs static control condition). The SMMHC-positive fraction after exposure to pressure-dominant forces (0.9% +/- 0.2%, 2.9% +/- 0.9%, and 12.6% +/- 0.8% for 7, 14, and 21 days of preincubation) or to combined forces (1.2% +/- 0.2%, 3.1% +/- 1.6%, and 15.5% +/- 2.8%) was higher than after flow-dominant stimulation (0, 1.2% +/- 0.1%, and 7.2% +/- 2.0%) (p < 0.01). In Western blotting, pressure-dominant or combined stimulation upregulated alphaSMA and SMMHC expression compared to static control condition. The long-term cell incubation and subsequent mechanical stimulation, especially compressive strain, promote expression of SMC-specific cytoskeletal protein in marrow stromal cells. (Keyword) Actins / Animals / Antigens, Surface / Blotting, Western / Bone Marrow Cells / Cell Differentiation / Cell Lineage / Cells, Cultured / Fibroblasts / Immunohistochemistry / Male / Mesenchymal Stem Cells / Microscopy, Fluorescence / Muscle, Smooth / Myosin Heavy Chains / Rats / Rats, Wistar / Stress, Mechanical / Stromal Cells (Link to Publication Site) ● Publication site (DOI): 10.1016/j.exphem.2004.08.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15588948 ● Search Scopus @ Elsevier (PMID): 15588948 ● Search Scopus @ Elsevier (DOI): 10.1016/j.exphem.2004.08.011 (DOI: 10.1016/j.exphem.2004.08.011, PubMed: 15588948)
498.	K Ohtani, K Egashira, KI Hiasa, Q Zhao, S Kitamoto, M Ishibashi, M Usui, S Inoue, Y Yonemitsu, K Sueishi, Masataka Sata, M Shibuya and K Sunagawa : Blockade of vascular endothelial growth factor suppresses experimental restenosis after intraluminal injury by inhibiting recruitment of monocyte lineage cells, Circulation, Vol.110, No.16, 2444-2452, 2004. (Summary) Therapeutic angiogenesis by delivery of vascular endothelial growth factor (VEGF) has attracted attention. However, the role and function of VEGF in experimental restenosis (neointimal formation) after vascular intraluminal injury have not been addressed. We report herein that blockade of VEGF by soluble VEGF receptor 1 (sFlt-1) gene transfer attenuated neointimal formation after intraluminal injury in rabbits, rats, and mice. sFlt-1 gene transfer markedly attenuated the early vascular inflammation and proliferation and later neointimal formation. sFlt-1 gene transfer also inhibited increased expression of inflammatory factors such as monocyte chemoattractant protein-1 and VEGF. Intravascular VEGF gene transfer enhanced angiogenesis in the adventitia but did not reduce neointimal formation. Increased expression and activity of VEGF are essential in the development of experimental restenosis after intraluminal injury by recruiting monocyte-lineage cells. (Keyword) Adenoviridae / Animals / Bone Marrow Transplantation / Carotid Artery Injuries / Catheterization / Cell Division / Cell Lineage / Constriction, Pathologic / Endothelium, Vascular / Extracellular Matrix Proteins / Femoral Artery / Gene Expression Regulation / Genetic Therapy / Genetic Vectors / Hyperplasia / Inflammation / Male / Mice / Mice, Transgenic / Monocytes / Myosin Heavy Chains / Neovascularization, Physiologic / Nonmuscle Myosin Type IIB / Proteins / Rabbits / Rats / Rats, Inbred WKY / Receptors, Vascular Endothelial Growth Factor / Recombinant Fusion Proteins / Recurrence / Regeneration / Solubility / Transduction, Genetic / Transfection / Tunica Intima / Vascular Endothelial Growth Factor A / Wound Healing (Link to Publication Site) ● Publication site (DOI): 10.1161/01.CIR.0000145123.85083.66 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15477409 ● CiNii @ National Institute of Informatics (CRID): 1363951793727132416 ● Search Scopus @ Elsevier (PMID): 15477409 ● Search Scopus @ Elsevier (DOI): 10.1161/01.CIR.0000145123.85083.66 (DOI: 10.1161/01.CIR.0000145123.85083.66, PubMed: 15477409, CiNii: 1363951793727132416)
499.	K Saito, N Ishizaka, T Aizawa, Masataka Sata, N Iso-O, E Noiri, M Ohno and R Nagai : Role of aberrant iron homeostasis in the upregulation of transforming growth factor-β1 in the kidney of angiotensin II-induced hypertensive rats., Hypertension Research, Vol.27, No.8, 599-607, 2004. (Summary) We have previously shown that abnormal iron metabolism might be one underlying mechanism of the renal damage observed in the angiotensin II-infused rat. Transforming growth factor-beta1 (TGF-beta1) is known to play a crucial role in the development of renal damage induced by activation of the renin-angiotensin-aldosterone system. The purpose of the present study was to examine the effects of an iron chelator and a free radical scavenger on the angiotensin II-induced upregulation of TGF-beta1 in the kidney. Rats were given angiotensin II (0.7 mg/kg/day) via osmotic minipumps for 7 days. The expressions of the mRNAs of TGF-beta1 and collagen types I and IV were significantly increased in response to angiotensin II treatment. Histologic analysis showed that TGF-beta1 expression was upregulated mainly in tubular epithelial cells, and occasionally in glomerular and perivascular cells, some of which were identified as monocytes and/or macrophages. Although tubular cells that overexpressed TGF-beta1 did not contain iron particles, angiotensin II-induced TGF-beta1 upregulation was suppressed by the iron chelator and the free radical scavenger. The free radical scavenger also suppressed angiotensin II-induced upregulation of heme oxygenase-1, an oxidative-stress sensitive gene. By contrast, administration of iron dextran to rats induced upregulation of TGF-beta1 mRNA. Collectively, these data suggest that the renal iron overload and presumed subsequent increase in oxidative stress play a role in angiotensin II-induced upregulation of the mRNAs of TGF-beta1 and collagen types I and IV in the kidney. (Keyword) Angiotensin II / Animals / Collagen / Ferritins / Fibrosis / Free Radical Scavengers / Heme Oxygenase (Decyclizing) / Heme Oxygenase-1 / Homeostasis / Hypertension, Renal / Iron / Iron Chelating Agents / Iron Overload / Kidney / Male / RNA, Messenger / Rats / Rats, Sprague-Dawley / Superoxides / Transforming Growth Factor beta / Transforming Growth Factor beta1 / Up-Regulation / Vasoconstrictor Agents (Link to Publication Site) ● Publication site (DOI): 10.1291/hypres.27.599 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15492480 ● Search Scopus @ Elsevier (PMID): 15492480 ● Search Scopus @ Elsevier (DOI): 10.1291/hypres.27.599 (DOI: 10.1291/hypres.27.599, PubMed: 15492480)
500.	H Ogawa, T Oohashi, Masataka Sata, Y Bekku, S Hirohata, K Nakamura, T Yonezawa, S Kusachi, Y Shiratori and Y Ninomiya : Lp3/Hapln3, a novel link protein which colocalizes with versican and is coordinately upregulated by platelet-derived growth factor in arterial smooth muscle cells, Matrix Biology, Vol.23, No.5, 287-298, 2004. (Summary) Link proteins (LPs) belong to the link-module superfamily, which can stabilize and enhance the binding of lecticans to hyaluronan. We report here the identification and characterization of a novel rat link protein gene (Lp3/Hapln3). The deduced protein sequence shares the typical modular elements of link proteins and has an estimated mass of 39 kDa. Examination of the rat genomic DNA sequence revealed that Lp3/Hapln3 and aggrecan genes were paired on chromosome 1q31. Another LP gene and the lectican gene were also paired at a different locus, as they are in the human and mouse genomes. Immunohistochemical analysis showed the prominent expression of Lp3/Hapln3 in the smooth muscle tissues of the vascular wall and gastrointestinal tract. Further comparative studies revealed that Lp3/Hapln3 was well co-localized with versican around the smooth muscle cells of blood vessels but not around endothelial cells. In vitro experiments using primary cultured rat arterial smooth muscle cells (ASMCs) demonstrated the coordinated up-regulation of Lp3/Hapln3 and versican by platelet-derived growth factor (PDGF). These data were supported by in vivo studies of a mechanical vascular injury model in mice. Altogether, our results suggest that Lp3/Hapln3 is involved, together with versican and hyaluronan, in the formation of the pericellular matrix of vascular smooth muscle cells. (Keyword) Amino Acid Sequence / Animals / Arteries / Blood Vessels / Carrier Proteins / Cells, Cultured / Chondroitin Sulfate Proteoglycans / Chromosome Mapping / DNA, Complementary / Hyaluronic Acid / Immunohistochemistry / Lectins, C-Type / Male / Molecular Sequence Data / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Platelet-Derived Growth Factor / RNA, Messenger / Rats / Rats, Sprague-Dawley / Tissue Distribution / Up-Regulation / Versicans (Link to Publication Site) ● Publication site (DOI): 10.1016/j.matbio.2004.07.001 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15464361 ● Search Scopus @ Elsevier (PMID): 15464361 ● Search Scopus @ Elsevier (DOI): 10.1016/j.matbio.2004.07.001 (DOI: 10.1016/j.matbio.2004.07.001, PubMed: 15464361)
501.	A Saiura, Masataka Sata, K Hiasa, S Kitamoto, M Washida, K Egashira, R Nagai and M Makuuchi : Anti-monocyte chemoattractant protein-1 gene therapy attenuates graft vasculopathy, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.24, No.10, 1886-1890, 2004. (Summary) Accelerated coronary arteriosclerosis remains a major problem in the long-term survival of cardiac transplant recipients. However, the pathogenesis of graft vasculopathy is poorly understood, and there is no effective therapy. Transplant arteriosclerosis is characterized by early mononuclear cell attachment on the transplanted vessel followed by development of concentric neointimal hyperplasia. Early and persistent expression of monocyte chemoattractant protein-1 (MCP-1) in cardiac allografts has been implicated for the pathogenesis of transplant arteriosclerosis. We investigated whether anti-MCP-1 gene therapy can inhibit the development of intima hyperplasia in a mouse model of cardiac transplantation. Either the dominant-negative form of MCP-1 (7ND) or control vector was transfected into the skeletal muscles of B10.D2 mice. Cardiac allografts from DBA/2 mice were transplanted heterotopically into B10.D2 mice. 7ND gene transfer was associated with a significant reduction of the number of mononuclear cells accumulating in the lumen of the graft coronary arteries at 1 week and an attenuation of the development of the lesion at 8 weeks (intima/media ratio 0.79+/-0.05 versus 0.48+/-0.04). The MCP-1/chemokine receptor 2 (CCR2) signaling pathway plays a critical role in the pathogenesis of graft vasculopathy. This new anti-MCP-1 gene therapy might be useful to treat graft vascular disease. (Keyword) Animals / Arteriosclerosis / Chemokine CCL2 / Coronary Vessels / Disease Models, Animal / Gene Therapy / Gene Transfer Techniques / Genes, Dominant / Heart Transplantation / Hyperplasia / Inflammation / Leukocytes, Mononuclear / Male / Mice / Mice, Inbred DBA / Mice, Inbred Strains / Muscle, Skeletal / Receptors, CCR2 / Receptors, Chemokine / Signal Transduction / Transplantation, Heterotopic / Transplantation, Homologous / Tunica Intima (Link to Publication Site) ● Publication site (DOI): 10.1161/01.ATV.0000141045.49616.6f (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15284091 ● Search Scopus @ Elsevier (PMID): 15284091 ● Search Scopus @ Elsevier (DOI): 10.1161/01.ATV.0000141045.49616.6f (DOI: 10.1161/01.ATV.0000141045.49616.6f, PubMed: 15284091)
502.	H Takahashi, Y Yanagi, Y Tamaki, K Muranaka, T Usui and Masataka Sata : Contribution of bone marrow derived cells to choroidal neovascularization, Biochemical and Biophysical Research Communications, Vol.320, No.2, 372-375, 2004. (Summary) We investigated the involvement of bone-marrow derived cells to experimental choroidal neovascularization (CNV) in mice, whose bone marrow was reconstituted by either unfractionated bone-marrow cells or Lin-c(-)Kit(+)Sca-1+ enriched presumable hematopoietic stem cells from the green fluorescent protein (GFP) transgeneic mice. Immunohistochemical analysis demonstrated the presence of GFP-positive cells in the CNV lesion after unfractionated bone-marrow transplantation, as well as Lin-c(-)Kit(+)Sca-1+ cell transplantation. Some of the GFP-expressing cells also expressed CD-31 and PanEC antigen, markers of vascular endothelial cells. Our results suggest that bone-marrow derived cells may contribute endothelial cells in CNV. (Keyword) Animals / Bone Marrow Cells / Choroidal Neovascularization / Fluorescent Antibody Technique / Green Fluorescent Proteins / Immunohistochemistry / Luminescent Proteins / Mice / Mice, Inbred C57BL / Mice, Transgenic (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2004.05.177 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15219837 ● Search Scopus @ Elsevier (PMID): 15219837 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2004.05.177 (DOI: 10.1016/j.bbrc.2004.05.177, PubMed: 15219837)
503.	D Nagata, R Takeda, Masataka Sata, H Satonaka, E Suzuki, T Nagano and Y Hirata : AMP-activated protein kinase inhibits angiotensin II-stimulated vascular smooth muscle cell proliferation, Circulation, Vol.110, No.4, 444-451, 2004. (Summary) AMP-activated protein kinase (AMPK) is a stress-activated protein kinase that works as a metabolic sensor of cellular ATP levels. Here, we investigated whether AMPK signaling has a role in the regulation of the angiotensin II (Ang II)-induced proliferation signal in rat vascular smooth muscle cells (VSMCs). Aminoimidazole-4-carboxamide-1-beta-ribofuranoside (AICAR) activated AMPK in rat VSMCs and inhibited Ang II-induced extracellular signal-regulated kinase 1/2 phosphorylation but not that of p38 MAPK or Akt/PKB. Although Ang II activated AMPK, this activation was significantly inhibited by catalase, N-acetylcysteine, and diphenyleneiodonium chloride, an NADPH oxidase inhibitor. Moreover, the observation that AMPK was activated by H2O2 suggests that AMPK is redox sensitive. The Ang II type 1 receptor antagonist valsartan but not the Ang II type 2 receptor antagonist PD123319 significantly inhibited Ang II-induced AMPK activation, suggesting that Ang II-induced AMPK activation was Ang II type 1 receptor dependent. Whereas 3H-thymidine incorporation by VSMCs treated with Ang II was significantly inhibited when the cells were pretreated with 1 mmol/L AICAR, the inhibition of AMPK by dominant-negative AMPK overexpression augmented Ang II-induced cell proliferation. Subcutaneous injection of AICAR (1 mg/g body weight per day) for 2 weeks suppressed neointimal formation after transluminal mechanical injury of the rat femoral artery. Our findings indicate that Ang II-induced AMPK activation is synchronized with extracellular signal-regulated kinase signaling and that AMPK works as an inhibitor of the Ang II proliferative pathway. AMPK signaling might serve as a new therapeutic target of vascular remodeling in cardiovascular diseases. (Keyword) AMP-Activated Protein Kinases / Aminoimidazole Carboxamide / Angiotensin II / Animals / Cell Division / Enzyme Activation / Extracellular Signal-Regulated MAP Kinases / Hydrogen Peroxide / Male / Multienzyme Complexes / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Protein-Serine-Threonine Kinases / Rats / Rats, Wistar / Recombinant Fusion Proteins / Ribonucleotides / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.1161/01.CIR.0000136025.96811.76 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15262850 ● Search Scopus @ Elsevier (PMID): 15262850 ● Search Scopus @ Elsevier (DOI): 10.1161/01.CIR.0000136025.96811.76 (DOI: 10.1161/01.CIR.0000136025.96811.76, PubMed: 15262850)
504.	Masataka Sata, H Nishimatsu, J.I. Osuga, K Tanaka, N Ishizaka, S Ishibashi, Y Hirata and R Nagai : Statins augment collateral growth in response to ischemia but they do not promote cancer and atherosclerosis, Hypertension, Vol.43, No.6, 1214-1220, 2004. (Summary) 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, or statins, are widely prescribed to lower cholesterol. Recent reports suggest that statins may promote angiogenesis in ischemic tissues. It remains to be elucidated whether statins potentially enhance unfavorable angiogenesis associated with tumor and atherosclerosis. Here, we induced hind limb ischemia in wild-type mice by resecting the right femoral artery and subsequently inoculated cancer cells in the same animal. Cerivastatin enhanced blood flow recovery in the ischemic hind limb as determined by laser Doppler imaging, whereas tumor growth was significantly retarded. Cerivastatin did not affect capillary density in tumors. Cerivastatin, pitavastatin, and fluvastatin inhibited atherosclerotic lesion progression in apolipoprotein E-deficient mice, whereas they augmented blood flow recovery and capillary formation in ischemic hind limb. Low-dose statins were more effective than high-dose statins in both augmentation of collateral flow recovery and inhibition of atherosclerosis. These results suggest that statins may not promote the development of cancer and atherosclerosis at the doses that augment collateral flow growth in ischemic tissues. (Keyword) Animals / Apolipoproteins E / Arteriosclerosis / Fatty Acids, Monounsaturated / Femoral Artery / Hindlimb / Hydroxymethylglutaryl-CoA Reductase Inhibitors / Hypercholesterolemia / Indoles / Ischemia / Male / Mice / Mice, Inbred C57BL / Mice, Knockout / Neovascularization, Pathologic / Neovascularization, Physiologic / Nitric Oxide Synthase / Nitric Oxide Synthase Type II / Nitric Oxide Synthase Type III / Pyridines / Quinolines (Link to Publication Site) ● Publication site (DOI): 10.1161/01.HYP.0000126186.29571.41 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15166180 ● Search Scopus @ Elsevier (PMID): 15166180 ● Search Scopus @ Elsevier (DOI): 10.1161/01.HYP.0000126186.29571.41 (DOI: 10.1161/01.HYP.0000126186.29571.41, PubMed: 15166180)
505.	K Hiasa, M Ishibashi, K Ohtani, S Inoue, Q Zhao, S Kitamoto, Masataka Sata, T Ichiki, A Takeshita and K Egashira : Gene transfer of stromal cell-derived factor-1α enhances ischemic vasculogenesis and angiogenesis via vascular endothelial growth factor/endothelial nitric oxide synthase-related pathway. Next-generation chemokine therapy for therapeutic neovascularization, Circulation, Vol.109, No.20, 2454-2461, 2004. (Summary) Stromal cell-derived factor-1alpha (SDF-1alpha) is implicated as a chemokine for endothelial progenitor cells (EPCs). We therefore hypothesized that SDF-1alpha gene transfer would induce therapeutic neovascularization in vivo by functioning as a chemokine of EPC. To examine SDF-1alpha-induced mobilization of EPC, we used bone marrow-transplanted mice whose blood cells ubiquitously express beta-galactosidase (LacZ). We produced unilateral hindlimb ischemia in the mice and transfected them with plasmid DNA encoding SDF-1alpha or empty plasmids into the ischemic muscles. SDF-1alpha gene transfer mobilized EPCs into the peripheral blood, augmented recovery of blood perfusion to the ischemic limb, and increased capillary density associated with partial incorporation of LacZ-positive cells into the capillaries of the ischemic limb, suggesting that SDF-1alpha induced vasculogenesis and angiogenesis. SDF-1alpha gene transfer did not affect ischemia-induced expression of vascular endothelial growth factor (VEGF) but did enhance Akt and endothelial nitric oxide synthase (eNOS) activity. Blockade of VEGF or NOS prevented all such SDF-1alpha-induced effects. SDF-1alpha gene transfer enhanced ischemia-induced vasculogenesis and angiogenesis in vivo through a VEGF/eNOS-related pathway. This strategy might become a novel chemokine therapy for next generation therapeutic neovascularization. (Keyword) Animals / Bone Marrow Cells / Bone Marrow Transplantation / Capillaries / Chemokine CXCL12 / Chemokines, CXC / Chemotaxis / Endothelium, Vascular / Genetic Therapy / Hindlimb / Ischemia / Male / Mice / Mice, Inbred C57BL / Mice, Knockout / Neovascularization, Physiologic / Nitric Oxide Synthase / Nitric Oxide Synthase Type II / Nitric Oxide Synthase Type III / Protein-Serine-Threonine Kinases / Proto-Oncogene Proteins / Proto-Oncogene Proteins c-akt / Signal Transduction / Stem Cells / Transfection / Vascular Endothelial Growth Factor A (Link to Publication Site) ● Publication site (DOI): 10.1161/01.CIR.0000128213.96779.61 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15148275 ● Search Scopus @ Elsevier (PMID): 15148275 ● Search Scopus @ Elsevier (DOI): 10.1161/01.CIR.0000128213.96779.61 (DOI: 10.1161/01.CIR.0000128213.96779.61, PubMed: 15148275)
506.	M Sekiya, J.I. Osuga, H Okazaki, N Yahagi, K Harada, W.J. Shen, Y Tamura, S Tomita, Y Iizuka, K Ohashi, M Okazaki, Masataka Sata, R Nagai, T Fujita, H Shimano, F.B. Kraemer, N Yamada and S Ishibashi : Absence of hormone-sensitive lipase inhibits obesity and adipogenesis in Lepob/ob mice, The Journal of Biological Chemistry, Vol.279, No.15, 15084-15090, 2004. (Summary) Hormone-sensitive lipase (HSL) plays a crucial role in the hydrolysis of triacylglycerol and cholesteryl ester in various tissues including adipose tissues. To explore the role of HSL in the metabolism of fat and carbohydrate, we have generated mice lacking both leptin and HSL (Lep(ob/ob)/HSL(-/-)) by cross-breeding HSL(-/-) mice with genetically obese Lep(ob/ob) mice. Unexpectedly, Lep(ob/ob)/HSL(-/-) mice ate less food, gained less weight, and had lower adiposity than Lep(ob/ob)/HSL(+/+) mice. Lep(ob/ob)/HSL(-/-) mice had massive accumulation of preadipocytes in white adipose tissues with increased expression of preadipocyte-specific genes (CAAT/enhancer-binding protein beta and adipose differentiation-related protein) and decreased expression of genes characteristic of mature adipocytes (CCAAT/enhancer-binding protein alpha, peroxisome proliferator activator receptor gamma, and adipocyte determination and differentiation factor 1/sterol regulatory element-binding protein-1). Consistent with the reduced food intake, hypothalamic expression of neuropeptide Y and agouti-related peptide was decreased. Since HSL is expressed in hypothalamus, we speculate that defective generation of free fatty acids in the hypothalamus due to the absence of HSL mediates the altered expression of these orexigenic neuropeptides. Thus, deficiency of both leptin and HSL has unmasked novel roles of HSL in adipogenesis as well as in feeding behavior. (Keyword) Adipocytes / Agouti-Related Protein / Animals / Blotting, Northern / Blotting, Western / Corticosterone / Crosses, Genetic / Feeding Behavior / Female / Hypothalamus / Immunoblotting / Immunohistochemistry / Intercellular Signaling Peptides and Proteins / Male / Mice / Mice, Inbred C57BL / Mice, Obese / Mice, Transgenic / Neuropeptide Y / Neuropeptides / Obesity / Oxygen Consumption / Proteins / Sterol Esterase / Temperature / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M310985200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14752112 ● Search Scopus @ Elsevier (PMID): 14752112 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M310985200 (DOI: 10.1074/jbc.M310985200, PubMed: 14752112)
507.	K Hiasa, K Egashira, S Kitamoto, M Ishibashi, S Inoue, W Ni, Q Zhao, S Nagata, M Katoh, Masataka Sata and A Takeshita : Bone marrow mononuclear cell therapy limits myocardial infarct size through vascular endothelial growth factor, Basic Research in Cardiology, Vol.99, No.3, 165-172, 2004. (Summary) No prior study has examined the effect of intravenous injection of bone marrow mononuclear cells (MNCs) on myocardial infarction size (IS). We tested the hypothesis that transplantation of MNCs decreases IS through the release of vascular endothelial growth factor (VEGF). Immediately after ligation of the left coronary artery of immunodeficient mice, PBS or MNCs were intravenously administered. Myocardial IS was significantly less in MNCs-treated mice than in PBS-treated mice. Trace experiments showed accumulation of exogenously administered MNCs into the vicinity of infarcted myocardium. Injection of MNCs did not affect capillary density after infarction, but did reduced myocardial cell apoptosis. Blockade of VEGF by a neutralizing antibody or by gene transfer of a soluble form of Flt-1 VEGF receptor diminished the IS-limiting effects of MNCs. In conclusion, injection of MNCs can reduce myocardial IS through the release of VEGF. The MNC therapy for acute myocardial infarction might improve prognosis of patients with myocardial infarction. (Keyword) Animals / Apoptosis / Bone Marrow Transplantation / Coronary Vessels / Disease Models, Animal / In Situ Nick-End Labeling / Leukocytes, Mononuclear / Mice / Mice, SCID / Myocardial Infarction / Myocardium / Vascular Endothelial Growth Factor A (Link to Publication Site) ● Publication site (DOI): 10.1007/s00395-004-0456-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15088101 ● Search Scopus @ Elsevier (PMID): 15088101 ● Search Scopus @ Elsevier (DOI): 10.1007/s00395-004-0456-9 (DOI: 10.1007/s00395-004-0456-9, PubMed: 15088101)
508.	N Ishizaka, K Saito, E Noiri, Masataka Sata, I Mori, M Ohno and R Nagai : Iron dextran causes renal iron deposition but not renal dysfunction in angiotensin ii-treated and untreated rats, Nephron. Physiology, Vol.98, No.4, 107-113, 2004. (Summary) Angiotensin II infusion into rats causes iron deposition in the kidney, which may augment the pro-proteinuric effects of this octapeptide. We have investigated whether administration of iron mimics the renal damage induced by angiotensin II. Rats were treated with iron dextran at a total dose of 960 mg/kg either with or without angiotensin II treatment at a dose of 0.7 mg/kg/day for 7 days. Protein expression of ferritin and heme oxygenase-1, an oxidative stress-sensitive gene, was determined by Western blot analysis and immunohistochemistry. Administration of iron dextran did not significantly increase proteinuria or decrease creatinine clearance in the rats with or without angiotensin II treatment. Prussian blue staining showed that iron deposition was observed mainly in the glomerular and medullar regions in the iron dextran-treated rats, but in the tubular epithelial cells in angiotensin II-infused rats. Administration of iron dextran upregulated ferritin, but not heme oxygenase-1. Iron dextran did not enhance or cause the renal dysfunction in the angiotensin II-treated or untreated rats, respectively. The distribution of deposited iron and presumably the type of iron compound administered may be important determinants of the development of renal injury. (Keyword) Angiotensin II / Animals / Blood Pressure / Body Weight / Ferritins / Heme Oxygenase (Decyclizing) / Iron / Iron Overload / Iron-Dextran Complex / Kidney / Kidney Diseases / Male / Proteinuria / Rats / Rats, Sprague-Dawley (Link to Publication Site) ● Publication site (DOI): 10.1159/000081559 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15627796 ● Search Scopus @ Elsevier (PMID): 15627796 ● Search Scopus @ Elsevier (DOI): 10.1159/000081559 (DOI: 10.1159/000081559, PubMed: 15627796)
509.	M Shoji, Masataka Sata, D Fukuda, K Tanaka, T Sato, Y Iso, M Shibata, H Suzuki, S Koba, E Geshi and T Katagiri : Temporal and spatial characterization of cellular constituents during neointimal hyperplasia after vascular injury: Potential contribution of bone marrow-derived progenitors to arterial remodeling, Cardiovascular Pathology, Vol.13, No.6, 306-312, 2004. (Summary) Exuberant smooth muscle cells (SMCs) hyperplasia is the major cause of postangioplasty restenosis. We suggested that circulating smooth muscle progenitor cells might contribute to lesion formation after vascular injury. We extensively investigated the cellular constituents during neointimal formation after mechanical vascular injury. A large wire was inserted into the mouse femoral artery, causing complete endothelial denudation and marked enlargement of the lumen with massive apoptosis of medial SMCs. At 2 h, the injured artery remained dilated with a thin media containing very few cells. A scanning electron microscopy showed fibrin and platelet deposition at the luminal side. One week after the injury, CD45-positive hematopoietic cells accumulated at the luminal side. Those CD45-positive cells gradually disappeared, whereas neointimal hyperplasia was formed with alpha-smooth muscle actin (SMA) positive cells. Bone marrow cells and peripheral mononuclear cells differentiated into alpha-SMA-positive cells in the presence of PDGF and basic FGF. Moreover, in bone marrow chimeric mice, bone-marrow-derived cells substantially contributed to neointimal hyperplasia after wire injury. These results suggest that early accumulation of hematopoietic cells may play a role in the pathogenesis of SMC hyperplasia under certain circumstances. (Keyword) Actins / Animals / Antigens, CD45 / Bone Marrow Cells / Cell Differentiation / Cell Proliferation / Cells, Cultured / Disease Models, Animal / Femoral Artery / Hematopoietic Stem Cells / Hyperplasia / Immunohistochemistry / Leukocytes, Mononuclear / Male / Mice / Mice, Inbred C3H / Microscopy, Electron, Scanning / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / RNA, Messenger / Tunica Intima (Link to Publication Site) ● Publication site (DOI): 10.1016/j.carpath.2004.08.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15556776 ● Search Scopus @ Elsevier (PMID): 15556776 ● Search Scopus @ Elsevier (DOI): 10.1016/j.carpath.2004.08.004 (DOI: 10.1016/j.carpath.2004.08.004, PubMed: 15556776)
510.	Y Matsui, A Saiura, Y Sugawara, Masataka Sata, K Naruse, H Yagita, T Kohro, C Mataki, A Izumi, T Yamaguchi, T Minami, T Sakihama, S Ihara, H Aburatani, T Hamakubo, T kodama and M Makuuchi : Identificaton of gene expression profile in tolerizing murine cardiac allograft by co-stimulatory blockade, Physiological Genomics, Vol.15, No.3, 199-208, 2003. (Summary) The induction of specific tolerance would be the ultimate achievement in transplant immunology, but the precise mechanisms of immunologic tolerance remain largely unknown. Here, we investigated global gene expression analysis in tolerizing murine cardiac allografts by means of oligonucleotide microarrays. Tolerance induction was achieved in cardiac allografts from BALB/c to C57BL/6 mice by daily intraperitoneal injection of anti-CD80 and anti-CD86 monoclonal antibodies (mAbs). Comparative analysis revealed 64 genes to be induced more extensively in the tolerizing than in the syngeneic isografts, and 16 genes than in the rejecting allografts. Two genes were specifically upregulated in the tolerizing allografts. In the tolerizing allografts there were induced marked expressions of a number of genes for pro-inflammatory factors, including interferon-gamma-inducible cytokines and chemokines, as well as apoptosis-related genes, which were also upregulated in the rejecting allografts. Moreover, these gene expression patterns continued to be upregulated more than 70 days posttransplant. These results provide evidence that immunologic tolerance can be induced and maintained in the presence of prominent pro-inflammatory gene expression in vivo. (Keyword) Animals / Antibodies, Monoclonal / Antigens, CD / Antigens, CD80 / Antigens, CD86 / Cluster Analysis / Gene Expression Profiling / Gene Expression Regulation / Graft Rejection / Graft Survival / Heart Transplantation / Immune Tolerance / Membrane Glycoproteins / Mice / Mice, Inbred BALB C / Mice, Inbred C57BL / Myocardium / Oligonucleotide Array Sequence Analysis / Reverse Transcriptase Polymerase Chain Reaction (Link to Publication Site) ● Publication site (DOI): 10.1152/physiolgenomics.00086.2003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12966135 ● Search Scopus @ Elsevier (PMID): 12966135 ● Search Scopus @ Elsevier (DOI): 10.1152/physiolgenomics.00086.2003 (DOI: 10.1152/physiolgenomics.00086.2003, PubMed: 12966135)
511.	T Natori, Masataka Sata, M Washida, Y Hirata, R Nagai and M Makuuchi : Nicotine enhances neovascularization and promotes tumor growth, Molecules and Cells, Vol.16, No.2, 143-146, 2003. (Summary) Solid tumors require vascularization for their growth. Bone marrow-derived endothelial progenitor cells participate in tumor angiogenesis. Here, we show that nicotine markedly accelerated growth of colon cancer cells inoculated subcutaneously in mice but had no effect on proliferation of carcinoma cells in vitro. We found that the tumor growth was associated with increased vascularization of the tumor and that bone marrow-derived cells contributed to the formation of the new blood vessels. Our findings show that nicotine promotes tumor growth, at least in part, by stimulating tumor-associated neovascularization. (Keyword) Animals / Bone Marrow Cells / Cell Division / Colonic Neoplasms / Male / Mice / Mice, Inbred C57BL / Neovascularization, Pathologic / Nicotine / Transplantation, Heterologous / Tumor Cells, Cultured (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14651253 ● Search Scopus @ Elsevier (PMID): 14651253 (PubMed: 14651253)
512.	K Fikino, Masataka Sata, Y Seko, Y Hirata and R Nagai : Genetic background influences therapeutic effectiveness of VEGF, Biochemical and Biophysical Research Communications, Vol.310, No.1, 143-147, 2003. (Summary) Therapeutic angiogenesis has emerged as a promising therapy, but some patients are refractory to exogenous growth factors. In order to identify the genetic determinants of post-natal angiogenesis and physiological vessel formation, we investigated the genetic factors that affected ischemia-induced development of collaterals in mice. An ischemic hindlimb model was generated in C57BL/6, C3H/He, and BALB/c mice. Angiogenesis was markedly different among the mice as determined by the restoration of blood perfusion and capillary density of the ischemic muscle. Impaired collateral vessel formation in BALB/c mice was associated with reduced expression of vascular endothelial cell growth factor (VEGF). Intramuscular gene transfer of VEGF promoted collateral formation in C57BL/6J mice, but not in BALB/c mice. Ineffectiveness of VEGF in BALB/c mice was associated with impaired expression of VEGF receptor. Our findings suggest that genetic background may influence spontaneous collateral formation and therapeutic effectiveness of exogenous VEGF. Alternative strategies other than administration of VEGF alone might be needed to attain optimal angiogenesis in some patients. (Keyword) Animals / Base Sequence / DNA Primers / Mice / Mice, Inbred BALB C / Neovascularization, Physiologic / Species Specificity / Transfection / Vascular Endothelial Growth Factor A (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2003.08.134 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14511661 ● Search Scopus @ Elsevier (PMID): 14511661 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2003.08.134 (DOI: 10.1016/j.bbrc.2003.08.134, PubMed: 14511661)
513.	K Tanaka, Masataka Sata, Y Hirata and R Nagai : Diverse contribution of bone marrow cells to neointimal hyperplasia after mechanical vascular injuries, Circulation Research, Vol.93, No.8, 783-790, 2003. (Summary) We and others have suggested that bone marrow-derived progenitor cells may contribute to the pathogenesis of vascular diseases. On the other hand, it was reported that bone marrow cells do not participate substantially in vascular remodeling in other experimental systems. In this study, three distinct types of mechanical vascular injuries were induced in the same mouse whose bone marrow had been reconstituted with that of GFP or LacZ mice. All injuries are known to cause smooth muscle cell (SMC) hyperplasia. At 4 weeks after wire-mediated endovascular injury, a significant number of the neointimal and medial cells derived from bone marrow. In contrast, marker-positive cells were seldom detected in the lesion induced by perivascular cuff replacement. There were only a few bone marrow-derived cells in the neointima after ligation of the common carotid artery. These results indicate that the origin of intimal cells is diverse and that contribution of bone marrow-derived cells to neointimal hyperplasia depends on the type of model. (Keyword) Actins / Animals / Arterial Occlusive Diseases / Arteries / Blood Vessels / Bone Marrow Cells / Bone Marrow Transplantation / Cell Differentiation / Hyperplasia / Inflammation / Ligation / Male / Mice / Mice, Inbred C57BL / Muscle, Smooth, Vascular / Stem Cells / Stress, Mechanical / Tunica Intima (Link to Publication Site) ● Publication site (DOI): 10.1161/01.RES.0000096651.13001.B4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14500338 ● Search Scopus @ Elsevier (PMID): 14500338 ● Search Scopus @ Elsevier (DOI): 10.1161/01.RES.0000096651.13001.B4 (DOI: 10.1161/01.RES.0000096651.13001.B4, PubMed: 14500338)
514.	A Saiura, Masataka Sata, M Washida, Y Sugawara, Y Hirata, R Nagai and M Makuuchi : Little evidence for cell fusion between recipient and donor-derived cells, The Journal of Surgical Research, Vol.113, No.2, 222-227, 2003. (Summary) Despite recent advances in immunosuppressive therapy, accelerated coronary atherosclerosis remains a major problem in the long-term survival of cardiac transplant recipients. However, the pathogenesis of the transplant-associated atherosclerosis remains largely unknown. Here, we investigated the origin of the vascular cells that contribute to graft vasculopathy. We performed heterotopic heart transplantation using genetically modified mice that express LacZ or green fluorescent protein (GFP) ubiquitously and constitutively. At 4 weeks after transplantation, the graft coronary arteries developed neointimal hyperplasia, expressing several smooth muscle cell markers. Most of the neointimal cells were composed of recipient cells but not graft medial smooth muscle cells. We seldom detected neointimal cells that were positive for both LacZ and GFP. When we transplanted wild-type cardiac allografts into the chimeric mice whose bone marrow cells had been replaced with those of LacZ-mice or GFP-mice, we observed that most of the neointimal cells were derived from the bone marrow. These findings suggest that recipient bone marrow-derived cells contribute to the pathogenesis of graft arteriosclerosis. Spontaneous cell fusion between recipient and donor-derived cells seems to be a rare event, if it occurs at all. (Keyword) Animals / Bone Marrow / Cell Fusion / Cell Movement / Coronary Artery Disease / Endothelium, Vascular / Green Fluorescent Proteins / Heart Transplantation / Indicators and Reagents / Lac Operon / Luminescent Proteins / Mice / Myocytes, Smooth Muscle (Link to Publication Site) ● Publication site (DOI): 10.1016/S0022-4804(03)00165-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12957133 ● Search Scopus @ Elsevier (PMID): 12957133 ● Search Scopus @ Elsevier (DOI): 10.1016/S0022-4804(03)00165-3 (DOI: 10.1016/S0022-4804(03)00165-3, PubMed: 12957133)
515.	Masataka Sata, K Tanaka, N Ishizaka, Y Hirata and R Nagai : Absence of p53 leads to accelerated neointimal hyperplasia after vascular injury, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.23, No.9, 1548-1552, 2003. (Summary) It has been suggested that deregulated expression of the tumor suppressor protein p53 may play a role in the pathogenesis of occlusive vascular remodeling. However, the role of p53 in cell proliferation and apoptosis in vascular lesions has been controversial. We tested the potential involvement of p53-mediated molecular signaling in lesion formation using a mouse model of vascular injury that may resemble balloon angioplasty. A large wire was inserted into the femoral artery of p53+/+ and p53-/- mice. There was no significant difference in the occurrence of rapid-onset apoptosis, that is, 4 hours after injury. At 2 weeks, the number of proliferating cells in the lesion of p53-/- mice was significantly higher than that observed in p53+/+ mice. The frequency of apoptotic cells was significantly lower in p53-/- mice than in p53+/+ mice. At 4 weeks, the neointimal hyperplasia of p53-/- mice was greater than that of p53+/+ mice. There was no significant difference in the frequency of apoptosis in the lesions. These results indicate a crucial role of p53 in pathological vascular remodeling after mechanical injury and provide the basis for the development of new therapies targeting p53 for a prophylactic treatment of vascular diseases. (Keyword) Actins / Animals / Apoptosis / Bone Marrow Cells / Cell Differentiation / Cell Division / Disease Models, Animal / Femoral Artery / Gene Expression Regulation / Genes, p53 / Hyperplasia / Male / Mice / Mice, Inbred C57BL / Mice, Mutant Strains / Muscle, Smooth, Vascular / Tumor Suppressor Protein p53 / Tunica Intima (Link to Publication Site) ● Publication site (DOI): 10.1161/01.ATV.0000089327.48154.32 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12893686 ● Search Scopus @ Elsevier (PMID): 12893686 ● Search Scopus @ Elsevier (DOI): 10.1161/01.ATV.0000089327.48154.32 (DOI: 10.1161/01.ATV.0000089327.48154.32, PubMed: 12893686)
516.	S Yamazaki, K Miki, K Hasegawa, Masataka Sata, T Takayama and M Makuuchi : Sera from liver failure patients and a demethylating agent stimulate transdifferentiation of murine bone marrow cells into hepatocytes in coculture with nonparenchymal liver cells, Journal of Hepatology, Vol.39, No.1, 17-23, 2003. (Summary) The plasticity of bone marrow cells (BMCs) is shown by their ability to differentiate into mesenchymal as well as endodermal and ectodermal lineages. Transdifferentiation of BMCs into hepatocytes has also been demonstrated, both in vitro and in vivo. In the present study we investigated the effects of liver nonparenchymal cells (NPCs) and sera from liver failure patients (HSLF) on the in vitro transdifferentiation of murine BMCs into hepatocytes. Liver NPCs from wild-type mice, and 5-azacytidine-treated BMCs from green fluorescence protein transgenic mice, were cocultured in medium containing HSLF in combination with several cytokines. Hepatocyte-specific gene expression in BMCs was identified by immunocytochemistry and reverse transcription-polymerase chain reaction. Bone marrow cell-derived hepatocyte-like colonies appeared after several days of coculture in medium containing HSLF, oncostatin M (OSM) and hepatocyte growth factor (HGF). These colonies expressed hepatocyte-specific genes. Transdifferentiation was enhanced by 5-azacytidine treatment, and by HSLF, OSM and HGF. It did not take place when the BMCs were separated from the NPCs in a dual chamber dish, or cultured with other mesenchymal cells. Direct interaction of murine BMCs with liver NPCs, as well as soluble factors in the HSLF and a demethylating agent, strongly stimulate transdifferentiation into hepatocytes. (Keyword) Animals / Antimetabolites, Antineoplastic / Azacitidine / Blood Proteins / Bone Marrow Cells / Cell Culture Techniques / Cell Differentiation / Child / Coculture Techniques / Hepatocytes / Humans / Liver / Liver Failure / Male / Methylation / Mice / Mice, Inbred C57BL / Mice, Transgenic / Middle Aged (Link to Publication Site) ● Publication site (DOI): 10.1016/S0168-8278(03)00150-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12821039 ● Search Scopus @ Elsevier (PMID): 12821039 ● Search Scopus @ Elsevier (DOI): 10.1016/S0168-8278(03)00150-8 (DOI: 10.1016/S0168-8278(03)00150-8, PubMed: 12821039)
517.	M Abe, Masataka Sata, H Nishimatsu, D Nagata, E Suzuki, Y Terauchi, T Kadowaki, N Minamino, K Kangawa, H Matsuo, Y Hirata and R Nagai : Adrenomedullin augments collateral development in response to acute ischemia, Biochemical and Biophysical Research Communications, Vol.306, No.1, 10-15, 2003. (Summary) Expression of adrenomedullin, discovered as a vasodilatory peptide, is markedly up-regulated under pathological conditions such as tissue ischemia and inflammation, which are associated with neovascularization. Here, we tested the hypothesis that overly expressed adrenomedullin may augment collateral flow to ischemic tissues. We induced hindlimb ischemia in wild-type mice and injected a naked plasmid expressing human adrenomedullin or an empty vector into the ischemic muscle, followed by in vivo electroporation. Adrenomedullin markedly enhanced blood flow recovery as determined by Laser Doppler imaging. The mice treated with an empty vector suffered frequent autoamputation of the ischemic toe, which was completely prevented by adrenomedullin. Anti-CD31 immunostaining revealed that adrenomedullin significantly increased capillary density. The angiogenic effect of adrenomedullin was abrogated in endothelial nitric oxide synthase (eNOS)-deficient mice. These results indicate that adrenomedullin may promote collateral growth in response to ischemia through activation of eNOS. (Keyword) Acute Disease / Adrenomedullin / Animals / Collateral Circulation / Female / Gene Expression / Gene Transfer Techniques / Humans / Ischemia / Mice / Mice, Inbred C3H / Mice, Inbred C57BL / Mice, Knockout / Neovascularization, Physiologic / Nitric Oxide / Nitric Oxide Synthase / Nitric Oxide Synthase Type II / Nitric Oxide Synthase Type III / Peptides / Recombinant Proteins / Vasodilation (Link to Publication Site) ● Publication site (DOI): 10.1016/S0006-291X(03)00903-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12788059 ● Search Scopus @ Elsevier (PMID): 12788059 ● Search Scopus @ Elsevier (DOI): 10.1016/S0006-291X(03)00903-3 (DOI: 10.1016/S0006-291X(03)00903-3, PubMed: 12788059)
518.	K Kumano, S Chiba, A Kunisato, Masataka Sata, T Saito, E Nakagami-Yamaguchi, T Yamaguchi, S Masuda, K Shimizu, T Takahashi, S Ogawa, Y Hamada and H Hirai : Notch1 but not notch2 is essential for generating hematopoietic stem cells from endothelial cells, Immunity, Vol.18, No.5, 699-711, 2003. (Summary) Hematopoietic stem cells (HSCs) are thought to arise in the aorta-gonad-mesonephros (AGM) region of embryo proper, although HSC activity can be detected in yolk sac (YS) and paraaortic splanchnopleura (P-Sp) when transplanted in newborn mice. We examined the role of Notch signaling in embryonic hematopoiesis. The activity of colony-forming cells in the YS from Notch1(-/-) embryos was comparable to that of wild-type embryos. However, in vitro and in vivo definitive hematopoietic activities from YS and P-Sp were severely impaired in Notch1(-/-) embryos. The population representing hemogenic endothelial cells, however, did not decrease. In contrast, Notch2(-/-) embryos showed no hematopoietic deficiency. These data indicate that Notch1, but not Notch2, is essential for generating hematopoietic stem cells from endothelial cells. (Keyword) Animals / Cell Differentiation / Endothelium, Vascular / Gene Expression Regulation, Developmental / Hematopoietic Stem Cells / Membrane Proteins / Mice / Receptor, Notch1 / Receptor, Notch2 / Receptors, Cell Surface / Transcription Factors / Yolk Sac (Link to Publication Site) ● Publication site (DOI): 10.1016/S1074-7613(03)00117-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12753746 ● CiNii @ National Institute of Informatics (CRID): 1363670318706988800 ● Search Scopus @ Elsevier (PMID): 12753746 ● Search Scopus @ Elsevier (DOI): 10.1016/S1074-7613(03)00117-1 (DOI: 10.1016/S1074-7613(03)00117-1, PubMed: 12753746, CiNii: 1363670318706988800)
519.	H Nishimatsu, Y Hirata, T Shindo, H Kurihara, E Suzuki, Masataka Sata, H Satonaka, R Takeda, D Nagata, M Kakoki, H Hayakawa, K Kangawa, H Matsuo, T Kitamura and R Nagai : Endothelial responses of the aorta from adrenomedullin transgenic mice and knockout mice, Hypertension Research, Vol.26 Suppl, S79-84, 2003. (Summary) Adrenomedullin (AM) is a potent vascular wall-derived vasorelaxing peptide which induces the release of nitric oxide (NO). To explore the role of endogenous AM in vascular function, we examined the effects of acetylcholine (ACh), AM, and AM receptor antagonists [AM (22-52), and calcitonin gene-related peptide (CGRP) (8-37)] on the isometric tension of aortic rings isolated from AM transgenic (TG) and knockout (KO) mice and wild type littermates (WT). ACh and AM caused a dose-dependent reduction of the isometric tension of aortic rings, but the degree of vasodilatation was smaller in TG than in KO or WT (% delta tension [10(-6) mol/l ACh]: KO -69 +/- 10%, WT -39 +/- 8%, TG -29 +/- 1%, p < 0.01). On the other hand, N(G)-nitro-L-arginine methyl ester, an NO synthase inhibitor, induced greater vasoconstriction in TG (% delta tension 10(-5)mol/l: KO +78 +/- 16%, WT +99 +/- 27%, TG +184 +/- 20%, p < 0.01), whereas E-4021, a cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase inhibitor, caused greater vasodilation in TG mice. Both AM antagonists increased tension in TG to a greater extent than in KO or WT mice (% delta tension [10(-6) mol/l CGRP (8-37)]: KO +24 +/- 5%, WT +51 +/- 6%, TG +75 +/- 7%, p < 0.01). Endothelial denudation of the aorta diminished the vasoconstriction caused by the AM antagonists. In conclusion, the amounts of AM expressed in the aortic endothelium influenced baseline NO release. AM antagonists increased vascular tone in WT as well as in TG, suggesting that endogenous AM plays a physiological role in the regulation of aortic tone. (Keyword) Acetylcholine / Adrenomedullin / Animals / Aorta, Thoracic / Calcitonin Gene-Related Peptide / Endothelium, Vascular / Enzyme Inhibitors / Male / Mice / Mice, Knockout / Mice, Transgenic / Miotics / Muscle Contraction / NG-Nitroarginine Methyl Ester / Peptide Fragments / Peptides / Phosphodiesterase Inhibitors / Piperidines / Quinazolines / Vasoconstriction / Vasodilator Agents (Link to Publication Site) ● Publication site (DOI): 10.1291/hypres.26.S79 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12630815 ● Search Scopus @ Elsevier (PMID): 12630815 ● Search Scopus @ Elsevier (DOI): 10.1291/hypres.26.S79 (DOI: 10.1291/hypres.26.S79, PubMed: 12630815)
520.	J Nitobe, S Yamaguchi, M Okuyama, N Nozaki, Masataka Sata, T Miyamoto, Y Takeishi, I Kubota and H Tomoike : Reactive oxygen species regulate FLICE inhibitory protein (FLIP) and susceptibility to Fas-mediated apoptosis in cardiac myocytes, Cardiovascular Research, Vol.57, No.1, 119-128, 2003. (Summary) Fas ligand (FasL) is a key cytokine which initiates apoptosis when FasL binds to its receptor, Fas. Cardiac myocytes are generally resistant to Fas-induced apoptosis. However, sublethal dose of doxorubicin (Dox) can sensitize cardiac myocytes to Fas-induced apoptosis. We investigated the molecular mechanism by which Dox sensitizes cardiac myocytes to Fas-induced apoptosis. FLICE inhibitory protein (FLIP) is a key molecule for blocking Fas-induced apoptosis by functioning as a caspase-8 dominant negative. FLIP was constitutively expressed in cultured neonatal rat cardiac myocytes. FLIP protein levels were markedly down-regulated by Dox in a time-dependent and dose-dependent manner. Next, we examined the relation of reactive oxygen species (ROS) by Dox to the expression of FLIP. Both of N-acetylcysteine (NAC) and the combination of superoxide dismutase and catalase restored the decreased FLIP in Dox-treated cardiac myocytes to the basal level. NAC also restored the increased formation of thiobarbituric acid-reactive substance after Dox-treatment. Concurrently, the susceptibility to Fas-mediated apoptosis disappeared with the treatments of the antioxidant agents. Hydrogen peroxide down-regulated FLIP in a dose-dependent fashion and also sensitized cardiac myocytes to Fas-induced apoptosis. FLIP, an inhibitor of apoptosis induced by cytokines of TNF family, contributes at least partly to Dox-induced sensitization to Fas-mediated apoptosis in cardiac myocytes. The expression of FLIP in cardiac myocytes is regulated by ROS. (Keyword) Acetylcysteine / Animals / Antibiotics, Antineoplastic / Apoptosis / Caspase 8 / Caspase 9 / Caspases / Catalase / Cells, Cultured / Dose-Response Relationship, Drug / Doxorubicin / Fas Ligand Protein / Membrane Glycoproteins / Myocytes, Cardiac / Rats / Rats, Wistar / Reactive Oxygen Species / Superoxide Dismutase / Thiobarbituric Acid Reactive Substances / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1016/S0008-6363(02)00646-6 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12504821 ● Search Scopus @ Elsevier (PMID): 12504821 ● Search Scopus @ Elsevier (DOI): 10.1016/S0008-6363(02)00646-6 (DOI: 10.1016/S0008-6363(02)00646-6, PubMed: 12504821)
521.	P Lee, Masataka Sata, D.J. Lefer, S.M. Factor, K Walsh and R.N. Kitsis : Fas pathway is a critical mediator of cardiac myocyte death and myocardial infarction during ischemia/reperfusion in vivo, American Journal of Physiology, Heart and Circulatory Physiology, Vol.284, No.2, H456-H463, 2003. (Summary) Fas is a widely expressed cell surface receptor that can initiate apoptosis when activated by its ligand (FasL). Whereas Fas abundance on cardiac myocytes increases in response to multiple pathological stimuli, direct evidence supporting its role in the pathogenesis of heart disease is lacking. Moreover, controversy exists even as to whether Fas activation induces apoptosis in cardiac myocytes. In this study, we show that adenoviral overexpression of FasL, but not beta-galactosidase, results in marked apoptosis both in cultures of primary neonatal cardiac myocytes and in the myocardium of intact adult rats. Myocyte killing by FasL is a specific event, because it does not occur in lpr (lymphoproliferative) mice that lack functional Fas. To assess the contribution of the Fas pathway to myocardial infarction (MI) in vivo, lpr mice were subjected to 30 min of ischemia followed by 24 h of reperfusion. Compared with wild-type mice, lpr mice exhibited infarcts that were 62.3% smaller with 63.8% less myocyte apoptosis. These data provide direct evidence that activation of Fas can induce apoptosis in cardiac myocytes and that Fas is a critical mediator of MI due to ischemia-reperfusion in vivo. (Keyword) Animals / Antigens, CD95 / Apoptosis / Cells, Cultured / Fas Ligand Protein / Male / Membrane Glycoproteins / Mice / Mice, Inbred C57BL / Mice, Mutant Strains / Myocardial Infarction / Myocardial Ischemia / Myocardial Reperfusion Injury / Myocytes, Cardiac (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpheart.00777.2002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12414449 ● Search Scopus @ Elsevier (PMID): 12414449 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpheart.00777.2002 (DOI: 10.1152/ajpheart.00777.2002, PubMed: 12414449)
522.	Takeshi Natori, Masataka Sata, Miwa Washida, Yasunobu Hirata, Ryozo Nagai and Masatoshi Makuuchi : G-CSF stimulates angiogenesis and promotes tumor growth: Potential contribution of bone marrow-derived endothelial progenitor cells, Biochemical and Biophysical Research Communications, Vol.297, No.4, 1058-1061, 2002. (Summary) Solid tumors require neovascularization for their growth. Recent evidence indicates that bone marrow-derived endothelial progenitor cells (EPCs) contribute to tumor angiogenesis. We show here that granulocyte colony-stimulating factor (G-CSF) markedly promotes growth of the colon cancer inoculated into the subcutaneous space of mice, whereas G-CSF had no effect on cancer cell proliferation in vitro. The accelerated tumor growth was associated with enhancement of neovascularization in the tumor. We found that bone marrow-derived cells participated in new blood vessel formation in tumor. Our findings suggest that G-CSF may have potential to promote tumor growth, at least in part, by stimulating angiogenesis in which bone marrow-derived EPCs play a role. (Keyword) Animals / Bone Marrow Cells / cell division / Colonic Neoplasms / Granulocyte Colony-Stimulating Factor / Hematopoietic Stem Cells / Humans / Kinetics / Male / Mice / Mice, Inbred C57BL / Neoplasms / Neovascularization, Pathologic / Recombinant Proteins (Link to Publication Site) ● Publication site (DOI): 10.1016/S0006-291X(02)02335-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12359263 ● Search Scopus @ Elsevier (PMID): 12359263 ● Search Scopus @ Elsevier (DOI): 10.1016/S0006-291X(02)02335-5 (DOI: 10.1016/S0006-291X(02)02335-5, PubMed: 12359263)
523.	N Ishizaka, K Saito, H Mitani, I Yamazaki, Masataka Sata, S Usui, I Mori, M Ohno and R Nagai : Iron overload augments angiotensin II-induced cardiac fibrosis and promotes neointima formation, Circulation, Vol.106, No.14, 1840-1846, 2002. (Summary) Abnormal iron deposition may cause oxidant-induced damage in various organs. We have previously reported that continuous administration of angiotensin II to rats results in an overt iron deposition in the renal tubular epithelial cells, which may have a role in angiotensin II-induced renal damage. In the present study, we investigated the role of iron in the development of cardiac injury induced by angiotensin II. Angiotensin II was continuously infused to rats at a dose of 0.7 mg/kg per day for 7 consecutive days. No iron deposits were observed in the hearts of untreated rats, whereas iron deposition was seen in the cells in the subepicardial and granulation regions after angiotensin II infusion. Concomitant administration of deferoxamine, an iron chelator, significantly reduced the extent of cardiac fibrosis, which suggests that iron deposition aggravates the cardiac fibrosis induced by angiotensin II. Iron overload caused by the administration of iron-dextran resulted in an augmentation of cardiac fibrosis and the generation of neointimal cells in the coronary artery in angiotensin II-infused rats. By contrast, neointima was not formed in the cardiac vessels in norepinephrine-infused rats with iron overload. Cardiac iron deposition may be involved in the development of cardiac fibrosis induced by angiotensin II. In addition, iron overload may enhance the formation of neointima under conditions of increased circulating angiotensin II but not catecholamines. (Keyword) Angiotensin II / Angiotensin Receptor Antagonists / Animals / Blood Pressure / Blotting, Western / Disease Models, Animal / Drug Synergism / Fibrosis / Heart / Heme Oxygenase (Decyclizing) / Heme Oxygenase-1 / Hypertension / Immunohistochemistry / Iron Chelating Agents / Iron Overload / Iron-Dextran Complex / Losartan / Male / Myocardium / Norepinephrine / Rats / Rats, Sprague-Dawley / Receptor, Angiotensin, Type 1 / Tunica Intima / Vasodilator Agents (Link to Publication Site) ● Publication site (DOI): 10.1161/01.CIR.0000031161.77536.02 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12356639 ● CiNii @ National Institute of Informatics (CRID): 1360292619578813568 ● Search Scopus @ Elsevier (PMID): 12356639 ● Search Scopus @ Elsevier (DOI): 10.1161/01.CIR.0000031161.77536.02 (DOI: 10.1161/01.CIR.0000031161.77536.02, PubMed: 12356639, CiNii: 1360292619578813568)
524.	A Saiura, Y Sugawara, Y Harihara, Masataka Sata, T Hamakubo, T Kodama and M Makuuchi : Gene expression profile during acute rejection in rat-to-mouse concordant cardiac xenograft by means of DNA microarray, Transplant International, Vol.15, No.11, 535-540, 2002. (Summary) Using a rat-to-mouse concordant cardiac transplantation model and DNA microarrays, we studied the gene expression profiles during acute rejection. We used inbred BALB/c and C3H/He mice and Lewis rats for our study, in which heterotopic cardiac transplantations were performed. Total RNA was isolated from xenografts (Lewis to C3H), allografts (BALB/c to C3H), rat isografts (Lewis to Lewis) and mouse isografts (C3H to C3H) on day 5 following transplantation. We screened for gene expression profiles in the xenografts, allografts, and mouse isografts by means of DNA microarrays. With a murine array, we determined that many IFN-gamma inducible genes were profoundly expressed in both the allografts and xenografts relative to the isografts. Mac-1 was specifically induced in the xenografts relative to the allografts. Using a rat array, we observed that the cardionatrin and atrial natriuretic factors were most profoundly expressed in the xenografts in comparison with the rat isografts. In addition to known genes, many expressed sequence tags were induced in the xenografts. We identified a group of genes, including Mac-1 induced specifically in xenografts, as well as many new genes upregulated in xenografts. (Keyword) Acute Disease / Animals / Gene Expression Profiling / Graft Rejection / Graft Survival / Heart Transplantation / Male / Mice / Mice, Inbred BALB C / Mice, Inbred C3H / Myocardium / Oligonucleotide Array Sequence Analysis / Rats / Rats, Inbred Lew / Time Factors / Transplantation, Heterologous / Transplantation, Heterotopic (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1432-2277.2002.tb00103.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12461656 ● Search Scopus @ Elsevier (PMID): 12461656 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1432-2277.2002.tb00103.x (DOI: 10.1111/j.1432-2277.2002.tb00103.x, PubMed: 12461656)
525.	Y Imai, T Shindo, K Maemura, Masataka Sata, Y Saito, Y Kurihara, M Akishita, J Osuga, S Ishibashi, K Tobe, H Morita, Y Oh-hashi, T Suzuki, H Maekawa, K Kangawa, N Minamino, Y Yazaki, R Nagai and H Kurihara : Resistance to neointimal hyperplasia and fatty streak formation in mice with adrenomedullin Overexpression, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.22, No.8, 1310-1315, 2002. (Summary) Several in vitro studies have implicated that adrenomedullin (AM) plays an important role in the pathogenesis of vascular injury and fatty streak formation. To test this possibility in vivo, we evaluated 2 experimental models using transgenic mice overexpressing AM in a vessel-selective manner (AMTg mice). Placement of a periarterial cuff on femoral arteries resulted in neointimal formation at 2 to 4 weeks to a lesser extent in AMTg mice than in their wild-type littermates (at 28 days, intima/media area ratio 0.45+/-0.14 versus 1.31+/-0.41, respectively; P<0.001). This vasculoprotective effect observed in AMTg mice was inhibited by N(omega)-nitro-L-arginine methyl ester. We further examined the effect of AM on hypercholesterolemia-induced fatty streak formation by crossing AMTg mice with apolipoprotein E knockout mice (ApoEKO mice). The extent of the formation of fatty streak lesions was significantly less in ApoEKO/AMTg mice than in ApoEKO mice (percent lesion area 12.0+/-3.9% versus 15.8+/-2.8%, respectively; P<0.05). Moreover, endothelium-dependent vasodilatation as indicative of NO production was superior in AMTg/ApoEKO mice compared with ApoEKO mice. Taken together, our data demonstrated that AM possesses a vasculoprotective effect in vivo, which is at least partially mediated by NO. (Keyword) Adipose Tissue / Adrenomedullin / Animals / Apolipoproteins E / Calcitonin Gene-Related Peptide / Femoral Artery / Hydralazine / Hyperplasia / Mice / Mice, Knockout / Mice, Transgenic / NG-Nitroarginine Methyl Ester / Nitric Oxide / Peptide Fragments / Peptides / Tunica Intima (Link to Publication Site) ● Publication site (DOI): 10.1161/01.ATV.0000024685.92243.E7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12171793 ● Search Scopus @ Elsevier (PMID): 12171793 ● Search Scopus @ Elsevier (DOI): 10.1161/01.ATV.0000024685.92243.E7 (DOI: 10.1161/01.ATV.0000024685.92243.E7, PubMed: 12171793)
526.	M Matsuda, I Shimomura, Masataka Sata, Y Arita, M Nishida, N Maeda, M Kumada, Y Okamoto, H Nagaretani, H Nishizawa, K Kishida, R Komuro, N Ouchi, S Kihara, R Nagai, T Funahashi and Y Matsuzawa : Role of adiponectin in preventing vascular stenosis -the missing link of adipo-vascular axis-, The Journal of Biological Chemistry, Vol.277, No.40, 37487-37491, 2002. (Summary) Obesity is more linked to vascular disease, including atherosclerosis and restenotic change, after balloon angioplasty. The precise mechanism linking obesity and vascular disease is still unclear. Previously we have demonstrated that the plasma levels of adiponectin, an adipose-derived hormone, decreases in obese subjects, and that hypoadiponectinemia is associated to ischemic heart disease. In current the study, we investigated the in vivo role of adiponectin on the neointimal thickening after artery injury using adiponectin-deficient mice and adiponectin-producing adenovirus. Adiponectin-deficient mice showed severe neointimal thickening and increased proliferation of vascular smooth muscle cells in mechanically injured arteries. Adenovirus-mediated supplement of adiponectin attenuated neointimal proliferation. In cultured smooth muscle cells, adiponectin attenuated DNA synthesis induced by growth factors including platelet-derived growth factor, heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF), basic fibroblast growth factor, and EGF and cell proliferation and migration induced by HB-EGF. In cultured endothelial cells, adiponectin attenuated HB-EGF expression stimulated by tumor necrosis factor alpha. The current study suggests an adipo-vascular axis, a direct link between fat and artery. A therapeutic strategy to increase plasma adiponectin should be useful in preventing vascular restenosis after angioplasty. (Keyword) Adenoviridae / Adiponectin / Animals / Cell Division / Cells, Cultured / Collagen / Coronary Disease / DNA Replication / Endothelium, Vascular / Intercellular Signaling Peptides and Proteins / Mice / Mice, Knockout / Obesity / Proteins / RNA, Messenger / Transcription, Genetic / Tunica Intima / Vascular Diseases (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M206083200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12138120 ● Summary page in Scopus @ Elsevier: 2-s2.0-0037020170 (DOI: 10.1074/jbc.M206083200, PubMed: 12138120, Elsevier: Scopus)
527.	T Shindo, I Manabe, Y Fukushima, K Tobe, K Aizawa, S Miyamoto, K Kawai-Kowase, N Moriyama, Y Imai, H Kawakami, H Nishimatsu, T Ishikawa, T Suzuki, H Morita, K Maemura, Masataka Sata, Y Hirata, M Komukai, H Kagechika, T Kadowaki, M Kurabayashi and R Nagai : Kruppel-like zinc-finger transcription factor KLF5/BTEB2 is a target for angiotensin signaling and an essential regulator of cardiovascular remodeling, Nature Medicine, Vol.8, No.8, 856-863, 2002. (Summary) We recently isolated a Krüppel-like zinc-finger transcription factor 5 (KLF5; also known as BTEB2 and IKLF), which is markedly induced in activated vascular smooth-muscle cells and fibroblasts. Here we describe our analysis of the in vivo function of KLF5 using heterozygous KLF5-knockout mice (Klf5(+/-)). In response to external stress, Klf5(+/-) mice showed diminished levels of arterial-wall thickening, angiogenesis, cardiac hypertrophy and interstitial fibrosis. Also, angiotensin II induced expression of KLF5, which in turn activated platelet-derived growth factor-A (PDGF-A) and transforming growth factor-beta (TGF-beta) expression. In addition, we determined that KLF5 interacted with the retinoic-acid receptor (RAR), that synthetic RAR ligands modulated KLF5 transcriptional activity, and that in vivo administration of RAR ligands affected stress responses in the cardiovascular system in a KLF5-dependent manner. KLF5 thus seems to be a key element linking external stress and cardiovascular remodeling. (Keyword) Angiotensin II / Animals / Blood Vessels / Cells, Cultured / Collagen Type IV / Dibenzazepines / Digestive System / Digestive System Physiological Phenomena / Female / Genes, Reporter / Humans / Kruppel-Like Transcription Factors / Male / Mice / Mice, Inbred C57BL / Mice, Knockout / Myocardium / Neoplasm Transplantation / Neovascularization, Physiologic / Platelet-Derived Growth Factor / Rats / Recombinant Fusion Proteins / Retinoids / Signal Transduction / Trans-Activators / Ventricular Remodeling / Zinc Fingers (Link to Publication Site) ● Publication site (DOI): 10.1038/nm738 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12101409 ● Search Scopus @ Elsevier (PMID): 12101409 ● Search Scopus @ Elsevier (DOI): 10.1038/nm738 (DOI: 10.1038/nm738, PubMed: 12101409)
528.	Masataka Sata, Y Hirata and R Nagai : Role of Fas/FasL interaction in ischemia-induced collateral vessel growth, Hypertension Research, Vol.25, No.4, 577-582, 2002. (Summary) Fas ligand (FasL) is a death factor that induces apoptosis in cells bearing its receptor, Fas. Accumulating evidence indicates that the Fas/FasL system is involved not only in apoptosis but also in cell-activation signals. Recently, it was reported that local stimulation of Fas in vivo using an agonistic antibody triggers inflammatory cell infiltration and neoangiogenesis independently of apoptosis. On the other hand, Fas/FasL interaction has been proposed to control the growth and development of new subretinal vessels. Here, we evaluated the potential involvement of Fas/FasL interaction in collateral development in response to tissue ischemia. Hindlimb ischemia was induced in C57BL/6J (wild-type), B6-gld(FasL -/-), and B6-lpr(Fas -/-) mice by resection of the right femoral artery. The blood flow recovery of FasL -/- or Fas -/- mice was similar to that of wild-type mice, as determined using a laser Doppler imaging system. There was no significant difference in capillary density of the ischemic calf muscle among the mice, as determined by anti-CD31 immunostaining. We did not find any difference in the number of infiltrating inflammatory cells or in vascular endothelial growth factor expression. These results indicate that postnatal angiogenesis in response to acute ischemia can occur independently of the endogenous Fas/FasL interaction. (Keyword) Acute Disease / Animals / Antigens, CD95 / Apoptosis / Blood Vessels / Collateral Circulation / Endothelial Growth Factors / Fas Ligand Protein / Hindlimb / Intercellular Signaling Peptides and Proteins / Ischemia / Lymphokines / Male / Membrane Glycoproteins / Mice / Mice, Inbred C57BL / Mice, Mutant Strains / Muscle, Skeletal / Regional Blood Flow / Vascular Endothelial Growth Factor A / Vascular Endothelial Growth Factors (Link to Publication Site) ● Publication site (DOI): 10.1291/hypres.25.577 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12358144 ● Search Scopus @ Elsevier (PMID): 12358144 ● Search Scopus @ Elsevier (DOI): 10.1291/hypres.25.577 (DOI: 10.1291/hypres.25.577, PubMed: 12358144)
529.	H Nishimatsu, Y Hirata, T Shindo, H Kurihara, M Kakoki, D Nagata, H Hayakawa, H Satonaka, Masataka Sata, A Tojo, E Suzuki, K Kangawa, H Matsuo, T Kitamura and R Nagai : Role of endogenous adrenomedullin in the regulation of vascular tone and ischemic renal injury. Studies on transgenic/knockout mice of adrenomedullin gene, Circulation Research, Vol.90, No.0, 657-663, 2002. (Summary) Adrenomedullin (AM) is a potent depressor peptide whose vascular action is suggested to involve nitric oxide (NO) release. To explore the role of endogenous AM in vascular and renal function, we examined the effects of acetylcholine (ACh), AM, and AM receptor antagonists AM(22-52) and CGRP(8-37) on the renal perfusion pressure (RPP) of kidneys isolated from AM transgenic (TG)/heterozygote knockout (KO) mice and wild-type littermates (WT). Furthermore, we evaluated the renal function and histology 24 hours after bilateral renal artery clamp for 45 minutes in TG, KO, and WT mice. Baseline RPP was significantly lower in TG than in KO and WT mice (KO 93.4+/-4.6, WT 85.8+/-4.2, TG 72.4+/-2.4 mm Hg [mean+/-SE], P<0.01). ACh and AM caused a dose-related reduction in RPP, but the degree of vasodilatation was smaller in TG than that in KO and WT (%DeltaRPP 10(-7) mol/L ACh: KO -48.1+/-3.9%, WT -57.5+/-5.6%, TG -22.8+/-4.8%, P<0.01), whereas N(G)-nitro-L-arginine methyl ester (L-NAME) caused greater vasoconstriction in TG (%DeltaRPP 10(-4) mol/L: KO 33.1+/-3.3%, WT 55.5+/-7.2%, TG 152.6+/-21.2%, P<0.01). Both AM antagonists increased RPP in TG to a greater extent compared with KO and WT mice (%DeltaRPP 10(-6) mol/L CGRP(8-37): KO 12.8+/-2.6%, WT 19.4+/-3.6%, TG 41.8+/-8.7%, P<0.01). In mice with ischemic kidneys, serum levels of urea nitrogen and renal damage scores showed smaller values in TG and greater values in KO mice (urea nitrogen: KO 104+/-5>WT 98+/-15>TG 38+/-7 mg/dL, P<0.05 each). Renal NO synthase activity was also greater in TG mice. However, the differences in serum urea nitrogen and renal damage scores among the 3 groups of mice were not observed in mice pretreated with L-NAME. In conclusion, AM antagonists increased renal vascular tone in WT as well as in TG, suggesting that endogenous AM plays a role in the physiological regulation of the vascular tone. AM is likely to protect renal tissues from ischemia/reperfusion injury through its NO releasing activity. (Keyword) Acetylcholine / Adrenomedullin / Animals / Cholinergic Agents / Enzyme Inhibitors / Gene Expression Regulation / In Vitro Techniques / Kidney / Mice / Mice, Knockout / Mice, Transgenic / NG-Nitroarginine Methyl Ester / Nitric Oxide Synthase / Peptides / Reperfusion Injury / Vasoconstriction / omega-N-Methylarginine (Link to Publication Site) ● Publication site (DOI): 10.1161/01.RES.0000013697.55301.E7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11934832 ● CiNii @ National Institute of Informatics (CRID): 1360292618537494912 ● Search Scopus @ Elsevier (PMID): 11934832 ● Search Scopus @ Elsevier (DOI): 10.1161/01.RES.0000013697.55301.E7 (DOI: 10.1161/01.RES.0000013697.55301.E7, PubMed: 11934832, CiNii: 1360292618537494912)
530.	Masataka Sata, A Saiura, A Kunisato, A Tojo, S Okada, T Tokuhisa, H Hirai, M Makuuchi, Y Hirata and R Nagai : Hematopoietic stem cells differentiate into vascular cells that participate in the pathogenesis of atherosclerosis, Nature Medicine, Vol.8, No.4, 403-409, 2002. (Summary) Excessive accumulation of smooth-muscle cells (SMCs) has a key role in the pathogenesis of vascular diseases. It has been assumed that SMCs derived from the outer medial layer migrate, proliferate and synthesize extracellular matrix components on the luminal side of the vessel. Although much effort has been devoted to targeting migration and proliferation of medial SMCs, there is no effective therapy that prevents occlusive vascular remodeling. We show here that in models of post-angioplasty restenosis, graft vasculopathy and hyperlipidemia-induced atherosclerosis, bone-marrow cells give rise to most of the SMCs that contribute to arterial remodeling. Notably, purified hematopoietic stem cells differentiate into SMCs in vitro and in vivo. Our findings indicate that somatic stem cells contribute to pathological remodeling of remote organs, and may provide the basis for the development of new therapeutic strategies for vascular diseases through targeting mobilization, homing, differentiation and proliferation of bone marrow-derived vascular progenitor cells. (Keyword) Animals / Apolipoproteins E / Arteriosclerosis / Cell Differentiation / Cell Division / Cell Movement / Cells, Cultured / Disease Models, Animal / Graft Occlusion, Vascular / Green Fluorescent Proteins / Hematopoietic Stem Cells / Lac Operon / Luminescent Proteins / Mice / Mice, Inbred C57BL / Mice, Knockout / Mice, Transgenic / Muscle, Smooth, Vascular / Rats (Link to Publication Site) ● Publication site (DOI): 10.1038/nm0402-403 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11927948 ● Search Scopus @ Elsevier (PMID): 11927948 ● Search Scopus @ Elsevier (DOI): 10.1038/nm0402-403 (DOI: 10.1038/nm0402-403, PubMed: 11927948)
531.	Masataka Sata, Akihiro Takahashi, Kimie Tanaka, Miwa Washida, Nobukazu Ishizaka, Junya Ako, Masao Yoshizumi, Yasuyoshi Ouchi, Takahiro Taniguchi, Yasunobu Hirata, Mitsuhiro Yokoyama, Ryozo Nagai and Kenneth Walsh : Mouse genetic evidence that tranilast reduces smooth muscle cell hyperplasia via a p21^WAF1-dependent pathway, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.22, No.8, 1305-1309, 2002. (Link to Publication Site) ● Publication site (DOI): 10.1161/01.ATV.0000026614.72957.E7 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1161/01.ATV.0000026614.72957.E7 (DOI: 10.1161/01.ATV.0000026614.72957.E7)
532.	A Saiura, Masataka Sata, Y Hirata, R Nagai and M Makuuchi : Tranilast inhibits transplant-associated coronary arteriosclerosis in a murine model of cardiac transplantation, European Journal of Pharmacology, Vol.433, No.2-3, 163-168, 2001. (Summary) Accelerated coronary arteriosclerosis remains a major problem for the long-term survival of cardiac transplant recipients. However, the pathogenesis of graft vasculopathy is poorly understood and there is no effective therapy. Tranilast is a promising drug that may prevent post-angioplasty restenosis. Here, we investigated whether orally administered tranilast inhibits the development of intima hyperplasia in a mouse model of cardiac transplantation. Cardiac allografts from BALB/c mice were transplanted heterotopically into C3H/He mice. Mice were administered either vehicle or tranilast everyday by gavage. Morphometrical analysis of the cardiac allografts harvested at 2 months revealed that the administration of tranilast significantly reduced the development of coronary atherosclerosis. In the mice treated with tranilast, up-regulation of the cyclin-dependent kinase inhibitor p21 was observed in the allografts, accompanied by a reduced number of proliferating cells. Tranilast also suppressed transforming growth factor-beta (TGF-beta) expression. Tranilast may be effective in preventing transplant-associated arteriosclerosis through its anti-inflammatory and anti-proliferative effects. (Keyword) Animals / Anti-Inflammatory Agents, Non-Steroidal / Cell Division / Coronary Artery Disease / Cyclin-Dependent Kinase Inhibitor p21 / Cyclins / Heart Transplantation / Hyperplasia / Mice / Mice, Inbred BALB C / Mice, Inbred C3H / Muscle, Smooth, Vascular / Transforming Growth Factor beta / ortho-Aminobenzoates (Link to Publication Site) ● Publication site (DOI): 10.1016/S0014-2999(01)01501-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11755148 ● Summary page in Scopus @ Elsevier: 2-s2.0-0035930840 (DOI: 10.1016/S0014-2999(01)01501-1, PubMed: 11755148, Elsevier: Scopus)
533.	Masataka Sata, S Sugiura, M Yoshizumi, Y Ouchi, Y Hirata and R Nagai : Acute and chronic smooth muscle cell apoptosis after mechanical vascular injury can occur independently of the Fas-death pathway, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.21, No.11, 1733-1737, 2001. (Summary) Vascular smooth muscle cell (VSMC) apoptosis has been demonstrated in vascular lesions, such as atherosclerotic and postangioplasty restenotic lesions. Balloon injury also induces VSMC apoptosis. Fas is a death factor that mediates apoptosis when it is activated by its ligand, FasL. Fas-mediated apoptosis was found to be implicated in the pathogenesis of vascular diseases in which Fas/FasL expression was detected. We investigated whether the Fas/FasL interaction mediated acute and chronic VSMC apoptosis and lesion formation in a vascular injury model that may resemble balloon angioplasty. A large spring wire was inserted into the femoral artery of C3H/HeJ (wild-type), C3H-gld (Fas ligand-/-), and C3H-lpr (Fas-/-) mice. The wire was left in place for 1 minute to denude and expand the artery. Massive apoptosis was observed in medial VSMCs from 1 to 7 hours later. There was no difference in the number of apoptotic cells among the 3 groups of mice 4 hours after injury. At 4 weeks, the injured arteries presented signs of concentric neointimal hyperplasia composed exclusively of VSMCs. There was no difference in the degree of neointima hyperplasia (intima/media ratios were as follows: wild type 1.4+/-0.3, gld 1.0+/-0.2, and lpr 1.3+/-0.2) or in the number of apoptotic nuclei among the 3 groups. These findings suggest the existence of other signaling pathways for acute and chronic VSMC apoptosis, at least that induced by mechanical vascular injury. (Keyword) Angioplasty, Balloon / Animals / Antigens, CD95 / Apoptosis / Arterial Occlusive Diseases / Fas Ligand Protein / Kinetics / Male / Membrane Glycoproteins / Mice / Mice, Inbred C3H / Mice, Knockout / Muscle, Smooth, Vascular / Signal Transduction / Stress, Mechanical (Link to Publication Site) ● Publication site (DOI): 10.1161/hq1201.098946 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11701458 ● Search Scopus @ Elsevier (PMID): 11701458 ● Search Scopus @ Elsevier (DOI): 10.1161/hq1201.098946 (DOI: 10.1161/hq1201.098946, PubMed: 11701458)
534.	Masataka Sata, H Nishimatsu, E Suzuki, S Sugiura, M Yoshizumi, Y Ouchi, Y Hirata and R Nagai : Endothelial nitric oxide synthase is essential for the HMG-CoA reductase inhibitor cerivastatin to promote collateral growth in response to ischemia, The FASEB journal, Vol.15, No.13, 2530-2532, 2001. (Summary) HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitors, or statins, are prescribed widely to lower cholesterol. Accumulating evidence indicates that statins have various effects on vascular cells, which are independent of their lipid-lowering effect. Here, we tested the hypothesis that statins may augment collateral flow to ischemic tissues. We induced hind-limb ischemia in wild-type mice and treated them with either saline or cerivastatin. Cerivastatin enhanced the blood flow recovery dramatically as determined by Laser Doppler imaging. The mice treated with saline displayed frequent autoamputation of the ischemic toe, which was prevented completely by cerivastatin. Anti-CD31 immunostaining revealed that cerivastatin significantly increased the capillary density. Endothelial nitric oxide synthase (eNOS) activity was enhanced markedly in the mice treated with cerivastatin. The angiogenic effect of cerivastatin was abrogated in eNOS deficient (eNOS-/-) mice. These results indicate that eNOS is essential for cerivastatin to promote collateral growth in response to ischemia. (Keyword) Animals / Capillaries / Collateral Circulation / Hydroxymethylglutaryl-CoA Reductase Inhibitors / Ischemia / Laser-Doppler Flowmetry / Mice / Mice, Inbred C3H / Mice, Inbred C57BL / Mice, Knockout / Nitric Oxide Synthase / Nitric Oxide Synthase Type II / Nitric Oxide Synthase Type III / Pyridines / Regional Blood Flow / Vasodilation (Link to Publication Site) ● Publication site (DOI): 10.1096/fj.01-0415fje (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11641268 ● Summary page in Scopus @ Elsevier: 2-s2.0-0035514486 (DOI: 10.1096/fj.01-0415fje, PubMed: 11641268, Elsevier: Scopus)
535.	H Nishimatsu, E Suzuki, D Nagata, N Moriyama, H Satonaka, K Walsh, Masataka Sata, K Kangawa, H Matsuo, A Goto, T Kitamura and Y Hirata : Adrenomedullin induces endothelium-dependent vasorelaxation via the phosphatidylinositol 3-kinase/Akt-dependent pathway in rat aorta, Circulation Research, Vol.89, No.1, 63-70, 2001. (Summary) To study the mechanisms by which adrenomedullin (AM) induces endothelium-dependent vasorelaxation, we examined whether AM-induced endothelium-dependent vasodilation was mediated by the phosphatidylinositol 3-kinase (PI3K)/Akt-dependent pathway in rat aorta, because it was recently reported that PI3K/Akt was implicated in the activation of endothelial NO synthase. AM-induced vasorelaxation in thoracic aorta with intact endothelium was inhibited by pretreatment with PI3K inhibitors to the same level as that in endothelium-denuded aorta. AM elicited Akt phosphorylation in a time- and dose-dependent manner. AM-induced Akt phosphorylation was inhibited by pretreatment with a calmodulin-dependent protein kinase inhibitor as well as with PI3K inhibitors. When an adenovirus construct expressing a dominant-negative Akt mutant (Ad/dnAkt) was injected into abdominal aortas so that the mutant was expressed predominantly in the endothelium layer, AM-induced vasodilation was diminished to the same level as that in endothelium-denuded aortas. Finally, AM-induced cGMP production, which was used as an indicator for NO production, was suppressed by PI3K inhibition or by Ad/dnAkt infection into the endothelium. These results suggested that AM induced Akt activation in the endothelium via the Ca(2+)/calmodulin-dependent pathway and that this was implicated in the production of NO, which in turn induced endothelium-dependent vasodilation in rat aorta. (Keyword) Adrenomedullin / Animals / Aorta / Calcium / Calmodulin / Culture Techniques / Cyclic GMP / Endothelium, Vascular / Enzyme Inhibitors / Male / Mutation / Nitric Oxide / Peptides / Phosphatidylinositol 3-Kinases / Phosphorylation / Protein-Serine-Threonine Kinases / Proto-Oncogene Proteins / Proto-Oncogene Proteins c-akt / Rats / Rats, Wistar / Signal Transduction / Vasodilation (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11440979 ● Summary page in Scopus @ Elsevier: 2-s2.0-0035816724 (PubMed: 11440979, Elsevier: Scopus)
536.	Masataka Sata, Z Luo and K Walsh : Fas ligand overexpression on allograft endothelium inhibits inflammatory cell infiltration and transplant-associated intimal hyperplasia, The Journal of Immunology, Vol.66, No.11, 6964-6971, 2001. (Summary) Despite recent advances in immunosuppressive therapy, accelerated coronary atherosclerosis remains a major problem in the long-term survival of transplant recipients. Chronic graft vasculopathy is believed to result from recipient inflammatory responses, and it is characterized by early mononuclear cell infiltration of the transplanted vessel. Here we show that endothelial cells can be genetically modified to overexpress functional, cell-surface Fas ligand (FasL) by adenovirus-mediated gene transfer without undergoing self-destruction. In a rodent model of transplant graft vasculopathy, endothelial overexpression of FasL attenuated T cell and macrophage infiltration at 1 wk posttransplantation. These vessels also displayed reduced neointima formation at one and 2 mo posttransplantation. These results indicate that inhibition of the early inflammatory response to allografted vessels by endothelial cell-specific overexpression of FasL may have utility in the treatment of transplant arteriosclerosis. (Keyword) Animals / Aorta / Arteriosclerosis / Carotid Artery, Common / Cell Movement / Cells, Cultured / Cytotoxicity, Immunologic / Endothelium, Vascular / Fas Ligand Protein / Gene Transfer Techniques / Humans / Hyperplasia / Inflammation / Jurkat Cells / Leukocytes, Mononuclear / Ligands / Male / Membrane Glycoproteins / Rats / Rats, Inbred ACI / Rats, Inbred WF / Transplantation, Homologous / Tunica Intima / fas Receptor (Link to Publication Site) ● Publication site (DOI): 10.4049/jimmunol.166.11.6964 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11359858 ● Summary page in Scopus @ Elsevier: 2-s2.0-0343773374 (DOI: 10.4049/jimmunol.166.11.6964, PubMed: 11359858, Elsevier: Scopus)
537.	A Saiura, Masataka Sata, Y Hirata, R Nagai and M Makuuchi : Circulating smooth muscle progenitor cells contribute to atherosclerosis, Nature Medicine, Vol.7, No.4, 382-383, 2001. (Keyword) Animals / Arteriosclerosis / Gene Expression / Genes, Reporter / Heart Transplantation / Lac Operon / Male / Mice / Mice, Inbred C3H / Mice, Transgenic / Muscle, Smooth, Vascular / Stem Cells / Transplantation, Homologous (Link to Publication Site) ● Publication site (DOI): 10.1038/86394 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11283635 ● Search Scopus @ Elsevier (PMID): 11283635 ● Search Scopus @ Elsevier (DOI): 10.1038/86394 (DOI: 10.1038/86394, PubMed: 11283635)
538.	Masataka Sata, Y Maejima, F Adachi, K Fukino, A Saiura, S Sugiura, T Aoyagi, Y Imai, H Kurihara, K Kimura, M Omata, M Makuuchi, Y Hirata and R Nagai : A mouse model of vascular injury that induces rapid onset of medial cell apoptosis followed by reproducible neointimal hyperplasia, Journal of Molecular and Cellular Cardiology, Vol.32, No.11, 2097-2104, 2000. (Summary) Genetically modified mice serve as a powerful tool to determine the role of specific molecules in a wide variety of biological phenomena including vascular remodeling. Several models of arterial injury have been proposed to analyze transgenic/knock-out mice, but many questions have been raised about their reproducibility and physiological significance. Here, we report a new mouse model of vascular injury that resembles balloon-angioplasty. A straight spring wire was inserted into the femoral artery via arterioctomy in a small muscular branch. The wire was left in place for one minute to denude and dilate the artery. After the wire was removed, the muscular branch was tied off and the blood flow of the femoral artery was restored. The lumen was enlarged with rapid onset of medial cell apoptosis. While the circumference of the external elastic lamina remained enlarged, the lumen was gradually narrowed by neointimal hyperplasia composed of smooth muscle cells. At 4 weeks, a concentric and homogeneous neointimal lesion was formed reproducibly in the region where the wire had been inserted. Similar exuberant hyperplasia could be induced in all strains examined (C57BL/6J, C3H/HeJ, BALB/c, and 129/SVj). This model may be widely used to study the molecular mechanism of post-angioplasty restenosis at the genetic level. (Keyword) Angioplasty, Balloon / Angioplasty, Balloon, Coronary / Animals / Apoptosis / Disease Models, Animal / Endothelium, Vascular / Femoral Artery / Hyperplasia / In Situ Nick-End Labeling / Male / Mice / Mice, Inbred BALB C / Mice, Inbred C3H / Mice, Inbred C57BL / Models, Animal / Recurrence / Reproducibility of Results / Species Specificity / Tunica Intima / Tunica Media (Link to Publication Site) ● Publication site (DOI): 10.1006/jmcc.2000.1238 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11040113 ● Summary page in Scopus @ Elsevier: 2-s2.0-0033750522 (DOI: 10.1006/jmcc.2000.1238, PubMed: 11040113, Elsevier: Scopus)
539.	D Nagata, E Suzuki, H Nishimatsu, M Yoshizumi, T Mano, K Walsh, Masataka Sata, M Kakoki, A Goto, M Omata and Y Hirata : Cyclin A downregulation and p21(cip1) upregulation correlate with GATA-6-induced growth arrest in glomerular mesangial cells, Circulation Research, Vol.87, No.8, 699-704, 2000. (Summary) The GATA-6 transcription factor is reported to be expressed in vascular myocytes. Because glomerular mesangial cells (GMCs) and vascular myocytes have similar properties, we examined whether GATA-6 was expressed in cultured GMCs and whether overexpression of GATA-6 induced cell cycle arrest in GMCs, using a recombinant adenovirus that expresses GATA-6 (Ad GATA-6). GATA-6 expression in GMCs was downregulated when quiescent GMCs were stimulated by serum to reenter the cell cycle. [(3)H]thymidine uptake was inhibited in GMCs infected with Ad GATA-6 in a dose- and time-dependent manner. The expression of cyclin A protein was decreased and that of the cyclin-dependent kinase inhibitor p21(cip1) was increased in GMCs infected with Ad GATA-6. Although the expression of p21(cip1) transcripts did not change remarkably, p21(cip1) protein was stabilized in GMCs infected with Ad GATA-6, suggesting a post-transcriptional regulation of p21(cip1) expression. Northern blot analysis showed that expression of the cyclin A transcript was decreased in Ad GATA-6-infected cells, whereas this decrease of cyclin A was not observed in GMCs derived from p21(cip1) null mice. Our results demonstrate that GATA-6 is endogenously expressed in GMCs and that overexpression of GATA-6 can induce cell cycle arrest. Our results also show that GATA-6-induced cell cycle arrest is associated with inhibition of cyclin A expression and p21(cip1) upregulation. Finally, our results indicate that the GATA-6-induced suppression of cyclin A expression depends on the presence of p21(cip1). (Keyword) Adenoviridae / Animals / Blood Proteins / Blotting, Northern / CDC2-CDC28 Kinases / Cell Cycle / Cell Cycle Proteins / Cell Division / Cells, Cultured / Cyclin A / Cyclin-Dependent Kinase 2 / Cyclin-Dependent Kinase Inhibitor p21 / Cyclin-Dependent Kinases / Cyclins / DNA-Binding Proteins / Dose-Response Relationship, Drug / Down-Regulation / GATA6 Transcription Factor / Gene Expression / Glomerular Mesangium / Humans / Muscle, Smooth, Vascular / Protein-Serine-Threonine Kinases / RNA, Messenger / Rats / Recombinant Proteins / Thymidine / Transcription Factors / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1161/01.RES.87.8.699 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11029406 ● Summary page in Scopus @ Elsevier: 2-s2.0-0034644607 (DOI: 10.1161/01.RES.87.8.699, PubMed: 11029406, Elsevier: Scopus)
540.	Masataka Sata and K Walsh : Fas ligand-deficient mice display enhanced leukocyte infiltration and intima hyperplasia in flow restricted vessels, Journal of Molecular and Cellular Cardiology, Vol.32, No.8, 1395-1400, 2000. (Summary) Fas ligand (FasL) is a death factor that induces apoptosis in Fas-bearing cells. To explore the role of FasL in vascular lesion formation, we analysed leukocyte infiltration and lesion formation in a flow-restriction model of vascular injury that results in neointima formation in the presence of intact endothelium. The left common carotid arteries of wild-type and FasL-deficient (gld) mice were ligated just proximal to the carotid bifurcation. Three days after the ligation, T lymphocyte and macrophage infiltration into the common carotid artery was notably enhanced in the gld mice relative to the wild-type C57BL/6J mice. Four weeks after the ligation, the common carotid arteries developed neointima-like lesions consisting primarily of alpha -smooth muscle actin-positive cells beneath an endothelial cell monolayer. Neointima formation was greater in the gld mice than in wild-type mice. These data provide mouse genetic evidence suggesting that Fas-mediated cell death can function to restrict inflammation and intimal hyperplasia during vascular remodelling. (Keyword) Actins / Animals / Fas Ligand Protein / Hyperplasia / Immunohistochemistry / Leukocyte Count / Leukocytes / Macrophages / Male / Membrane Glycoproteins / Mice / Mice, Inbred C57BL / Mice, Mutant Strains / Point Mutation / Time Factors / Tunica Intima (Link to Publication Site) ● Publication site (DOI): 10.1006/jmcc.2000.1176 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10900166 ● Summary page in Scopus @ Elsevier: 2-s2.0-0033864287 (DOI: 10.1006/jmcc.2000.1176, PubMed: 10900166, Elsevier: Scopus)
541.	Masataka Sata, M Kakoki, D Nagata, H Nishimatsu, E Suzuki, T Aoyagi, S Sugiura, H Kojima, T Nagano, K Kangawa, H Matsuo, M Omata, R Nagai and Y Hirata : Adrenomedullin and nitric oxide inhibit human endothelial cell apoptosis via a cGMP-independent mechanism, Hypertension, Vol.36, No.1, 83-88, 2000. (Summary) Adrenomedullin, which was discovered as a vasodilating peptide, has been reported to be produced in various organs, in which adrenomedullin regulates not only vascular tone but also cell proliferation and differentiation in an autocrine/paracrine manner. We evaluated the effect of adrenomedullin on endothelial cell apoptosis. Human umbilical vein endothelial cells underwent apoptosis when cultured in serum-free medium. Treatment with adrenomedullin reduced the number of cells with pyknotic nuclei (Hoechst 33258 staining) and inhibited cell death (dimethylthiazol-diphenyltetrazolium bromide assay) in a dose-dependent manner. The administration of adrenomedullin did not alter the expression levels of Bcl-2 family proteins. Experiments with analogs of cAMP or a cAMP-elevating agonist demonstrated that elevation of the intracellular cAMP concentration does not mediate the antiapoptotic effect of adrenomedullin. The coadministration of N-nitro-L-arginine methyl ester (2 mmol/L), an inhibitor of nitric oxide synthase, abrogated the effect of adrenomedullin. Lower doses of sodium nitroprusside (1 to 10 micromol/L), a nitric oxide donor, mimicked the antiapoptotic effect of adrenomedullin. The antiapoptotic effect of sodium nitroprusside was not attenuated by the inhibition of soluble guanylyl cyclase with 1 micromol/L oxadiazolo-quinoxalin-1-one nor could apoptosis be inhibited by the incubation of human umbilical vein endothelial cells with 1 mmol/L 8-bromo-cGMP, a cell-permeant cGMP analog. These results indicate that adrenomedullin and nitric oxide inhibit endothelial cell apoptosis via a cGMP-independent mechanism. (Keyword) Adrenomedullin / Apoptosis / Cell Survival / Cells, Cultured / Cyclic AMP / Cyclic GMP / Endothelium, Vascular / Humans / Nitric Oxide / Peptides / Proto-Oncogene Proteins c-bcl-2 (Link to Publication Site) ● Publication site (DOI): 10.1161/01.HYP.36.1.83 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10904017 ● Search Scopus @ Elsevier (PMID): 10904017 ● Search Scopus @ Elsevier (DOI): 10.1161/01.HYP.36.1.83 (DOI: 10.1161/01.HYP.36.1.83, PubMed: 10904017)
542.	Y Eto, K Yonekura, M Sonoda, N Arai, Masataka Sata, S Sugiura, K Takenaka, A Gualberto, ML Hixon, MW Wagner and T Aoyagi : Calcineurin is activated in rat hearts with physiological left ventricular hypertrophy induced by voluntary exercise training, Circulation, Vol.101, No.18, 2134-2137, 2000. (Summary) Calcineurin may play a pivotal role in the signaling of cardiac hypertrophy; since this hypothesis was first put forward, controversial reports have been published using various experimental models. This study was designed to compare the physiological left ventricular hypertrophy (LVH) induced by voluntary exercise with LVH induced by aortic constriction and to determine whether calcineurin participates in the signaling of exercise-induced LVH. Wistar rats were assigned to 1 of the following 5 groups: 10 weeks of voluntary exercise (EX), a sedentary regimen, a 1-week (AC1) or 4-week (AC4) ascending aortic constriction period, or a sham operation. EX rats ran 2.4+/-0.7 km/day voluntarily in specially manufactured cages; this was associated with an increase of LV diastolic dimension and stroke volume. Myocardial calcineurin activity markedly increased in EX rats (46.4+/-8.3 versus 18.4+/-0.5 pmol. min(-1). mg(-1) in sedentary rats; P<0.001) and in AC1 rats (44.9+/-6.7 versus 22.1+/-3.7 pmol. min(-1). mg(-1) in sham-operated rats; P<0.001), but not in AC4 rats (29.0+/-3.4 pmol. min(-1). mg(-1)). Treatment with cyclosporin A completely inhibited the development of LVH in EX rats, but it only partially attenuated the development of LVH in AC4 rats. Calcineurin was activated in exercise-induced physiological LVH and in the developing phase of LVH (AC1), but not in decompensated pressure-overload hypertrophy (AC4). Cyclosporin therapy for the prevention of LVH may be harmful because it does not block the development of pathological hypertrophy but rather that of favorable adaptive hypertrophy. (Keyword) Animals / Calcineurin / Hypertrophy, Left Ventricular / Physical Conditioning, Animal / Rats / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.1161/01.CIR.101.18.2134 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10801751 ● CiNii @ National Institute of Informatics (CRID): 1572824499409617792 ● Summary page in Scopus @ Elsevier: 2-s2.0-0034625078 (DOI: 10.1161/01.CIR.101.18.2134, PubMed: 10801751, CiNii: 1572824499409617792, Elsevier: Scopus)
543.	H Perlman, Masataka Sata, K Krasinski, T Dorai, R Buttyan and K Walsh : Adenovirus-encoded hammerhead ribozyme to Bcl-2 inhibits neointimal hyperplasia and induces vascular smooth muscle cell apoptosis, Cardiovascular Research, Vol.45, No.3, 570-578, 2000. (Summary) The balance between apoptosis and cell proliferation is vital for cellular homeostasis, yet little is known about the mechanisms that coordinate these two cell fates, particularly in the vessel wall. It is well established that the members of Bcl-2-gene family are regulators of apoptosis, but their role in cellular proliferation is less clear. We analyzed the effects of disrupting Bcl-2 expression in vascular smooth muscle cells (VSMCs) by adenoviral-mediated delivery of a hammerhead ribozyme against bcl-2 mRNA (Ad-Rbz-Bcl-2). Forced ablation of Bcl-2 in balloon-injured rat carotid arteries reduced cell number and inhibited neointimal hyperplasia. In vitro, VSMCs transduced with the Ad-Rbz-Bcl-2 underwent apoptosis as indicated by a reduction in cell number and DNA fragmentation. Ad-Rbz-Bcl-2-transduced cells also exhibited aberrations in both G1- and S-phases of the cell cycle. However, forced perturbations in cell cycle activity by serum-stimulation or treatment with chemical inhibitors did not affect Ad-Rbz-Bcl-2-induced cell death, indicating that these cell cycle changes are not essential for apoptosis. These data show that physiological levels of Bcl-2 are essential for VSMC viability and that ablation of Bcl-2 alters cell cycle activity through the execution of the apoptotic process. (Keyword) Adenoviridae / Analysis of Variance / Animals / Aorta, Thoracic / Apoptosis / Blotting, Western / Carotid Artery Injuries / Catheterization / Cell Cycle / Cells, Cultured / Flow Cytometry / Genes, bcl-2 / Genetic Vectors / Male / Muscle, Smooth, Vascular / RNA, Catalytic / Rats / Rats, Sprague-Dawley / Reverse Transcriptase Polymerase Chain Reaction (Link to Publication Site) ● Publication site (DOI): 10.1016/S0008-6363(99)00346-6 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10728378 ● Summary page in Scopus @ Elsevier: 2-s2.0-0033979269 (DOI: 10.1016/S0008-6363(99)00346-6, PubMed: 10728378, Elsevier: Scopus)
544.	Masataka Sata, T Suhara and K Walsh : Vascular endothelial cells and smooth muscle cells differ in expression of Fas and Fas ligand and in sensitivity to Fas Ligand induced cell death: Implications for vascular disease and therapy, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.20, No.2, 309-316, 2000. (Summary) Fas ligand (FasL) is a death factor that induces apoptosis in cells bearing its receptor, Fas. Fas and FasL have been detected in the vessel wall, and it has been proposed that Fas-mediated apoptosis has a role in physiological and pathological cell turnover in the vasculature. Here, we evaluated the expression of Fas in the presence and absence of cytokines on both endothelial cells (ECs) and vascular smooth muscle cells (VSMCs). We also examined the sensitivity of ECs and VSMCs to Fas-mediated apoptosis induced by exposure to multiple Fas agonists: soluble FasL, anti-Fas antibody, and membrane-bound FasL resulting from transduction with a replication-defective adenovirus expressing FasL (Adeno-FasL). Cell-surface FasL expression was detected on human ECs with the use of 4 anti-FasL antibodies, whereas cell-surface FasL expression was not detected on VSMCs. Unstimulated ECs expressed relatively low levels of Fas, but expression was upregulated after treatment with tumor necrosis factor-alpha (TNF-alpha) or interferon gamma (IFN-gamma). In contrast, VSMCs expressed relatively high levels of Fas, and treatment with TNF-alpha or IFN-gamma induced little or no upregulation under the conditions of these assays. ECs were resistant to death after exposure to soluble FasL or agonist anti-Fas antibody and also after infection with Adeno-FasL in the presence or absence of cytokine treatment. In contrast, VSMCs remained viable in the presence of soluble FasL or agonist anti-Fas antibody, but they underwent apoptosis after infection with Adeno-FasL. IFN-gamma enhanced Adeno-FasL-induced death of VSMCs, but TNF-alpha did not. These findings provide insights about the potential role of Fas-mediated apoptosis in the vessel wall and suggest strategies to treat proliferative vascular diseases by exploiting the differential sensitivity of ECs and VSMCs to FasL-induced cell death. (Keyword) Antigens, CD95 / Apoptosis / Cell Survival / Cells, Cultured / Endothelium, Vascular / Fas Ligand Protein / Gene Expression Regulation / Humans / Membrane Glycoproteins / Muscle, Smooth, Vascular / Vascular Diseases (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10669625 ● Summary page in Scopus @ Elsevier: 2-s2.0-0033980167 (PubMed: 10669625, Elsevier: Scopus)
545.	Masataka Sata and K Walsh : Cyclosporine downregulates Fas ligand expression on vascular endothelial cells: Implication for accelerated vasculopathy by immunosuppressive therapy, Biochemical and Biophysical Research Communications, Vol.263, No.2, 430-432, 1999. (Summary) Although the introduction of cyclosporine A (CyA) and FK506 for immunosuppressive therapy has dramatically enhanced the early survival of organ transplant recipients, administration of these immunosuppresants is correlated with high incidence of transplant arteriosclerosis. Transplant-associated arteriosclerosis is believed to result from recipient inflammatory responses to the allograft, as it is characterized by early mononuclear cell infiltration of the transplanted vessel. We reported that vascular endothelial cells naturally express a death factor, Fas ligand, that may function to inhibit detrimental leukocyte infiltration. Here, we show that CyA or FK506 downregulates FasL expression on endothelial cells with accompanying decrease in the cytotoxicity toward Fas-bearing cells. Our findings not only demonstrate a novel biological action of these drugs, but also suggest a mechanism by which immunosupressive treatment contributes to atherogenesis. (Keyword) Arteriosclerosis / Cyclosporine / Down-Regulation / Endothelium, Vascular / Fas Ligand Protein / Immunosuppressive Agents / Membrane Glycoproteins / Organ Transplantation / Tacrolimus (Link to Publication Site) ● Publication site (DOI): 10.1006/bbrc.1999.1392 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10491310 ● Summary page in Scopus @ Elsevier: 2-s2.0-0033600707 (DOI: 10.1006/bbrc.1999.1392, PubMed: 10491310, Elsevier: Scopus)
546.	Z Luo, Masataka Sata, T Nguyen, J.M. Kaplan, G.Y. Akita and K Walsh : Adenovirus-mediated delivery of Fas ligand inhibits intimal hyperplasia following balloon injury in immunologically-primed animals, Circulation, Vol.99, No.14, 1776-1779, 1999. (Summary) Adenoviral constructs have been used for studies of injury-induced vascular hyperplasia in immunologically naive laboratory animals, but their usefulness for intra-arterial gene therapy may be limited by the prevalence of preexisting immunity to adenovirus in the patient population. Here, we explored the efficacy of adenovirus-mediated transfer of Fas ligand, a cytotoxic gene with immunomodulatory properties, in inhibiting injury-induced vascular lesion formation in both naive and immunologically primed animals. Lesion formation was evaluated in balloon-injured carotid arteries of naive and adenovirus-immunized rats that were infected with adenoviral constructs expressing Fas ligand (Ad-FasL), the cyclin-dependent kinase inhibitor p21 (Ad-p21), or beta-galactosidase (Ad-betagal). In naive rats, Ad-FasL induced apoptosis in medial vascular smooth muscle cells and inhibited intimal hyperplasia by 60% relative to Ad-betagal-treated vessels (P<0.05), whereas the cytostatic agent Ad-p21 decreased lesion size by 58% (P<0.05). In animals preimmunized with an adenoviral vector containing no transgene, Ad-FasL significantly inhibited neointima formation (73% reduction, P<0.05), but Ad-p21 failed to inhibit neointima formation relative to controls. Immunologically primed rats displayed robust T-cell infiltration in Ad-p21- and Ad-betagal-treated vessels, but T-cell infiltration was markedly attenuated in Ad-FasL-treated vessels. Our data demonstrate that adenovirus-mediated Fas ligand delivery can inhibit intimal hyperplasia in both immunologically primed and naive animals, whereas the efficacy of an adenovirus-mediated p21 delivery is limited to immunologically naive animals. This study documents, for the first time, the therapeutic efficacy of intravascular adenoviral gene transfer in animals with preexisting immunity to adenovirus. (Keyword) Adenoviridae / Animals / Carotid Arteries / Carotid Artery Diseases / Catheterization / Fas Ligand Protein / Gene Transfer Techniques / Hyperplasia / Immunization / Male / Membrane Glycoproteins / Rats / Rats, Sprague-Dawley / Tunica Intima / Vasculitis (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10199871 ● Summary page in Scopus @ Elsevier: 2-s2.0-0033551097 (PubMed: 10199871, Elsevier: Scopus)
547.	Z.F. Cheema, S.B. Wade, Masataka Sata, K Walsh, F Sohrabji and R.C. Miranda : Fas/Apo [Apoptosis]-1 and associated proteins in the differentiating cerebral cortex: Induction of caspase dependent cell death and activation of NF-κB, The Journal of Neuroscience, Vol.19, No.5, 1754-1770, 1999. (Summary) The developing cerebral cortex undergoes a period of substantial cell death. The present studies examine the role of the suicide receptor Fas/Apo[apoptosis]-1 in cerebral cortical development. Fas mRNA and protein are transiently expressed in subsets of cells within the developing rat cerebral cortex during the peak period of apoptosis. Fas-immunoreactive cells were localized in close proximity to Fas ligand (FasL)-expressing cells. The Fas-associated signaling protein receptor interacting protein (RIP) was expressed by some Fas-expressing cells, whereas Fas-associated death domain (FADD) was undetectable in the early postnatal cerebral cortex. FLICE-inhibitory protein (FLIP), an inhibitor of Fas activation, was also expressed in the postnatal cerebral cortex. Fas expression was more ubiquitous in embryonic cortical neuroblasts in dissociated culture compared to in situ within the developing brain, suggesting that the environmental milieu partly suppresses Fas expression at this developmental stage. Furthermore, FADD, RIP, and FLIP were also expressed by subsets of dissociated cortical neuroblasts in culture. Fas activation by ligand (FasL) or anti-Fas antibody induced caspase-dependent cell death in primary embryonic cortical neuroblast cultures. The activation of Fas was also accompanied by a rapid downregulation of Fas receptor expression, non-cell cycle-related incorporation of nucleic acids and nuclear translocation of the RelA/p65 subunit of the transcription factor NF-kappaB. Together, these data suggest that adult cortical cell number may be established, in part, by an active process of receptor-mediated cell suicide, initiated in situ by killer (FasL-expressing) cells and that Fas may have functions in addition to suicide in the developing brain. (Keyword) Adaptor Proteins, Signal Transducing / Aging / Animals / Antigens, CD95 / Apoptosis / CASP8 and FADD-Like Apoptosis Regulating Protein / Carrier Proteins / Caspases / Cell Cycle / Cell Death / Cell Differentiation / Cell Nucleus / Cerebral Cortex / Down-Regulation / Fas Ligand Protein / Fas-Associated Death Domain Protein / Intracellular Signaling Peptides and Proteins / Membrane Glycoproteins / NF-kappa B / Neurons / Proteins / RNA, Messenger / Rats / Rats, Sprague-Dawley / Time Factors (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10024361 ● Summary page in Scopus @ Elsevier: 2-s2.0-0033103344 (PubMed: 10024361, Elsevier: Scopus)
548.	A Matsumoto, S Momomura, S Sugiura, H Fujita, T Aoyagi, Masataka Sata, M Omata and Y Hirata : Effect of inhaled nitric oxide on gas exchange in patients with congestive heart failure. A randomized,controlled trial, Annal.Int.Med., Vol.130, 40-44, 1999.
549.	Masataka Sata and K Walsh : Endothelial cell apoptosis induced by oxidized LDL is associated with the downregulation of the cellular caspase inhibitor FLIP, The Journal of Biological Chemistry, Vol.273, 33103-33106, 1998.
550.	Masataka Sata and K Walsh : Oxidized LDL activates Fas-mediated endothelial cell apoptosis, The Journal of Clinical Investigation, Vol.102, 1682-1689, 1998.
551.	H.R. Perlman, Masataka Sata, T Sedlak, D Branellec and K Walsh : Bax-mediated cell death by the Gax homeoprotein requires mitogen-activation but is independent of cell cycle activity, The EMBO Journal, Vol.13, 3576-3586, 1998.
552.	Masataka Sata and K Walsh : TNFα regulation of Fas ligand expression on the vascular endothelium modulates leukocyte extravasation, Nature Medicine, Vol.4, No.4, 415-420, 1998. (Summary) It is generally believed that the vascular endothelium serves as an inflammatory barrier by providing a nonadherent surface to leukocytes. Here, we report that Fas ligand (FasL) is expressed on vascular endothelial cells (ECs) and that it may function to actively inhibit leukocyte extravasation. TNFalpha downregulates FasL expression with an accompanying decrease in EC cytotoxicity toward co-cultured Fas-bearing cells. Local administration of TNFalpha to arteries downregulates endothelial FasL expression and induces mononuclear cell infiltration. Constitutive FasL expression markedly attenuates TNFalpha-induced cell infiltration and adherent mononuclear cells undergo apoptosis under these conditions. These findings suggest that endothelial FasL expression can negatively regulate leukocyte extravasation. (Keyword) Antigens, CD95 / Aorta / Apoptosis / Cell Adhesion / Cell Survival / Cells, Cultured / Chromatin / Coculture Techniques / DNA Fragmentation / Endothelium, Vascular / Fas Ligand Protein / Gene Expression Regulation / Humans / Leukocytes / Leukocytes, Mononuclear / Membrane Glycoproteins / Microcirculation / Tumor Necrosis Factor-alpha / Umbilical Veins (Link to Publication Site) ● Publication site (DOI): 10.1038/nm0498-415 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9546786 ● Search Scopus @ Elsevier (PMID): 9546786 ● Search Scopus @ Elsevier (DOI): 10.1038/nm0498-415 (DOI: 10.1038/nm0498-415, PubMed: 9546786)
553.	Masataka Sata, H Perlman, D.A. Muruve, M Silver, M Ikebe, T.A. Libermann, P Oettgen and K Walsh : Fas ligand gene transfer to the vessel wall inhibits neointima formation and overrides the adenovirus-mediated T cell response, Proceedings of the National Academy of Sciences of the United States of America, Vol.95, 1213-1217, 1998.
554.	M Ikebe, T Kanbara, W.F. Stafford, Masataka Sata, E Katayana and R Ikebe : A hinge at the central helix of the regulatory light chain of myosin is critical for phosphrylation-dependent regulation of smooth muscle myosin motor activity, The Journal of Biological Chemistry, Vol.273, 17702-17707, 1998.
555.	Masataka Sata, W.F. Safford, K Mabuchi and M Ikebe : The motor domain and the regulatory domain of myosin solely dictate enzymatic activity and phosphorylation dependent regulation, respectively, Proceedings of the National Academy of Sciences of the United States of America, Vol.94, 91-96, 1997.
556.	Masataka Sata and M Ikebe : Functional analysis of the mutations in the human cardiac β-myosin that are responsible for familial hypertrophic cardiomyopathy: Implication for the clinical outcome, The Journal of Clinical Investigation, Vol.98, 2866-2873, 1996.
557.	Masataka Sata, M Matsuura and M Ikebe : Characterization of the motor and enzymatic properties of smooth muscle long S1 and short HMM: Role of the two headed structure on the activity and regulation of myosin motor, Biochemistry, Vol.35, 11113-11118, 1996.
558.	T Zhu, Masataka Sata and M Ikebe : Functional expression of mammalian myosin Iβ: Analysis of its motor activity, Biochemistry, Vol.35, 513-522, 1996.
559.	Masataka Sata, S Sugiura, H Yamashita, S Momomura and T Serizawa : Coupling between myosin ATPase cycle and creatine kinase cycle facilitates cardiac actomyosin sliding in vitro: A clue to mechanical dysfunction during myocardial ischemia, Circulation, Vol.93, 310-317, 1996.
560.	S Sugiura, H Yamashita, Masataka Sata, S Momomura, T Serizawa, K Oiwa, S Chaen, T Shimmen and H Sugi : Force-velocity relations of rat cardiac myosin isozymes sliding on algal actin cables in vitro, Biochem.Biophysic.Acta., Vol.1231, 69-75, 1995.
561.	A Matsumoto, Y Hirata, S Momomura, E Suzuki, I Yokoyama, Masataka Sata, Y Ohtani and T Serizawa : Effects of exercise on plasma level of brain natriuretic peptide in congestive heart failure with and without left ventricular dysfunction, American Heart Journal, Vol.129, 139-145, 1995.
562.	Masataka Sata, S Sugiura, H Yamashita, T Aoyagi, S Momomura and T Serizawa : Pimobendan directly sensitizes reconstituted thin filament sliding on cardiac myosin, Eur.J.Pharmacol.-Molcular Pharmacology section, Vol.290, 55-59, 1995.
563.	Masataka Sata, S Sugiura, H Yamashita, H Fujita, S Momomura and T Serizawa : MCI-154 increases Ca²⁺ sensitivity of reconstituted thin filament. A study using a novel in vitro motility assay technique, Circulation Research, Vol.76, 626-633, 1995.
564.	Masataka Sata, H Yamashita, S Sugiura, H Fujita, S Momomura and T Serizawa : A new in vitro motility assay technique to evaluate calcium sensitivity of the cardiac contractile proteins, Pflügers Archiv : European Journal of Physiology, Vol.429, 443-445, 1995.
565.	A Matsumoto, Y Hirata, S Momomura, H Fujita, A Yao and Masataka Sata : Increased nitric oxide production during exercise, The Lancet, Vol.343, 849-850, 1994.
566.	H Yamashita, Masataka Sata, S Sugiura, S Momomura, S Serizawa and M Iizuka : ADP inhibits the slidingvelocity of fluorescent actin filaments on cardiac and skeletal myosins, Circulation Research, Vol.74, 1027-1033, 1994.
567.	Masataka Sata, S Sugiura, H Yamashita, S Momomura and T Serizawa : Dynamic interaction between cardiac myosin isoforms modifies velocity of actomyosin sliding in vitro., Circulation Research, Vol.73, No.4, 696-704, 1993.
568.	H Yamashita, S Sugiura, Masataka Sata, T Serizawa, M Iizuka, T Shimmen and S Momomura : Depressed sliding velocity of isolated cardiac myosin from cardiomypathic hamsters: evidence for an alteration in mechanical interaction of actomyosin, Molecular and Cellular Biochemistry, Vol.119, 79-88, 1993.
569.	Masataka Sata, S Sugiura, H Yamashita, S Momomura and T Serizawa : Dynamic interaction between cardiac myosin isoforms modifies velocity of actomyosin sliding in vitro., Circulation Research, Vol.73, 696-704, 1993.
570.	Masataka Sata, S Momomura, K Takenaka, T Aoyagi, T Takahashi, T Serizawa and T Sugimoto : Dynamic left ventricular outflow tract obstruction 4 years after aortic valve replacement., American Heart Journal, Vol.124, 1085-1088, 1992.
571.	Masataka Sata, K Kimura, N Yagi, S Nanba, A Tojo, Y Hirata, H Matsuoka and T Sugimoto : A case of membranous nephropathy complicated by interstitial nephritis due to Sjogren's syndrome, Journal of Nephrology, Vol.4, 251-254, 1991.

Academic Paper (Unrefereed Paper):

1.	Issei Yagi, Shusuke Yagi, Keisuke Nakanishi, Kazuki Tezuka, K Matsuyama, Y Aibara, T Ishida, H Yoneda, M Yamamoto, Takayuki Ise, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Tetsuya Kitagawa, Yasuhiko Nishioka and Masataka Sata : Critical Limb Threatening Ischemia Due to Severe Polyarteritis Nodosa-A Case Report, Internal Medicine, 2024. (Tokushima University Institutional Repository) ● Metadata: 119631 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.4149-24 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39370254 ● Search Scopus @ Elsevier (PMID): 39370254 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.4149-24 (Tokushima University Institutional Repository: 119631, DOI: 10.2169/internalmedicine.4149-24, PubMed: 39370254)
2.	TOMONORI Takahashi, Tetsuzo Wakatsuki, Takayuki Ise and Masataka Sata : Spontaneous thrombosis of a giant aneurysm complicated with the coronary-to-pulmonary artery fistula: a case report, European Heart Journal. Case Reports, Vol.8, No.5, ytae227, 2024. (Tokushima University Institutional Repository) ● Metadata: 119332 (Link to Publication Site) ● Publication site (DOI): 10.1093/ehjcr/ytae227 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38736999 ● Search Scopus @ Elsevier (PMID): 38736999 ● Search Scopus @ Elsevier (DOI): 10.1093/ehjcr/ytae227 (Tokushima University Institutional Repository: 119332, DOI: 10.1093/ehjcr/ytae227, PubMed: 38736999)
3.	W Liu, Y Higashikuni and Masataka Sata : Optimizing antihypertensive therapy in patients with diabetes mellitus, Hypertension Research, Vol.46, No.3, 797-800, 2023. (Tokushima University Institutional Repository) ● Metadata: 117985 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41440-022-01150-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36577847 ● Search Scopus @ Elsevier (PMID): 36577847 ● Search Scopus @ Elsevier (DOI): 10.1038/s41440-022-01150-5 (Tokushima University Institutional Repository: 117985, DOI: 10.1038/s41440-022-01150-5, PubMed: 36577847)
4.	平田陽一郎 and Masataka Sata : YS-1402皮下投与および心筋投与における虚血性心筋症に対する効果の検討, BIO INDUSTRY, Vol.78, No.2, 191-196, 2020.
5.	田中君枝 and Masataka Sata : 5血小板・血栓, 動脈硬化診療のすべて A.成因:基礎研究，日本医師会雑誌生涯教育シリーズ-97 磯部光章他監修・編集, Vol.148, No.(2), 567-569, 2019.
6.	Masataka Sata : EPA・DHAと心血管疾患, 日本食品安全協会会誌, Vol.14, No.2, 93-102, 2019.
7.	PMC Davy, DC Willcox, Michio Shimabukuro, TA Donlon, T Torigoe, M Suzuki, M Higa, H Masuzaki, Masataka Sata, R Chen, R Murkofsky, BJ Morris, E Lim, RC Allsopp and BJ Willcox : Minimal shortening of leukocyte telomere length across age groups in a cross-sectional study for carriers of a longevity-associated FOXO3 allele., The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences, Vol.73, No.11, 1448-1452, 2018. (Summary) FOXO3 is one of the most prominent genes demonstrating a consistently reproducible genetic association with human longevity. The mechanisms by which these individual gene variants confer greater organismal lifespan are not well understood. We assessed the effect of longevity-associated FOXO3 alleles on age-related leukocyte telomere dynamics in a cross-sectional study comprised of samples from 121 healthy Okinawan-Japanese donors aged 21-95 years. We found that telomere length for carriers of the longevity associated allele of FOXO3 single nucleotide polymorphism rs2802292 displayed no significant correlation with age, an effect that was most pronounced in older (>50 years of age) participants. This is the first validated longevity gene variant identified to date showing an association with negligible loss of telomere length with age in humans in a cross-sectional study. Reduced telomere attrition may be a key mechanism for the longevity-promoting effect of the FOXO3 genotype studied. (Link to Publication Site) ● Publication site (DOI): 10.1093/gerona/gly071 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29688278 ● Summary page in Scopus @ Elsevier: 2-s2.0-85052888295 (DOI: 10.1093/gerona/gly071, PubMed: 29688278, Elsevier: Scopus)
8.	Masataka Sata and 松岡優 : (巻頭言) 特集心筋梗塞から身を守る-発作が起こる前と起こってからできること-, Shikoku Acta Medica, Vol.67, No.3-4, 103, 2011. (Tokushima University Institutional Repository) ● Metadata: 83830 (Tokushima University Institutional Repository: 83830)
9.	Koji Yamaguchi and Masataka Sata : 血管保護をふまえた脂質異常症の薬物治療, MEDICAMENT NEWS, No.2021, 8-11, 2010.
10.	Masataka Sata : 動脈硬化とRA系, Hypertens Scope, Vol.9, 5-6, 2010.
11.	Masataka Sata : 待たれる脂肪入れ替え術の臨床試験, Japan Medicine MONTHLY, Vol.4, 7, 2010.
12.	Koji Yamaguchi and Masataka Sata : 狭心症の薬物療法スタチンに関する最近の話題―strong statinとvascular statinをどのように選択するのか?, Medical Practice, Vol.27, No.5, 825-831, 2010.
13.	Tetsuzo Wakatsuki, K Yamaguchi, T Niki, Kenya Kusunose, K Koshiba, Hirotsugu Yamada, Takeshi Soeki, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Masataka Sata : Long-term endothelial dysfunction after coronary artery stenting with drug-eluting stent associated with local inflammatory response., Circulation, Vol.118, S_749, 2008.
14.	K Yamaguchi, Tetsuzo Wakatsuki, T Niki, Kenya Kusunose, K Koshiba, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Local hypercoagulability and endothelial dysfunction after sirolimus-eluting stent implantation: implication for late stent thrombosis., Circulation, Vol.118, S_651, 2008.
15.	Tetsuzo Wakatsuki, K Yamaguchi, Kenya Kusunose, T Niki, K Koshiba, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Long-term local inflammatory response after coronary artery stenting with drug-eluting stent., Eur Heart J, Vol.29, 505-732, 2008.

Academic Letter:

1.	Masataka Sata : Message From the Editor-in-Chief Circulation Reports: 4 Years of Progress After Launch, Circulation Reports, Vol.5, No.1, 1-3, 2023. (Keyword) General Medicine (Tokushima University Institutional Repository) ● Metadata: 118528 (Link to Publication Site) ● Publication site (DOI): 10.1253/circrep.CR-66-0010 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390294719108171264 ● Search Scopus @ Elsevier (DOI): 10.1253/circrep.CR-66-0010 (Tokushima University Institutional Repository: 118528, DOI: 10.1253/circrep.CR-66-0010, CiNii: 1390294719108171264)
2.	Kenya Kusunose, Hirotsugu Yamada, Yoshihito Saijo, Susumu Nishio, Yukina Hirata, Takayuki Ise, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Preload Stress Echocardiography for the Assessment of Heart Failure With Preserved Ejection Fraction, JACC. Cardiovascular Imaging, Vol.15, No.2, 375-378, 2022. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jcmg.2021.09.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34656477 ● Summary page in Scopus @ Elsevier: 2-s2.0-85123584116 (DOI: 10.1016/j.jcmg.2021.09.005, PubMed: 34656477, Elsevier: Scopus)
3.	Kenya Kusunose, K Matsunaga, Hirotsugu Yamada and Masataka Sata : Identifying the extent of oral fluid droplets on echocardiographic machine consoles in COVID-19 era, Journal of Echocardiography, Vol.18, No.4, 268-270, 2020. (Keyword) COVID-19 / Echocardiography / Equipment Contamination / Fomites / Humans / Infection Control / Language / Masks / Saliva / Speech (Link to Publication Site) ● Publication site (DOI): 10.1007/s12574-020-00491-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32946008 ● Search Scopus @ Elsevier (PMID): 32946008 ● Search Scopus @ Elsevier (DOI): 10.1007/s12574-020-00491-9 (DOI: 10.1007/s12574-020-00491-9, PubMed: 32946008)
4.	Kenya Kusunose, Hirotsugu Yamada, Rino Suzukawa, Yukina Hirata, Masami Yamao, Takayuki Ise, Shusuke Yagi, Masashi Akaike and Masataka Sata : Effects of Transthoracic Echocardiographic Simulator Training on Performance and Satisfaction in Medical Students., Journal of the American Society of Echocardiography, Vol.29, No.4, 375-377, 2016. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.echo.2015.12.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26743736 ● Summary page in Scopus @ Elsevier: 2-s2.0-84960912424 (DOI: 10.1016/j.echo.2015.12.002, PubMed: 26743736, Elsevier: Scopus)

Review, Commentary:

1.	Masataka Sata and Hiroshi Sakaue : 特集生活習慣病を克服して,健康寿命を延伸するために【巻頭言】, Shikoku Acta Medica, Vol.77, No.5,6, 173, Dec. 2021. (Tokushima University Institutional Repository) ● Metadata: 117125 (Tokushima University Institutional Repository: 117125)
2.	Masataka Sata : 動脈硬化性疾患におけるΩ3脂肪酸の役割, Medical Science Digest, Vol.46, No.3, 137-140, Mar. 2020.
3.	Masataka Sata and 田中君枝 : 心外膜下脂肪と冠動脈硬化, 伊藤浩編集，そうだったんだ脂質異常症治療の新潮流を探る第2版, 134-135, Mar. 2020.
4.	Koji Yamaguchi and Masataka Sata : その他XIV 動脈硬化のスクリーニング検査, 循環器疾患最新の治療2020-2021, 357-360, Jan. 2020.
5.	Koji Yamaguchi and Masataka Sata : 特集Endovascular Therapyはどこまできたか識る6 いかにEVT後の再狭窄?, Heart View, Vol.24, No.1, 39-44, Jan. 2020.
6.	Masataka Sata : 編集後記, 循環器専門医, Vol.23, 174, 2019.
7.	Masataka Sata and 田中君枝 : 心外膜脂肪と心疾患, Journal of JCS Cardiologists, Vol.23, 73-79, 2019. (Link to Publication Site) ● Publication site (DOI): 10.1253/jjcsc.28.0_73 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390564227302382336 ● Search Scopus @ Elsevier (DOI): 10.1253/jjcsc.28.0_73 (DOI: 10.1253/jjcsc.28.0_73, CiNii: 1390564227302382336)
8.	Yuta Torii, Kenya Kusunose, Hirotsugu Yamada, Y Saijo, Hiromitsu Seno, Susumu Nishio, Yukina Hirata and Masataka Sata : Pre-Discharge LV Filling Pressure and Pulmonary Artery Pressure Were Associated With Hospital Readmission in Heart Failure With Reduced and Preserved Ejection Fraction, AHA Scientific Sessions2017, Nov. 2017.
9.	高島啓 and Masataka Sata : omega-3 polyunsaturated fatty acid reduces the risk of cardiovascular events in the patients with ischemic heart disease, The Journal of the Japanese Society of Internal Medicine, Vol.106, No.2, 226-231, Feb. 2017. (Keyword) ω3系不飽和脂肪酸 / 虚血性心疾患 / EPA / DHA (Link to Publication Site) ● Publication site (DOI): 10.2169/naika.106.226 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520853831989032832 ● Search Scopus @ Elsevier (DOI): 10.2169/naika.106.226 (DOI: 10.2169/naika.106.226, CiNii: 1520853831989032832)
10.	Shusuke Yagi and Masataka Sata : 非薬物降圧治療の可能性-RDN, デバイス，遠隔モニタリング, Journal of Clinical and Experimental Medicine, Vol.260, No.5, 484-485, Feb. 2017.
11.	Masataka Sata, 小川佳宏, Michio Shimabukuro and 髙橋尚彦 : 座談会異所性脂肪と循環器疾患, CARDIAC PRACTICE, Vol.27, No.4, 63-67, Nov. 2016.
12.	Masataka Sata : 総論 (特集循環器疾患と異所性脂肪), CARDIAC PRACTICE, Vol.27, No.4, 15, Nov. 2016.
13.	Koji Yamaguchi and Masataka Sata : 4. 虚血性心疾患を治す b. 労作性狭心症での使い方, Heart View, Vol.20, No.12, 124-129, Nov. 2016.
14.	平田有紀奈, Hirotsugu Yamada and Masataka Sata : 【循環器疾患と異所性脂肪】心外膜下脂肪を測定する意義, Cardiac Practice, Vol.27, No.4, 279-284, Nov. 2016.
15.	Daiju Fukuda and Masataka Sata : 肥満によって増加するDNA断片の遊離が，脂肪組織の炎症とインスリン抵抗性を惹起する, 尿酸と血糖, Vol.2, No.4, 37-39, Oct. 2016.
16.	Masataka Sata : いまから寒さに備え血管の健康を保つ, まいんど, Vol.28, No.10, 18-19, Oct. 2016.
17.	田中君枝 and Masataka Sata : Ⅱ．PPARαと疾患 2．動脈硬化とPPARα, The Lipid, Vol.27, No.4, 47-53, Oct. 2016. (Keyword) PPARα / 動脈硬化病変 / 血管内皮細胞 / 血管平滑筋細胞 / 炎症細胞
18.	Masataka Sata : Coronary Atherosclerosis and Epicardial Adipose Tissue, Respiration & Circulation, Vol.64, No.8, 791-797, Aug. 2016. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390002209966920832 (CiNii: 1390002209966920832)
19.	Masataka Sata : 第45回日本心脈管作動物質学会, 血圧, Vol.23, No.7, 90-91, Jul. 2016.
20.	Michio Shimabukuro, 益崎裕章 and Masataka Sata : Ⅲ アディポサイエンス・クリニカル ②異所性脂肪のフロンティア, Diabetes Frontier, Vol.3, No.27, 343-349, Jun. 2016. (Keyword) 異所性脂肪 / 心臓脂肪 / 内臓肥満症 / diabetes mellitus / insulin resistance
21.	平田有紀奈 and Masataka Sata : ECHO・CTで診る異所性脂肪, TOTAL VASCULAR MANAGEMENT, Vol.2, 4-7, Jun. 2016.
22.	山下静也, Libby Peter, 横手幸太郎, 大内乗有, 筒井裕之 and Masataka Sata : (座談会)アテローム血栓症と動脈硬化性疾患-ACS発症リスク因子のパラダイムシフト-, TOTAL VASCULAR MANAGEMENT, Vol.1, 8-15, Apr. 2016.
23.	田中君枝 and Masataka Sata : 血管のアンチエイジング, Medical Science Digest, Vol.42, No.3, 9-12, Mar. 2016. (Keyword) aging / atherosclerosis / vascular function / cardiovascular disease / erectile dysfunction
24.	Shusuke Yagi and Masataka Sata : 7 心臓病と肥満 -メタボリックシンドロームを中心に-, 循環器疾患最新の治療2016-2017(監修堀正二，編集長井良三，伊藤浩), 509-511, Mar. 2016.
25.	橋本洋一郎, 平野照之, 長谷川泰弘, Masataka Sata and 藤城光弘 : 大出血ハイリスク例における抗凝固療法, Cardio-Coagulation, Vol.3, No.1, 6-14, Mar. 2016.
26.	石井亜由美, 西川幸治, Takayuki Ise, 門田宗之, Shusuke Yagi, Takashi Iwase, Hajime Kinoshita, Miho Sakata, Yasunobu Hayabuchi, Tetsuya Kitagawa, Masashi Akaike, Shinsuke Katoh and Masataka Sata : 単心室症患児の開心術後にフェイススケールを用いて心臓リハビリテーションを試みた1症例, Heart, Vol.48, No.2, 181-186, Feb. 2016. (Keyword) 心臓リハビリテーション / infant / フェイススケール
27.	田中君枝 and Masataka Sata : 巻頭総説動脈硬化病変における血管周囲脂肪組織と血管外膜微小血管の役割, Japanese Journal of Circulation Research, Vol.38, No.3, 95-107, Oct. 2015.
28.	Masataka Sata : 序文 (特集血管機能検査を臨床に活かす), Cardioangiology, Vol.78, No.3, 78, Sep. 2015. (Keyword) vascular function / atherosclerosis / endothelial dysfunction
29.	田中君枝 and Masataka Sata : PDE5阻害薬の臨床 2)PDE5阻害薬と血管機能, 腎臓内科・泌尿器科, Vol.2, No.1, 54-61, Jul. 2015. (Keyword) PDE5 infibitor / erectile dysfunction / cardiovascular disease / endothelial dysfunction / vascular dysfunction
30.	Daiju Fukuda and Masataka Sata : 23 ACE阻害薬の抗動脈硬化作用に関して教えて下さい, 実はすごい!ACE阻害薬エキスパートからのアドバイス50(編集伊藤浩), 111-114, Jul. 2015.
31.	田中君枝 and Masataka Sata : 血管外の組織はACSの発症に関与しているのか?(I. 虚血性心疾患 A. 急性冠症候群), EBM 循環器疾患の治療2015-2016 (監修小室一成), 25-29, May 2015.
32.	Hirotsugu Yamada, Mika Bando, 西尾進, 天野里江, 鳥居裕太, Koji Yamaguchi, Tetsuzo Wakatsuki and Masataka Sata : 超音波後方散乱信号を用いた頸動脈プラークの性状診断とその臨床応用, Neurosonology, Vol.28, No.suppl-1, 94, May 2015.
33.	Kenya Kusunose and Masataka Sata : atrial appendage occlusion (左心耳閉鎖デバイス), Journal of JCS Cardiologists, Vol.23, No.1, 85, Mar. 2015. (Link to Publication Site) ● Publication site (DOI): 10.1253/jjcsc.23.1_86 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282763011288192 ● Search Scopus @ Elsevier (DOI): 10.1253/jjcsc.23.1_86 (DOI: 10.1253/jjcsc.23.1_86, CiNii: 1390282763011288192)
34.	榎本操一郎, 墨誠 and Masataka Sata : 小口径人工血管 7-2 ラットへの移植評価 (ワイド特集シルクによる再生医療材料の開発-衣料から医療へ-), 工業材料, Vol.63, No.2, 68-72, Feb. 2015.
35.	Masataka Sata : 冠動脈疾患における心外膜脂肪の役割, Medical Science Digest, Vol.41, No.1, 16-19, Jan. 2015. (Keyword) atherosclerosis / angiogenesis / 心外膜脂肪 / 不安定プラーク / 心筋梗塞
36.	Masataka Sata : 特集臓器連関企画にあたって, 腎・高血圧の最新治療, Vol.5, No.1, 4, Jan. 2015.
37.	Takayuki Ise, 高木恵理, Takashi Iwase, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心臓サルコイドーシス再燃に対してメトトレキサートの併用が有効であった1例, The Journal of the Japanese Society of Internal Medicine, Vol.104, No.6, 1175-1179, 2015. (Summary) 心臓サルコイドーシスの標準的治療はステロイドであるが，ステロイドを投与中であっても再燃を認めることも多く，またステロイドの多岐にわたる副作用も問題となることが多い．症例は70歳代，女性．心臓サルコイドーシスの診断でプレドニンを維持量5 mg/日で加療されていた．定期検査で施行した心電図で陰性T波，前壁心尖部に新規の左室壁運動異常を認めた．FDG-PET，Gaシンチグラフィーで壁運動異常部位に一致して集積を認め，心臓サルコイドーシスの再燃と判断した．本症例では，ステロイドの副作用として糖尿病，肥満，白内障などを認めており，ステロイド増量が躊躇され，メトトレキサートの併用を開始した．メトトレキサート開始後，特に副作用を認めず，心電図ならびに左室壁運動異常の改善が認められた．ステロイド投与で再燃を認める心臓サルコイドーシス症例にはメトトレキサート併用も考慮すべきであると考えられた． (Keyword) 心臓サルコイドーシス / 再燃 / steroid / メトトレキサート / 副作用 (Link to Publication Site) ● Publication site (DOI): 10.2169/naika.104.1175 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001206449318272 ● Search Scopus @ Elsevier (DOI): 10.2169/naika.104.1175 (DOI: 10.2169/naika.104.1175, CiNii: 1390001206449318272)
38.	Masataka Sata : 私の健康法, 臨床高血圧 CLINICAL HYPERTENSION, Vol.6, No.20, 70-71, Sep. 2014.
39.	今田久美子, Shusuke Yagi, Koji Yamaguchi, Tetsuzo Wakatsuki, Takayuki Ise, 太田理絵, 門田宗之, 高島啓, 松浦朋美, Takeshi Tobiume, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Efficacy of percutaneous transluminal renal angioplasty for renovascular hypertension complicated with heart failure, Shikoku Acta Medica, Vol.70, No.3, 4, 87-92, Aug. 2014. (Summary) 【Background】 Percutaneous transluminal renal angioplasty (PTRA) is recommended for patients with heart failure due to renovascular hypertension ; however, the clinical characteristics of the patients and the effects of PTRA on heart failure and cardiorenal function have not been elucidated. 【Methods】 We retrospectively analyzed data for 4 PTRA-treated patients (male/female, 1/3 ; mean age, 70.0±10 years ; mean left ventricular ejection fraction, 51.5±15.2%) with heart failure due to renovascular hypertension and evaluated the effects of PTRA on heart failure and cardiorenal function 6 months after treatment. 【Results】 All patients had pro-arteriosclerotic diseases including diabetes mellitus, essential thrombocythemia, heparin cofactor II deficency, metabolic syndrome, and familial hypercholesterolemia, and 3 patients had ischemic heart disease. No abdominal bruit was heard and mean plasma renin activity was 4.5±3.6 ng/ml/hr, which was not elevated, contrary to expectation. All contralateral kidneys of PTRA were nonfunctioning, suggesting bilateral kidneys were disturbed in all patients. In all patients, PTRA was successfully performed and resolved heart failure. PTRA resulted in decreases in systolic blood pressure from 157±18 to 124±8.6 mmHg, mean serum creatinine from 3.2±2.6 to 2.7±2.2 mg/dl, and mean BNP from 919±998 to 243±291 pg/ml at 6 months after treatment. PTRA did not change left ventricular ejection fraction, a parameter of systolic fraction evaluated by an echocardiogram ; however, PTRA improved E/e', a parameter of left ventricular diastolic fraction, from 16.1±5.2 to 9.7±3.7. None of the patients were hospitalized due to heart failure during the 6-month period after PTRA. 【Conclusions】 Patients with heart failure with cardiovascular risk factors should be screened for renovascular hypertension regardless of abdominal bruit or plasma renin activity. PTRA is effective for resolving heart failure and for improving renal and cardiac diastolic functions in patients with renovascular hypertension complicated with heart failure. (Keyword) heart failure / cardiac disturbance syndrome / percutaneous transluminal renal angioplasty (Tokushima University Institutional Repository) ● Metadata: 109759 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050001337734629888 (Tokushima University Institutional Repository: 109759, CiNii: 1050001337734629888)
40.	Shusuke Yagi and Masataka Sata : 血圧日内変動を考慮したRAAS抑制薬による高血圧治療 (特集血圧サーカディアンリズム : 24時間血圧管理の重要性) -- (24時間パーフェクト血圧管理をめざした治療), Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.72, No.8, 1466-1471, Aug. 2014.
41.	田中君枝 and Masataka Sata : 粥状動脈硬化 (特集:循環器における炎症性疾患-病態から診療へ-), 臨床循環器 CIRCULATION, Vol.4, No.4, 45-53, Jul. 2014.
42.	Shusuke Yagi and Masataka Sata : 文献紹介「Stenting and medical therapy for atherosclerotic renal-artery stenosis」, 腎・高血圧の最新治療, Vol.3, No.3, 170-171, Jul. 2014.
43.	Masataka Sata : 特集保存期腎不全の集学的治療企画にあたって, 腎・高血圧の最新治療, Vol.3, No.3, 128, Jul. 2014.
44.	Masataka Sata : 異所性脂肪としての血管周囲脂肪組織の役割と臨床的意味, Cardio-Lipidology, Vol.8, No.1, 12-17, May 2014. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1521980706050001920 (CiNii: 1521980706050001920)
45.	Masataka Sata : 脂肪酸とプラークの炎症, The Lipid, Vol.25, No.2, 13-18, Apr. 2014. (Keyword) n-3脂肪酸 / 血管炎症反応 / 白血球 / プラーク
46.	Masataka Sata : 心外膜脂肪と冠動脈疾患, The Lipid, Vol.25, No.2, 13-18, Apr. 2014. (Summary) ヒトの動脈硬化は, 従来考えられていたよりかなり早期から始まり, 生活習慣病の進行とともに急速に増悪し, 突然イベントを誘発する. その病態においては, 従来研究されてきた脂質の沈着や細胞増殖だけでなく, 血管周囲のvasa vasorumからの新生血管を介した細胞流入や微小出血が関与することがわかってきた. また, 血管, 特に冠動脈周囲には豊富に心外膜脂肪組織が存在し, 血管の慢性炎症に深く関与し, プラークの進展と不安定化に重要な役割を担っていることが明らかとなった. 心外膜脂肪を利用した, 新しい冠動脈疾患の診断や治療の開発が期待される. [はじめに] 最近の研究により, 半数以上の心筋梗塞は内腔の有意狭窄を伴わず虚血を引き起こさないような軽度の病変が原因として生じていることが明らかとなった. そのため, イベントを未然に防ぐためには, 動脈硬化病変が破綻してイベントを引き起こしそうな不安定プラークを検出しなければならない.
47.	Michio Shimabukuro and Masataka Sata : 異所性脂肪と心臓脂肪:心臓血管病における新たな病態, 心血管薬物療法, Vol.2, No.1, 35-40, Mar. 2014. (Keyword) 異所性脂肪 / 心臓脂肪 / 内臓肥満症 / 心臓血管病 / insulin resistance
48.	Masataka Sata : J-ISCP会誌「心血管薬物療法」第二巻発行にあたり, 心血管薬物療法, Vol.2, No.1, 2, Mar. 2014.
49.	高木恵理 and Masataka Sata : 妊娠を契機に発見され,出産が可能であった先天性アンチトロンビンIII欠損症の1例(症例検討), Journal of JCS Cardiologists, Vol.22, No.1, 109-115, Mar. 2014. (Keyword) 先天性アンチトロンビンIII欠損症 / 栓友病 / 常染色体優性遺伝 (Link to Publication Site) ● Publication site (DOI): 10.1253/jjcsc.22.1_109 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390564237986910464 ● Search Scopus @ Elsevier (DOI): 10.1253/jjcsc.22.1_109 (DOI: 10.1253/jjcsc.22.1_109, CiNii: 1390564237986910464)
50.	Masataka Sata : Recent progress in diagnosis, treatment, and prevention of coronary artery disease, The Journal of the Japanese Society of Internal Medicine, Vol.103, No.3, 687-692, Mar. 2014. (Keyword) atherosclerosis / 心筋梗塞 / 冠動脈CT / AED (Link to Publication Site) ● Publication site (DOI): 10.2169/naika.103.687 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24796137 ● CiNii @ National Institute of Informatics (CRID): 1390001206447465216 ● Summary page in Scopus @ Elsevier: 2-s2.0-84902673536 (DOI: 10.2169/naika.103.687, PubMed: 24796137, CiNii: 1390001206447465216, Elsevier: Scopus)
51.	田中君枝 and Masataka Sata : [Expertise]糖尿病による動脈硬化のメカニズムはどこまで解明されたか?(特集:心血管系疾患と糖尿病―どう対応していくか), Heart View, Vol.18, No.4, 47-53, Mar. 2014.
52.	Masataka Sata : (特集長期予後を見据えたアプローチ4)心腎連関を考慮した高血圧治療-将来の心血管イベント抑制に向けて, 循環plus, Vol.14, No.4, 2-6, Dec. 2013.
53.	Masataka Sata : オメガ3系多価不飽和脂肪酸の作用機序動脈硬化抑制の多面的作用を考える, CardioVascular Contemporary, Vol.2, No.4, 14-19, Dec. 2013.
54.	西尾進, Hirotsugu Yamada and Masataka Sata : 頸動脈エコー検査による頸動脈内膜中膜複合体肥厚度(IMT)の評価, Cardio-Renal Diabetes, Vol.2, No.4, 4-7, Nov. 2013. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1521136281138006656 (CiNii: 1521136281138006656)
55.	Daiju Fukuda and Masataka Sata : The role of RAA system in endothelial function and vascular remodeling, Fluid Management Renaissance, Vol.3, No.4, 34-42, Nov. 2013. (Summary) レニン-アンジオテンシン-アルドステロン(RAA)系は，血圧や体液電解質の調節だけではなく生体内でさまざまな生理活性をもっている．多くの細胞・組織にRAA系の構成因子が発現していることが知られるようになり，循環RAA系よりも組織的RAA系が血管の炎症である動脈硬化病変の形成に重要であることが示されている．RAA系は，活性酵素種の産生をもとにした炎症反応の惹起・血管内皮機能障害・血管リモデリングなどさまざまな機序で動脈硬化病変の増悪に関与し，心血管疾患の発症とその後の病態の進展に重要な役割を果たしている．また，RAA系を対象にしたさまざまな薬品の開発が進み，その降圧作用のみならず抗炎症効果など多面的な効果が注目されている． (Keyword) inflammation / atherosclerosis / 活性酵素 / 組織レニン-アンジオテンシン-アルドステロン系 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520291856204070784 (CiNii: 1520291856204070784)
56.	Takeshi Soeki and Masataka Sata : 高血圧の炎症・免疫バイオマーカー, 血圧, Vol.20, No.11, 30-34, Nov. 2013. (Keyword) 高感度CRP / inflammatory cytokine / PTX3 / アディポネクチン / micro RNA
57.	Masataka Sata : 特集今，動脈硬化はこう治療する巻頭言, Mebio, Vol.30, No.9, 7, Sep. 2013.
58.	Masataka Sata : (特集:今，動脈硬化はこう治療する) 今，動脈硬化はこう予防する ω3不飽和脂肪酸, Mebio, Vol.30, No.9, 98-107, Sep. 2013.
59.	Michio Shimabukuro and Masataka Sata : 異所性脂肪と心臓血管病【特集異所性脂肪-糖尿病診療における新しい視点】, 糖尿病の最新治療, Vol.4, No.4, 202-208, Aug. 2013. (Summary) 内臓肥満症に脂質異常症, 耐糖能障害, 高血圧症が重積する背景には, インスリン抵抗性および相対的なインスリン分泌障害がある. また, 内臓脂肪蓄積と共存あるいは独立して, 脂肪細胞以外の臓器における脂肪蓄積(異所性脂肪)も関与が疑われる. 異所性脂肪が蓄積すると, 肝臓, 筋肉の慢性炎症やインスリン抵抗性が起こること, さらに, 脂質異常症, 耐糖能障害, 高血圧症のリスクが重なり, 心臓血管病が起こりやすくなる. 異所性脂肪は心臓血管系にもみられ, (1)流血中および血管局所の脂肪, (2)心筋細胞内脂肪, 心筋細胞外脂肪, (3)血管周囲脂肪, (4)心外膜周囲脂肪に分けられる. 心臓脂肪は, 心臓血管系の機能やリモデリングに関わるという知見も出てきており, 耐糖能障害, 2型糖尿病での検討も課題であろう. 「はじめに」内臓肥満症では, 脂質異常症, 耐糖能障害, 高血圧症のリスクが重積しやすく, 心臓血管病の発症リスクとなる. (Keyword) 内臓肥満症 / 異所性脂肪 / 心臓脂肪 / insulin resistance (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1522262181036674048 (CiNii: 1522262181036674048)
60.	Koji Yamaguchi and Masataka Sata : The effect of antihypertensive therapy on ischemic heart disease, Cardioangiology, Vol.73, No.6, 667-671, Jun. 2013. (Keyword) antihypertensive therapy / ischemic heart disease / angina pectoris / myocardial infarction (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1522825130065508352 (CiNii: 1522825130065508352)
61.	Koji Yamaguchi and Masataka Sata : ACSの病態, 月刊循環器 CIRCULATION, Vol.3, No.5, 25-31, Apr. 2013.
62.	Koji Yamaguchi and Masataka Sata : 球形吸着炭:クレメジン®は心血管疾患を制御できるか, 腎・高血圧の最新治療, Vol.2, No.2, 92-97, Apr. 2013. (Keyword) インドキシル硫酸 / uremic toxin / クレメジン / 抗動脈硬化作用 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520010381228211328 (CiNii: 1520010381228211328)
63.	Masataka Sata : 特集3 循環器疾患における新たなる知見, 循環plus, Vol.13, No.7, 2-6, Apr. 2013.
64.	平田陽一郎 and Masataka Sata : 心臓周囲脂肪組織の炎症から血管疾患をみる, Vascular Medicine, Vol.9, No.1, 29-34, Apr. 2013.
65.	Masataka Sata : 特集慢性炎症から血管疾患をみる特集にあたって, Vascular Medicine, Vol.9, No.1, 12, Apr. 2013.
66.	Koji Yamaguchi and Masataka Sata : 血管保護をふまえた脂質異常症・高血圧の薬物治療, 心血管薬物療法, Vol.1, No.1, 3-9, Mar. 2013. (Keyword) スタチン / 多面的効果 / プラーク安定化 / ストロングスタチン
67.	Shusuke Yagi, Masayoshi Ishida and Masataka Sata : 用語解説マイクロRNAと循環器疾患, Journal of JCS Cardiologists, Vol.21, No.1, 97, Mar. 2013. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390564237987988864 (CiNii: 1390564237987988864)
68.	Kenya Kusunose and Masataka Sata : 用語解説TAVR(transcatheter aortic valve replacement), Journal of JCS Cardiologists, Vol.21, No.1, 16, Mar. 2013. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001288034034432 (CiNii: 1390001288034034432)
69.	Takayuki Ise and Masataka Sata : 専門医トレーニング問題Ⅱ, 循環器専門医, Vol.21, No.1, 132-134, Mar. 2013.
70.	Masataka Sata : 複合心血管病変に対する治療戦略-内科の立場から-, 日本冠疾患学会雑誌, Vol.19, No.1, 36, Mar. 2013.
71.	足立克仁, Takashi Iwase, Masashi Akaike, 斎藤美穂, 柏木節子, 橋口修二, Masataka Sata, Shoichiro Takao, Masafumi Harada and 川井尚臣 : Late Gadolinium Enhancement of Cardiac Magnetic Resonance and Computed Tomography of Skeletal Muscle at Lower Legs in Female Carriers of Duchenne Muscular Dystrophy, Japanese Journal of National Medical Services, Vol.67, No.2, 63-69, Feb. 2013. (Keyword) Duchenne型筋ジストロフィー / 保因者 / 心臓MRI / ガドリニウム遅延造影 / 心機能障害 / CT (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1522262181098698368 ● Summary page in Scopus @ Elsevier: 2-s2.0-84876390340 (CiNii: 1522262181098698368, Elsevier: Scopus)
72.	Shusuke Yagi, Daiju Fukuda, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : RAS研究 -ラボの最前線- 徳島大学大学院ヘルスバイオサイエンス研究部循環器内科学・心臓血管病態医学, Angiotensin Research, Vol.10, No.1, 59-63, Jan. 2013.
73.	Hirotsugu Yamada, 西尾進 and Masataka Sata : 血管機能不全(後編)血管弾性, Vascular Lab, Vol.10, No.4, 452-456, 2013.
74.	西尾進, Hirotsugu Yamada and Masataka Sata : 血管機能不全(前編)血管内皮機能検査, Vascular Lab, Vol.10, No.3, 343-347, 2013.
75.	Masataka Sata : 冠動脈疾患の最新の動向 (第26回日本臨床内科医学会教育講演), 日本臨床内科医会会誌, Vol.27, No.4, 412-417, Dec. 2012.
76.	Masataka Sata : 企画にあたって (特集腎性高血圧と動脈硬化), 腎・高血圧の最新治療, Vol.1, No.1, 6, Oct. 2012.
77.	Masataka Sata : 脂肪組織の慢性炎症と循環器疾患, Inflammation & Immunology, Vol.20, No.5, 28-32, Aug. 2012. (Keyword) atherosclerosis / angiogenesis / 心外膜脂肪 / 不安定プラーク / 心筋梗塞
78.	Masataka Sata : 特集:ω3系脂肪酸の魅力にせまる ω3系脂肪酸の多面的な作用心・血管系, 実験治療, Vol.708, 233-238, Aug. 2012.
79.	Masataka Sata : 冠動脈疾患における心外膜脂肪の意義, Heart, Vol.44, No.7, 965-969, Jul. 2012.
80.	室原豊明, 葛谷雅文, Masataka Sata and 大屋祐輔 : (座談会)血管老化の基礎と臨床, CARDIAC PRACTICE, Vol.23, No.3, 71-78, Jul. 2012.
81.	Michio Shimabukuro, Daiju Fukuda, Masataka Sata and 益崎裕章 : 血管内皮機能障害, 最新臨床糖尿病学(下) -糖尿病学の最新動向-, Vol.70, No.5, 236-242, Jul. 2012.
82.	Shusuke Yagi, Ken-ichi Aihara, Yasumasa Ikeda, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Effects of Statins on Cardiorenal Syndrome., International Journal of Vascular Medicine, Vol.2012, 162545, Jun. 2012. (Summary) Cardiovascular disease and renal disease have a close relationship that forms a vicious cycle as a cardiorenal syndrome (CRS). Oxidative stress, endothelial dysfunction, and vascular inflammation could be therapeutic targets when the renin-angiotensin-aldosterone system is activated by accumulation of conventional cardiovascular risk factors; however, a strategy for management of CRS has not been established yet. Statins, HMG-CoA reductase inhibitors, have not only cholesterol-lowering effects but also pleiotropic effects on cardiovascular systems, including anti-inflammatory and antioxidant effects and improvement of nitric oxide bioavailability. Since recent studies have indicated that statins have beneficial effects on chronic kidney disease and heart failure as well as coronary artery disease in cholesterol-lowering-dependent/independent manners, treatment with statins might be a successful strategy for preventing deterioration of CRS. (Link to Publication Site) ● Publication site (DOI): 10.1155/2012/162545 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22792467 ● Search Scopus @ Elsevier (PMID): 22792467 ● Search Scopus @ Elsevier (DOI): 10.1155/2012/162545 (DOI: 10.1155/2012/162545, PubMed: 22792467)
83.	原知也 and Masataka Sata : ACSの概念と成因, 月刊循環器 CIRCULATION, Vol.2, No.7, 6-7, Jun. 2012.
84.	Takayuki Ise and Masataka Sata : 心不全予防としての睡眠呼吸障害の診断と介入, 臨床医のための循環器診療, Vol.16, 16-18, Jun. 2012.
85.	田中君枝 and Masataka Sata : Insulin resistance and atherosclerosis : The role of inflammation in atherosclerosis, Cardioangiology, Vol.71, No.5, 401-405, May 2012. (Keyword) insulin resistance / inflammation / atherosclerosis / perivascular adipose tissue / vasa vasorum (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1524232505677074048 (CiNii: 1524232505677074048)
86.	Takeshi Soeki, 木谷光宏 and Masataka Sata : 循環器専門医が考えるCa拮抗薬の選択ポイント(動脈硬化), 循環Plus, Vol.12, No.8, 7-9, May 2012.
87.	小室一成, 苅尾七臣, 堀内正嗣 and Masataka Sata : (座談会) 脳心血管イベント抑制に着目した高血圧治療とは-ミカルディスのポテンシャル-, Japan Medical Journal, Vol.4591, C1-C4, Apr. 2012.
88.	小室一成, 苅尾七臣, 森下竜一 and Masataka Sata : (座談会)心血管イベント抑制を目指す高血圧治療における"メタボサルタン''への期待, 日経メディカル, Vol.4, No.533, 135-138, Apr. 2012.
89.	Michio Shimabukuro, 益崎裕章 and Masataka Sata : 大血管障害抑制の視点からみた速効型インスリン分泌刺激薬, Angiology Frontier, Vol.11, No.1, 21-26, Mar. 2012.
90.	Masataka Sata, 横山光宏, 板倉弘重 and 山下智也 : (座談会)循環器領域における脂肪酸バランス(EPA/AA比)の重要性を考える-JELIS脂肪酸サブ解析からみえてくる新たな治療戦略-, Mebio, 14-24, Feb. 2012.
91.	田中君枝 and Masataka Sata : Diabetes and vascular aging, Anti-aging Science, Vol.4, No.1, 6-9, Feb. 2012. (Keyword) 血管老化 / テロメア / サーチュイン遺伝子 / AGEs-RAGE系 / p53 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520010381217585536 (CiNii: 1520010381217585536)
92.	原知也 and Masataka Sata : NEW ARRIVAL & COMMENT : NT5E mutations and arterial calcifications, O.li.v.e., Vol.2, No.1, 28-34, Feb. 2012. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1521417756108763776 (CiNii: 1521417756108763776)
93.	Masataka Sata : 慢性炎症としての動脈硬化, Cardiovascular Frontier, Vol.3, No.1, 43-49, Feb. 2012.
94.	Michio Shimabukuro, Masataka Sata, 山川研 and 益崎裕章 : 【ステロイドホルモンと脂質代謝-最近の進歩と臨床の新展開-】コルチゾールと脂質代謝, The Lipid, Vol.23, No.1, 35-41, Jan. 2012.
95.	Michio Shimabukuro and Masataka Sata : 糖尿病における内膜の障害とそのメカニズム, 月刊糖尿病, Vol.3, No.13, 27-31, Dec. 2011.
96.	Michio Shimabukuro and Masataka Sata : (海外文献紹介) 糖尿病は，プラーク退縮におけるマクロファージ形質を負に制御する, Angiology Frontier, Vol.10, No.4, 334-336, Dec. 2011.
97.	Michio Shimabukuro, Asuka Shiota, 山川研, 益崎裕章 and Masataka Sata : (海外文献紹介) 2型糖尿病患者における代謝因子，脂肪細胞，PAI-1レベル:Look AHEAD試験, Angiology Frontier, Vol.10, No.3, 68, Sep. 2011.
98.	光山勝慶, 平田健一 and Masataka Sata : (座談会) 動脈硬化研究の新展開, Cardiovascular Frontier, Vol.2, No.4, 7-12, Aug. 2011.
99.	平田陽一郎, 高岡稔 and Masataka Sata : The Role of Perivascular Adipose Tissue in Vascular Inflammation and Atherogenesis, Journal of the The Japan Diabetes Society, Vol.54, No.7, 483-486, Jul. 2011. (Keyword) diabetes mellitus / 慢性炎症 / atherosclerosis / blood vessel / 周囲 / 脂肪組織 / 役割 (Link to Publication Site) ● Publication site (DOI): 10.11213/tonyobyo.54.483 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001204905774208 ● Summary page in Scopus @ Elsevier: 2-s2.0-80052066540 (DOI: 10.11213/tonyobyo.54.483, CiNii: 1390001204905774208, Elsevier: Scopus)
100.	Masataka Sata : (監訳) n-3 PUFAのうち，EPAがアテローム性プラークに取り込まれ，炎症性低下および安定性増強に関与 (原著:Abbie L. Cawoodほか), 動脈硬化予防, Vol.10, No.2, 92-94, Jul. 2011.
101.	Masataka Sata : (巻頭言) 被災地医療支援の日本の現状, Respiration & Circulation, Vol.59, No.6, 543, Jun. 2011. (Link to Publication Site) ● Publication site (DOI): 10.11477/mf.1404101719 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390846634896730880 ● Search Scopus @ Elsevier (DOI): 10.11477/mf.1404101719 (DOI: 10.11477/mf.1404101719, CiNii: 1390846634896730880)
102.	Michio Shimabukuro and Masataka Sata : 慢性関節リウマチと糖尿病における動脈硬化症の程度の比較, Angiology Frontier, Vol.10, No.2, 160-161, Jun. 2011.
103.	Michio Shimabukuro, 山川研, 益崎裕章 and Masataka Sata : 食後高血糖と血管内皮機能, 月刊糖尿病, Vol.3, No.5, 39-46, May 2011. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520854806150325248 (CiNii: 1520854806150325248)
104.	Michio Shimabukuro, 山川研, 益崎裕章 and Masataka Sata : Ectopic fat disposition and lipotoxicity, The Journal of the Japanese Society of Internal Medicine, Vol.100, No.4, 983-988, Apr. 2011. (Summary) 遊離脂肪酸はエネルギー基質であると同時にさまざまなシグナル分子の基質でもあり，インスリン作用，インスリン合成・分泌に影響を与える．肥満症にともなう過剰な遊離脂肪酸は，耐糖能を悪化させる．遊離脂肪酸によるインスリン作用の障害を(広義の)脂肪毒性，インスリン分泌能に及ぼす悪影響を膵β細胞脂肪毒性(狭義の脂肪毒性)と呼ぶ．最近，脂肪組織以外の臓器に蓄積する脂肪(異所性脂肪)の動態に注目が集まっており，各臓器で何らかの病的意義を有する可能性がある． (Keyword) 内臓肥満症 / 異所性脂肪 / 脂肪毒性 / 遊離脂肪酸 / インスリン抵抗性 (Link to Publication Site) ● Publication site (DOI): 10.2169/naika.100.983 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21626835 ● CiNii @ National Institute of Informatics (CRID): 1390282681420646784 ● Summary page in Scopus @ Elsevier: 2-s2.0-79960048326 (DOI: 10.2169/naika.100.983, PubMed: 21626835, CiNii: 1390282681420646784, Elsevier: Scopus)
105.	堀内正継, 吉村道博, 光山勝慶 and Masataka Sata : (座談会) Ca拮抗薬のRAAS抑制作用を探る-特にN型Ca拮抗薬の臓器障害抑制にフォーカスをあてて-, Therapeutic Research, Vol.32, No.2, 135-142, Feb. 2011.
106.	檜垣實男, 山岸昌一 and Masataka Sata : (座談会) メタボリックシンドロームを伴う高血圧の治療戦略ミカルディスとミカロム配合錠への期待, 日経メディカル, Vol.519, No.2, 107-110, Feb. 2011.
107.	Yoichiro Hirata and Masataka Sata : Synergistic protection against vascular inflammation with a calcium channel blocker and a statin., Hypertension Research, Vol.34, No.4, 441-442, Jan. 2011. (Keyword) Amlodipine / Animals / Calcium Channel Blockers / Disease Models, Animal / Dose-Response Relationship, Drug / Drug Synergism / Drug Therapy, Combination / Femoral Artery / Heptanoic Acids / Hydroxymethylglutaryl-CoA Reductase Inhibitors / Leukocytes / Mice / Pyrroles / Vasculitis (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2010.275 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21270818 ● Search Scopus @ Elsevier (PMID): 21270818 ● Search Scopus @ Elsevier (DOI): 10.1038/hr.2010.275 (DOI: 10.1038/hr.2010.275, PubMed: 21270818)
108.	Y Hirata and Masataka Sata : CAVI, a new parameter that detects arterial stiffness change after smoking., Circulation Journal, Vol.75, No.3, 548-549, Jan. 2011. (Keyword) Aorta / Atherosclerosis / Blood Flow Velocity / Elasticity / Femoral Artery / Humans / Male / Smoking / Tibial Arteries / Vascular Resistance (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-10-1319 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21282874 ● Search Scopus @ Elsevier (PMID): 21282874 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-10-1319 (DOI: 10.1253/circj.CJ-10-1319, PubMed: 21282874)
109.	Shusuke Yagi and Masataka Sata : Pre-clinical data on the role of mineralocorticoid receptor antagonists in reversing vascular inflammation., European Heart Journal Supplements, No.13, B15-B20, 2011. (Link to Publication Site) ● Publication site (DOI): 10.1093/eurheartj/sur012 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1093/eurheartj/sur012 (DOI: 10.1093/eurheartj/sur012)
110.	Masataka Sata and D. Fukuda : Chronic inflammation and atherosclerosis: A critical role for renin angiotensin system that is activated by life-style related diseases., Inflammation and Regeneration, Vol.31, 245-255, 2011. (Link to Publication Site) ● Publication site (DOI): 10.2492/inflammregen.31.245 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.2492/inflammregen.31.245 (DOI: 10.2492/inflammregen.31.245)
111.	Masataka Sata : Pathogenesis of coronary artery diseases, Shikoku Acta Medica, Vol.66, No.5, 6, 151-156, Dec. 2010. (Summary) Recent evidence suggests that acute coronary syndrome(ACS)results from plaque rupture in most of the cases. Vulnerable plaques are characterized by thinning of fibrous cap, increased lipid content, decreased smooth muscle cell content, and enhanced infiltration of inflammatory cells. However, the molecular mechanism of plaque destabilization is not fully understood. Thus, there is no established method to predict and prevent ACS. We have been studying the pathogenesis of plaque progression and destabilization, using animal models and clinical specimen. ApoE-deficient mice showed exaggerated atherosclerotic lesions with aging. Accumulation of macrophages in adventitia was first detected prior to plaque formation. Proliferation of vasa vasorum was observed only after atherosclerotic lesion formation. Local delivery of an angiogenic growth factor promoted lesion formation with enhanced neovascularization in the adventitia. Periadventitial fat is distributed ubiquitously around arteries. By using fat transplantation method, we found that periadventitial fat may protect against neointimal formation after angioplasty under physiological conditions and that inflammatory changes in the periadventitial fat may play a crucial role in the pathogenesis of vascular disease accelerated by obesity. Elucidation of the pathogenesis of coronary artery diseases leads to development of new strategies to diagnose and treat acute coronary syndrome. (Keyword) coronary artery disease / epicardial adipose tissue / angiogenesis / inflammation / obesity (Tokushima University Institutional Repository) ● Metadata: 110335 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050564287418523008 (Tokushima University Institutional Repository: 110335, CiNii: 1050564287418523008)
112.	Masataka Sata : 冠動脈疾患の病態解明と新しい診断治療技術の開発, Shikoku Acta Medica, Vol.66, No.3, 4, 151-156, Aug. 2010.
113.	Hirotsugu Yamada, Kenya Kusunose, 西尾進, Takeshi Soeki and Masataka Sata : Atrial fibrillation and thromboembolic stroke: when and how can it be treated, Shikoku Acta Medica, Vol.66, No.3, 63-70, Aug. 2010. (Summary) Atrial fibrillation(AF)is a common arrhythmia and the prevalence of this arrhythmia is increasing as aging. Secondary AF is defined as AF with organic heart disease and lone AF as AF without it. The AF is divided into paroxysmal, persistent and chronic by its onset and persistence. It is clinically important that any type AF causes thromboembolic stroke. The preventive Qumadin therapy should be applied to patients with AF. Transesophageal echocardiography has been utilized for the diagnosis of left atrial thrombus and for the prediction of stroke. CHADS2 score is a clinical prediction rule for estimating the risk of stroke in patients with non-rheumatic AF. Patients with CHADS2 score_1should be treated with Qumadin. Rhythm control and rate control are two different strategies for the treatment of AF. There is no evidence that indicate better choice between rhythm control and rate control. Recently, inhibitors of the renin-angiotensin system have a potential to prevent new onset of AF in patients who has risk factors. (Keyword) atrial fibrillation / thrombosis / stroke / transesophageal echocardiography / qumadin (Tokushima University Institutional Repository) ● Metadata: 110316 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050845762395229952 (Tokushima University Institutional Repository: 110316, CiNii: 1050845762395229952)
114.	J Sainz and Masataka Sata : When EPC says: I2 shall limit neointima formation!, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.30, No.3, 457-458, Mar. 2010. (Keyword) Animals / Endothelium, Vascular / Epoprostenol / Mesenchymal Stromal Cells / Mice / Mice, Knockout / Models, Animal / Neovascularization, Physiologic / Receptors, Epoprostenol / Signal Transduction / Tunica Intima (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.109.201517 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20167663 ● Search Scopus @ Elsevier (PMID): 20167663 ● Search Scopus @ Elsevier (DOI): 10.1161/ATVBAHA.109.201517 (DOI: 10.1161/ATVBAHA.109.201517, PubMed: 20167663)
115.	Masataka Sata and Daiju Fukuda : Crucial role of renin-angiotensin system in the pathogenesis of atherosclerosis, The Journal of Medical Investigation : JMI, Vol.57, No.1, 2, 12-25, Feb. 2010. (Summary) The renin-angiotensin system (RAS) has been demonstrated to play a critical role in the initiation and progression of atherosclerosis, thereby contributing to development of cardiovascular diseases. Angiotensin II (Ang II), a major substrate in RAS, stimulates atherosclerosis through various deleterious effects such as endothelial dysfunction, cellular proliferation and inflammation. Recently, local RAS in vasculature is reported to play an important role. Many of these atherogenic actions of Ang II are mediated by reactive oxygen species (ROS). Investigation of the role of ROS and inflammation induced by RAS may provide a clue to understanding the pathophysiology of atherosclerotic diseases, and may lead to a new therapeutic strategy. (Keyword) Angiotensin II / atherosclerosis / Bone Marrow / Humans / reactive oxygen species / Receptor, Angiotensin, Type 1 / Receptor, Angiotensin, Type 2 / Renin-angiotensin System (Tokushima University Institutional Repository) ● Metadata: 66339 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.57.12 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20299739 ● Search Scopus @ Elsevier (PMID): 20299739 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.57.12 (Tokushima University Institutional Repository: 66339, DOI: 10.2152/jmi.57.12, PubMed: 20299739)
116.	山下静也, 前村浩二, 江頭健輔, Tomlinson Brain and Masataka Sata : (座談会)コレステロール吸収阻害がもたらす臨床的ベネフィットを検証する, 日経メディカル, Vol.4, 143-145, 2010.
117.	筒井裕之, 堀内正嗣, 大屋祐輔 and Masataka Sata : (座談会)アリスキレンの高血圧患者における心保護作用への期待, Progress in Medicine, Vol.30, No.2, 419-425, 2010.
118.	J Sainz and Masataka Sata : Is PIGF a Plaque Growth Factor?, Cardiovascular Research, Vol.86, No.1, 4-5, 2010. (Link to Publication Site) ● Publication site (DOI): 10.1093/cvr/cvq037 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1093/cvr/cvq037 (DOI: 10.1093/cvr/cvq037)
119.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Heparin Cofactor II as a Novel Vascular Protective Factor Against Atherosclerosis., Journal of Atherosclerosis and Thrombosis, Vol.16, No.5, 523-531, Sep. 2009. (Summary) Heparin cofactor II (HCII) specifically inhibits thrombin action at the site of vascular wall injury. We encountered a congenital HCII deficiency patient with advanced multiple atherosclerotic lesions. This patient led us to conduct clinical studies to examine the role of HCII against atherosclerosis. We found that the incidence of in-stent restenosis after percutaneous coronary intervention, severity of carotid atherosclerosis and prevalence of peripheral arterial disease are inversely associated with plasma HCII activity. In order to clarify the vascular protective action of HCII, we generated HCII- deficient mice by gene targeting. In contrast to a previous study, HCII(-/-) mice were embryonically lethal. In HCII(+/-) mice, accelerated intimal hyperplasia and frequent thrombosis were observed after cuff or wire injury of femoral arteries. The number of protease-activated receptor-1 (PAR-1) -positive cells and the gene expression levels of inflammatory cytokines and chemokines were increased in the thickened vascular walls of HCII(+/-) mice. The accelerated intimal hyperplasia in HCII+/- mice with vascular injury was attenuated by human HCII administration. Furthermore, HCII deficiency exaggerated aortic plaque formation with increased oxidative stress in apolipoprotein E(-/-) mice. These results demonstrate that HCII protects against thrombin-induced vascular remodeling in both humans and mice and suggest that HCII is a predictive biomarker and therapeutic target for atherosclerosis. (Keyword) Animals / atherosclerosis / Female / Heparin Cofactor II / Humans / knockout mice / knockout mice / Recombinant Proteins (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.1552 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19729870 ● Search Scopus @ Elsevier (PMID): 19729870 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.1552 (DOI: 10.5551/jat.1552, PubMed: 19729870)
120.	J Sainz and Masataka Sata : When p66ShcA is away, mice EPCs sweetly play., Cardiovascular Research, Vol.82, No.3, 388-389, Apr. 2009. (Keyword) Animals / Diabetic Angiopathies / Endothelial Cells / Glucose / Male / Mice / Mice, Knockout / Oxidative Stress / Shc Signaling Adaptor Proteins / Stem Cells (Link to Publication Site) ● Publication site (DOI): 10.1093/cvr/cvp111 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19351737 ● Search Scopus @ Elsevier (PMID): 19351737 ● Search Scopus @ Elsevier (DOI): 10.1093/cvr/cvp111 (DOI: 10.1093/cvr/cvp111, PubMed: 19351737)
121.	K Tanaka and Masataka Sata : Role of vascular progenitor cells in cardiovascular disease., Current Pharmaceutical Design, Vol.15, No.24, 2760-2768, 2009. (Summary) It is a widely accepted view that vascular repair results from migration and proliferation of adjacent vascular cells. On the other hand, accumulating evidence suggests that bone marrow cells can give rise to endothelial-like cells and smooth muscle-like cells that potentially contribute to vascular healing, remodeling and lesion formation under physiological and pathological conditions. However, some recent reports indicated controversial results and cast a doubt on the specificity of the method to detect differentiation of ectopic cells. Here, we overview recent findings on the role of vascular progenitor cells in cardiovascular diseases and provide possible explanation why different conclusions have been drawn from different animal experiments. (Keyword) Animals / Arteriosclerosis / Cardiovascular Diseases / Cell Fusion / Endothelial Cells / Heart Transplantation / Hematopoietic Stem Cells / Humans / Hyperplasia / Hypertension, Pulmonary / Muscle, Smooth, Vascular / Tunica Intima (Link to Publication Site) ● Publication site (DOI): 10.2174/138161209788923868 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19689346 ● Search Scopus @ Elsevier (PMID): 19689346 ● Search Scopus @ Elsevier (DOI): 10.2174/138161209788923868 (DOI: 10.2174/138161209788923868, PubMed: 19689346)
122.	K Tanaka and Masataka Sata : Contribution of circulating vascular progenitors in lesion formation and vascular healing: lessons from animal models., Current Opinion in Lipidology, Vol.19, No.5, 498-504, Oct. 2008. (Summary) It is a widely accepted view that vascular repair results from migration and proliferation of adjacent cells in animal models. On the contrary, accumulating evidence suggests that bone marrow can give rise to endothelial-like cells and smooth muscle like cells that potentially contribute to vascular healing, remodeling, and lesion formation under physiological and pathological conditions. The aim of this article is to review recent findings obtained from animal models of vascular diseases regarding bone marrow derived progenitor cells. Studies using chimeric animals revealed that bone marrow derived cells exist at the sites of vascular healing and lesion formation after injury. High-resolution histological analyses revealed that those bone marrow derived cells do express some markers for endothelial cells or smooth muscle cells. Peripheral mononuclear cells could differentiate into endothelial-like cells or smooth muscle like cells in vitro according to the culture conditions. Circulating progenitors significantly contribute to vascular repair and lesion formation. These findings provide the basis for the development of new therapeutic strategies that involve targeting the mobilization, homing, differentiation, and proliferation of bone marrow- derived vascular progenitor cells. (Keyword) Animals / Bone Marrow Cells / Cell Differentiation / Disease Models, Animal / Endothelial Cells / Humans / Models, Biological / Muscle, Smooth, Vascular / Stem Cells / Vascular Diseases (Link to Publication Site) ● Publication site (DOI): 10.1097/MOL.0b013e32830dd566 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18769231 ● Search Scopus @ Elsevier (PMID): 18769231 ● Search Scopus @ Elsevier (DOI): 10.1097/MOL.0b013e32830dd566 (DOI: 10.1097/MOL.0b013e32830dd566, PubMed: 18769231)
123.	H Iwata and Masataka Sata : The origin of the cells that contribute to neointima growth., Circulation, Vol.117, No.24, 3060-3061, Jun. 2008. (Keyword) Animals / Bone Marrow Cells / Bone Marrow Transplantation / Cell Division / Cytoskeletal Proteins / Mice / Muscle, Smooth, Vascular / Tunica Intima / Vascular Diseases (Link to Publication Site) ● Publication site (DOI): 10.1161/CIRCULATIONAHA.108.782961 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18559712 ● Search Scopus @ Elsevier (PMID): 18559712 ● Search Scopus @ Elsevier (DOI): 10.1161/CIRCULATIONAHA.108.782961 (DOI: 10.1161/CIRCULATIONAHA.108.782961, PubMed: 18559712)
124.	Daiju Fukuda and Masataka Sata : Role of bone marrow renin angiotensin system in the pathogenesis of atherosclerosis., Pharmacology & Therapeutics, Vol.118, No.2, 268-276, Mar. 2008. (Summary) The renin-angiotensin system (RAS) has been considered to be a circulating hormonal system that regulates blood pressure, blood flow, fluid volume and electrolyte balance. A growing body of evidence indicates local effects of an activated RAS, particularly in the cardiac, vascular, and renal systems. It is now well established that RAS, especially angiotensin II (Ang II) and Ang II type 1 receptor (AT1R) pathway, has significant pro-inflammatory actions on the vessel wall, leading to progression of atherosclerosis. Recent reports suggest that an activated RAS has local effects in bone marrow (BM), which contributes to the regulation of normal and malignant hematologic processes. We reported that AT1aR in BM cells participate in the pathogenesis of atherosclerosis by analyzing several BM chimeric mice whose BM cells were positive or negative for AT1aR. These results suggest that blockade of AT1R not only in vascular cells but also in BM could be an important strategy to prevent atherosclerosis. In this review, we overview recent findings on a role of RAS in the pathogenesis of atherosclerosis, and discuss functional contribution of a local RAS in BM to progression and destabilization of atherosclerotic plaque. (Keyword) Angiotensin II / Animals / atherosclerosis / Bone Marrow / Humans / Inflammation / Mice / knockout mice / Receptor, Angiotensin, Type 1 / Renin-angiotensin System (Link to Publication Site) ● Publication site (DOI): 10.1016/j.pharmthera.2008.02.007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18439685 ● Search Scopus @ Elsevier (PMID): 18439685 ● Search Scopus @ Elsevier (DOI): 10.1016/j.pharmthera.2008.02.007 (DOI: 10.1016/j.pharmthera.2008.02.007, PubMed: 18439685)
125.	J Sainz and Masataka Sata : Open sesame! CXCR4 blockade recruits neutrophils into the plaque., Circulation Research, Vol.102, No.2, 154-156, Feb. 2008. (Keyword) Animals / Atherosclerosis / Chemokine CXCL12 / Chemotaxis / Humans / Neutrophils / Pyridines / Receptors, CXCR4 (Link to Publication Site) ● Publication site (DOI): 10.1161/CIRCRESAHA.107.170241 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18239145 ● Search Scopus @ Elsevier (PMID): 18239145 ● Search Scopus @ Elsevier (DOI): 10.1161/CIRCRESAHA.107.170241 (DOI: 10.1161/CIRCRESAHA.107.170241, PubMed: 18239145)
126.	K Tanaka and Masataka Sata : Potential role of statins in re-endothelialization., Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry, Vol.8, No.2, 151-155, 2008. (Link to Publication Site) ● Publication site (DOI): 10.2174/187152208784587917 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.2174/187152208784587917 (DOI: 10.2174/187152208784587917)
127.	D Fukuda and Masataka Sata : Renin-angiotensin system: a potential modulator of endothelial progenitor cells., Hypertension Research, Vol.30, No.11, 1017-1018, Nov. 2007. (Keyword) Endothelium, Vascular / Humans / Hypertension / Losartan / Neovascularization, Pathologic / Renin-Angiotensin System / Stem Cells (Link to Publication Site) ● Publication site (DOI): 10.1291/hypres.30.1017 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18250549 ● Search Scopus @ Elsevier (PMID): 18250549 ● Search Scopus @ Elsevier (DOI): 10.1291/hypres.30.1017 (DOI: 10.1291/hypres.30.1017, PubMed: 18250549)
128.	H Iwata and Masataka Sata : Potential contribution of bone marrow-derived precursors to vascular repair and lesion formation: lessons from animal models of vascular diseases, Frontiers in Bioscience, Vol.12, 4157-4167, May 2007. (Summary) Atherosclerosis is responsible for more than half of all deaths in western countries. Numerous studies have reported that exuberant accumulation of smooth muscle cells (SMCs) plays a principal role in the pathogenesis of occlusive vascular diseases. It has been assumed that SMCs derived from the adjacent medial layer migrate towards the atherosclerotic lesion, proliferate and synthesize extracellular matrix, thus contributing to atheroma growth. Although much effort has been devoted to targeting the migration and proliferation of medial SMCs, no effective therapy to prevent occlusive vascular remodeling has been established. By taking advantage of genetically-modified mice, we recently reported that bone marrow cells substantially contribute to the pathogenesis of vascular diseases. It was suggested that bone marrow cells may have the potential to give rise to vascular progenitor cells that home in the damaged vessels and differentiate into smooth muscle cells or endothelial cells, thereby contributing to vascular repair, remodeling, and lesion formation. This article summarizes what we learned from genetically-modified animals regarding the origins and the fates of vascular cells that contribute to lesion formation. (Keyword) Animals / Bone Marrow Cells / Cell Differentiation / Cell Fusion / Disease Models, Animal / Mice / Muscle, Smooth, Vascular / Stem Cells / Vascular Diseases (Link to Publication Site) ● Publication site (DOI): 10.2741/2377 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17485364 ● Search Scopus @ Elsevier (PMID): 17485364 ● Search Scopus @ Elsevier (DOI): 10.2741/2377 (DOI: 10.2741/2377, PubMed: 17485364)
129.	J Sainz and Masataka Sata : CXCR4, a key modulator of vascular progenitor cells, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.27, No.2, 263-265, Feb. 2007. (Keyword) Animals / Atherosclerosis / Cell Differentiation / Cell Proliferation / Chemokine CXCL12 / Chemokines, CXC / Endothelium, Vascular / Macrophage Colony-Stimulating Factor / Mice / Receptors, CXCR4 / Stem Cells / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1161/01.ATV.0000256727.34148.e2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17229969 ● Search Scopus @ Elsevier (PMID): 17229969 ● Search Scopus @ Elsevier (DOI): 10.1161/01.ATV.0000256727.34148.e2 (DOI: 10.1161/01.ATV.0000256727.34148.e2, PubMed: 17229969)
130.	K Tanaka and Masataka Sata : Therapeutic application of bone marrow-derived progenitor cells for vascular diseases: Magic bullets having the good without the bad, International Journal of Gerontology, Vol.1, 10-21, 2007. (Link to Publication Site) ● Publication site (DOI): 10.1016/S1873-9598(08)70019-X (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/S1873-9598(08)70019-X (DOI: 10.1016/S1873-9598(08)70019-X)
131.	堀内正嗣, 森下竜一, Julius Stevo, 浦信行, Masataka Sata, Michio Shimabukuro, 島田朗, 鈴木大輔, 山内敏正, 中里雅光, 寺内康夫, 西村理明, 森保道, 綿田裕孝 and 小川渉 : 高血圧発症におけるレニン・アンジオテンシン系の役割, Pharma Medica, Vol.24, No.9, 107-112, Sep. 2006.
132.	J Sainz and Masataka Sata : Maintenance of Vascular Homeostasis by Bone Marrow-derived Cells, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.26, No.6, 1196-1197, Jun. 2006. (Keyword) Animals / Blood Vessels / Bone Marrow Cells / Cell Differentiation / Homeostasis / Humans / Stem Cells (Link to Publication Site) ● Publication site (DOI): 10.1161/01.ATV.0000220378.06854.35 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16709951 ● Search Scopus @ Elsevier (PMID): 16709951 ● Search Scopus @ Elsevier (DOI): 10.1161/01.ATV.0000220378.06854.35 (DOI: 10.1161/01.ATV.0000220378.06854.35, PubMed: 16709951)
133.	J Sainz and Masataka Sata : Targeting bone marrow to treat vascular diseases: Accelerated vascular healing by colony stimulating factor, Cardiovascular Research, Vol.70, No.1, 3-5, Feb. 2006. (Keyword) Animals / Arteries / Cell Differentiation / Cell Movement / Cell Proliferation / Colony-Stimulating Factors / Endothelial Cells / Humans / Interleukin-6 / Stem Cells / Vascular Diseases / Wound Healing (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cardiores.2006.01.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16472791 ● Search Scopus @ Elsevier (PMID): 16472791 ● Search Scopus @ Elsevier (DOI): 10.1016/j.cardiores.2006.01.006 (DOI: 10.1016/j.cardiores.2006.01.006, PubMed: 16472791)
134.	Masataka Sata : The role of circulating vascular progenitors in angiogenesis, vascular healing and pulmonary hypertension: Lessons from animal models, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.26, No.5, 1008-1014, Feb. 2006. (Summary) Accumulating evidence suggests that circulating progenitors contribute to vascular healing and remodeling under physiological and pathological conditions. Although there is growing enthusiasm for therapeutic and diagnostic application of bone marrow-derived progenitors, there are concerns that transplanted precursors or bone marrow cells may participate in the pathogenesis of unfavorable diseases such as cancer, retinopathy, and atherosclerosis. This review summarizes recent findings obtained from animal models to examine the roles of circulating vascular progenitor cells in angiogenesis, pulmonary hypertension, and vascular healing. (Keyword) Animals / Atherosclerosis / Bone Marrow Cells / Endothelial Cells / Hematopoietic Stem Cell Transplantation / Hematopoietic Stem Cells / Humans / Hypertension, Pulmonary / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Neovascularization, Physiologic / Regeneration (Link to Publication Site) ● Publication site (DOI): 10.1161/01.ATV.0000206123.94140.f3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16456096 ● Search Scopus @ Elsevier (PMID): 16456096 ● Search Scopus @ Elsevier (DOI): 10.1161/01.ATV.0000206123.94140.f3 (DOI: 10.1161/01.ATV.0000206123.94140.f3, PubMed: 16456096)
135.	Masataka Sata, F Fukuda, K Tanaka, Y Kaneda, H Yashiro and I Shirakawa : The role of circulating precursors in vascular repair and lesion formation, Journal of Cellular and Molecular Medicine, Vol.9, No.3, 557-568, 2005. (Summary) The accumulation of smooth muscle cells (SMCs) plays a principal role in atherogenesis, post-angioplasty restenosis and transplantation-associated vasculopathy. Therefore, much effort has been expended in targeting the migration and proliferation of medial smooth muscle cells to prevent occlusive vascular remodeling. Recent evidence suggests that bone marrow-derived circulating precursors can also give rise to endothelial cells and smooth muscle cells that contribute to vascular repair, remodeling, and lesion formation under physiological and pathological conditions. This article overviews recent findings on circulating vascular progenitor cells and describes potential therapeutic strategies that target these cells to treat occlusive vascular diseases. (Keyword) Animals / Arteriosclerosis / Bone Marrow Cells / Graft Occlusion, Vascular / Humans / Stem Cell Transplantation / Stem Cells / Vascular Diseases (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1582-4934.2005.tb00488.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16202205 ● Search Scopus @ Elsevier (PMID): 16202205 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1582-4934.2005.tb00488.x (DOI: 10.1111/j.1582-4934.2005.tb00488.x, PubMed: 16202205)
136.	Masataka Sata, K Tanaka and R Nagai : Circulating Osteoblast-Lineage Cells., The New England Journal of Medicine, Vol.353, 737-738, 2005.
137.	Masataka Sata and R Nagai : Origin of neointimal cells in autologous vein graft, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.24, No.7, 1147-1149, Jul. 2004. (Keyword) Animals / Blood Vessel Prosthesis / Cell Lineage / Cell Survival / Endothelium, Vascular / Femoral Artery / Graft Occlusion, Vascular / Graft Survival / Humans / Hyperplasia / Jugular Veins / Mice / Models, Animal / Thrombosis / Transplantation, Autologous / Tunica Intima / Vascular Patency (Link to Publication Site) ● Publication site (DOI): 10.1161/01.ATV.0000134296.22448.eb (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15237090 ● Search Scopus @ Elsevier (PMID): 15237090 ● Search Scopus @ Elsevier (DOI): 10.1161/01.ATV.0000134296.22448.eb (DOI: 10.1161/01.ATV.0000134296.22448.eb, PubMed: 15237090)
138.	Masataka Sata and R Nagai : Inflammation,angiogenesis,and endothelial progenitor cells: How do EPCs find their place?, Journal of Molecular and Cellular Cardiology, Vol.36, No.4, 459-463, Apr. 2004. (Keyword) Animals / Bone Marrow Cells / Endothelial Cells / Endothelium, Vascular / Humans / Inflammation / Models, Biological / Neovascularization, Pathologic / Neovascularization, Physiologic / Stem Cells (Link to Publication Site) ● Publication site (DOI): 10.1016/j.yjmcc.2004.01.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15081305 ● Search Scopus @ Elsevier (PMID): 15081305 ● Search Scopus @ Elsevier (DOI): 10.1016/j.yjmcc.2004.01.011 (DOI: 10.1016/j.yjmcc.2004.01.011, PubMed: 15081305)
139.	Masataka Sata and R Nagai : Mouse models of vein graft., Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.24, e185-e187, 2004. (Link to Publication Site) ● Publication site (DOI): 10.1161/01.ATV.0000142809.94325.af (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1161/01.ATV.0000142809.94325.af (DOI: 10.1161/01.ATV.0000142809.94325.af)
140.	Masataka Sata : Molecular strategies to treat vascular disease; Circulating vascular progenitor cell as a potential target for prophylactic treatment of atherosclerosis, Circulation Journal, Vol.67, No.12, 983-991, Dec. 2003. (Summary) Atherosclerosis is responsible for more than half of all deaths in Western countries. Numerous studies have reported that accumulation of smooth muscle cells (SMCs) plays a principal role in atherogenesis, post-angioplasty restenosis and transplantation-associated vasculopathy. Although much effort has been devoted to targeting the migration and proliferation of medial SMCs, effective therapy to prevent occlusive vascular remodeling has not been established. Recently, it was suggested that bone marrow-derived precursors can give rise to vascular cells that contribute to the repair, remodeling, and lesion formation of the arterial wall under certain circumstances. This review highlights the recent findings on circulating vascular precursors and describes the potential therapeutic strategies for vascular diseases, targeting mobilization, homing, differentiation and proliferation of circulating progenitor cells. (Keyword) Animals / Arteriosclerosis / Bone Marrow Transplantation / Cell Differentiation / Disease Models, Animal / Fas Ligand Protein / Genetic Therapy / Humans / Membrane Glycoproteins / Stem Cell Transplantation / Vascular Diseases (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.67.983 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14639011 ● Search Scopus @ Elsevier (PMID): 14639011 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.67.983 (DOI: 10.1253/circj.67.983, PubMed: 14639011)
141.	Masataka Sata : Circulating vascular progenitor cells contribute to vascular repair, remodeling and lesion formation, Trends in Cardiovascular Medicine, Vol.13, No.6, 249-253, Aug. 2003. (Summary) Exuberant accumulation of smooth muscle cells (SMCs) plays a principal role in the pathogenesis of vascular diseases. It has been assumed that SMCs derived from the adjacent medial layer migrate, proliferate, and synthesize extracellular matrix. Although much effort has been devoted to understanding the molecular pathways regulating migration and proliferation of medial SMCs, no effective therapy to prevent occlusive vascular remodeling has been established. It was recently reported that bone marrow cells substantially contribute to the pathogenesis of vascular diseases, in models of postangioplasty restenosis, graft vasculopathy, and hyperlipidemia-induced atherosclerosis. It was suggested that bone marrow cells may have the potential to give rise to vascular progenitor cells that home in on the damaged vessels and differentiate them into smooth muscle cells or endothelial cells, thereby contributing to vascular repair, remodeling, and lesion formation. The present findings may provide the basis for the development of new therapeutic strategies for vascular diseases, targeting mobilization, homing, differentiation, and proliferation of circulating vascular progenitor cells. (Keyword) Animals / Arteriosclerosis / Bone Marrow Cells / Hematopoietic Stem Cells / Humans / Myocytes, Smooth Muscle / Pluripotent Stem Cells / Transplantation / Vascular Diseases (Link to Publication Site) ● Publication site (DOI): 10.1016/S1050-1738(03)00106-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12922022 ● Search Scopus @ Elsevier (PMID): 12922022 ● Search Scopus @ Elsevier (DOI): 10.1016/S1050-1738(03)00106-3 (DOI: 10.1016/S1050-1738(03)00106-3, PubMed: 12922022)
142.	Masataka Sata, K Tanaka and R Nagai : Origin of smooth muscle progenitor cells: Different conclusions from different models., Circulation, Vol.107, No.16, e106-e107, Apr. 2003. (Keyword) Animals / Aorta / Arteriosclerosis / Bone Marrow Cells / Cell Lineage / Disease Models, Animal / Mice / Mice, Transgenic / Muscle, Smooth, Vascular / Stem Cells (Link to Publication Site) ● Publication site (DOI): 10.1161/01.CIR.0000067689.02650.98 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12719293 ● Search Scopus @ Elsevier (PMID): 12719293 ● Search Scopus @ Elsevier (DOI): 10.1161/01.CIR.0000067689.02650.98 (DOI: 10.1161/01.CIR.0000067689.02650.98, PubMed: 12719293)
143.	Masataka Sata : Biphasic effect of statins on angiogenesis, Circulation, Vol.106, e47, 2002.
144.	Masataka Sata and R Nagai : Phosphatidylinosotol 3-kinase. A key regulator of vascular tone?, Circulation Research, Vol.91, 273-275, 2002.
145.	K Walsh and Masataka Sata : Nagative regulation of inflammation by Fas ligand expression on the vascular endothelium, Trends Cardiovasc Med., Vol.9, 34-41, 1999.
146.	K Walsh and Masataka Sata : Is extravasation a Fas-regulated process?, Mol.Med.Today., Vol.7, 61-67, 1999.

Proceeding of International Conference:

1.	Natsumi Yamaguchi, TOMONORI Takahashi, Susumu Nishio, Robert Zheng, Yoshihito Saijyo, Muneyuki Kadota, Yutaka Kawabata, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Elevated left atrial stiffness index is a poor prognostic factor in heart failure with preserved ejection fraction undergoing transcatheter aortic valve replacement, EUROECHO 2024, Dec. 2024.
2.	Bavuu Oyunbileg, Masataka Sata and Daiju Fukuda : Blockade of Mineralocorticoid Receptor by Esaxerenone Improves Insulin Sensitivity in Obese Mice, AHA2024, Chicago, Nov. 2024.
3.	Tezuka Kazuki, Takeshi Soeki, Tomoko Takahashi, Tomomi Matsuura, Akihiro Tani, Ryo Bando, R Zheng, TOMONORI Takahashi, Yoshihito Saijo, Tomoya Hara, Muneyuki Kadota, Yutaka Kawabata, Rie Ueno, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Risk Factors For Intraoperative Instability In Sedated Patients Undergoing Pulmonary Vein Isolation Ablation, Sydney, Sep. 2024.
4.	Tomoko Takahashi, Takeshi Soeki, Tezuka Kazuki, TOMONORI Takahashi, Yoshihito Saijo, Tomoya Hara, Yutaka Kawabata, Muneyuki Kadota, Rie Ueno, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : NAFLD score predicts the onset of atrial fibrillation, APHRS 2024, Sydney, Sep. 2024.
5.	TOMONORI Takahashi, K Yamaji, S Kohsaka, H Ishii, Y Mori, Tetsuzo Wakatsuki, Koji Yamaguchi, D Nisioka, Kenya Kusunose, T Amano and Masataka Sata : Drug-Coated Balloon versus Drug-Eluting Stent for DeNovo Culprit Lesion in Acute Coronary Syndromes: A Report from Nationwide Registry in Japan, ESC 2024, London, Aug. 2024.
6.	Yoshihito Saijo, Hirotsugu Yamada, Robert Zheng, TOMONORI Takahashi, Yutaka Kawabata, Rie Ueno, Muneyuki Kadota, Tomoya Hara, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Differential echocardiographic profiles in immunoglobulin light chain and transthyretin amyloid cardiomyopathy: insights from speckle tracking analysis, ESC 2024, London, Aug. 2024.
7.	R Bando, Tetsuzo Wakatsuki, Koji Yamaguchi, TOMONORI Takahashi, Takayuki Ise, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Clinical outcome of DCB vs DES for de novo large coronary lesion in HBR patients, Euro PCR 2024, Paris, May 2024.
8.	Kumiko Suto, Tomoya Hara, Sachiko Nishimoto, S Kaneyama, Masataka Sata and Daiju Fukuda : Macrophage-Specific DNaseII Deficiency Plays a Critical Role in Vascular Inflammation and Atherosclerosis in Apolipoprotein E-Deficient Mice, AHA2023, Philadelphia, Nov. 2023.
9.	W Liu, Y Higashikuni, T Obana, Y Tanaka, Y Hirata and Masataka Sata : The DEAD-Box RNA Helicase Ddx41 Contributes to Adverse Cardiac Remodeling During Pressure Overload Through Modulation of RNA Metabolism, AHA2023, Philadelphia, Nov. 2023.
10.	Kohei Nagano, TOMONORI Takahashi, Tetsuzo Wakatsuki, Robert Zheng, Yoshihito Saijyo, Muneyuki Kadota, Yutaka Kawabata, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Long-Term Outcome of Stentless Coronary Intervention With Drug-Coated Balloon in Patients With High Bleeding Risk, AHA2023, Philadelphia, Nov. 2023.
11.	N Yamaguchi, Kenya Kusunose, Yukina Hirata, Susumu Nishio, TOMONORI Takahashi, Yoshihito Saijo, Muneyuki Kadota, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Improved Pressure-Flow Relationship With Sacubitril/Valsartan: A 6-min Walk Stress Echocardiographic Study, AHA2023, Philadelphia, Nov. 2023.
12.	TOMONORI Takahashi, Tetsuzo Wakatsuki, Kenya Kusunose, Takayuki Ise and Masataka Sata : The aneurysm that vanished into thin air:Spontaneous thrombosis of a giant aneurysm complicated with the coronary to pulmonary artery fistula, ESC2023, Amsterdam, Aug. 2023.
13.	Ryou Bando, Tetsuzo Wakatsuki, Koji Yamaguchi, Yutaka Kawabata, TOMONORI Takahashi, Yoshihito Saijyo, Muneyuki Kadota, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, S Yagi, Hirotsugu Yamada, T Soeki, M Akaike and Masataka Sata : Two-year outcomes of drug-coated balloon only strategy for de novo lesions in large coronary vessels, ESC2023, Amsterdam, Aug. 2023.
14.	Munkhjargal Uugantsetseg, Daiju Fukuda and Masataka Sata : A selective mineralocorticoid receptor blocker, esaxerenone, attenuates vascular dysfunction and inhibits atherogenesis in apolipoprotein E-deficient mice, ESC2023, Amsterdam, Aug. 2023.
15.	Shusuke Yagi, Tserensonom Munkhtsetseg and Masataka Sata : Lipoprotein (a) is a Residual Risk Factor of Aortic Valve Calcification in Patients With High Risk of Atherosclerotic, AHA 2022, Chicago, Nov. 2022.
16.	Kenya Kusunose, Yukina Hirata, T Tsuji, J Kotoku and Masataka Sata : Deep Learning Approach for Analyzing Chest X-rays to Predict Cardiac Events in Heart Failure, AHA 2022, Chicago, Nov. 2022.
17.	Akihiro Tani, Takeshi Soeki, Yuji Ozaki, Ken-ichi Aihara and Masataka Sata : Impact of Sarcopenia and Atrial Fibrillation on the Incidence of Heart Failure in Elderly Patients, The 29th Scientific Meeting of the International Society of Hypertension, Oct. 2022.
18.	Masataka Sata : Updated research on statin and atherosclerosis:What is the role of statin for primary prevention? International Symposium on Vascular Hearth under COVID-19 Status, Annual Meeting of Taiwan Society of Lipids &Atherosclerosis 2022, Sep. 2022.
19.	Y Okushi, Kenya Kusunose, Hiromitsu Seno, TOMONORI Takahashi, Yoshihito Saijyo, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : The Impact of Surveillance of Cancer Therapeutics-Related Cardiac Dysfunction by Periodic Echocardiography, ASE2022, Seattle, Jun. 2022.
20.	Kumiko Suto, Daiju Fukuda and Masataka Sata : Macrophage-specific Dnase II Deficiency Stimulates Atherosclerosis In Apolipoprotein E-deficient Mice, AHA, Nov. 2021.
21.	Masataka Sata : Rivaroxaban, a Direct Oral Anticoagulant, Attenuates Atherosclerotic Plaque Progression and Destabilization by Inhibiting FXa-PAR2 Pathway, ISA2021, Kyoto, Oct. 2021.
22.	Kumiko Suto, Daiju Fukuda and Masataka Sata : Macrophage-specific DNaseII deficiency stimulates atherosclerosis in apolipoprotein E-deficient mice, ISA2021, Kyoto, Oct. 2021.
23.	Masataka Sata : Roles of Epicardial Adipose Tissue in the Progression of Coronary Atherosclerosis, International Society of Atherosclerosis 2021, Kyoto, Oct. 2021.
24.	Koji Yamaguchi, Tetsuzo Wakatsuki, Y Okushi, Kumiko Suto, Kazuhisa Matsumoto, Tomonori Takahashi, Muneyuki Kadota, Yutaka Kawabata, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Early and chronic phased local coagulative responses following bioresorbable-polymer drug-eluting stent implantation, European Heart Journal, Vol.42, No.S1, ehab724.1245, Aug. 2021. (Link to Publication Site) ● Publication site (DOI): 10.1093/eurheartj/ehab724.1245 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1093/eurheartj/ehab724.1245 (DOI: 10.1093/eurheartj/ehab724.1245)
25.	Pham Tran Phuong, Daiju Fukuda and Masataka Sata : Genetic Deletion of Stimulator of Interferon Genes Attenuates Atherogenesis in Apolipoprotein E-deficient Mice, American Heart Association, Dallas, Nov. 2020.
26.	Yukina Hirata, Kenya Kusunose, Hirotsugu Yamada, T Tsuji, K Fujimori, J Kotoku and Masataka Sata : Deep Learning For Detection Of Elevated Pulmonary Artery Wedge Pressure Using Standard Chest X-ray, The Canadian Journal of Cardiology, Dallas, Nov. 2020. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cjca.2021.02.007 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85108436549 (DOI: 10.1016/j.cjca.2021.02.007, Elsevier: Scopus)
27.	Miharu Arase, Kenya Kusunose, Sae Morita, N Yamaguchi, Yukina Hirata, Susumu Nishio, Takayuki Ise, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Clinical Utility of Noninvasive Assessment of Flow-pressure Relationship in Scleroderma, American Heart Associeition, Dallas, Nov. 2020.
28.	Y Okushi, Kenya Kusunose, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Differences ofCancer Types in Hospital Mortality in Patients With Venous Thromboembolism, American Heart Association, Dallas, Nov. 2020. (Link to Publication Site) ● Publication site (DOI): 10.1161/circ.142.suppl_3.13145 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1161/circ.142.suppl_3.13145 (DOI: 10.1161/circ.142.suppl_3.13145)
29.	Koji Yamaguchi, Tetsuzo Wakatsuki, Tomonori Takahashi, Muneyuki Kadota, Yutaka Kawabata, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Suppressed Local Coagulative Response After Newer-generation Ultrathin Strut SES Implantation Compared to Older-generation SES Implantation, American Heart Association, Dallas, Nov. 2020. (Link to Publication Site) ● Publication site (DOI): 10.1161/circ.142.suppl_3.12894 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1161/circ.142.suppl_3.12894 (DOI: 10.1161/circ.142.suppl_3.12894)
30.	Masataka Sata : Primary Prevention-Balancing efficacy and safety, The Annual Scientific Meeting of Taiwan Society of Lipids &Aterosclerosis 2020 and The 19th Taipei International Vascular Biology Symposium, Sep. 2020.
31.	Takeshi Soeki, Kazuhisa Matsumoto, Daiju Fukuda, E Uematsu, Tomomi Matsuura, Takeshi Tobiume, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Toll-like receptor 9 is a novel therapeutic target to prevent atrial fibrillation, European Heart Journal, Vol.41, No.S2, ehaa946.0463, Aug. 2020. (Link to Publication Site) ● Publication site (DOI): 10.1093/ehjci/ehaa946.0463 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1093/ehjci/ehaa946.0463 (DOI: 10.1093/ehjci/ehaa946.0463)
32.	Yukina Hirata, Kenya Kusunose, Natumi Yamaguchi, Sae Morita, Susumu Nishio, Yuichiro Okushi, Tomonori Takahashi, Hirotsugu Yamada, T Tsuji, K Fujimori, J Kotoku and Masataka Sata : Deep learning for screening of pulmonary hypertension using standard chest X-Ray, European Heart Journal, Amsterdam, Aug. 2020. (Link to Publication Site) ● Publication site (DOI): 10.1093/ehjci/ehaa946.2246 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1093/ehjci/ehaa946.2246 (DOI: 10.1093/ehjci/ehaa946.2246)
33.	Natsumi Yamaguchi, Kenya Kusunose, S Haga, Sae Morita, Yukina Hirata, Yuta Torii, Susumu Nishio, Yuichiroh Ohkushi, Tomonori Takahashi, Hirotsugu Yamada, nao Yamada and Masataka Sata : Assessment of left ventricular ejection fraction from echocardiographic images using machine learning algorithm, Euro Echo 2019, Wien, Dec. 2019.
34.	Tomonori Takahashi, Kenya Kusunose, Shuji Hayashi, Sae Morita, Yuta Torii, Yukina Hirata, M Yamao, Susumu Nishio, Yuichiroh Ohkushi, M Abe, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Updated prevalence of lambls excrescences using the latest three-dimensional tansesophageal echocardiography, Euro Echo 2019, Wien, Dec. 2019.
35.	Kenya Kusunose, Nishio Susumu, Hirata Yukina, Takayuki Ise, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Pulmonary Artery Hypertension Specific Therapy Improves Exercise Tolerance and Outcomes in Exercise-Induced Pulmonary Hypertension, JACC. Cardiovascular Imaging, Vol.12, No.12, 2576-2579, Dec. 2019. (Keyword) Adult / Aged / Antihypertensive Agents / Arterial Pressure / Disease Progression / Echocardiography, Stress / Exercise / Exercise Tolerance / Female / Humans / Male / Middle Aged / Progression-Free Survival / Prospective Studies / Pulmonary Arterial Hypertension / Pulmonary Artery / Recovery of Function / Time Factors / Vasodilator Agents / Walk Test (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jcmg.2019.07.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31422131 ● Search Scopus @ Elsevier (PMID): 31422131 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jcmg.2019.07.002 (DOI: 10.1016/j.jcmg.2019.07.002, PubMed: 31422131)
36.	Yutaka Kawabata, Kenya Kusunose, Shusuke Yagi, Hirotsugu Yamada, Daiju Fukuda, Takeshi Soeki and Masataka Sata : The relationship among local epicardial adipose tissue, coronary intraplaque microluminal structure, and coronary plaque formation -a fresh cadaveric study, AHA2019, Philadelphia, Nov. 2019.
37.	Yukina Hirata, Masataka Sata, Kenya Kusunose, Hirotsugu Yamada, Yuta Torii, Susumu Nishio, nao Yamada, Koji Yamaguchi, Takeshi Soeki and Tetsuzo Wakatsuki : Usefulness of echocardiographic epicardial adipose tissue thickness for predicting coronary artery disease regardless of body mass index, AHA2019, Philadelphia, Nov. 2019.
38.	B Ganbaatar, Daiju Fukuda, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : S1p2 Receptor Antagonist Attenuates Endothelial Dysfunction And Inhibits Atherogenesis In Apolipoprotein-e-deficient Mice, AHA2019, Philadelphia, Nov. 2019.
39.	Yuta Torii, Kenya Kusunose, Yukina Hirata, Hirotsugu Yamada and Masataka Sata : Clinical utility of left atrial strain to predict functional recovery in patients with optimal treatments of heart failure, AHA2019, Philadelphia, Nov. 2019.
40.	Kenya Kusunose, A Haga, T Abe, Daiju Fukuda, Hirotsugu Yamada and Masataka Sata : Assessment of left ventricular ejection fraction from echocardiographic images using deep learning algorithm, AHA2019, Philadelphia, Nov. 2019.
41.	Sutou Kumiko, Daiju Fukuda, B Ganbaatar, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Pemafibrate, a novel selective peroxisome proliferator-activated receptor-a modulator, ameliorated diabetes-induced endothelial dysfunction, AHA2019, Philadelphia, Nov. 2019.
42.	A Tanaka, Masataka Sata, S Ueda, T Murohara and K Node : Effects of canagliflozin in patients with type 2 diabetes and chronic heart failure: A randomized clinical trial (CANDLE), AHA2019, Philadelphia, Nov. 2019.
43.	A Kunduziayi, Daiju Fukuda, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Vildagliptin, a DPP-4 inhibitor, attenuates endothelial dysfunction and atherogenesis independent of its glucose lowering effect in apolipoprotein e-deficient mice, AHA2019, Philadelphia, Nov. 2019.
44.	Shusuke Yagi and Masataka Sata : Increased advanced glycation end products are a risk factor of epicardial adipose tissue thickness, AHA2019, Philadelphia, Nov. 2019.
45.	Byambasuren Ganbaatar, Daiju Fukuda, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Empagliflozin, a SGLT2 inhibitor, attenuates endothelial dysfuntion and atherogenesis by inhibiting inflammatory responses in the vasculature and adipose tissue in disbetic apolipoprotein E-deficient, ESC Congress 2019, Paris, Sep. 2019.
46.	Takeshi Soeki, Kazuhisa Matsumoto, Daiju Fukuda, 植松悦子, Tomomi Matsuura, Takeshi Tobiume, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Vildagliptin reduces inducitiligy of arterial fibrillation in hypertensive rats complicated with diabetes mellitus, ESC Congress 2019, Paris, Sep. 2019.
47.	Koji Yamaguchi, Tetsuzo Wakatsuki, Rie Ueno, Yutaka Kawabata, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : The improvement of chronic local coagulative response according to the progress of drug eluting stent, ESC Congress 2019, Paris, Sep. 2019.
48.	Maimaituxun Gulinu, Kenya Kusunose, Daiju Fukuda, Shusuke Yagi, Yuta Torii, Yukina Hirata, Susumu Nishio, nao Yamada, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata and Michio Shimabukuro : Impact of epicardial adipose tissue on global longitudinal strain: a study in patients with normal left ventricular ejection fraction, ESC Congress 2019, Paris, Sep. 2019.
49.	Maimaituxun Gulinu, Daiju Fukuda, Shusuke Yagi, Shoichiro Takao, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masafumi Harada, Masataka Sata and Michio Shimabukuro : Adipose tissue surrounding the kidney and its impact on coronary artery disease, ESC Congress 2019, Paris, Sep. 2019.
50.	Rahadian Arief, Daiju Fukuda, Hotimah Masdan Salim, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Glycemic control with canagliflozin, a SGLT-2 inhibitor, attenuates atherosclerosis and endothelial dysfuntion in diabetic apolipoprotein e-deficient mice, ESC Congress 2019, Paris, Aug. 2019.
51.	Masataka Sata : SGL T2 and CHF, The 49th Annual Convention & Scientific Session of the Taiwan Society of Cardiology, Taipei, May 2019.
52.	Phuong Tran Pham, D Fukuda, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Rivaroxaban, a Direct Inhibitor of Factor Xa, Attenuates Endothelial Dysfunction in Streptozotocin-Induced Diabetic Mice Through the Inhibition of Protease-Activated Receptor 2 Signaling, AHA, Chicago, Nov. 2018.
53.	Daiju Fukuda, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Inhibition of Thrombin-PARs Signaling by Dabigatran, a Direct Thrombin Inhibitor, Attenuates Endothelial Dysfunction in Diabetic Mice, AHA, Chicago, Nov. 2018.
54.	Y Saijo, Kenya Kusunose, Hirotsugu Yamada, Susumu Nishio, Yuta Torii, Y Hirata, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Right Ventricular Contractile Function Predicts Cardiac Events in Passive and Reactive Pulmonary Hypertension, AHA, Chicago, Nov. 2018.
55.	Kenya Kusunose, T Abe, A Haga, Hirotsugu Yamada, Daiju Fukuda, M Harada and Masataka Sata : A Deep Learning Approach for Automated Diagnosis of Regional Wall Motion Abnormality on Echocardiography, AHA, Chicago, Nov. 2018.
56.	Yukina Hirata, Kenya Kusunose, Hirotsugu Yamada, Susumu Nishio, O Harada, N Miyazato, A Haraguni, A Ito, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Epicardial Adipose Tissue Thickness Measured by Echocardiography is Useful Marker for Predicting Coronary Artery Disease, AHA, Chicago, Nov. 2018.
57.	Ganbaatar Byambasuren, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Inhibition of S1P2 receptor ameliorates endothelial dysfunction and prevents atherogenesis in apolipoprotein-E-deficient Mice, ESC2018, Munich, Aug. 2018.
58.	Takeshi Soeki, E Uematsu, Tomomi Matsuura, Takeshi Tobiume, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : C-type natriuretic peptide improves left ventricular diastolic dysfunction and ischemia/reperfusion injury-associated ventricular arrhythmias., ESC2018, Munich, Aug. 2018.
59.	Masataka Sata : Role of epicardial fat in cardiovascular disease, ESC2018, Munich, Aug. 2018.
60.	Hiroyuki Ito, Tetsuzo Wakatsuki, Koji Yamaguchi, Daiju Fukuda, Yutaka Kawabata, Takafumi Todoroki, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Growth of vasa vasorum is associated with local inflammation around coronary plaque in fresh cadavers, ESC2018, Munich, Aug. 2018.
61.	Ganbaatar Byambasuren, Daiju Fukuda, HM Salim, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Atheroprotective effects of ticagrelor, a P2Y12 antagonist, in apolipoprotein-E-deficient mice, ESC2018, Munich, Aug. 2018.
62.	Y Saijo, Kenya Kusunose, Mika Bando, H Seno, Robert Zheng, Susumu Nishio, Yukina Hirata, Y Tori, R Amano, Hirotsugu Yamada and Masataka Sata : Localization of myocardial injury in anthracycline-induced cardiotoxicity: evaluation using two-dimensional speckle tracking echocardiography, ESC2018, Munich, Aug. 2018.
63.	Maimaituxun Gulinu, Michio Shimabukuro, Daiju Fukuda, Shusuke Yagi, Hirata Yukina, Takashi Iwase, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Gender disparities of distribution of epicardial adipose tissue and its impact on coronary artery disease, ESC2018, Munich, Aug. 2018.
64.	Susumu Nishio, K Kusunose, Yukina Hirata, Yuta Torii, R Amano, Y Saijo, Hirotsugu Yamada and Masataka Sata : The effect of gender difference in patients with cardiovascular disease on various vascular functional indices., EACVI meeting 2018, Dec. 2017.
65.	M Bando, Hirotsugu Yamada, K Kusunose, Yukina Hirata, Junya Kuwahata, R Amano, Susumu Nishio and Masataka Sata : Change in Ultrasonic Tissue Characteristics of Carotid Artery Plaque Reflects That of Coronary Artery Plaque, EACVI meeting 2018, Dec. 2017.
66.	Junya Kuwahata, Y Saijo, Hirotsugu Yamada, Kenya Kusunose, Hiromitsu Seno, Y Okushi, Susumu Nishio, Yukina Hirata, Torii Yuta and Masataka Sata : Detection of Subtle Changes in Stroke Volume during Pre-load Stress Echocardiography by Three-dimensional Echocardiography using Automated Adaptive Analytics Algorithm, EACVI meeting 2018, Dec. 2017.
67.	Yukina Hirata, Kenya Kusunose, Hirotsugu Yamada, R Shimizu, Yuta Torii, Susumu Nishio, Y Okushi, Hiromitsu Seno, Y Saijo, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Quantitative Classification of Left Atrial Appendage is Superior to Visual Classification for Risk Stratification of Stroke in Atrial Fibrillation, EACVI meeting 2018, Dec. 2017.
68.	J. Kuwahata, Y. Saijo, Hirotsugu Yamada, Kenya Kusunose, H. Seno, Y. Okushi, S. Nishio, Y. Hirata, Y. Torii, S. Morita and Masataka Sata : Detection of subtle changes in stroke volume during pre-load stress echocardiography by three-dimensional echocardiography using automated adaptive analytics algorithm, Euro Echo 2017, Portugal, Dec. 2017.
69.	Y. Hirata, Kenya Kusunose, Hirotsugu Yamada, J. Kuwahata, R. Shimizu, Y. Torii, R. Amano, M. Yamao, S. Nishio, H. Seno, Y. Saijo, Takeshi Soeki and Masataka Sata : Association between left atrial appendage morphology and stroke in atrial fibrillation: comparison between quantitative and visual classification, Euro Echo 2017, Portugal, Dec. 2017.
70.	Takeshi Soeki, Tomomi Matsuura, E Uematsu, Takeshi Tobiume, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Epicardial Adipose Tissue Produces Proinflammatory Cytokines and Influences the Pathogenesis of Atrial Fibrillation, AHA Scientific Sessions2017, California, America, Nov. 2017.
71.	Yukina Hirata, Kenya Kusunose, Hirotsugu Yamada, J Kuwahata, Y Torii, S Nishio, H Seno, Y Saijo, Koji Yamaguchi, Tetsuzo Wakatsuki and Masataka Sata : Detection of Coronary Artery Stenosis by Epicardial Adipose Tissue Thickness in Type 2 Diabetes, AHA Scientific Sessions2017, California, America, Nov. 2017.
72.	Maimaituxun. Gulinu, Michio Shimabukuro, Y Hirata, Takashi Iwase, S Takao, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, M Harada and Masataka Sata : Local Epicardial Adipose Tissue Thickness in Left Anterior Descending Artery Provides a New Prediction Model for Coronary Artery Disease, AHA Scientific Sessions2017, California, America, Nov. 2017.
73.	Kenya Kusunose, Hirotsugu Yamada, S Nishio, Y Torii, Yukina Hirata, H Seno, Y Saijo, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Echocardiography Predicts Outcomes in Patients With Preserved Ejection Fraction and Low Gradient Aortic Stenosis, AHA Scientific Sessions2017, California, America, Nov. 2017.
74.	Takeshi Soeki, Tomomi Matsuura, Daiju Fukuda, Etsuko Uematsu, Takeshi Tobiume, T Hara, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Activated Factor X Signaling Pathway via Protease-Activated Receptor-2 is a Novel Therapeutic Target to Prevent Atrial Fibrillation, AHA Scientific Sessions2017, California, America, Nov. 2017.
75.	Koji Yamaguchi, Tetsuzo Wakatsuki, Yutaka Kawabata, H Ito, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Preserved Endothelial Function and Suppressed Local Coagulative and Inflammatory Response After Biodegradable Polymer SES Implantation Compared to Durable Polymer SES, AHA Scientific Sessions2017, California, America, Nov. 2017.
76.	Tomomi Matsuura, Takeshi Tobiume, Takeshi Soeki, R Kato, M Hara, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Direct Slow Pathway Capture: A New Electrophysiological Method of Catheter Ablation for Atrioventricular Nodal Reentrant Tachycardia, AHA Scientific Sessions2017, California, America, Nov. 2017.
77.	Susumu Nishio, Kenya Kusunose, Hirotsugu Yamada, Yukina Hirata, H Seno, Y Saijo, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Echocardiographic Epicardial Adipose Tissue Thickness is a Marker for the Detection of Vasospastic Angina, ASE2017, Baltimore, Jun. 2017.
78.	Y Saijo, Hirotsugu Yamada, Kenya Kusunose, H Seno, Y Okushi, Susumu Nishio, Yukina Hirata, Y Torii and Masataka Sata : Left Atrial Dysfunction in Patients with Infarction of Proximal Left Circumflex Artery, ASE2017, Baltimore, Jun. 2017.
79.	Kenya Kusunose, Hirotsugu Yamada, Susumu Nishio, Y Hirata, Hiromitsu Seno, Y Saijo, Takayuki Ise, Koji Yamaguchi, Shuusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Right Ventricular Myocardial Strain during Preload Augmentation is Associated with Exercise Capacity, ASE2017, Baltimore, Jun. 2017.
80.	Shusuke Yagi, Takayuki Ise, Masashi Akaike and Masataka Sata : Adaptive Servo-ventilation Supported Exercise Increases Exercise Capacity in Patients With Severe Heart Failure, AHA Scientific Sessions 2016, New Orleans, Nov. 2016.
81.	Yukina Hirata, Hirotsugu Yamada, Kenya Kusunose, R Shimizu, Yuta Torii, Susumu Nishio, Hiromitsu Seno, Y Saijo, S Hayashi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Impact of Age on the Morphology of Left Atrial Appendage I Atrial Fibrillation, AHA Scientific Sessions 2016, New Orleans, Nov. 2016.
82.	Y Torii, Hirotsugu Yamada, Kenya Kusunose, H Seno, Y Saijo, Y Okushi, S Nishio, Y Hirata, R Amano and Masataka Sata : Effect of Direct Oral Anticoagulants on Carotid Artery Sclerosis in Patients with Atrial Fibrillation, AHA Scientific Sessions 2016, New Orleans, Nov. 2016.
83.	H Seno, Hirotsugu Yamada, Kenya Kusunose, R Amano, M Matsushita, M Nanasato, T Murohara, H Kamiya and Masataka Sata : Effect of Sitagliptin on Left Ventricular Function in Patients With Type 2 Diabetes a Sub Analysis of the PROLOGUE Study, AHA Scientific Sessions 2016, New Orleans, Nov. 2016.
84.	Kenya Kusunose, Hirotsugu Yamada, Y Saijo, H Seno, Y Hirata, Y Torii, S Nishio, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Longitudinal Strain Distribution is a Powerful Predictor for Functional Recovery in Patients With Tachycardia-induced Cardiomyopathy, AHA Scientific Sessions 2016, New Orleans, Nov. 2016.
85.	Masataka Sata : Role of innate immunity in chronic inflammation in arterial wall and adipose tissue, 19th International Vascular Biology Meeting, Boston, Nov. 2016.
86.	HMM Salim, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Dabigatran, a direct thrombin inhibitor, prevents the development of endothelial dysfunction in diabetic mice, 19th International Vascular Biology Meeting, Boston, Nov. 2016.
87.	HMM Salim, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Glycemic control with canagliflozin, a SGLT2 inhibitor, inhibited inflammation in the vascular and adipose tissue, and ameliorated vascular complication in diabetic mice, 19th International Vascular Biology Meeting, Boston, Nov. 2016.
88.	Shusuke Yagi and Masataka Sata : Reduced levels of eicosapentaenoic acid and docosahexaenoic acid on admission predict in-stent restenosis in patients with acute coronary syndrome, 19th International Vascular Biology Meeting, Boston, Nov. 2016.
89.	Shusuke Yagi and Masataka Sata : The effects of edoxaban on thrombin generation and anti-coagrant systems in patients with acute venous thromboembolism, 19th International Vascular Biology Meeting, Boston, Nov. 2016.
90.	Daiju Fukuda, S Nishimoto, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Cell free DNA/Toll-like receptor 9 axis plays a pivotal role in chronic inflammation induced by metabolic disorders, leading to atherogenesis and insulin resistance, 19th International Vascular Biology Meeting, Boston, Nov. 2016.
91.	Nishimoto Sachiko, Daiju Fukuda, Higashikuni Yasutomi, Tanaka Kimie, Hirata Yoichiro, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata : Genetic deletion of TLR9 promotes blood flow recovery in hind limb ischemia, 19th International Vascular Biology Meeting, Nov. 2016.
92.	Kenya Kusunose, Hirotsugu Yamada, H Seno, Y Saijo, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Longitudinal Strain Distribution is a Powerful Predictor for Functional Recovery in Patients with Tachycardia-induced Cardiomyopathy, KSC2016(The 60th Annual Scientific Meeting of The Korean Society of Cardiology), Seoul, Sep. 2016.
93.	Takeshi Soeki, Tomomi Matsuura, E Uematsu, S Bando, Takeshi Tobiume, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Increased local production of C-type natriuretic peptide in patients with vasospastic angina, ESC Congress 2016, Rome, Aug. 2016.
94.	Koji Yamaguchi, Tetsuzo Wakatsuki, R Ueno, H Ito, Takayuki Ise, Tomomi Matsuura, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Paclitaxel eluting balloon angioplasty equals everolimus eluting stent implantation in local coagulative and inflammatory responses in stable angina patients, ESC Congress 2016, Rome, Aug. 2016.
95.	T Matsuura, Takeshi Soeki, E Uematsu, S Bando, Takeshi Tobiume, T Hara, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Oral Direct Factor Xa Inhibitor Prevents Atrial Fibrillation by Inhibiting Inflammation in Rapidly Paced Spontaneously Hypertensive Rats, ESC Congress 2016, Rome, Aug. 2016.
96.	Y Saijo, Hirotsugu Yamada, Kenya Kusunose, H Seno, S Nishio, R Amano, Y Hirata and Masataka Sata : Clinical Utility of Preload Stress Echocardiography for Predicting Future Pseudo-normal Transmitral Flow Pattern, ASE2016, Seattle, Jun. 2016.
97.	Hirotsugu Yamada, Kenya Kusunose, Y Torii, Y Saijo, H Seno, Y Hirata, R Amano, S Nishio and Masataka Sata : Criteria for Exercise-induced Pulmonary Hypertension Using 6-minute Walk Stress Echocardiography in Patients with Collagen Tissue Disease., ASE2016, Seattle, Jun. 2016.
98.	Y Saijo, Kenya Kusunose, Hirotsugu Yamada, S Nishio, R Amano, Y Hirata, H Seno and Masataka Sata : Echocardiographic Predictors for Worsening of 6-minute Walk Distance in Patients with Connective Tissue Disease, ASE2016, Seattle, Jun. 2016.
99.	R Amano, Hirotsugu Yamada, Mika Bando, R Tamai, Y Torii, S Nishio, H Seno, Kenya Kusunose and Masataka Sata : Quantitative Ultrasound Evaluation of the Changes on Tissue Characteristics of Carotid Plaques by Lipid Lowering Therapy, ASE2016, Seattle, Jun. 2016.
100.	Hirotsugu Yamada, Kenya Kusunose, Y Saijo, H Seno, S Nishio, Y Torii, Y Hirata, R Amano and Masataka Sata : Echocardiographic Diagnosis of Exercise-induced Pulmonary Hypertension in Patients with Connective Tissue Diseases, AAE 2016 (4th Annual Scientific Sessions of the Asian-Pacific Association of Echocardiography), Osaka, Apr. 2016.
101.	Y Saijo, Hirotsugu Yamada, Kenya Kusunose, H Seno, S Nishio, R Amano, Y Hirata, Y Torii and Masataka Sata : Clinical Utility of Preload Stress Echocardiography for Predict Future Pseudo -normal Transmitral Flow Pattern in Patients with Various Cardiac Diseases, AAE 2016 (4th Annual Scientific Sessions of the Asian-Pacific Association of Echocardiography), Osaka, Apr. 2016.
102.	H Seno, Kenya Kusunose, Hirotsugu Yamada, Y Saijo, S Nishio, Y Hirata, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Comparison of Right Ventricular Global Longitudinal Strain Between Vender-Dependent and Vender-Independent Two-Dimensional Speckle Tracking Software, ACC Scientific Sessions 2016, Chicago, Apr. 2016.
103.	K Tanaka, I Komuro and Masataka Sata : Vascular Cells Originating From Perivascular Adipose Tissue Contribute to Vasa Vasorum Neovascularization in Atherosclerosis., AHA Scientific Sessions 2015, Orlando, Nov. 2015.
104.	S Bando, Takeshi Soeki, Tomomi Matsuura, Takeshi Tobiume, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Atrial Late Potentials and Atrial Substrate Remodeling in Patients With Atrial Fibrillation., AHA Scientific Sessions 2015, Orlando, Nov. 2015.
105.	HM Salim, Daiju Fukuda, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Dipeptidyl Peptidase-4 Inhibitor, Linagliptin, Ameliorates Endothelial Dysfunction and Atherogenesis in Apolipoprotein-e Deficient Mice Through GLP-1 Dependent and Independent Manners., AHA Scientific Sessions 2015, Orlando, Nov. 2015.
106.	Y Hirata, Hirotsugu Yamada, Kenya Kusunose, S Nishio, Mika Bando, Koji Yamaguchi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Clinical Utility of Echocardiographic Epicardial Adipose Tissue Thickness Measured Using a High-frequency Linear Probe in Patients with Coronary Artery Disease., AHA Scientific Sessions 2015, Orlando, Nov. 2015.
107.	Takeshi Soeki, S Bando, Tomomi Matsuura, Takeshi Tobiume, E Uematsu, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Combination Of Clinical, Electrocardiographic and Echocardiographic Parameters Predict the Onset of Atrial Fibrillation., AHA Scientific Sessions 2015, Orlando, Nov. 2015.
108.	A Takashima, Daiju Fukuda, K Tanaka, Y Higashikuni, Y Hirata, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : N-3 Polyunsaturated Fatty Acids Inhibit Inflammatory Responses in Macrophages by the Reduction of Toll-like Receptor 4 Expression in Lipid Rafts, Leading to the Suppression of Atherogenesis in Apolipoprotein E Deficient Mice., AHA Scientific Sessions 2015, Orlando, Nov. 2015.
109.	T Hara, Daiju Fukuda, K Tanaka, Y Higashikuni, Y Hirata, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Hematopoietic Protease-activated Receptor-2 Plays a Critical Role in Vascular Inflammation and Atherosclerosis in ApoE-Deficient Mice., AHA Scientific Sessions 2015, Orlando, Nov. 2015.
110.	S Nishimoto, Daiju Fukuda, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata : Toll-like Receptor 9 Plays a Pivotal Role in Angiotensin II-induced Atherosclerosis., AHA Scientific Sessions 2015, Orlando, Nov. 2015.
111.	Kenya Kusunose, Hirotsugu Yamada, Mika Bando, S Nishio, Y Hirata, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Pressure-flow Relationship of Pulmonary Circulation Determines Six-minute Walk Distance in Connective Tissue Disease., AHA Scientific Sessions 2015, Orlando, Nov. 2015.
112.	Masataka Sata : The Functional Implication of Novel Inflammatory Mediators on the Atherogenesis and Metabolic Derangement., The 59th Annual Scientific Meeting of The Korean Society of Cardiology, Seoul, Oct. 2015.
113.	Masataka Sata : How do you treat AF patients with CAD and what does the evidence tell us?, The Annual Scientific Meeting of Taiwan Society of Lipids & Atherosclerosis 2015 and The 15th Taipei International Vascular Biology Symposium, Taipei, Sep. 2015.
114.	Masataka Sata : The role of innate immunity in the pathogenesis of atherosclerosis., The Annual Scientific Meeting of Taiwan Society of Lipids & Atherosclerosis 2015 and The 15th Taipei International Vascular Biology Symposium, Taipei, Sep. 2015.
115.	Masataka Sata : The role of NOAC in atherosclerotic disease., The Annual Scientific Meeting of Taiwan Society of Lipids & Atherosclerosis 2015 and The 15th Taipei International Vascular Biology Symposium, Taipei, Sep. 2015.
116.	R Hashimoto, Michio Shimabukuro, HM Salim, T Hara, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Antagonism of protease-activated receptor 2 (PAR-2) rescues vascular endothelial dysfunction in diabetic mice., ESC Congress 2015, London, Aug. 2015.
117.	S Nishimoto, Daiju Fukuda, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata : The activation of toll-like receptor 9 deteriorates blood flow recovery after hind-limb ischemia., ESC Congress 2015, London, Aug. 2015.
118.	Y Torii, Kenya Kusunose, Hirotsugu Yamada, Mika Bando, S Hayashi, S Nishio, M Yamao, R Amano, Y Hirata and Masataka Sata : Impact of atrial fibrillation on tricuspid annular plane systolic excursion in patients without organic cardiovascular disease., ASE 2015, Boston, Jun. 2015.
119.	Kenya Kusunose, Hirotsugu Yamada, J Hotchi, Mika Bando, S Nishio, Y Hirata, Jun Kishi and Masataka Sata : Prediction of future overt pulmonary hypertension by sixminute walk stress echocardiography in connective tissue disease., ASE 2015, Boston, Jun. 2015.
120.	Mika Bando, Hirotsugu Yamada, Junko Hotsuchi, S Hayashi, Y Saijo, Y Takagawa, N Sawada, S Nishio, Y Hirata and Masataka Sata : Association of CHADS2 and CHA2DS2-VASc scores with left atrial appendage dysfunction in patients with atrial fibrillation., Euro Echo Imaging 2014, Wien, Dec. 2014.
121.	Koji Yamaguchi, Tetsuzo Wakatsuki, A Takashima, Mika Bando, S Bando, Tomomi Matsuura, Takayuki Ise, Junko Hotsuchi, Takeshi Tobiume, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Differential response of local coagulation after implantation of new generation drug-eluting stents compared with sirolimus-eluting stent., AHA Scientific Sessions 2014, Chicago, Nov. 2014.
122.	Y Higashikuni, Daiju Fukuda, Masataka Sata and I Komuro : The inducible nuclear protein IB plays a pivotal role in the transition from adaptive to maladaptive cardiac hypertrophy during pressure overload., AHA Scientific Sessions 2014, Chicago, Nov. 2014.
123.	Y Higashikuni, Masataka Sata and I Komuro : The central nervous system regulates inflammation and cardiac remodeling during pressure overload through NLRP3 inflammasome activation., AHA Scientific Sessions 2014, Chicago, Nov. 2014.
124.	S Nishimoto, Daiju Fukuda, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata : Genetic deletion of toll-like receptor 9 accelerates blood flow recovery after hindlimb ischemia., AHA Scientific Sessions 2014, Chicago, Nov. 2014.
125.	T Hara, D Fukuda, K Tanaka, Y Higashikuni, Y Hirata, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Rivaroxaban, a direct factor Xa inhibitor, attenuates neointima formation after mechanical vascular injury., AHA Scientific Sessions 2014, Chicago, Nov. 2014.
126.	H Yamazaki, Tetsuzo Wakatsuki, Koji Yamaguchi, K Imada, K Matsumoto, Y Takagawa, E Takagi, Y Saijo, T Hara, Y Saito, Mika Bando, A Takashima, S Bando, Tomomi Matsuura, Takayuki Ise, Junko Hotsuchi, Takeshi Tobiume, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Differential responses of local coagulation after implantation of second-generation drug-eluting stent compared with first-generation drug-eluting stents., AHA Scientific Sessions 2014, Chicago, Nov. 2014.
127.	Michio Shimabukuro, Sachiko Matsumoto, Daiju Fukuda, T Hara, Takeshi Soeki and Masataka Sata : Antagonism of protease-activated receptors salvages vascular endothelial dysfunction in KK-Ay diabetic mice: a novel mechanism of rivaroxaban, an oral factor Xa inhibitor., ESC 2014, Barcelona, Aug. 2014.
128.	Michio Shimabukuro, Masayoshi Ishida, Shusuke Yagi, Daiju Fukuda, Takeshi Soeki and Masataka Sata : Post-transcriptional regulation of adiponectin by microRNA-378 in adipose tissue: a novel mechanism for hypoadiponectinemia., ESC 2014, Barcelona, Aug. 2014.
129.	S Nishio, Hirotsugu Yamada, M Yamano, Y Hirata, K Mori, S Matsuoka and Masataka Sata : Echocardiographic screening for congenital heart disease in infants and preschool children: 12 years experience in a civic event for children care., ESC 2014, Barcelona, Aug. 2014.
130.	Tomomi Matsuura, Takeshi Soeki, E Uematsu, S Bando, Takeshi Tobiume, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : A renin inhibitor prevents atrial endocardial dysfunction in rapidly paced rats with streptozotocin-induced diabetes., ESC 2014, Barcelona, Aug. 2014.
131.	Takeshi Soeki, E Uematsu, S Bando, Tomomi Matsuura, Takeshi Tobiume, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Relationship between local production of microRNA-328 and atrial substrate remodeling in atrial fibrillation., ESC 2014, Barcelona, Aug. 2014.
132.	S Bando, Takeshi Soeki, Takeshi Tobiume, Tomomi Matsuura, E Uematsu, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Atrial late potentials and atrial substrate remodeling in patients with atrial fibrillation., ESC 2014, Barcelona, Aug. 2014.
133.	S Bando, Daiju Fukuda, Takeshi Soeki, E Uematsu, Michio Shimabukuro and Masataka Sata : Relationship between NLRP3 inflammasome activation in adipose tissue and atherosclerosis., ESC 2014, Barcelona, Aug. 2014.
134.	T Hara, Daiju Fukuda, K Tanaka, Y Higashikuni, Y Hirata, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, M Shimabukuro and Masataka Sata : Rivaroxaban, a direct factor Xa inhibitor, attenuates neointima formation following vascular injury in the mouse through the inhibition of proliferative activation of vascular smooth muscle cells., ESC 2014, Barcelona, Aug. 2014.
135.	T Hara, Daiju Fukuda, K Tanaka, Y Higashikuni, Y Hirata, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, M Shimabukuro and Masataka Sata : Rivaroxaban, a direct factor Xa inhibitor, attenuates plaque progression and destabilization in ApoE-deficient mice by inhibiting macrophage activation., ESC 2014, Barcelona, Aug. 2014.
136.	Hirotsugu Yamada, S Akiyama, Junko Hotsuchi, Mika Bando, Y Saijo, S Nishio, M Yamano, Y Torii, Y Hirata and Masataka Sata : Relationships between 3-Dimensional and 2-Dimensional/Doppler Echocardiographic Variables for Evaluating Right Ventricular Systolic Function., ASE 2014, Portland, Jun. 2014.
137.	Junko Hotsuchi, Hirotsugu Yamada, Y Saijo, Mika Bando, S Hayashi, S Nishio, M Yamano, Y Torii, Y Hirata, R Amano, Takayuki Ise, Koji Yamaguchi, Takeshi Tobiume, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Serial Changes of Exercise Stress Echocardiographic Parameters in Patients with Connective Tissue Disease without Overt Pulmonary Hypertension., ASE 2014, Portland, Jun. 2014.
138.	Mika Bando, Hirotsugu Yamada, S Nishio, R Amano, Y Hirata, Junko Hotsuchi, Y Saijo, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Predicting Restenosis of Coronary Artery Stents by Ultrasound Tissue Characteristics of Carotid Artery Plaque., ASE 2014, Portland, Jun. 2014.
139.	Michio Shimabukuro, C Okawa, XF Lei, JR Kim-Kaneyama, Hirotsugu Yamada, Hirotsugu Kurobe, Daiju Fukuda, M Sato, Tetsuya Kitagawa and Masataka Sata : Effects of ezetimibe on oxidized cholesterol components in epicardial fat and myocardium: a gas chromatography-mass spectrometry analysis., EAS 2014, Madrid, May 2014.
140.	Hirotsugu Kurobe, T. Motoki, Y. Hirata, Mikio Sugano, T. Nakayama, Hajime Kinoshita, Tamotsu Kanbara, Eiki Fujimoto, Takashi Kitaichi, Takaki Hori, H. Sogabe, Masataka Sata and Tetsuya Kitagawa : PPAR-γ Agonist Administration Attenuates inflammation In Patients With Aortic Aneurysm., AATS Aortic Symposium 2014, New York, Apr. 2014.
141.	Masataka Sata : Epicardial adipose tissue plays a role in the pathogenesis of atherosclerosis., The 18th International Vascular Biology Meeting, Kyoto, Apr. 2014.
142.	Y Higashikuni, Masataka Sata and I Komuro : NLRP3 inflammasome activation through the heart-brain interaction is important for adaptive cardiac hypertrophy in response to pressure overload., The 18th International Vascular Biology Meeting, Kyoto, Apr. 2014.
143.	Y Saijo, Hirotsugu Yamada, Junko Hotsuchi, S Nishio, S Hayashi, Mika Bando, Y Hirata, R Amano, Takayuki Ise, Shusuke Yagi, Koji Yamaguchi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Right ventricular systolic dysfunction in patients with exercise-induced pulmonary hypertension associated with connective tissue disease., ACC 2014, Washington, D.C., Mar. 2014.
144.	Masataka Sata : Novel insights into the pathogenesis of atherosclerosis : epicardial adipose tissue vasa vasorum, and anti-aging genes, 2014 Metabosartan Expert Summit, Taipei, Mar. 2014.
145.	Junko Hotsuchi, Hirotsugu Yamada, S Nishio, Mika Bando, S Hayashi, Y Hirata, R Amano, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Right ventricular dysfunction in patients with exercise-induced pulmonary hypertension associated with connective tissue disease : an assessment using tricuspid annular motion velocities., Euro Echo Imaging 2013, Istanbul, Dec. 2013.
146.	Y Higashikuni, R Nagai, Masataka Sata and I Komuro : NLRP3 Inflammasome Activation Through the Heart-Brain Interaction Contributes to Adaptive Cardiac Hypertrophy in Response to Pressure Overload., American Heart Association AHA 2013, Dallas, Nov. 2013.
147.	Y Higashikuni, R Nagai, Masataka Sata and I Komuro : Toll-Like Receptor 2-Mediated Inflammation Induces Adaptive Cardiac Hypertrophy in Response to Pressure Overload., American Heart Association AHA 2013, Dallas, Nov. 2013.
148.	S Hayashi, Hirotsugu Yamada, Junko Hotsuchi, Mika Bando, Takayuki Ise, Koji Yamaguchi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Noninvasively Obtained Augmentation Index is Not a Reliable Maker for Vascular Sclerosis in Elderly Subjects., American Heart Association AHA 2013, Dallas, Nov. 2013.
149.	T Hara, Daiju Fukuda, K Tanaka, Y Higashikuni, Y Hirata, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Rivaroxaban, A Novel Oral Anticoagulant, Attenuates Plaque Progression in ApoE-Deficient Mice Through the Inhibition of Pro-Inflammatory Activation of Macrophages., American Heart Association AHA 2013, Dallas, Nov. 2013.
150.	Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki, Takayuki Ise, Takeshi Tobiume, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada and Masataka Sata : Impact Of Indoxy1 Sulfate, A Uremic Toxin, On Non-culprit Coronary Plaque Composition Assessed By Integrated Backscatter Intravascular Ultrasound In Patients With Coronary Artery Disease., American Heart Association AHA 2013, Dallas, Nov. 2013.
151.	Koji Yamaguchi, Tetsuzo Wakatsuki, Takayuki Ise, Takeshi Tobiume, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Decreased Local Hypercoagulation after Implantation of Everolimus-Eluting and Zotarolimus-Eluting Stents Compared with Early-Generation Drug-Eluting Stents in patients with stable angina., American Heart Association AHA 2013, Dallas, Nov. 2013.
152.	Koji Yamaguchi, Tetsuzo Wakatsuki, Takayuki Ise, Takeshi Tobiume, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Time-dependent Changes Of Local Vascular Response And Angiographic Peri-stent Contrast Staining Up To Five Years After Zotarolimus-eluting, Sirolimus-eluting, And Bare Metal Stent Implantation., American Heart Association AHA 2013, Dallas, Nov. 2013.
153.	S Nishimoto, Daiju Fukuda, Michio Shimabukuro, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Yutaka Nakaya and Masataka Sata : Macrophage Toll-like Receptor 9 Signaling Contributes to the Development of Insulin Resistance through the Promotion of Inflammation in Adipose Tissue., American Heart Association AHA 2013, Dallas, Nov. 2013.
154.	Masayoshi Ishida, Michio Shimabukuro, Shusuke Yagi, Daiju Fukuda, Takeshi Soeki, H Sato, E Uematsu, Hirofumi Izaki, Hiro-omi Kanayama and Masataka Sata : Post-Transcriptional Regulation of Adiponectin by Micro-RNA 378 in Human Visceral and Subcutaneous Adipose Tissue., American Heart Association AHA 2013, Dallas, Nov. 2013.
155.	Taisuke Nakayama, Hirotsugu Kurobe, Noriko Sugasawa, Hajime Kinoshita, Yasushi Yoshida, Yoichiro Hirata, Mie Sakata, Mark Webster Maxfield, Michio Shimabukuro, Yousuke Takahama, Masataka Sata, Toshiaki Tamaki, Tetsuya Kitagawa and Shuhei Tomita : Macrophage-Specific Hypoxia-Inducible Factor (HIF)-1-Deficient Mice Suppress the Vascular Remodeling and Regulate M2 Macrophage Polarization, American Heart Association AHA 2013, Nov. 2013.
156.	S Bando, Takeshi Soeki, T Matsuura, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro, Kenji Kangawa and Masataka Sata : Plasma Brain Natriuretic Peptide (BNP) level is elevated in patients with cancer., ESC Congress 2013, Amsterdam, Aug. 2013.
157.	Michio Shimabukuro, T Saito, T Higa, K Nakamura and Masataka Sata : Gender-based risk stratification of coronary artery disease in asymptomatic diabetic subjects: a multi-clinic study using multi-detector computed tomography., ESC Congress 2013, Amsterdam, Aug. 2013.
158.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, Takayuki Ise, Shusuke Yagi, Koji Yamaguchi, Hirotsugu Yamada, Yasuhiko Nishioka, Masafumi Harada and Masataka Sata : Differentiation of left ventricular systolic dysfunction related to cardiac sarcoidosis and other heart diseases using contrast-enhanced cardiovascular magnetic resonance., ESC Congress 2013, Amsterdam, Aug. 2013.
159.	S Bando, Takeshi Soeki, E Uematsu, T Matsuura, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro, Kenji Kangawa and Masataka Sata : Ghrelin ameliorates the progression of experimental autoimmune myocarditis., ESC Congress 2013, Amsterdam, Aug. 2013.
160.	Takeshi Soeki, S Bando, T Matsuura, E Uenmatsu, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Electrophysiological correlation and prognostic impact of pentraxin 3 as a local inflammatory marker in atrial fibrillation., ESC Congress 2013, Amsterdam, Aug. 2013.
161.	Tetsuzo Wakatsuki, Koji Yamaguchi, Toshiyuki Niki, Yoshio Taketani, Takayuki Ise, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : The tissue characteristics of coronary plaque with microchannel structure assessed by optical coherence tomography associated with local inflammatory response., ESC Congress 2013, Amsterdam, Aug. 2013.
162.	K Nishikawa, Shusuke Yagi, Takayuki Ise, Yuka Ueda, Takashi Iwase, Masashi Akaike, Michio Shimabukuro, Shinsuke Katoh and Masataka Sata : Visceral fat mass is associated with daily physical activity, leg skeletal muscle mass and fiber intake in healthy men., ESC Congress 2013, Amsterdam, Aug. 2013.
163.	Koji Yamaguchi, Tetsuzo Wakatsuki, Toshiyuki Niki, Yoshio Taketani, Takayuki Ise, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Differential responses of local coagulation after implantation of everolimus-eluting and zotarolimus-eluting stents compared with early-generation drug-eluting stents in patients with stable angina., ESC Congress 2013, Amsterdam, Aug. 2013.
164.	S Nishimoto, Daiju Fukuda, Michio Shimabukuro, S Matsumoto, Masayoshi Ishida, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Yutaka Nakaya and Masataka Sata : Genetic ablation of TLR9 improves insulin resistance through macrophage accumulation in adipose tissue., ESC Congress 2013, Amsterdam, Aug. 2013.
165.	Masayoshi Ishida, Michio Shimabukuro, Shusuke Yagi, Daiju Fukuda, Takeshi Soeki, H Sato, E Uematsu, Hirofumi Izaki, Hiro-omi Kanayama and Masataka Sata : MicroRNA-100 regulates a cluster of adipocytokine expression: A human biopsy study in subcutaneous and visceral adipose tissue., ESC Congress 2013, Amsterdam, Aug. 2013.
166.	Masayoshi Ishida, Michio Shimabukuro, Shusuke Yagi, Daiju Fukuda, Takeshi Soeki, H Sato, E Uematsu, Hirofumi Izaki, Hiro-omi Kanayama and Masataka Sata : MicroRNA miR-378 regulates adipocytokine fate by targeting transcriptional factors in human visceral and subctaneous adipose tissue., ESC Congress 2013, Amsterdam, Aug. 2013.
167.	Takeshi Soeki, K Yamaguchi, S Bando, T Matsuura, E Uematsu, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Cardiospecific microRNA plasma levels are associated with coronary plaque vulnerability., ESC Congress 2013, Amsterdam, Aug. 2013.
168.	Y Hirata, Hirotsugu Yamada, S Nishio, Mika Bando, S Hayashi, Junko Hotsuchi, T Tomofuji, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Echocardiographic epicardial adipose tissue thickness in anterior interventricular groove is a marker for the presence and severity of coronary artery disease., ESC Congress 2013, Amsterdam, Aug. 2013.
169.	S Hayashi, Hirotsugu Yamada, Junko Hotsuchi, S Nishio, Mika Bando, Y Hirata and Masataka Sata : Peak Systolic Mitral Annular Motion Velocity Reflects the Status of Ventricular-Arterial Coupling: A Clinical Study., ASE 2013, Minneapolis, Jun. 2013.
170.	S Hayashi, Hirotsugu Yamada, Junko Hotsuchi, S Nishio, Mika Bando, Y Hirata and Masataka Sata : Assessment of Optimal Method for Analysing Left Atrial Strain using Speckle Tracking Imaging., ASE 2013, Minneapolis, Jun. 2013.
171.	M Nakagawa, Hirotsugu Yamada, S Nishio, S Hayashi, Junko Hotsuchi, Mika Bando, Y Hirata, T Tomofuji and Masataka Sata : Clinical Significance of Mitral L-wave in Patients with Atrial Fibrillation and Preserved Ejection Fraction., ASE 2013, Minneapolis, Jun. 2013.
172.	Hirotsugu Yamada, S Nishio, S Hayashi, Junko Hotsuchi, Mika Bando, Y Hirata, T Tomofuji and Masataka Sata : Effect of Aging and Gender on Tricuspid Annular Motion Velocities and Displacement., ASE 2013, Minneapolis, Jun. 2013.
173.	S Hayashi, Hirotsugu Yamada, S Nishio, N Tomita, J Hotchi, Mika Bando, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Augmentation Index Measured by Tonometry Significantly Underestimates Atrial Stiffness in Ischemic Heart Disease in Japanese Population., 第77回日本循環器学会学術集会, Yokohama, Mar. 2013.
174.	Mika Bando, Hirotsugu Yamada, Toshiyuki Niki, S Nishio, R Tamai, J Hotchi, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Change in Ultrasonic Tissue Characteristics of Carotid Artery Plaque Reflects That of Coronary Artery Plaque., American College of Cardiology (ACC) 2013 Scientific Sessions, San Francisco, Mar. 2013.
175.	Tomoya Kinouchi, Yoshitaka Kurashiki, 北里慶子, Kenji Shimada, Kenji Yagi, Yoshiteru Tada, Nobuhisa Matsushita, Manabu Sumiyoshi, Junichiro Satomi, Masataka Sata and Shinji Nagahiro : Post-stroke PPAR activation promotes the proliferation and differentiation of innate- and bone marrow-derived stem cells insubventricular zone, leading to vasogenesis and neurogenesis in cortex, International STROKE Conference 2013, Honolulu, Feb. 2013.
176.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Androgen Receptor is Required for Cellular Survival and Angiogenesis in Response to Ischemia via Activation of VEGF Receptor Signaling Pathway Regardless of Sex, American Heart Association Scientific Session 2012, Nov. 2012.
177.	Taisuke Nakayama, Hirotsugu Kurobe, Noriko Sugasawa, Hajime Kinoshita, Mayuko Higashida, Yuki Matsuoka, Yasushi Yoshida, Yoichiro Hirata, Mie Sakata, Mark Webster Maxfield, Yousuke Takahama, Masataka Sata, Toshiaki Tamaki, Tetsuya Kitagawa and Shuhei Tomita : Role of Macrophage-derived Hif-1a as a Mediator of Vascular Remodeling, American Heart Association Scientific Sessions 2012, Nov. 2012.
178.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Masataka Sata, Masashi Akaike, Toshio Matsumoto and Toshiaki Tamaki : Heparin Cofactor II Promotes Angiogenesis in Response to Ischemic Hindlimb via an AMPK-eNOS-dependent Manner, American Heart Association Scientific Sessions 2012, Nov. 2012.
179.	Yusaku Maeda, Shuhei Tomita, Masaki Murakami, Hirotsugu Kurobe, Masaki Imanishi, Yasushi Yoshida, Yoichiro Hirata, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Tetsuya Kitagawa, Masataka Sata and Toshiaki Tamaki : Deficiency of Hypoxia Inducible Factor-1a in SM-22a-Expressing Bone Marrow-Derived Cells Alleviates Neointimal Formation Following Wire-induced Vascular Formation, American Heart Association Scientific Sessions 2012, Nov. 2012.
180.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Eicosapentaenoic acid administration ameliorates cardiac remodeling in humans and protects against Ang II-induced cardiovascular remodeling via attenuation of oxidative stress in mice., American Heart Association Scientific Sessions 2012, ロサンゼルス, Nov. 2012.
181.	Takayuki Ise, Shusuke Yagi, Takashi Iwase, Masashi Akaike, M Kadota, T Hara, S Bando, Toshiyuki Niki, J Hotchi, N Tomita, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Acute Hemodynamic Effects of Adaptive Servo-Ventilation in Patients with Chronic Left Heart Failure., AHA Scientific Sessions 2012, ロサンゼルス, Nov. 2012.
182.	Koji Yamaguchi, Tetsuzo Wakatsuki, Takeshi Soeki, Toshiyuki Niki, Yoshio Taketani, H. Oeduka, Mika Bando, K. Ogasawara, S. Bando, J. Hotchi, Takayuki Ise, Takashi Iwase, Hirotsugu Yamada and Masataka Sata : Telmisartan Reduces Coronary Plaque Vulnerability and Instent-neointimal Proliferation in Hypertensive Patients., AHA Scientific Sessions 2012, ロサンゼルス, Nov. 2012.
183.	Y. Higashikuni, R. Nagai and Masataka Sata : Toll-Like Receptor 2 Mediates Cardiac Adaptive Response to Pressure Overload., AHA Scientific Sessions 2012, ロサンゼルス, Nov. 2012.
184.	Michio Shimabukuro, N. Kuwae, K. Oba, M. Kakazu, M. Tamashiro, O. Arasaki, T. Shinjo, K. Yamakawa, M. Higa, Y. Shiohira and Masataka Sata : Low Left Ventircular Contractile Capacity and Low eGFR Are Significant Predictors for Hyperkalemia in 364 Patients with Heart Failure., AHA Scientific Sessions 2012, ロサンゼルス, Nov. 2012.
185.	Toshiyuki Niki, Tetsuzo Wakatsuki, Mika Bando, K. Ogasawara, S. Bando, T. Matsuura, J. Hotch, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, N. Tomita, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Effects of Additional Eicosapentaenoic Acid to Statin Therapy on Inflammatory Cytokines and the Tissue Characterization of Coronary Plaque Assessed by Integrated Backscatter Intravascular Ultrasound Systems., AHA Scientific Sessions 2012, Nov. 2012.
186.	H. Sato, M. Shimabukuro, Y. Hirata, M. Tabata, D. Munkhbaatar, D. Fukuda, Hirotsugu Kurobe, T. Soeki, S. Takanashi, Tetsuya Kitagawa and Masataka Sata : The Innate Immune System, Nlrp3 Inflammasome is Intensified in Epicardial Adipose Tissue around Coronary Arterial Lesions: Evidence from Biopsied Adipose Tissue in Coronary Artery Bypass Surgery., AHA Scientific Sessions 2012, ロサンゼルス, Nov. 2012.
187.	A. Takashima, Takayuki Ise, Masashi Akaike, Yuka Ueda, Takashi Iwase, T. Hara, M. Kadota, R. Ohta, K. Ogasawara, Toshiyuki Niki, J. Hotchi, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Cardiac Rehabilitation Reduces Levels of Oxidized LDL., AHA Scientific Sessions 2012, ロサンゼルス, Nov. 2012.
188.	K. Tanaka, Y. Hirata, Y. Tabata, Y. Ouchi and Masataka Sata : Locally Applied Suramin inhibits Angiogenesis in Adventitia and Arterial Lesion Progression in Apolipoprotein E-deficient Mice., AHA Scientific Sessions 2012, ロサンゼルス, Nov. 2012.
189.	S. Bando, Takeshi Soeki, E. Uematsu, T. Matsuura, M. Kadota, T. Hara, R. Ohta, Y. Kawabata, K. Ogasawara, Mika Bando, Toshiyuki Niki, Takayuki Ise, J. Hotchi, N. Tomita, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Relationship Between Nlrp3 Inflammasome and Coronary Atherosclerosis., AHA Scientific Sessions 2012, ロサンゼルス, Nov. 2012.
190.	S. Kimura, Yuka Ueda, Takayuki Ise, Takashi Iwase, K. Maeda, K. Nishikawa, K. Ogasawara, Mika Bando, S. Bando, Toshiyuki Niki, J. Hotchi, Koji Yamaguchi, N. Tomita, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Effect of Cardiac Rehabilitation with Supervised Exercise Training on Urinary Albumin Excretion in Patients with Cardiovascular Disease., AHA Scientific Sessions 2012, ロサンゼルス, Nov. 2012.
191.	Masataka Sata : Inflammation in atherosclerosis and adipose tissue., The 12th Biennial International Endotoxin & Innate Immunity Society (IEIIS) Meeting 2012, Tokyo, Oct. 2012.
192.	Takeshi Soeki, S. Bando, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Kenji Kangawa and Masataka Sata : Ghrelin protects the heart against ischemia-induced arrhythmias by modulating autonomic nerve activity., ESC Congress 2012, Munich, Aug. 2012.
193.	Takeshi Soeki, M. Kitani, Hirotsugu Yamada, Tetsuzo Wakatsuki, T. Kawano, S. Orino, K. Kawano, A. Kakutani, S. Bando and Masataka Sata : Renoprotective effect of cilnidipine via the antioxidant activity in hypertensive patients., ESC Congress 2012, Munich, Aug. 2012.
194.	H. Sato, Michio Shimabukuro, Y. Hirata, Hirofumi Izaki, M. Higashida, Hirotsugu Kurobe, Hiro-omi Kanayama, Hiroshi Sakaue, Yutaka Nakaya and Masataka Sata : Region-specific regulation of the innate immune system, NLRP3 inflammasome, in human abdominal adipose tissue., ESC Congress 2012, Munich, Aug. 2012.
195.	H. Sato, Y. Hirata, Michio Shimabukuro, M. Tabata, Hirotsugu Kurobe, M. Higashida, S. Takanashi, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : The innate immune system, NLRP3 inflammasome, in epicardial adipose tissue intensifies human coronary atherosclerosis., ESC Congress 2012, Munich, Aug. 2012.
196.	M. Dagvasumberel, Michio Shimabukuro, Junji Ueno, T. Nishiuchi, Takeshi Soeki, Takashi Iwase, Shoichiro Takao, Hirotsugu Yamada, Tetsuya Kitagawa and Masataka Sata : Gender disparities in the association of epicardial adipose tissue volume and coronary atherosclerosis: a 256-slice multidetector computed tomography study., ESC Congress 2012, Aug. 2012.
197.	Toshiyuki Niki, Tetsuzo Wakatsuki, Koji Yamaguchi, Yoshio Taketani, S Bando, Takayuki Ise, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : The tissue characteristics of coronary plaque with microchannel structure in patients with Coronary Artery Disease assessed by OCT and IB-IVUS., ESC Congress 2012, Munich, Aug. 2012.
198.	K Tanaka, Y Hirata, Y Tabata, Y Ouchi and Masataka Sata : Locally applied suramin inhibits angiogenesis in adventitia and arterial lesion progression in apolipoprotein E-deficient mice., ESC Congress 2012, Munich, Aug. 2012.
199.	S Hayashi, Hirotsugu Yamada, N Tomita, J Hotchi, Mika Bando, S Nishio, R Tamai, M Nakagawa, D Hirota, Y Hirata and Masataka Sata : Differentiation of Left Atrial Dysfunction From Pseudonormal/Restrictive Transmitral Flow Velocity Pattern in Patients With Preserved Ejection Fraction., American Society of Echocardiography (ASE) 23rd Annual Scientific Sessions, Maryland, Jun. 2012.
200.	Mika Bando, Hirotsugu Yamada, N Tomita, S. Nishio, R. Tamai, S. Hayashi, J. Hotchi, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Left Ventricular Geometry and Function in Patients with Sigmoid Septum., American Society of Echocardiography (ASE) 23rd Annual Scientific Sessions, Maryland, Jun. 2012.
201.	S Hayashi, Hirotsugu Yamada, N Tomita, J Hotchi, Mika Bando, S Nishio, R Tamai, M Nakagawa, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Differentiation Between Hypertrophic Cardiomyopathy and Hypertensive Heart Disease Using Tricuspid Annular Motion Velocity., American Society of Echocardiography (ASE) 23rd Annual Scientific Sessions, Maryland, Jun. 2012.
202.	Mika Bando, Hirotsugu Yamada, S Nishio, R Tamai, N. Tomita, S. Hayashi, J. Hotchi, M. Nakagawa, D. Hirota, Y. Hirata, S. Bando, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Effect of Statin Therapy on Regression of Carotid Artery Plaque Assessed by High-Resolution Color Mapping Method Based on Integrated Backscatter., American Society of Echocardiography (ASE) 23rd Annual Scientific Sessions, Maryland, Jun. 2012.
203.	J. Hotchi, Hirotsugu Yamada, S Nishio, Kenya Kusunose, N Tomita, S Hayashi, Mika Bando, R Tamai, M Nakagawa, D Hirota, Y Hirata, K Ogasawara, S Bando, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Efficacy of Six-minute Walk Stress Echocardiography for Detection of Pulmonary Arterial Hypertension in Patients With Connective Tissue Disease., American Society of Echocardiography (ASE) 23rd Annual Scientific Sessions, Maryland, Jun. 2012.
204.	J. Hotchi, Hirotsugu Yamada, R. Tamai, S. Nishio, N. Tomita, S. Hayashi, Mika Bando, S. Bando, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Assessment of Tricuspid Annular Motion Velocities in Pulmonary Hypertension of Various Etiologies., American Society of Echocardiography (ASE) 23rd Annual Scientific Sessions, Maryland, Jun. 2012.
205.	S. Nishio, Hirotsugu Yamada, R. Tamai, Y. Hirata, M. Sato, H. Hioraoka, S. Hayashi, N. Tomita, J. Hotchi, Mika Bando, M. Nakagawa, D. Hirota and Masataka Sata : Non-invasive Assessment of Left Atrial-Left Ventricular-Arterial Coupling in Patients With Diabetes Mellitus., American Society of Echocardiography (ASE) 23rd Annual Scientific Sessions, Maryland, Jun. 2012.
206.	Masataka Sata : Epicardial adipose tissue plays a role in the pathogenesis of Atherosclerosis., APSC Subspecialty Congress-Intervention and Imaging 2012, Taipei, May 2012.
207.	Yuki Matsuoka, Hirotsugu Kurobe, Noriko Sugasawa, Yoichiro Hirata, M Higashida, Taisuke Nakayama, Chika Nishio, Takaki Hori, Hitoshi Sogabe, Michio Shimabukuro, Masataka Sata and Tetsuya Kitagawa : Azelnidipine Suppress The Progression of Aortic Aneurysm in Wild Mice Model Through Anti-inflammatory Effects, AORTIC SYMPOSIUM2012, New York, Apr. 2012.
208.	Yusaku Maeda, Shuhei Tomita, Masaki Murakami, Hirotsugu Kurobe, Masaki Imanishi, Yasushi Yoshida, Yoichiro Hirata, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Tetsuya Kitagawa, Masataka Sata and Toshiaki Tamaki : Deficiency of Hypoxia Inducible Factor-1 in SM-22-Expressing Bone Marrow-Derived Cells Alleviates Neointimal Formation Following Wire-induced Vascular Formation, AHA SCIENTIFIC SESSIONS 2012, 2012.
209.	Y. Higashikuni, R. Nagai and Masataka Sata : The Role of the ATP-Binding Cassette Transporter ABCG2 in Antioxidant Response in the Heart., The 28th Annual Meeting of the International Society for Heart Research Japanese Section., Tokyo, Dec. 2011.
210.	Y. Higashikuni, R. Nagai and Masataka Sata : The ATP-binding cassette transporter ABCG2 protects against pressure overload-induced cardiac hypertrophy and heart failure by promoting angiogenesis and antioxidant response., AHA Scientific Sessions 2011, Orlando, Nov. 2011.
211.	Kenya Kusunose, Hirotsugu Yamada, S. Nishio, N. Tomita, S. Hayashi, J. Hotchi, R. Tamai, D. Hirota, Y. Hirata, Mika Bando, K. Ogasawara, A. Takashima, H. Yamazaki, S. Bando, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Single-Beat Assessment of Left Ventricular Systolic and Diastolic Function during Atrial Fibrillation using Myocardial Strain and Strain Rate., AHA Scientific Sessions 2011, Orlando, Nov. 2011.
212.	M. Higashida, Y. Hirata, Hirotsugu Kurobe, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : HMGB1 Signal via TLR9 Plays Critical Role in Vascular Remodeling., AHA Scientific Sessions 2011, Orlando, Nov. 2011.
213.	Takeshi Soeki, S. Bando, Toshiyuki Niki, H. Yamazaki, A. Takashima, K. Ogasawara, Mika Bando, Takayuki Ise, H. Takeuchi, N. Tomita, Yuka Ueda, Kenya Kusunose, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Pentraxin 3 is a Local Inflammatory Maker in Atrial Fibrillation., AHA Scientific Sessions 2011, Orlando, Nov. 2011.
214.	Mika Bando, Hirotsugu Yamada, S. Nishio, E. Uematsu, S. Hayashi, J. Hotchi, Kenya Kusunose, N. Tomita, R. Tamai, Y. Hirata, D. Hirota, M. Nakagawa, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Ultrasonic Tissue Characterization of Carotid Artery Plaque using High-resolution Integrated Backscatter Imaging;Validation Study with Histological Correlation., AHA Scientific Sessions 2011, Orlando, Nov. 2011.
215.	Koji Yamaguchi, Tetsuzo Wakatsuki, Takeshi Soeki, Toshiyuki Niki, Yoshio Taketani, H. Oezuka, S. Bando, N. Tomita, Kenya Kusunose, Takashi Iwase, Hirotsugu Yamada and Masataka Sata : Effects of Telmisartan on Inflammatory Cytokines and Coronary Plaque Component Assessed by Integrated Backscatter Intravascular Ultrasound in Hypertensive Patients., AHA Scientific Sessions 2011, Orlando, Nov. 2011.
216.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, Takayuki Ise, Toshiyuki Niki, Kenya Kusunose, Yuka Ueda, N. Tomita, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Ken-ichi Aihara, Tetsuzo Wakatsuki, Masafumi Harada and Masataka Sata : Detection of Cardiac Involvement in Patients with Sarcoidosis Using Cardiac Magnetic Resonance., AHA Scientific Sessions 2011, Orlando, Nov. 2011.
217.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Yoshitaka Kihira, Keisuke Ishizawa, Yuki Izawa-Ishizawa, Shuhei Tomita, Masataka Sata, Masashi Akaike, Shigeki Kato, Toshio Matsumoto and Toshiaki Tamaki : Heparin Cofactor Promotes Angiogenesis via an AMPK-eNOS Signaling Pathway, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
218.	M. Higashida, Y. Hirata, Hirotsugu Kurobe, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : HMGB1/TLR9 pathway plays a critical role in chronic inflammation and vascular remodeling after endovascular injury., ESC Congress 2011, Paris, Aug. 2011.
219.	Y. Hirata, Hirotsugu Kurobe, M. Higashida, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : GLP-1 receptor agonist attenuates vascular remodeling after endovascular injury., ESC Congress 2011, Paris, Aug. 2011.
220.	S. Nishio, Hirotsugu Yamada, R. Tamai, K. Endo, S. Hayashi, Kenya Kusunose, Takeshi Soeki, Tetsuzo Wakatsuki, Y. Sakai and Masataka Sata : Deterioration of right ventricular myocardial systolic function in monocrotaline-induced pulmonary arterial hypertension canine model: echocardiographic evaluation by 2D speckle tracking., ESC Congress 2011, Paris, Aug. 2011.
221.	Koji Yamaguchi, Tetsuzo Wakatsuki, Toshiyuki Niki, Yoshio Taketani, S. Bando, Kenya Kusunose, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Differential response of local persistent hypercoagulability after zotarolimus-eluting, paclitaxel-eluting, sirolimus-eluting and bare-metal stent implantation in patients with stable angina., ESC Congress 2011, Paris, Aug. 2011.
222.	Koji Yamaguchi, Tetsuzo Wakatsuki, Toshiyuki Niki, Yoshio Taketani, S. Bando, Kenya Kusunose, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Time-dependent changes of local coagulative response up to five years after sirolimus-eluting and bare-metal stent implantation in patients with stable angina., ESC Congress 2011, Paris, Aug. 2011.
223.	Takeshi Soeki, S. Bando, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Elevated concentration of pentraxin 3 is associated with local inflammation in atrial fibrillation., ESC Congress 2011, Paris, Aug. 2011.
224.	Tetsuzo Wakatsuki, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Kenya Kusunose, S. Bando, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Long-term local inflammatory and coagulative responses after coronary artery stenting with drug-eluting stent., ESC Congress 2011, Paris, Aug. 2011.
225.	Michio Shimabukuro, M. Higa, K. Yamakawa, H. Masuzaki and Masataka Sata : Impact of abdominal obesity and insulin resistance on cardiovascular events in Japanese obesity-endemic area: Okinawa Tomishiro Cohort Study., ESC Congress 2011, Paris, Aug. 2011.
226.	R. Tamai, Hirotsugu Yamada, S. Nishio, Kenya Kusunose, N. Tomita, S. Hayashi, M. Sato, H. Hiraoka, J. Miki, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Comparison of Tricuspid Annular Motion Velocities in Patients with Pulmonary Arteril Hypertension Secondary to Heart Failure., American Society of Echocardiography 2011. 22st Annual Scientific Sessions. Montreal, Montreal, Jun. 2011.
227.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 林修司, 玉井利奈, 坂東左知子, 久岡白陽花, Toshiyuki Niki, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : ストレインイメージング法を用いた心房細動例の左室心筋機能評価―左室圧曲線との同時記録による検討―, 第98回日本循環器学会中国・四国合同地方会, Tokushima, May 2011.
228.	S Nishio, Hirotsugu Yamada, R Tamai, K Endo, S Hayashi, Kenya Kusunose, N Tomita, J Miki, S Bando, S Hisaoka, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Relationship Between Carotid Artery Stiffness Parameter β and Brachial Artery Flow-mediated Dilation in coronary Artery Disease., American College of Cardiology 2011, New Orleans, Apr. 2011.
229.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Androgen receptor is essential for cell survival and neovascularization after ischemia., American Heart Association Scientific Sessions 2010, Chicago, Nov. 2010.
230.	Y. Higashikuni, J. Sainz, K. Nakamura, M. Takaoka, S. Enomoto, H. Iwata, M. Sahara, K. Tanaka, R. Nagai and Masataka Sata : The ATP-binding Cassette Transporter BCRP1/ABCG2 Plays a Pivotal Role in Cardiac Repair After Myocardial Infarction via Modulation of Microvascular Endothelial Cell Survival and Function., American Heart Association 2010, Chicago, Nov. 2010.
231.	Koji Yamaguchi, Tetsuzo Wakatsuki, Toshiyuki Niki, Yoshio Taketani, S. Bando, S. Hisaoka, Kenya Kusunose, Yuka Ueda, H. Takeuchi, Takashi Iwase, N. Tomita, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Time-dependent Changes Of Local Coagulative Response Up To Five Years After Sirolimus-eluting Stent Implantation., American Heart Association 2010, Chicago, Nov. 2010.
232.	Tetsuzo Wakatsuki, Koji Yamaguchi, Toshiyuki Niki, Kenya Kusunose, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Long-Term Local Inflammatory and Coagulative Responses after Coronary Artery Stenting with Drug-Eluting Stent., American Heart Association 2010, Chicago, Nov. 2010.
233.	H. Iwata, Masataka Sata, J. Ando, H. Fujita, D. Sawaki, M. Takahashi, Y. Hirata and R. Nagai : Significant Correlation between Primitive Cells in Intracoronary Thrombi in Patients with Myocardial Infarction and Lesion Progression., American Heart Association 2010, Chicago, Nov. 2010.
234.	K. Tanaka, D. Nagata, Y. Hirata, Y. Tabata, R. Nagai and Masataka Sata : Enhanced Angiogenesis in Adventitia Promotes Plaque Formation in Abdominal Aorta of Apolipoprotein E-deficient Mice., American Heart Association 2010, Chicago, Nov. 2010.
235.	Kenya Kusunose, Hirotsugu Yamada, S. Nishio, N. Tomita, S. Hayashi, S. Bando, S. Hisaoka, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Left Ventricular Dyssynchrony during Lower Leg Positive Pressure Assessed by Real-time 3-dimensional Echocardiography., American Heart Association 2010, Chicago, Nov. 2010.
236.	Takeshi Soeki, Toshiyuki Niki, S. Bando, S. Hisaoka, H. Takeuchi, Kenya Kusunose, Koji Yamaguchi, Y. Hirata, N. Tomita, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike, K. Kangawa and Masataka Sata : Ghrelin Protects Heart Against Ischemia-Induced Arrhythmias by Preserving Connexin43 Protein., American Heart Association 2010, Chicago, Nov. 2010.
237.	Y. Hirata, T. Motoki, Hirotsugu Kurobe, Masashi Akaike, M. Tabata, S. Takanashi, T. Igarashi, Tetsuya Kitagawa and Masataka Sata : Macrophage Polarization in Epicardial Adipose Tissue is Correlated with Severity of Human Coronary Artery Disease., American Heart Association 2010, Chicago, Nov. 2010.
238.	S. Yoshida, Ken-ichi Aihara, Yasumasa Ikeda, T. Ise, Yuka Ueda, Takashi Iwase, Masashi Akaike, Masataka Sata and T. Matsumoto : Androgen Receptor is Essential for Cell Survival and Neovascularization after Ischemia., American Heart Association 2010, Chicago, Nov. 2010.
239.	Kenya Kusunose, Hirotsugu Yamada, S. Nishio, N. Tomita, S. Hayashi, S. Bando, S. Hisaoka, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Time Difference between Onset of Mitral Inflow and Onset of Early Diastolic Mitral Annulus Velocity Predicts Left Ventricular End-diastolic Pressure: Assessment by Dual Doppler Echocardiography., American Heart Association 2010, Chicago, Nov. 2010.
240.	Takeshi Soeki, Toshiyuki Niki, S. Bando, S. Hisaoka, H. Takeuchi, Kenya Kusunose, Koji Yamaguchi, Y. Hirata, N. Tomita, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike, K. Kangawa and Masataka Sata : Ghrelin Attenuates Myocardial Ischemia/Reperfusion Injury via the Extracellular Signal-Regulated Kinase 1/2 and Phosphatidylinositol 3-Kinase/Akt Pathway., American Heart Association 2010, Chicago, Nov. 2010.
241.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Androgen receptor participants in ischemia-induced tissue damage and angiogenesis in male mice, 23rd Scientific Meeting of the International Society of Hypertension Vancouver, Vancouver, Sep. 2010.
242.	Takashi Iwase, S. Takao, Masashi Akaike, K. Adachi, Yuka Ueda, M. Harada, H. Nishitani and Masataka Sata : Detection of Myocardial Damage in Female Carriers of Duchenne Muscular Dystrophy Using Cardiac Magnetic Resonance., ESC CONGRESS 2010, Stockholm, Aug. 2010.
243.	Toshiyuki Niki, Tetsuzo Wakatsuki, Koji Yamaguchi, Kenya Kusunose, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Impact of Statin Theraphy on Local Coagulative Response after sirolimus-eluting Stent Implantation in late chronic Phase., ESC CONGRESS 2010, Stockholm, Aug. 2010.
244.	Masataka Sata : Vascular injury and repair: beyond the endothelium., ESC CONGRESS 2010, Stockholm, Aug. 2010.
245.	Masataka Sata : Strategy to prevent cardiovasucular events in patients with metabolic syndrome: Insights from atherosclerosis research and hypertension management., The 6th International Conference on the Biology, Chemistry and Therapeutic Applications of Nitric Oxide, Jun. 2010.
246.	Kenya Kusunose, Hirotsugu Yamada, S Nishio, N Tomita, K Endo, H Takashima, C Mimura, M Yamanaka, J Miki, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Effect of Preload on Left Ventricular Dyssynchrony in Patients with Dilated Cardiomyopathy: Assessment with Real-Time Three-Dimensional Echocardiography., American Society of Echocardiography 2010 21st Annual Scientific Sessions, San Diego, Jun. 2010.
247.	H Takashima, Hirotsugu Yamada, Kenya Kusunose, S Nishio, N Tomita, C Mimura, K Endo, M Yamanaka, J Miki, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Association of Carotid Artery Atherosclerosis with Aortic Valve Sclerosis., American Society of Echocardiography 2010 21st Annual Scientific Sessions, San Diego, Jun. 2010.
248.	Hirotsugu Yamada, Kenya Kusunose, S Nishio, J Miki, N Tomita, H Takashima, C Mimura, M Yamanaka, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Identification of Pseudonormal / Restrictive Transmitral Flow Velocity Pattern Using its Response to Nitroglycerin Spray Oral Administration., American Society of Echocardiography 2010 21st Annual Scientific Sessions, San Diego, Jun. 2010.
249.	Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Sumiko Yoshida, Yasumasa Ikeda, Uemoto Ryoko, Shusuke Yagi, Takashi Iwase, Hirata Yoichiro, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Plasma heparin cofactor II activity is an independent determinant for cardiac remodeling in subjects with cardiovascular risk factors, 20th International Society for Heart Research(ISHR), Kyoto, May 2010.
250.	Ken-ichi Aihara, Yuka Ueda, Takayuki Ise, Sumiko Yoshida, Yasumasa Ikeda, Uemoto Ryoko, Shusuke Yagi, Takashi Iwase, Hirata Yoichiro, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Heparin cofactor II is a novel anticardiac remodeling factor against angiotensin II excess, 20th International Society for Heart Research(ISHR), Kyoto, May 2010.
251.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Exacerbation of cell survival and impaired neovascularization after hindlimb ischemia in male androgen receptor null mice, 20th International Society for Heart Research(ISHR), Kyoto, May 2010.
252.	S. Yoshida, K. Aihara, Yuka Ueda, Yasumasa Ikeda, T. Iwase, Masashi Akaike, Masataka Sata and T. Matsumoto : Exacerbation of Cell Survival and Impaired Neovascularization after Hindlimb Ischemia in Male Androgen Receptor Null Mice., XXth World Congress of the International Society for Heart Research 2010, Kyoto, May 2010.
253.	Y. Hirata, Hirotsugu Kurobe, Masashi Akaike, F. Chikugo, Takaki Hori, Tetsuya Kitagawa and Masataka Sata : CD-8 Positive T-lymphocyte Infiltration in Epicardial Adipose Tissue in Patients with Coronary Artery Disease., XXth World Congress of the International Society for Heart Research 2010, Kyoto, May 2010.
254.	Masashi Akaike, Ken-ichi Aihara, Yasumasa Ikeda, K. Ishikawa, S. Yoshida, Yuka Ueda, Shusuke Yagi, Takashi Iwase, T. Matsumoto and Masataka Sata : Glucocorticoid causes vascular endothelial dysfunction through activation of mineralocorticoid receptor., XXth World Congress of the International Society for Heart Research 2010, Kyoto, May 2010.
255.	Ken-ichi Aihara, T. Ise, Yuka Ueda, S. Yoshida, Yasumasa Ikeda, R. Uemoto, Shusuke Yagi, Takashi Iwase, Y. Hirata, Masashi Akaike, Masataka Sata and T. Matsumoto : Plasma heparin cofactor II activity is an independent determinant for cardiac remodeling in subjects with cardiovascular risk factors., XXth World Congress of the International Society for Heart Research 2010, Kyoto, May 2010.
256.	Y. Hirata, Masashi Akaike, S. Nagahiro and Masataka Sata : Increased expression of HMGB1 in human and murine atherosclerotic lesions., XXth World Congress of the International Society for Heart Research 2010, Kyoto, May 2010.
257.	Yuka Ueda, Ken-ichi Aihara, T. Ise, S. Yoshida, Yasumasa Ikeda, R. Uemoto, Shusuke Yagi, Takashi Iwase, Y. Hirata, Masashi Akaike, Masataka Sata and T. Matsumoto : Heparin cofactor II is a novel anticardiac remodeling factoragainst angiotensin II excess., XXth World Congress of the International Society for Heart Research 2010, Kyoto, May 2010.
258.	Tatsuo Motoki, Hirotsugu Kurobe, Y Hirata, A Terahashi, Y Arai, M Sugano, Homare Yoshida, Tamotsu Kanbara, Takashi Kitaichi, Masataka Sata and Tetsuya Kitagawa : Piolitazone may suppres the progression of aortic aneuysm, Aortic symposium 2010, New York, Apr. 2010.
259.	Tatsuo Motoki, Hirotsugu Kurobe, Y Hirata, A Terahashi, Y Arai, M Sugano, Homare Yoshida, Tamotsu Kanbara, Takashi Kitaichi, Masataka Sata and Tetsuya Kitagawa : Pioglitazone attenuates inframmatory changes in abdominal aortic aneurysm, Arteriosclerosis, Thrombosis and Vascular Biology 2010 Scientific Sessions, San Francisco, Apr. 2010.
260.	Ken-ichi Aihara, Yuichi Fujinaka, Mizuho Kinouchi, Sumiko Yoshida, Yuka Ueda, Kurahashi Kiyoe, Itsuro Endo, Uemoto Ryoko, Shusuke Yagi, Takashi Iwase, Hirata Yoichiro, Suzuki Reiko, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Albuminuria is an independent aggravating factor for visceral fat obesity regardless of diabetes mellitus: a study using abdominal CT scan imaging, 14th International Congress of Endocrinology, Kyoto, Mar. 2010.
261.	Hirotsugu Yamada, Kenya Kusunose, S Nishio, N Tomita, J Miki, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Identification of Pseudonormal Transmitral Flow Velocity Pattern using its Change by Nitroglycerin Spray Oral Administration., American College of Cardiology 2010, Mar. 2010.
262.	Kenya Kusunose, Hirotsugu Yamada, S Nishio, N Tomita, J Miki, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Doppler Echocardiographic Estimation of Left Ventricular End-diastolic Pressure in Challenging, 第74回日本循環器学会総会・学術集会, Mar. 2010.
263.	S Nishio, Hirotsugu Yamada, Kenya Kusunose, N Tomita, J Miki, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Evaluation of Secondary Pulmonary Hypertension by Tricuspid Annular Velocity Profile Using Pulsed Tissue Doppler Imaging., 第74回日本循環器学会総会・学術集会, Mar. 2010.
264.	N Tomita, Hirotsugu Yamada, Kenya Kusunose, S Nishio, K Endo, H Takashima, C Mimura, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Detection of Patent Foramen Ovale by Contrast Realtime 3-dimensional Transesophageal Echocardiography., 第74回日本循環器学会総会・学術集会, Mar. 2010.
265.	K Endo, Hirotsugu Yamada, Kenya Kusunose, S Nishio, N Tomita, J Miki, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Ken Saito and Masataka Sata : N-3 Fatty Acids, IMT and CKD as Risk Factors in Coronary Artery Disease., 第74回日本循環器学会総会・学術集会, Mar. 2010.
266.	S Nishio, Hirotsugu Yamada, Kenya Kusunose, N Tomita, J Miki, K Endo, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Clinical Evaluation of Stiffness Parameter beta of Common Carotid Artery Obtained by Echo-tracking Method in Coronary Heart Disease., 第74回日本循環器学会総会・学術集会, Mar. 2010.
267.	T Niki, Takeshi Soeki, Kunihiko Koshiba, Kenya Kusunose, Koji Yamaguchi, Y Hirata, N Tomita, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Role of Circulating High-Mobility Group Box-1 (HMGB1) in Patients with Coronary Artery Disease., 第74回日本循環器学会総会・学術集会, Mar. 2010.
268.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, K Adachi, Y Sumitomo, Shusuke Yagi, T Niki, Kenya Kusunose, N Tomita, Y Hirata, Koji Yamaguchi, Kunihiko Koshiba, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Ken-ichi Aihara, Masafumi Harada, Hiromu Nishitani and Masataka Sata : Utility of Cardiac Magnetic Resonance for Detection of Cardiac Involvement in Female Carriers of Duchenne Muscular Dystrophy., 第74回日本循環器学会総会・学術集会, Mar. 2010.
269.	Tetsuzo Wakatsuki, Koji Yamaguchi, T Niki, Kenya Kusunose, Kunihiko Koshiba, Takashi Iwase, Yoshio Taketani, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Long-Term Local Inflammatory and Coagulative Responses after Coronary Artery Stenting with Drug-Eluting Stent., 第74回日本循環器学会総会・学術集会, Mar. 2010.
270.	Takeshi Soeki, Kunihiko Koshiba, T Niki, Kenya Kusunose, Koji Yamaguchi, Y Hirata, N Tomita, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike, Kenji Kangawa and Masataka Sata : Ghrelin Protects Heart against Ischemia-Induced Arrhythmias by Preserving Connexin43 Protein., 第74回日本循環器学会総会・学術集会, Mar. 2010.
271.	Kenya Kusunose, Hirotsugu Yamada, S Nishio, N Tomita, J Miki, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Detection of Myocardial Amyloid Involvement Using 2-Dimentional Speckle Tracking Echocardiography: Utilization of Inner and Outer Myocardial Strain and Strain Rate., 第74回日本循環器学会総会・学術集会, Mar. 2010.
272.	Koji Yamaguchi, Tetsuzo Wakatsuki, T Niki, Kenya Kusunose, Kunihiko Koshiba, Yoshio Taketani, Takashi Iwase, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Time-Dependent Changes of Local Coagulative Response up to Five Years after Sirolimus-Eluting Stent Implantation., 第74回日本循環器学会総会・学術集会, Mar. 2010.
273.	C Mimura, Hirotsugu Yamada, Kenya Kusunose, S Nishio, N Tomita, J Miki, H Takashima, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Predictive Value of Subepicardial Fat Thickness in Coronary Artery Sclerosis in Comparison with Intima-media Thickness, 第74回日本循環器学会総会・学術集会, Mar. 2010.
274.	Ken-ichi Aihara, Yuichi Fujinaka, Mizuho Kinouchi, Sumiko Yoshida, Takashi Iwase, Masashi Akaike, Yuka Ueda, Kurahashi Kiyoe, Itsuro Endo, Uemoto Ryoko, Shusuke Yagi, Takashi Iwase, Hirata Yoichiro, Suzuki Reiko, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Albuminuria is an independent aggravating factor for visceral fat obesity regardless of diabetes mellitus: a study using abdominal CT scan imaging, 14th International Congress of Endocrinology, Kyoto, Japan, Mar. 2010.
275.	Ken-ichi Aihara, Sumiko Yoshida, Yuka Ueda, Uemoto Ryoko, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Rosuvastatin attenuates left ventricular mass even in subjects without cardiac hypertrophy, 14th International Congress of Endocrinology, Kyoto, Japan, Mar. 2010.
276.	Y. Higashikuni, S. Julie, K. Nakamura, M. Takaoka, S. Enomoto, H. Iwata, M. Sahara, M. Tanaka, N. Koibuchi, Masataka Sata and R. Nagai : The ATP-binding Cassette Transporter BCRP1-ABCG2 Plays a Critical Role in Cardiac Repair after Myocardial Infarction via Protection of Microvascular Endothelial Cells., International Symposium on Cardiovascular Endocrinology and Metabolism. CVEM 2010, Nara, Mar. 2010.
277.	Yuka Ueda, Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Shusuke Yagi, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Exacerbation of Angiotensin ll-induced Cardiac Remodeling through Enhancement of NADPH oxidase-TGF- 1 Pathway in Heparin Cofactor ll-Deficient Mice, Scientific Sessions 2009, American Heart Association, Florida, Nov. 2009.
278.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Shusuke Yagi, Yasumasa Ikeda, Takashi Iwase, Kurahashi Kiyoe, Itsuro Endo, Yuichi Fujinaka, Nishio Susumu, Hirotsugu Yamada, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Dehydroepiandrosterone sulfate is an endothelial function-independent protective factor against carotid atherosclerosis., Scientific Sessions 2009, American Heart Association, Florida, Nov. 2009.
279.	Koji Yamaguchi, Tetsuzo Wakatsuki, T Niki, Kenya Kusunose, Kunihiko Koshiba, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Predictors of Local Persistent Hypercoagulability After Sirolimus-eluting Stent Implantation: Implication for Correlates of Late Stent Thrombosis., American Heart Association 2009, Nov. 2009.
280.	Hirotsugu Yamada, Kenya Kusunose, S Nishio, N Tomita, K Endo, H Takashima, C Mimura, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Prognostic Value of Changes in Transmitral Flow Velocity Pattern During Leg Positive Pressure in Mild Heart Failure: A Clinical Application of "Preload Stress Echocardiography", American Heart Association 2009, Nov. 2009.
281.	Tetsuzo Wakatsuki, T Niki, Kenya Kusunose, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, N Tomita, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Long-Term Local Inflammatory Response After Coronary Artery Stenting. Bare Metal vs Sirolimus-Eluting vs Paclitaxel-Eluting Stent., American Heart Association 2009, Nov. 2009.
282.	Tetsuzo Wakatsuki, T Niki, Kenya Kusunose, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, N Tomita, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Long-Term Local Inflammatory Response After Coronary Artery Stenting with Drug-Eluting Stent., American Heart Association 2009, Nov. 2009.
283.	Kunihiko Koshiba, Takeshi Soeki, T Niki, Kenya Kusunose, Y Hirata, Koji Yamaguchi, Shusuke Yagi, N Tomita, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike, Kenji Kangawa and Masataka Sata : C-type Natriuretic Peptide Ameliorates the Progression of Experimental Autoimmune Myocarditis., American Heart Association 2009, Nov. 2009.
284.	S Nishio, Hirotsugu Yamada, Kenya Kusunose, N Tomita, Y Tadatsu, M Sato, H Hiraoka and Masataka Sata : Usefulness of B-Flow Imaging in Carotid Artery Ultrasound Examination., 12th World Congress of the World Federation for Ultrasound in Medicine and Biology, Aug. 2009.
285.	Hirotsugu Yamada, Kenya Kusunose, N Tomita, Y Tadatsu, S Nishio, M Sato, H Hiraoka and Masataka Sata : Enhance of Early Diastolic Left Ventricular Mismatch between Wall Motion and Inflow by Preload Augmentation: Assessment by Dual-Doppler Echocardiography., 12th World Congress of the World Federation for Ultrasound in Medicine and Biology, Aug. 2009.
286.	Tetsuzo Wakatsuki, Koji Yamaguchi, T Niki, Kenya Kusunose, Kunihiko Koshiba, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Long-term local inflammatory response after coronary artery stenting -BMS vs SES vs PES-., ESC Congress 2009, Aug. 2009.
287.	Takeshi Soeki, T Niki, Kunihiko Koshiba, Kenya Kusunose, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Plasma concentration of pentraxin 3 is a useful marker for monitoring the anti-plaque effect of telmisartan., ESC Congress 2009, Aug. 2009.
288.	Koji Yamaguchi, Tetsuzo Wakatsuki, T Niki, Kenya Kusunose, Kunihiko Koshiba, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Local persistent hypercoagulability after drug-eluting stent implantation: siroliumus-eluting stent vs. paclitaxel-eluting stent., ESC Congress 2009, Aug. 2009.
289.	Y Fukuda, Takeshi Soeki, N Fukuda, S Morishita, K Sakabe, H Shinohara, Y Tamura, Masashi Akaike, Tetsuzo Wakatsuki, Hirotsugu Yamada, Takashi Iwase, Shusuke Yagi, Kunihiko Koshiba, Koji Yamaguchi, Kenya Kusunose, T Niki and Masataka Sata : Pentraxin 3, a Novel Inflammatory Marker, Predicts Left Ventricular Remodeling in Patients with Acute Myocardial Infarction., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
290.	Shusuke Yagi, Masashi Akaike, Takashi Iwase, Kenya Kusunose, T Niki, Y Hirata, Koji Yamaguchi, Kunihiko Koshiba, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, S Yoshida, Y Sumitomo, Ken-ichi Aihara, Toshio Matsumoto and Masataka Sata : Bosentan, an Endothelin Receptor Antagonist, Exerts Protective Actions against Systemic Sclerosis-related Peripheral Circulation Insufficiency., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
291.	Y Hirata, H Iwata, K Nakamura, Y Sakai, N Tomita, T Niki, Kenya Kusunose, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Synthetic Prostacycline Agonist, ONO-1301, Ameliorates Left Ventricular Dysfunction and Cardiac Fibrosis in Cardiomyopathic Hamsters., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
292.	Kenya Kusunose, Hirotsugu Yamada, S Nishio, N Tomita, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Prediction of Cardiac Response to Preload Augmentation by Dual Doppler Echocardiography and Left Arial Volume Auto Tracking System., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
293.	M Yamanaka, Hirotsugu Yamada, Kenya Kusunose, N Tomita, S Nishio, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Shinji Nagahiro and Masataka Sata : Utilization of Echocardiography in Stroke Care Unit of Tokushima University Hospital., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
294.	Takeshi Soeki, T Niki, Kunihiko Koshiba, Y Hirata, N Tomita, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike, H Satoh and Masataka Sata : Plasma Concentration of Pentraxin 3 is a Useful Marker for Monitoring the Anti-plaque Effect of Telmisartan., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
295.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, S Yoshida, Y Sumitomo, Kenya Kusunose, T Niki, Y Hirata, Koji Yamaguchi, Kunihiko Koshiba, Takashi Iwase, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Pitavastatin Exerts LDL Cholesterol Reduction-independent Protective Action for Cardiac and Renal Function in Patients with Dyslipidemia., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
296.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, S Yoshida, Y Sumitomo, Kenya Kusunose, T Niki, Y Hirata, Koji Yamaguchi, Kunihiko Koshiba, Takashi Iwase, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Plasma Aldosterone Concentration is Associated with Cognitive Impairement in Patients with Hypertension., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
297.	Koji Yamaguchi, Tetsuzo Wakatsuki, T Niki, Kenya Kusunose, Kunihiko Koshiba, N Tomita, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Local Persistent Hypercoagulability after Drug-Eluting Stent Implantation: Sirolimus-Eluting Stent vs. Paclitaxel-Eluting Stent., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
298.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, K Adachi, Y Sumitomo, Shusuke Yagi, T Niki, Kenya Kusunose, N Sakamoto, Y Hirata, Koji Yamaguchi, Kunihiko Koshiba, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Ken-ichi Aihara, Masafumi Harada, Hiromu Nishitani and Masataka Sata : Early Detection of Myocardial Damage in Female Carriers of Duchenne Muscular Dystrophy - the Utility of Cardiac Magnetic Resonance., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
299.	Hirotsugu Yamada, Kenya Kusunose, N Tomita, S Nishio, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Angiotensin-II Receptor Blocker Prevents the Deterioration of Left Ventricular Geometry and Diastolic Function in Hypertrophic Cardiomyopathy., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
300.	Takeshi Soeki, Kunihiko Koshiba, T Niki, Y Hirata, N Tomita, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Effect of Ghrelin on Autonomic Activity in Healthy Volunteers., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
301.	Kenya Kusunose, Hirotsugu Yamada, S Nishio, N Tomita, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Elevation of Left Ventricular End-diastolic Pressure Enhances Mismatch between Mitral Inflow and Annular Motion., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
302.	S Nishio, Hirotsugu Yamada, Kenya Kusunose, N Tomita, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Clinical utility of B-Flowimaging on ultrasound examination of carotid artery., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
303.	M Yamanaka, Kenya Kusunose, Hirotsugu Yamada, S Nishio, N Tomita, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Postsystolic Shortening is Superior to Peak Systolic Strain on the Prediction of Ischemia in Normal Wall Motion Segments., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
304.	Tetsuzo Wakatsuki, Koji Yamaguchi, T Niki, Kenya Kusunose, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Long-Term Local Inflammatory Response after Coronary Artery Stenting -BMS vs. SES vs. PES-, 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
305.	Hirotsugu Yamada, Kenya Kusunose, S Nishio, N Tomita, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : The Mitral L-wave Predicts Adverse Response to Volume Overloading in Patients with Atrial Fibrillation., 58th American College of Cardiology, Mar. 2009.
306.	S Nishio, Hirotsugu Yamada, Kenya Kusunose, N Tomita, T Niki, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Tricuspid Annular Velocity Profile by Pulsed Tissue Doppler Imaging for the Assessment of Serial Change of Pulmonary Artery Pressure in Secondary Pulmonary Hypertension., 58th American College of Cardiology, Mar. 2009.
307.	Ken-ichi Aihara, Sumiko Yoshida, Takayuki Ise, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Kurahashi Kiyoe, Itsuro Endo, Yuichi Fujinaka, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Increased serum triglyceride but not LDL cholesterol is associated with left ventricular diastolic dysfunction., Scientific Sessions 2008, American Heart Association, New Orleans, Nov. 2008.
308.	Takayuki Ise, Ken-ichi Aihara, Sumiko Yoshida, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Ishikawa Kazue, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Plasma Heparin Cofactor II Activity Is Inversely Associated with Left Atrial Volume and Left Ventricular Diastolic Dysfunction., Scientific Sessions 2008, American Heart Association, New Orleans, Nov. 2008.
309.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Kurahashi Kiyoe, Itsuro Endo, Yuichi Fujinaka, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Dehydroepiandrosterone sulfate is an antivascular remodeling factor in elderly individuals., Scientific Sessions 2008, American Heart Association, New Orleans, Nov. 2008.
310.	Takashi Iwase, Hirotsugu Kurobe, Masashi Akaike, Shunji Nakano, Sumiko Yoshida, Sumitomo Yuka, Shusuke Yagi, Ken-ichi Aihara, Shuji Ozaki, Masahiro Abe, Natsuo Yasui, Toshio Matsumoto, Tetsuya Kitagawa and Masataka Sata : Erythropoietin administration with autologous blood donation - a novel strategy to enhance mobilization of circulating progenitor cells, American Heart Association Sessions 2008, New Orleans, Nov. 2008.
311.	Masashi Akaike, Ken-ichi Aihara, Yasumasa Ikeda, Shusuke Yagi, Ishikawa Kazue, Sumitomo Yuka, Sumiko Yoshida, Takashi Iwase, Toshio Matsumoto and Masataka Sata : Pitavastatin, an HMG-CoA Reductase Inhibitor, Prevents Glucocorticoid-induced Hypertension through Ameliorating Imbalance of Oxidative Stress and Nitric Oxide Production, American Heart Association Sessions 2008, New Orleans, Nov. 2008.
312.	Tetsuzo Wakatsuki, K Yamaguchi, T Niki, Kenya Kusunose, K Koshiba, Hirotsugu Yamada, Takeshi Soeki, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Masataka Sata : Long-term endothelial dysfunction after coronary artery stenting with drug-eluting stent associated with local inflammatory response., American Heart Association 2008, New Orleans, Nov. 2008.
313.	K Yamaguchi, Tetsuzo Wakatsuki, T Niki, Kenya Kusunose, K Koshiba, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Local hypercoagulability and endothelial dysfunction after sirolimus-eluting stent implantation: implication for late stent thrombosis., American Heart Association 2008, New Orleans, Nov. 2008.
314.	Masataka Sata : Vascular Regeneration Utilizing Circulating Prigenitors and Novel Biomaterials., The Second International Cell Therapy Conference, Seoul, Nov. 2008.
315.	Tetsuzo Wakatsuki, K Yamaguchi, Kenya Kusunose, T Niki, K Koshiba, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Long-term local inflammatory response after coronary artery stenting with drug-eluting stent., ESC Congress 2008, Munich, Aug. 2008.
316.	Masataka Sata : Maintenace of Vascular Homeostasis by Circulating Progenitors and Periadvential Adipose Tissue, The New Frontiers in Biomedical Science Conference, Taipei, Nov. 2007.
317.	Masataka Sata : Potential role of periadventitial adipose tissue in regulation of vascular homeostasis and remodeling, The SEOUL Conference, Seoul, Oct. 2007.
318.	Masataka Sata : Maintenance of vascular homeostasis by bone marrow-derived progenitors, Carwile LeRoy Memorial International Workshop on Scleroderma Secretariat, Tokyo, May 2007.
319.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Yasumasa Ikeda, Shusuke Yagi, Takashi Iwase, Sumitomo Yuka, Masataka Sata, Kato Shigeaki and Toshio Matsumoto : Heparin Cofactor II Deficiency Causes Accelerated Thrombosis and Atherosclerosis in Mice, American Heart Association Scientific Sessions 2006, Chicago, USA, Nov. 2006.
320.	Masataka Sata : Maintenance of vascular homeostasis by bone marrow-derived progenitors, The 32nd Autumn Congress of Korean Diabetes Association, Gyeongju,Korea, Nov. 2006.
321.	Masataka Sata : Vascular Regeneration Utilizing Somatic Stem Cells and Novel Biomaterials, 6th Taipei vascular molecular biology symposium, Taipei,Taiwan, Aug. 2006.
322.	Masataka Sata : Circulating progenitors contribute to vascular repair and lesion formation, 5th Congress of Asian-Pacific Society of Atherosclerosis and Vascular Disease, Apr. 2006.
323.	Masataka Sata : Bone Marrow-Derived Stem Cells in Vascular Disease, American Heart Association Scientific Sessions 2005, Dallas, Nov. 2005.
324.	Masataka Sata : Do blood cells turn into vessels?, International Cardiovascular Symposium-Clinical Implications of Stem Cells in Cardiovasucular Disease, Taiwan, Sep. 2005.
325.	Masataka Sata : Use of animal models to elucidate the role of stem cells in the cardiovascular system, European Atherosclerosis Society 75th EAS Congress, Czech Republic, Apr. 2005.
326.	Masataka Sata : Smooth muscle stem cells, Swedish National Network for Cardiovascular Research Conclusion Symposium, Sweden,Gotenborg, Nov. 2004.
327.	Masataka Sata : Potential Roles of Circulating Vascular Progenitor Cells in Progression and Remodeling of Atherosclerotic Lesions, The 48th Annual Scientific Session of Korean Society of Circulation, Seoul, Oct. 2004.
328.	Masataka Sata : Circulating progenitors contribute to vascular repair and remodeling, 4th Taipei vascular molecular biology symposium, Taipei, Sep. 2004.
329.	Masataka Sata : Bone marrow-derived progenitor cells participate in the pathogenesis of atherosclerosis, 1st Euregio-Symposium Workshop on Atherosclerosis-Molecular Basis of an Inflammatory Disease, Vaals,Netherlands, Sep. 2003.
330.	Masataka Sata : Bone marrow-derived progenitor cells contribute to vascular repair and atherosclerosis, Annual Spring Conference of the Korean Society of Circulation, Cheju, Apr. 2003.
331.	R Bando, Koji Yamaguchi, Tetsuzo Wakatsuki, Takayuki Ise, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Predictors of late lumen enlargement after drug coated balloon angioplasty for denovo coronary lesions, ACC 2024, Atlanta, Apr. 202.

Proceeding of Domestic Conference:

1.	TAKAHASHI Tomoko, Takeshi Soeki, Kazuki Tezuka, Tomomi Matsuura and Masataka Sata : クライオアブレーションが奏功した心房中隔起源上室頻拍の2例, カテーテルアブレーション関連秋季大会, Oct. 2024.
2.	玉上大暉, 森西啓介, 平良竣也, 野田康裕, 林昌晃, 近田優介, 大藤純, BANDO Ryo, TOMONORI Takahashi, Yutaka Kawabata, Takayuki Ise, Koji Yamaguchi, Tetsuzo Wakatsuki and Masataka Sata : ローターブレーターのドライブシャフトシース破損の検証実験, 第30回日本心血管インターベンション治療学会(CVIT)中国四国地方会 2024年9月7日(土)∼8日(日) 岡山, Sep. 2024.
3.	野田康裕, 森西啓介, 平良竣也, 玉上大暉, 林昌晃, 近田優介, 大藤純, BANDO Ryo, TOMONORI Takahashi, Yutaka Kawabata, Takayuki Ise, Koji Yamaguchi, Tetsuzo Wakatsuki and Masataka Sata : Impella挿入患者の搬送に伴う人員と機器選定に苦慮した一例, 第30回日本心血管インターベンション治療学会(CVIT)中国四国地方会, Sep. 2024.
4.	Yutaka Kawabata, Takayuki Ise, BANDO Ryo, Robert Zheng, TOMONORI Takahashi, Rie Ueno, Koji Yamaguchi, Tetsuzo Wakatsuki and Masataka Sata : 弓部大動脈に高度屈曲を有する外科的大動脈弁置換術後の人工弁機能不全に対して TF-TAVIを施行した1例, 第30回日本心血管インターベンション治療学会(CVIT)中国四国地方会, Sep. 2024.
5.	BANDO Ryo, Koji Yamaguchi, TOMONORI Takahashi, Yutaka Kawabata, Takayuki Ise, Tetsuzo Wakatsuki and Masataka Sata : 高出血リスク患者の急性冠症候群に対して薬剤塗布バルーンで治療を行い遠隔期に冠動脈瘤形成を認めた一例, 第30回日本心血管インターベンション治療学会(CVIT)中国四国地方会, Sep. 2024.
6.	TOMONORI Takahashi, Tetsuzo Wakatsuki, TAKAHASHI Tomoko, BANDO Ryo, Zengu Robahto, Yutaka Kawabata, Rie Ueno, Takayuki Ise, Koji Yamaguchi and Masataka Sata : 弁の石灰化と動脈蛇行の合併はTAVR術後の予後不良因子である:大動脈弁狭窄症患者のサブタイプ解析, 第30回日本心血管インターベンション治療学会(CVIT)中国四国地方会, Sep. 2024.
7.	Koji Yamaguchi, Tetsuzo Wakatsuki, BANDO Ryo, TOMONORI Takahashi, Yutaka Kawabata, Takayuki Ise and Masataka Sata : 高度石灰化病変に対して使用したDrug coated balloonが抜去困難・断裂した一例, 第30回日本心血管インターベンション治療学会(CVIT)中国四国地方会, Sep. 2024.
8.	八木一成, Shusuke Yagi, 相原泰, 松山和男, Masaki Yamamoto, 石田卓也, Hiroto Yoneda, Keisuke Nakanishi, Yasuhiko Nishioka, Masataka Sata and Tetsuya Kitagawa : 一般演題1「末梢動脈1(手技，合併症)」急激に指趾壊疽が進行した1例, 日本血管外科学会中国四国地方会第54回総会, Aug. 2024.
9.	Koji Yamaguchi, Tetsuzo Wakatsuki, BANDO Ryo, TOMONORI Takahashi, Yutaka Kawabata, Takayuki Ise and Masataka Sata : アブレーション後に生じた肺静脈厚土井狭窄病変に対する薬剤塗布バルーン有効2症例, 第32回日本心血管インターベンション治療学会; CVIT 2024, Jul. 2024.
10.	S Kashima, TOMONORI Takahashi, K Nagano, R Bando, Yutaka Kawabata, Takayuki Ise, Koji Yamaguchi, Tetsuzo Wakatsuki and Masataka Sata : Association of High Lipoprotein(a) Levels with Adverse Outcomes in Patients with Stable Angina Undergoing Stentless PCI with Drug-coated balloon, 第32回日本心血管インターベンション治療学会; CVIT 2024, Jul. 2024.
11.	Tomoko Takahashi, Takeshi Soeki, Kazuki Tezuka, Tomomi Matsuura and Masataka Sata : A case of Tetralogy of Fallot in which a 3D sheath was useful for CRT-D system implantation, Jul. 2024.
12.	Masataka Sata : 循環器医としての矜持:心疾患患者の予後改善に向けた動脈硬化のサイエンスと心臓リハビリテーション, 第30回日本心臓リハビリテーション学会学術集会, Jul. 2024.
13.	FUJIMOTO Saori, 古本みゆ, 石井亜由美, 西川幸治, 小河ゆか, 筑後桃子, 橋本脩平, 小笠有加, Muneyuki Kadota, Takayuki Ise, Shusuke Yagi, 鈴木佳子, Masataka Sata and 阪上浩 : 経口補助食品を用いた栄養・水分管理が有効であった冠状動脈バイパス術後の透析患者の一例, 第30回日本心臓リハビリテーション学会学術集会, Jul. 2024.
14.	三浦伸一郎, 嶺井陽, 藤見幹太, 島田和典, 白石裕一, 中村幸志, 有馬久富, 田倉智之, 井澤英夫, 福間長知, Masataka Sata, 大屋祐輔 and 牧田茂 : 高度医療・短期入院時代における急性心筋梗塞患者に対する心臓リハビリテーションの効果, 第30回日本心臓リハビリテーション学会学術集会, Jul. 2024.
15.	古本みゆ, FUJIMOTO Saori, 石井亜由美, 西川幸治, 東條恵, 濱野愛莉沙, 粟田由佳, 西麻希, 山田静恵, Muneyuki Kadota, Takayuki Ise, Shusuke Yagi, Yoshiko Suzuki, Masataka Sata and 阪上浩 : 体組成評価を用いた栄養管理が効果的であった高度肥満合併の若年心不全患者の心臓リハビリの一例, 第30回日本心臓リハビリテーション学会学術集会, Jul. 2024.
16.	Yoshiko Suzuki, FUJIMOTO Saori, 古本みゆ, 石井亜由美, 西川幸治, Muneyuki Kadota, Takayuki Ise, Shusuke Yagi, Masataka Sata and 阪上浩 : 徳島大学病院の心臓リハビリテーションでの栄養管理の取り組み, 第30回日本心臓リハビリテーション学会学術集会, Jul. 2024.
17.	石井亜由美, Takayuki Ise, Muneyuki Kadota, Shusuke Yagi and Masataka Sata : 心リハ専従看護師の役割と他部門連携, 第30回日本心臓リハビリテーション学会学術集会, Jul. 2024.
18.	Takayuki Ise, 石井亜由美, 西川幸治, Muneyuki Kadota, Rie Ueno, Shusuke Yagi, Hirokazu Ohminami, Yutaka Taketani and Masataka Sata : 進歩するSHDに対する治療と心臓リハビリテーション, 第30回日本心臓リハビリテーション学会学術集会, Jul. 2024.
19.	髙坂佳孝, Kenya Kusunose and Masataka Sata : AI技術によるHCM患者のLGE予測精度向上に向けた研究, 第45回日本循環制御医学会総会・学術集会, Jun. 2024.
20.	Tserensonom Munkhtsetseg, Shusuke Yagi, Takayuki Ise, Yutaka Kawabata, Muneyuki Kadota, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 経カテーテル的大動脈弁置換術後血清Lp【a】の上昇は予後不良のリスクファクター, 第45回日本循環制御医学会総会・学術集会, Jun. 2024.
21.	Masataka Sata : 映像でみる動脈硬化の新知見とイメージング技術への応用, 第45回日本循環制御医学会総会・学術集会, Jun. 2024.
22.	Yoshihito Saijyo, Hirotsugu Yamada, Zengu Robahto, TOMONORI Takahashi, BANDO Ryo, TAKAHASHI Tomoko, Tomoya Hara, Muneyuki Kadota, Yutaka Kawabata, Rie Ueno, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki, 笹聡一郎, 滝沢宏光 and Masataka Sata : Mechanical circulatory supportを要した重症がん治療関連心機能障害の1例, 第124回日本循環器学会中国・四国合同地方会, Jun. 2024.
23.	八木一成, Shusuke Yagi, Yoshihito Saijyo, TAKAHASHI Tomoko, Zengu Robahto, BANDO Ryo, TOMONORI Takahashi, Tomoya Hara, Muneyuki Kadota, Yutaka Kawabata, Rie Ueno, Tomomi Matsuura, 伊勢孝之, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, 秦広樹 and 菅野幹雄 : 心室中隔欠損症・感染性心内膜炎を合併した大動脈縮窄証による二次性高血圧症の一例, 第124回日本循環器学会中国・四国合同地方会, Jun. 2024.
24.	Shusuke Yagi, BANDO Ryo, Koji Yamaguchi, Takeshi Soeki, Masashi Akaike, Tetsuzo Wakatsuki and Masataka Sata : 腎血管性高血圧を合併した左室駆出率の保たれた心不全の1例, 第130回日本内科学会四国地方会, Jun. 2024.
25.	Shusuke Yagi, Takeshi Soeki, Masashi Akaike and Masataka Sata : 高血圧患者における塩分摂取量の特徴の検討, 第130回日本内科学会四国地方会, Jun. 2024.
26.	Yoshihito Saijyo, Hirotsugu Yamada, Zengu Robahto, TOMONORI Takahashi, YAMAGUCHI Natsumi, Yukina Hirata, Susumu Nishio and Masataka Sata : AL および TTR アミロイドーシスにおける心エコー所見の相違に関する検討, 第97回日本超音波医学会学術集会, May 2024.
27.	MATSUMOTO Rikizo, Kei Daizumoto, Susumu Nishio, Asami Yuasa, Yukina Hirata, Junya Furukawa and Masataka Sata : ロボット手術後の腎エコー, 第97回日本超音波医学会学術集会, May 2024.
28.	YAMAGUCHI Natsumi, Susumu Nishio, TAKAHASHI Tomoko, NOMURA Yuka, Yukina Hirata, Zengu Robahto, TOMONORI Takahashi, Yoshihito Saijyo, Hirotsugu Yamada and Masataka Sata : 左房内膜肉腫の 1 例, 第97回日本超音波医学会学術集会, May 2024.
29.	Yukina Hirata, NOMURA Yuka, YAMAGUCHI Natsumi, Susumu Nishio, Zengu Robahto, TOMONORI Takahashi, Yoshihito Saijyo, Hirotsugu Yamada, Masataka Sata and Kenya Kusunose : 心臓超音波検査における全自動解析システムによる精度と時間短縮の検証, 第35回日本心エコー図学会学術集会, Apr. 2024.
30.	Yoshihito Saijyo, 楠瀬健也, TOMONORI Takahashi, Hirotsugu Yamada, Masataka Sata, 佐藤希美, Noor Albakaa, 石津智子 and 瀬尾由広 : 経カテーテル的大動脈弁置換術における混合型」大動脈弁疾患の左室形状と予後への影響:多施設共同研究からの知見, 第35回日本心エコー図学会学術集会, Apr. 2024.
31.	Masataka Sata : 心不全のGDMT:診療ガイドライン推奨の心不全治療アップデート, SLENDER CLUB JAPAN2024, Apr. 2024.
32.	BOLLOS CHRISTINE ANNE LEAH LOCSIN, Ryosuke Kasai, Hideki Otsuka, Youichi Otomi, Tomomi Matsuura, Tamaki Otani, BANDOH Takanori, UEKI Yuya, MATSUDA Noritake, 高志智, Shota Azane, Yamato Kunikane, Shoichiro Takao, Shusuke Yagi, Masataka Sata, Hitoshi Ikushima and Masafumi Harada : Ventilation/Perfusion Mismatch in Pulmonary Vein Stenosis After Atrial Fibrillation Ablation, 第268回徳島医学会学術集会, Mar. 2024.
33.	YUKA Nomura, Yukina Hirata, YAMAGUCHI Natsumi, Sae Morita, Susumu Nishio, Zengu Robahto, TOMONORI Takahashi, Yoshihito Saijyo, Hirotsugu Yamada, Masataka Sata and Kenya Kusunose : 心臓超音波検査における全自動解析システムを用いた左室・左房ストレインの計測精度に関する検討, 第88回日本循環器学会学術集会, Mar. 2024.
34.	東邦康智, Yoichiro Hirata and Masataka Sata : Rbm15b is an RNA-Binding Protein that Protects against Adverse Cardiac Remodeling during Pressure Overload, 第88回日本循環器学会学術集会, Mar. 2024.
35.	Masataka Sata : 維持期心臓リハビリテーションに有用な医療者向けガイドブックの作成，複合疾患および回復期・維持期の心臓リハビリテーション:第二期循環器病対策推進基本計画に向けて, 第88回日本循環器学会学術集会, Mar. 2024.
36.	Ryo Bando, Koji Yamaguchi, Tetsuzo Wakatsuki, Yutaka Kawabata, TOMONORI Takahashi, Hayato Orino, Issei Yagi, TOMONORI Takahashi, Zheng Robert, Yoshihito Saijyo, Tomoya Hara, Muneyuki Kadota, Tomomi Matsuura, Takayuki Ise, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Predictors of Late Lumen Enlargement after Drug Coated Balloon Angioplasty for de Novo Coronary Lesions, 第88回日本循環器学会学術集会 JCS2024, Mar. 2024.
37.	Tomoya Hara, Daiju Fukuda and Masataka Sata : Activated Factor X/Protease-activated Receptor-2 Axis Plays a Pivotal Role in Vascular Inflammation and Atherosclerosis, 第88回日本循環器学会学術集会 JCS2024, Mar. 2024.
38.	Bavuu Oyunbileg, Tran Phuong Pham, Daiju Fukuda and Masataka Sata : The Role of STING Signaling in Hyperglycemia-induced Endothelial Dysfunction, 第88回日本循環器学会学術集会 JCS2024, Mar. 2024.
39.	Kumiko Suto, Tomoya Hara, Sachiko Nishimoto, S Kaneyama, Masataka Sata and Daiju Fukuda : Macrophage-Specific DNaseII Deficiency Stimulates Vascular Inflammation and Atherosclerosis, 第88回日本循環器学会学術集会 JCS2024, Mar. 2024.
40.	Yutaka Kawabata, Koji Yamaguchi, Tetsuzo Wakatsuki, TOMONORI Takahashi, BANDO Ryo, Yoshihito Saijyo, Muneyuki Kadota, Tomomi Matsuura, Takayuki Ise, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Microvasculature and Gene Expression in Pericoronary Adipose Tissue According to Coronary Plaque Progression Stage in Fresh Cadavers, 第88回日本循環器学会学術集会, Mar. 2024.
41.	東邦康智, 平田陽一郎 and Masataka Sata : The DEAD-box RNA Helicase Ddx41 Contributes to Adverse Cardiac Remodeling Induced by Pressure Overload through Modulation of RNA Metabolism, 第88回日本循環器学会学術集会, Mar. 2024.
42.	Yoshihito Saijyo, Hirotsugu Yamada, 長野絋平, 折野逸人, 八木一成, TAKAHASHI Tomoko, Zengu Robahto, BANDO Ryo, TOMONORI Takahashi, Tomoya Hara, Muneyuki Kadota, Yutaka Kawabata, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Incremental Value of Relative Apical Sparing Index for Discrimination of Cardiac Amyloidosis Subtypes, 第88回日本循環器学会学術集会, Mar. 2024.
43.	Yukina Hirata, YUKA Nomura, YAMAGUCHI Natsumi, Susumu Nishio, Zengu Robahto, TOMONORI Takahashi, Yoshihito Saijyo, Hirotsugu Yamada, Masataka Sata and Kenya Kusunose : 心臓超音波検査における全自動解析システムの可能性, 第88回日本循環器学会学術集会, Mar. 2024.
44.	M Tserensonom, Shusuke Yagi, Takayuki Ise, Yutaka Kawabata, Muneyuki Kadota, Tomoya Hara, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : High Serum lipoprotein (a) level is a risk factor of poor prognosis after transcatheter aortic valve implantation, 第88回日本循環器学会学術集会 JCS2024, Mar. 2024.
45.	Masataka Sata : 複合疾患および回復期・維持期の心臓リハビリテーション:第二期循環器病対策推進基本計画に向けて, 第88回日本循環器学会学術集会 JCS2024, Mar. 2024.
46.	西川幸治, Takayuki Ise, 石井亜由美, Hirokazu Ohminami, Muneyuki Kadota, Shusuke Yagi and Masataka Sata : 心不全を伴う若年の高度肥満患者に対する心臓リハビリテーションの経験, 日本心臓リハビリテーションン学会第7回四国支部地方会, Mar. 2024.
47.	赤井美佳, Yuka Ueda, 小山美華, 前田高宏, 住友辰次, Yoshihito Saijyo and Masataka Sata : 地域連携により術後心タンポナーデに介入できた1例, 日本心臓リハビリテーション学会第7回四国支部地方会, Mar. 2024.
48.	Masataka Sata : 徳島県循環器病対策推進計画∼心疾患地域連携ネットワークと脳卒中・心臓病等総合支援センター∼, 日本心臓リハビリテーション学会第7回四国支部地方会, Mar. 2024.
49.	南野哲男 and Masataka Sata : 循環器病対策推進基本計画における心臓リハビリテーション, 日本心臓リハビリテーション学会第7回四国支部地方会, Mar. 2024.
50.	Masataka Sata : 維持期心臓リハビリテーションに有用な医療者向けガイドブックの作成，複合疾患および回復期・維持期の心臓リハビリテーション, 第88回日本循環器学会学術集会, Mar. 2024.
51.	Hirokazu Ohminami, KITAMURA Ayano, Masashi Masuda, Takayuki Ise, Shusuke Yagi, Masataka Sata and Yutaka Taketani : 心不全マウスに対する高脂肪食と運動の併用効果，優秀演題アワードセッショ, 日本心臓リハビリテーション学会第7回四国支部地方会, Mar. 2024.
52.	八木一成, Yoshihito Saijyo, 長野絋平, 折野逸人, Naofumi Yoshida, TAKAHASHI Tomoko, Zengu Robahto, BANDO Ryo, TOMONORI Takahashi, Tomoya Hara, Muneyuki Kadota, Yutaka Kawabata, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : ALおよびATTR心アミロイドーシス間のエコー図検査的特徴の相違に関する検討, 第123回日本循環器学会四国支部地方会, Dec. 2023.
53.	國松明日子, Susumu Nishio, Sae Morita, Asami Yuasa, MATSUMOTO Rikizo, Yukina Hirata, 山上紘規 and Masataka Sata : ランレオチド酢酸塩投与中の先端巨大症患者に認めた胆管拡張の1例, 第33回日本超音波医学会四国地方会学術集会, Oct. 2023.
54.	Asami Yuasa, Susumu Nishio, Sae Morita, MATSUMOTO Rikizo, Yukina Hirata, Tomohiro Kagawa, Hirohisa Ogawa, Yoshimi Bando and Masataka Sata : 深部静脈血栓症を契機に発見された子宮内膜症性嚢胞を伴う卵巣甲状腺腫の1例, 第33回日本超音波産学会四国地方会学術集会, Oct. 2023.
55.	MATSUMOTO Rikizo, Susumu Nishio, Sae Morita, Asami Yuasa, Yukina Hirata, Yu Saitou, Tetsu Tomonari, Takeshi Oya, Yoshimi Bando and Masataka Sata : 術前診断が困難であった肝臓原発リンパ管腫の1例, 第33回日本超音波産学会四国地方会学術集会, Oct. 2023.
56.	TOMONORI Takahashi, Shuji Hayashi, YAMAGUCHI Natsumi, Sae Morita, Yukina Hirata, Susumu Nishio, Zengu Robahto, Yoshihito Saijyo, Hirotsugu Yamada and Masataka Sata : 3次元経食道超音波時代におけるランブル疣贅の頻度と形態評価, 第33回日本超音波産学会四国地方会学術集会, Oct. 2023.
57.	Ren Nonaka, Susumu Nishio, Yukina Hirata, YUKA Nomura, YAMAGUCHI Natsumi, Sae Morita, Yoshihito Saijyo, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : RAWデータおよびDICOMデータにおけるストレイン解析の差異に関する検討, 第33回日本超音波産学会四国地方会学術集会, Oct. 2023.
58.	YAMAGUCHI Natsumi, Kenya Kusunose, Muneyuki Kadota, Takayuki Ise, Shusuke Yagi and Masataka Sata : ARNI投与による慢性心不全患者の安静時および運動時心機能に対する影響:負荷エコーを用いた検討, 第27回日本心不全学会学術集会, Oct. 2023.
59.	Yukina Hirata, Kenya Kusunose, YAMAGUCHI Natsumi, Sae Morita, Asami Yuasa, MATSUMOTO Rikizo, Susumu Nishio, Zengu Robahto, TOMONORI Takahashi, Yoshihito Saijyo, Hirotsugu Yamada and Masataka Sata : 上腕動脈における血管柔軟性と性差・加齢との関係 ∼ViewWaveを用いた検討∼, 第71回日本心臓病学会学術集会，2023年9月8日(金)∼10日(日)，東京, Sep. 2023.
60.	石井亜由美, 西川幸治, Muneyuki Kadota, Kenya Kusunose, Shusuke Yagi, Hirokazu Ohminami, 内藤紘一, Yutaka Taketani and Masataka Sata : 情報発信WEB 「リカバルクラブ」を用いた多職種患者教育の取り組み, 第71回日本心臓病学会学術集会，2023年9月8日(金)∼10日(日)，東京, Sep. 2023.
61.	Susumu Nishio, Kenya Kusunose, YUKA Nomura, YAMAGUCHI Natsumi, Asami Yuasa, MATSUMOTO Rikizo, Yukina Hirata, Zheng Robert, TOMONORI Takahashi, Yoshihito Saijyo, Hirotsugu Yamada and Masataka Sata : HFpEFに対する脈波増大指数の影響∼SphygmoCor-XCEL®を用いた検討∼, 第71回日本心臓病学会学術集会, Sep. 2023.
62.	BANDO Ryo, Koji Yamaguchi, Tetsuzo Wakatsuki, Takayuki Ise, Yutaka Kawabata, TOMONORI Takahashi, Zengu Robahto, TAKAHASHI Tomoko, Naofumi Yoshida and Masataka Sata : 薬剤塗布バルーン治療後に認めた遠隔期血管内腔拡大の長期観察, 第29回日本心血管インターヘンション治療学会(CVIT)中国四国地方会, Sep. 2023.
63.	Kohei Nagano, TOMONORI Takahashi, 折野逸人, Keita Ohtani, Yusuke Negishi, 八木一成, Naofumi Yoshida, Zengu Robahto, BANDO Ryo, Yutaka Kawabata, Takayuki Ise, Koji Yamaguchi, Tetsuzo Wakatsuki and Masataka Sata : 高血圧リスク患者に対する薬剤コーティングバルーンを用いたstentless PCI 治療の長期成績, 第29回日本心血管インターヘンション治療学会(CVIT)中国四国地方会, Sep. 2023.
64.	Ryo Bando, Tetsuzo Wakatsuki, Koji Yamaguchi, Yutaka Kawabata, TOMONORI Takahashi, Takayuki Ise and Masataka Sata : Association of coronary plaque characteristics with vasa vasorum and local inflammation of epicardial adipose tissue in fresh cadavers, CVIT2023, Aug. 2023.
65.	Koji Yamaguchi, Tetsuzo Wakatsuki, Ryo Bando, TOMONORI Takahashi, Yutaka Kawabata, Takayuki Ise and Masataka Sata : Limitations of treatment for severely calcified lesions of renal arteries, CVIT2023, Aug. 2023.
66.	Takayuki Ise, 石井亜由美, 西川幸治, 上野理恵, Muneyuki Kadota, Shusuke Yagi, Hirokazu Ohminami, 内藤紘一, Yutaka Taketani and Masataka Sata : 遠隔伴走型心リハ「リカバル」による新たな在宅心リハの取り組み, 第29回日本心臓リハヒリテーション学会学術集会, Jul. 2023.
67.	Hirokazu Ohminami, Ayano KITAMURA, MINA Matsubara, Masashi Masuda, Takayuki Ise, Shusuke Yagi, Masataka Sata and Yutaka Taketani : 動物モデルから探る心リハ栄養としての糖・脂質組成の意義, 第29回日本心臓リハビリテーション学会学術集会, Jul. 2023.
68.	石井亜由美, Takayuki Ise, 西川幸治, Hirokazu Ohminami, Muneyuki Kadota, Shusuke Yagi, Tetsuya Matsuura and Masataka Sata : 心リハ専従看護師としての働き方, 第29回日本心臓リハビリテーション学会学術集会, Jul. 2023.
69.	菅崎幹樹, Shingen Nakamura, 新井慎平, 漆原南実, 寺本継脩, 秦真公人, 井上雄介, Takayuki Nakao, Yasuhiko Nishioka and Masataka Sata : 新規変異BβCys76Pheを伴った低フィブリノゲン血症の1症例, 日本検査血液学会雑誌, Vol.24, S147, Jul. 2023. (Keyword) Fibrinogen 変異先天性低フィブリノーゲン血症(診断) ヒト成人(19∼44) 女
70.	MATSUMOTO Rikizo, Susumu Nishio, Kei Daizumoto, Sae Morita, Asami Yuasa, Yukina Hirata, 山尾雅美, Yu Saitou, Kenya Kusunose, Hirotsugu Yamada, Mitsuo Shimada and Masataka Sata : 後腹膜リンパ節転移を生じたBurned-out testicular tumorの1例, 第48回日本超音波検査学会学術集会, Jun. 2023.
71.	Sae Morita, Susumu Nishio, MATSUMOTO Rikizo, YAMAGUCHI Natsumi, Asami Yuasa, Yukina Hirata, 山尾雅美, Yu Saitou, Kenya Kusunose, Hirotsugu Yamada, Mitsuo Shimada and Masataka Sata : 分枝膵管型IPMNに由来した膵管内乳頭粘液性腺癌の一例, 第48回日本超音波検査学会学術集会, Jun. 2023.
72.	Yukina Hirata, Susumu Nishio, 岩本紗英, YUKA Nomura, YAMAGUCHI Natsumi, Sae Morita, Asami Yuasa, MATSUMOTO Rikizo, 山尾雅美, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 検査経験別にみた2次元および3次元超音波による測定精度の比較, 第48回日本超音波検査学会学術集会, Jun. 2023.
73.	YAMAGUCHI Natsumi, Susumu Nishio, Yukina Hirata, YUKA Nomura, Sae Morita, Asami Yuasa, MATSUMOTO Rikizo, TOMONORI Takahashi, Yoshihito Saijyo, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : コロナウイルス感染後に左室心筋に高度の石灰化をきたした1例, 第48回日本超音波検査学会学術集会, Jun. 2023.
74.	Susumu Nishio, Kenya Kusunose, Yukina Hirata, YAMAGUCHI Natsumi, Zengu Robahto, TOMONORI Takahashi, Hiromitsu Seno, Yoshihito Saijyo, Hirotsugu Yamada and Masataka Sata : マルチモダリティによる心筋ストレイン評価, 第48回日本超音波検査学会学術集会, Jun. 2023.
75.	Hirotsugu Yamada, Kenya Kusunose, Susumu Nishio and Masataka Sata : 卒前・卒後の超音波研修:医師の超音波離れをどうするか．徳島大学病院の卒後研修プログラムにおける超音波研修, 第96回日本超音波医学会学術集会, May 2023.
76.	YAMAGUCHI Natsumi, Hirotsugu Yamada, Muneyuki Kadota, Sae Morita, Yukina Hirata, Susumu Nishio, TOMONORI Takahashi, Yoshihito Saijyo, Kenya Kusunose and Masataka Sata : 心サルコイドーシスとの鑑別に苦慮した巨細胞性心筋炎の1 例, 第96回日本超音波医学会学術集会, May 2023.
77.	Yukina Hirata, Hirotsugu Yamada, YAMAGUCHI Natsumi, Sae Morita, Asami Yuasa, MATSUMOTO Rikizo, 山尾雅美, Susumu Nishio, Kenya Kusunose and Masataka Sata : Point-of-Care の心臓超音波検査(FoCUS)の普及に向けて．当院における技師による簡易エコー(POCUS)の取り組み, 第96回日本超音波医学会学術集, May 2023.
78.	Yukina Hirata, Hirotsugu Yamada, YAMAGUCHI Natsumi, Sae Morita, Susumu Nishio, TOMONORI Takahashi, Yoshihito Saijyo, Kenya Kusunose, Takeshi Soeki and Masataka Sata : マラソンと左房機能:スポーツ後の Cardiac fatigue とは, 96回日本超音波医学会学術集会, May 2023.
79.	Masataka Sata : 生活習慣病として動脈硬化症などの循環器疾患に対するアプローチ, 第66回春季日本歯周病学会学術集会, 80, May 2023.
80.	TOMONORI Takahashi, Kenya Kusunose, 岩野弘幸, 柴山謙太郎, 北井豪, 田中秀和, Hirotsugu Yamada and Masataka Sata : 急性心不全における非侵襲的Forrester分類の臨床的有用性,, 第34回日本心エコー図学会学術集会, Apr. 2023.
81.	TOMONORI Takahashi, Hirotsugu Yamada, 和田靖明, 衣川尚知, 木村靖子, 野坂淳子, 井伊稚佳子, 米山里果, 内海郁恭, Kenya Kusunose and Masataka Sata : 心不全ステージAの糖尿病患者における糖尿病性心筋症とその臨床背景および心エコー図指標に関する検討, 第37回日本心エコー図学会学術集会, Apr. 2023.
82.	Yoshihito Saijyo, Kenya Kusunose, Hirotsugu Yamada, Zengu Robahto, Hiromitsu Seno, TOMONORI Takahashi, Susumu Nishio, Yukina Hirata, Sae Morita, YAMAGUCHI Natsumi and Masataka Sata : 心房細動患者において心機能が左房憩室に与える影響の検討, 第37回日本心エコー図学会学術集会, Apr. 2023.
83.	Zengu Robahto, Muneyuki Kadota, Keita Ohtani, Hayato Orino, Yusuke Negishi, Tomoko Takahashi, Ryo Bando, Hiromitsu Seno, TOMONORI Takahashi, Yoshihito Saijyo, Yutaka Kawabata, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : A Case of Biopsy-Proven Giant Cell Myocarditis, 第37回日本心エコー図学会学術集会, Apr. 2023.
84.	Yukina Hirata, Susumu Nishio, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : ストレイン法を加えると，何がわかりますか?, 第37回日本心エコー図学会学術集会, Apr. 2023.
85.	Yoshihito Saijyo, Kenya Kusunose, Hirotsugu Yamada, Hiromitsu Seno, TOMONORI Takahashi, Zengu Robahto, Susumu Nishio, Yukina Hirata, Sae Morita, YAMAGUCHI Natsumi and Masataka Sata : Mixed aortic valve diseaseにおいて中等度以上の大動脈弁膜症の併存が左室形態および予後に与える影響の検討, 第37回日本心エコー図学会学術集会, Apr. 2023.
86.	Hirotsugu Yamada, Yuichiro Okushi, Kenya Kusunose, Robert Zheng, TOMONORI Takahashi, Yoshihito Saijyo, Susumu Nishio, Yukina Hirata, Takeshi Soeki and Masataka Sata : 乳癌の薬物療法における心エコー図検査を用いた心毒性サーベイランスの有用性, 第37回日本心エコー図学会学術集会, Apr. 2023.
87.	Asami Yuasa, Susumu Nishio, YAMAGUCHI Natsumi, Sae Morita, MATSUMOTO Rikizo, Yukina Hirata, 山尾雅美, Zengu Robahto, Yuichiro Okushi, Hiromitsu Seno, TOMONORI Takahashi, Yoshihito Saijyo, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : ヘルスクロノスを用いた冠動脈狭窄検出の試み, 第8回日本血管不全学会学術集会, Apr. 2023.
88.	Takayuki Ise, 石井亜由美, 西川幸治, Muneyuki Kadota, Shusuke Yagi, Hirokazu Ohminami, Yutaka Taketani and Masataka Sata : 遠隔伴走型心臓リハヒリテーション「リカバル」を用いた新たな取り組み, 日本心臓リハヒリテーション学会第6回四国支部地方会, Mar. 2023.
89.	Ryota Miyamoto, Takayuki Ise, Muneyuki Kadota, Shusuke Yagi, Takaaki Samura, 石井亜由美, 西川幸治 and Masataka Sata : 急性僧帽弁閉鎖不全症に対してImpella 5.5留置下にリハビリを進め，MICS-MVPに繋げた一例, 日本心臓リハヒリテーション学会第6回四国支部地方会, Mar. 2023.
90.	西川幸治, Takayuki Ise, 石井亜由美, Hirokazu Ohminami, Muneyuki Kadota, Shusuke Yagi and Masataka Sata : 心不全を伴う若年の高度肥満患者に対する心臓リハヒリテーションの経験, 日本心臓リハヒリテーション学会第6回四国支部地方会, Mar. 2023.
91.	Yuichiro Okushi, Hiromu Yamazaki, Tetsuzo Wakatsuki and Masataka Sata : Predicting the Efficacy of n-3 Polyunsaturated Fatty Acids for Secondary Prevention of Coronary Artery Disease, 第87回日本循環器学会学術集会, Mar. 2023.
92.	Akihiro Tani, Takeshi Soeki, 小崎裕司, Ken-ichi Aihara and Masataka Sata : Concomitant Sarcopenia and Atrial Fibrillation is Associated with Heart Failure in Elderly Patients, 第87回日本循環器学会学術集会, Mar. 2023.
93.	Susumu Nishio, Kenya Kusunose, Yukina Hirata, YAMAGUCHI Natsumi, Zengu Robahto, TOMONORI Takahashi, Hiromitsu Seno, Yoshihito Saijyo, Hirotsugu Yamada and Masataka Sata : 心エコー図検査における2Dストレイン計測の現状と課題, 第87回日本循環器学会学術集会, Mar. 2023.
94.	Ryo Bando, Tetsuzo Wakatsuki, Koji Yamaguchi, Yutaka Kawabata, Ryota Miyamoto, Zengu Robahto, TOMONORI Takahashi, Yoshihito Saijyo, Rie Ueno, Muneyuki Kadota, Tomoya Hara, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Two-year Outcomes of Drug-coated Balloon-only Strategy for De Novo Lesions in Large Coronary Vessels, 第87回日本循環器学会学術集会, Mar. 2023.
95.	Yoshihito Saijyo, Yuichiro Okushi, Kenya Kusunose, Hirotsugu Yamada, Zengu Robahto, TOMONORI Takahashi, Hiromitsu Seno, Susumu Nishio, Rie Ueno, Muneyuki Kadota, Tomoya Hara, Yutaka Kawabata, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Utility of Periodic Echocardiographic Surveillance for Early Detection of Cardiac Dysfunction from Chemotherapy in Breast Cancer Patients, 第87回日本循環器学会学術集会, Mar. 2023.
96.	Yutaka Kawabata, Tetsuzo Wakatsuki, Koji Yamaguchi, BANDO Ryo, Yoshihito Saijyo, Rie Ueno, Muneyuki Kadota, Tomoya Hara, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : The Impact of Coronary Plaque Progression Stage on Coronary Neovascularization Structures in Fresh Cadavers, 第87回日本循環器学会学術集会, Mar. 2023.
97.	Takayuki Ise, Shusuke Yagi, Rie Ueno, Muneyuki Kadota, Keita Ohtani, Yusuke Negishi, Ryota Miyamoto, BANDO Ryo, Zengu Robahto, Hiromitsu Seno, TOMONORI Takahashi, Yutaka Kawabata, Yoshihito Saijyo, Tomomi Matsuura, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Novel Home-based Cardiac Telerehabilitation System Using a Wearable Device and a Web Application, 第87回日本循環器学会学術集会, Mar. 2023.
98.	Shusuke Yagi and Masataka Sata : Epicardial Adipose Tissue as a Novel Target of Pemafibrate in Preventing Cardiovascular Disease through Reduction of Triglyceride and Oxidative Stress, 第87回日本循環器学会学術集会, Mar. 2023.
99.	S Yamaguchi, M Maeda, K Ohba, M Glinu, O Arasaki, Shusuke Yagi, Kenya Kusunose, Takeshi Soeki, Hirotsugu Yamada, Daiju Fukuda, H Masuzaki, Masataka Sata and Michio Shimabukuro : Sex Differences in the Association between Epicardial Adipose Tissue Volume and Left Atrial Volume Index, 第87回日本循環器学会学術集会, Mar. 2023.
100.	Hirokazu Ohminami, 北村彩乃, 松原未奈, Masashi Masuda, Takayuki Ise, Shusuke Yagi, Masataka Sata and Yutaka Taketani : 動物モデルから探る病期別心リハ栄養の可能性, 第12回日本リハビリテーション栄養学会学術集会, Jan. 2023.
101.	北村彩乃, Hirokazu Ohminami, 松原未奈, Masashi Masuda, Takayuki Ise, Shusuke Yagi, Masataka Sata and Yutaka Taketani : 高脂肪食が心不全マウスの骨格筋エネルギー代謝に及ぼす影響, 第26回日本病態栄養学会年次学術集会, Jan. 2023.
102.	Kenya Kusunose, Tetsuzo Wakatsuki and Masataka Sata : 心エコー図法におけるAI医療の現状と未来像, 第33回日本心血管画像動態学会, Jan. 2023.
103.	Masataka Sata : 地域で取り組む循環器病対策, 第121回日本循環器学会四国地方会, Dec. 2022.
104.	吉田知哉, Takayuki Ise, 宮本亮太, BANDO Ryo, Zengu Robahto, Hiromitsu Seno, Tomonori Takahashi, Yutaka Kawabata, Tomomi Matsuura, Yoshihito Saijyo, Muneyuki Kadota, Kenya Kusunose, Takeshi Soeki, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki, 飯間努, 山本浩史 and Masataka Sata : 劇症型心筋炎に対してECPELLA導入で救命しえた症例, 第121回日本循環器学会四国地方会, Dec. 2022.
105.	Tomonori Takahashi, Kenya Kusunose, Zheng Robert, Seno Hiromitsu, Yoshihito Saijyo, Muneyuki Kadota, Yutaka Kawabata, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心房細動患者におけるイソプロテレノール負荷経食堂心エコー図法の有用性, 第121回日本循環器学会四国地方, Dec. 2022.
106.	YUKA Nomura, Susumu Nishio, Yukina Hirata, 山尾雅美, YAMAGUCHI Natsumi, Sae Morita, Yoshihito Saijyo, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : RAW data と DICOM data で計測した左室長軸方向ストレイン値の差異, 第32回日本超音波医学会四国地方会学術集会, Oct. 2022.
107.	Sae Morita, Susumu Nishio, Asami Yuasa, 松本力三, Yukina Hirata, 山尾雅美, Kenya Kusunose, Hirotsugu Yamada, 菅野幹雄 and Masataka Sata : 無症状で経過した VSD 合併バルサルバ洞動脈瘤破裂の一例, 第32回日本超音波医学会四国地方会学術集会, Oct. 2022.
108.	Natsumi Yamaguchi, 山尾雅美, 奥村和正, Yukina Hirata, Susumu Nishio, 乾友浩, 笹聡一郎, 青山万理子, 井上寛章 and Masataka Sata : 経過観察に超音波検査が有用であった乳腺結核疑いの 1 例, 第32回日本超音波医学会四国地方会学術集会, Oct. 2022.
109.	松本力三, Susumu Nishio, Sae Morita, Asami Yuasa, Yukina Hirata, 山尾雅美, 田中貴大, 岡田泰行 and Masataka Sata : 多発膵嚢胞を契機に診断された von Hippel-Lindau 病の 1 例, 第32回日本超音波医学会四国地方会学術集会, Oct. 2022.
110.	折野逸人, Yoshihito Saijyo, Kenya Kusunose, Zengu Robahto, Tomonori Takahashi, Hiromitsu Seno, 山尾雅美, Susumu Nishio, Hirotsugu Yamada and Masataka Sata : 心房細動患者における左房憩室の頻度および形態学的特徴に関する検討, 第32回日本超音波医学会四国地方会学術集会, Oct. 2022.
111.	Masataka Sata : Ischemia Study 私の解釈, Slender Club Japan, Live Demonstration &Annual Meeting 2022 in Tokyo, Oct. 2022.
112.	吉田知哉, Tetsuzo Wakatsuki, 山木浩二, Yoshihito Saijyo, Yutaka Kawabata, Takayuki Ise, Kenya Kusunose, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : 冠動脈入口部および鎖骨下動脈に特徴的な血管内超音波所見を認めた高安動脈炎の2例, 第70回日本心臓病学会学術集会, Sep. 2022.
113.	Takayuki Ise, 内藤紘一, 佐藤聡見, 小野慎太郎, 石井亜由美, 西川幸治, Muneyuki Kadota, Shusuke Yagi and Masataka Sata : ウェアラブルデバイスとコミュニケーションアプリを用いた遠隔伴走型心リハシステムの開発, 第70回日本心臓病学会学術集会, Sep. 2022.
114.	Yuichiroh Ohkushi, Kenya Kusunose, Hiromitsu Seno, Tomonori Takahashi, Yoshihito Saijyo, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心エコー検査によるサーベイランスのがん治療関連心筋障害への影響, 第5回日本腫瘍循環器学会学術集会, Sep. 2022.
115.	Masataka Sata : 心血管イベント抑制に向けた脂質栄養学, 日本脂質栄養学会第31回大会, Sep. 2022.
116.	Tomonori Takahashi, Koji Yamaguchi, Tetsuzo Wakatsuki, 宮本亮太, 坂東遼, Yutaka Kawabata, Takayuki Ise and Masataka Sata : 腫瘍塞栓が疑われた肺動脈塞栓症に対して下大静脈フィルターを腎静脈上部へ長期留置し得た1例, 第28回日本心血管インターベンション治療学会(CVIT)中国四国地方会, Sep. 2022.
117.	BANDO Ryo, Tetsuzo Wakatsuki, Yutaka Kawabata, Koji Yamaguchi, 宮本亮太, Tomonori Takahashi, Takayuki Ise and Masataka Sata : 未個体遺体における冠動脈Lipid-richプラークと外膜vasa vasorumおよび局所心臓周囲脂肪の関連性の検討, 第28回日本心血管インターベンション治療学会(CVIT)中国四国地方会, Sep. 2022.
118.	松崎慶仁, Yoshihito Saijyo, Takayuki Ise, 太田啓太, 折野逸人, 吉田知哉, 根岸佑典, 宮本亮太, 坂東遼, Rovert Zheng, Hiromitsu Seno, Tomonori Takahashi, Rie Ueno, Muneyuki Kadota, Tomoya Hara, Yutaka Kawabata, Tomomi Matsuura, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 急性A型大動脈解離をきたしたMarfan症候群の一例, 第265回徳島県医学学術集会, Jul. 2022.
119.	Yusuke Negishi, Muneyuki Kadota, Koji Yamaguchi, Hirotsugu Yamada, 折野逸人, 太田啓太, 吉田知哉, 宮本亮太, BANDO Ryo, Zheng Rovert, Hiromitsu Seno, Tomonori Takahashi, Yoshihito Saijyo, Rie Ueno, Tomoya Hara, Yutaka Kawabata, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki, 田蒔昌憲 and Masataka Sata : 腎動脈拡張術により心不全の著名な改善を認めたCardiac Disturbance syndrome の1例, 第265回徳島県医学学術集会, Jul. 2022.
120.	Kenya Kusunose, Tetsuzo Wakatsuki and Masataka Sata : AI画像診断技術を用いた心筋梗塞の診断, 第30回日本心血管インターベンション治療学会学術集会, Jul. 2022.
121.	Koji Yamaguchi, Tetsuzo Wakatsuki, TOMONORI Takahashi, Yutaka Kawabata, Takayuki Ise and Masataka Sata : The impact of polymer duration on local coagulative responses following drug-eluting stent implantation, 第30回日本心血管インターベンション治療学会学術集会, Jul. 2022.
122.	Shusuke Yagi, Takayuki Ise, Muneyuki Kadota, Yutaka Kawabata, Tomoya Hara, Rie Ueno, Yoshihito Saijyo, Tomomi Matsuura, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : パンデミック下の臨床実習におけるオンライン医学教育の実際と問題点, 第265回徳島県医学学術集会, Jun. 2022.
123.	北村彩乃, Hirokazu Ohminami, Masashi Masuda, Hisami Okumura, Takayuki Ise, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Masataka Sata and Yutaka Taketani : 運動介入中の脂質摂取の違いが心不全マウスの病態に及ぼす影響, 第28回日本心臓リハビリテーション学会学術集会, Jun. 2022.
124.	石井亜由美, Muneyuki Kadota, 西川幸治, 大南博和, Takayuki Ise, Shusuke Yagi and Masataka Sata : 外来心リハ患者に対するアンケート調査から, Jun. 2022.
125.	西川幸治, Takayuki Ise, 石井亜由美, 大南博和, Muneyuki Kadota, Shusuke Yagi and Masataka Sata : コロナ禍における外来心リハ患者の体重変化と健康意識調査, 第28回日本心臓リハビリテーション学術集会, Jun. 2022.
126.	Takayuki Ise, 内藤紘一, 佐藤聡見, 小野慎太郎, 石井亜由美, 西川幸治, Muneyuki Kadota, Shusuke Yagi and Masataka Sata : ウェアラブルデバイスとコミュニケーションアプリを用いた遠隔伴走型心リハシステムの開発, 第28回日本心臓リハビリテーション学術集会, Jun. 2022.
127.	Takayuki Ise, 石井亜由美, 西川幸治, Muneyuki Kadota, Shusuke Yagi, Hirotsugu Yamada, 竹谷豊 and Masataka Sata : Withコロナに対応した心リハオンライン臨床実習システムの構築, 第28回日本心臓リハビリテーション学術集会, Jun. 2022.
128.	林昌晃, Takeshi Soeki, 玉上大暉, 野田康裕, 森西啓介, 近田優介, Kazuhisa Matsumoto, Tomomi Matsuura, 大西芳明 and Masataka Sata : 心房細動アズレーション時の鎮静不安定化に寄与する因子の検討, 第68回日本不整脈心電学会学術大会, Jun. 2022.
129.	Masataka Sata : 心不全治療フォーカスアップデート, 第66回四国支部生涯教育講演会, Jun. 2022.
130.	Rikako Takahashi, Muneyuki Kadota, Takayuki Ise, Yoshihito Saijyo, Yutaka Kawabata, Tomomi Matsuura, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 免疫抑制療法の導入により心機能が劇的に改善した巨細胞性心筋炎の一例, 第120回日本循環器学会中国・四国合同地方会, May 2022.
131.	Muneyuki Kadota, Kenya Kusunose, Shusuke Yagi, Yutaka Kawabata, Yoshihito Saijyo, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 慢性心不全におけるサクビトリル / バルサルタンのナトリウム利尿ペプチドに対する急性反応の検討, 第120回日本循環器学会中国・四国合同地方会, May 2022.
132.	Susumu Nishio, Kei Daizumoto, Yukina Hirata, 松本力三, Asami Yuasa, Sae Morita, YAMAGUCHI Natsumi, 山尾雅美, 高橋正幸 and Masataka Sata : 造影超音波検査による術前シミュレーションが有用であったパラガングリオーマの 1 例, 日本超音波医学会第95回学術集会, May 2022.
133.	KOSAKA Yoshitaka, Kenya Kusunose, 芳賀昭宏, YAMAGUCHI Natsumi, 竹田泰治, 田中秀和, 三宅誠, 森内健史, Hirotsugu Yamada and Masataka Sata : 人工知能による左室駆出率予測モデルの施設間差についての検討, 日本超音波医学会第95回学術集会, May 2022.
134.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 心毒性を有する薬物投与時の心機能評価, 日本超音波医学会第95回学術集会, May 2022.
135.	Yoshihito Saijyo, Hirotsugu Yamada, Kenya Kusunose, Hiromitsu Seno, Tomonori Takahashi, YAMAGUCHI Natsumi, Sae Morita, Yukina Hirata, Susumu Nishio and Masataka Sata : 心エコー図検査を用いたがん治療関連心機能障害サーベイランス, 日本超音波医学会第95回学術集会, May 2022.
136.	楠瀬賢也, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 大動脈弁閉鎖不全症の評価法, 第32回日本心血管画像動態学会, May 2022.
137.	Munkhtsetseg Tserensonom, Shusuke Yagi, Takayuki Ise, Daiju Fukuda, Muneyuki Kadota, Yutaka Kawabata, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 動脈硬化性疾患の高リスク患者において大動脈弁の石灰化と血清リポ蛋白との関連, 第9回日本心血管脳卒中学会学術集会, Apr. 2022.
138.	Uugantsetseg Munkhjargal, Daiju Fukuda and Masataka Sata : Esaxerenone, attenuates vascular dysfunction in diabetic C57BL/6 mice, 第9回日本心血管脳卒中学会学術集会, Apr. 2022.
139.	Shusuke Yagi, Oyunbileg Bavuu, Daiju Fukuda and Masataka Sata : The novel non-steroidal mineralocorticoid receptor blocker esaxerenoneameliorates insulin resistance, 第9回日本心血管脳卒中学会学術集会, Apr. 2022.
140.	Takeshi Soeki, Daiju Fukuda and Masataka Sata : 動脈効果の炎症性バイオマーカーの探求, 第7回日本血管不全学会, Apr. 2022.
141.	Masataka Sata : 心臓脂肪蓄積と冠動脈硬化, 第42回日本肥満学会, Mar. 2022.
142.	Y Saijo, Kenya Kusunose, Yuichiro Okushi, Hirotsugu Yamada and Masataka Sata : Predictive Value of Speckle Tracking Echocardiography for Cancer Therapy Related Cardiac Dysfunction, 第86回日本循環器学会学術集会, Mar. 2022.
143.	Y Okushi, Kenya Kusunose, Zheng Robert, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Findings from the JROAD-DPC Registry across 6 Studies Conducted in a Year, 第86回日本循環器学術集会, Mar. 2022.
144.	Bavuu Oyunbileg, Daiju Fukuda and Masataka Sata : Esaxerenone, a Selective Mineralocorticoid Receptor Blocker, Improves Insulin Sensitivity in High Fat-fed C57BL/6 Mice, 第86回日本循環器学会学術集会, Mar. 2022.
145.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : Artificial Intelligence in Echocardiography, Special Session12 Artificial Intelligence in Cardiology, 第86回日本循環器学会学術集会, Mar. 2022.
146.	Yutaka Kawabata, Tetsuzo Wakatsuki, Koji Yamaguchi, Daiju Fukuda, Yoshihito Saijyo, Muneyuki Kadota, Tomomi Matsuura, 伊勢孝之, Kenya Kusunose, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : First Assessment of Coronary Plaque Vulnerability and Lipid Core Burden Assessed by Near-Infrared Spectroscopy-Intravascular Ultrasound in a Fresh Cadaver, 第86回日本循環器学会学術集会, Mar. 2022.
147.	Daiju Fukuda and Masataka Sata : The Innate Immune System: A Possible Link between Lifestyle-related Diseases and Atherosclerosis, 第86回日本循環器学会学術集会, Mar. 2022.
148.	Munkhjargal Uugantsetseg, Daiju Fukuda and Masataka Sata : A Selective Mineralocorticoid Receptor Blocker, Esaxerenone, 第86回日本循環器学会学術集会, Mar. 2022.
149.	YAMAGUCHI Natsumi, Kenya Kusunose, Akihiro Haga, Yukina Hirata, Susumu Nishio, Hirotsugu Yamada and Masataka Sata : 人工知能を用いた左室壁運動異常の検出, 第86回日本循環器学会学術集会, Mar. 2022.
150.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : Clinical Utility of Stress Echocardiography in Pulmonary Hypertension, 第86回日本循環器学会学術集会, Mar. 2022.
151.	Tserensonom Munkhtsetseg, Shusuke Yagi and Masataka Sata : The Association of Lp(a) with Aortic Calcium Score in Patients with High Risk of Atherosclerotic Disease, 第86回日本循環器学会学術集会, Mar. 2022.
152.	Tomonori Takahasi, Kenya Kusunose, Yukina Hirata, Susumu Nisio, Yuichiro Okushi, Hiromitsu Seno, Y Saijo, Muneyuki Kadota, Yutaka Kawabata, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Cardiovascular Risk Factors Associated with Left Ventricular Strain Distribution in Patients without Known Cardiovascular Disease, 第86回日本循環器学会学術集会, Mar. 2022.
153.	Hirata Yukina, Kenya Kusunose, 辻拓将, 古徳純一, Susumu Nishio, Hirotsugu Yamada and Masataka Sata : 胸部X線画像に人工知能を組み合わせた肺高血圧の検出∼今後の展望と課題点について∼, 第86回日本循環器学会学術集会, Mar. 2022.
154.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : Potential of AI-based Echocardiographic Analysis and Quantification in Clinical Practice, 第86回日本循環器学会学術集会, Mar. 2022.
155.	Hirata Yukina, Susumu Nishio, 中尾隆之, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : SGLT-2阻害薬が心機能へ与える効果と心外膜下脂肪厚軽減との関連, 第18回日本臨床検査医学合同地方会, Feb. 2022.
156.	Tomoko Kawanishi, 河野裕美, 坂東典子, Yoko Kagawa, 谷美紀, 平岡葉月, 中尾隆之, Yasuhiko Nishioka, Masataka Sata and 谷口浩一郎 : α波の出現部位がPSG検査の睡眠ステージ判定に有用であった1症例, 第18回日本臨床検査医学合同地方会, Feb. 2022.
157.	Akira Hatakeyama, Masashi Miyoshi, 中尾隆之 and Masataka Sata : フェリチン測定試薬FER-ラテックススRX「生研」の性能評価, 第18回日本臨床検査医学合同地方会, Feb. 2022.
158.	Minami Urushihara, Keisuke Teramoto, 秦真公人, 菅崎幹樹, 中尾隆之, Yasuhiko Nishioka and Masataka Sata : 自動分析装置による幼若血小板比率の検討, 第18回日本臨床検査医学合同地方会, Feb. 2022.
159.	Ayano Kitamura, Hirokazu Ohminami, Masashi Masuda, Hisami Okumura, Takayuki Ise, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Masataka Sata and Yutaka Taketani : 運動および栄養介入が心不全マウスの病態に及ぼす影響, 日本心臓リハビリテーション学会第 5 回四国支部地方会, Jan. 2022.
160.	Muneyuki Kadota, 石井亜由美, Takayuki Ise, 西川幸治, Shusuke Yagi, 大南博和, 竹谷豊 and Masataka Sata : 当院における末期心不全に患者に対する緩和ケアの取り組み, 日本心臓リハビリテーション学会第5回四国支部地方会, Jan. 2022.
161.	石井亜由美, Muneyuki Kadota, 西川幸治, 大南博和, Takayuki Ise, Shusuke Yagi and Masataka Sata : 外来心リハ患者に対するACPアンケート調査から, 日本心臓リハビリテーション学会第5回四国支部地方会, Jan. 2022.
162.	西川幸治, Takayuki Ise, 石井亜由美, 大南博和, Muneyuki Kadota, Shusuke Yagi and Masataka Sata : 心リハ研修施設としての活動報告, 日本心臓リハビリテーション学会第5回四国支部地方会, Jan. 2022.
163.	Takayuki Ise, 石井亜由美, 西川幸治, Muneyuki Kadota, Shusuke Yagi, 大南博和, 竹谷豊 and Masataka Sata : Withコロナに対応したオンライン臨床実習システムの構築, 日本心臓リハビリテーション学会第5回四国支部地方会, Jan. 2022.
164.	Munkhtsetseg Tserensonom, Shusuke Yagi and Masataka Sata : 動脈硬化性疾患の高リスク患者において大動脈弁の石灰化と血清リポ蛋白との関連, 第33回日本老年医学会四国地方会, Jan. 2022.
165.	Munkhjargal uugantsettseg, Daiju Fukuda and Masataka Sata : A selective mineralocorticoid receptor antagonist,esaxerenone,sttenuates vascular function and atherosclerosis, 第33回日本老年医学会四国地方会, Jan. 2022.
166.	Bavuu Oyunbileg, Daiju Fukuda and Masataka Sata : A selective mineralocorticoid receptor blocker,esaxerenone,improves insulin sensitivity in diet induced obese mice, 第33回日本老年医学会四国地方会, Jan. 2022.
167.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : ポータブル心エコー機器の AI による進化, POP超音波研究会, Jan. 2022.
168.	Masataka Sata : 生活習慣病における動脈硬化での血管外膜ならびに心外膜脂肪の役割, 第57回高血圧関連疾患モデル学会学術総会, Dec. 2021.
169.	Yoshihito Saijyo, Takaaki Samura, Tomoko Takahashi, Yuichiroh Ohkushi, Hiromitsu Seno, 高橋智紀, Muneyuki Kadota, Yutaka Kawabata, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Hiroki Hata and Masataka Sata : 滲出性収縮性心膜炎の1例, 第119回日本循環器学会四国地方会, Dec. 2021.
170.	Kumiko Suto, Daiju Fukuda, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : マクロファージ特異的DNaseII欠損が動脈硬化に与える影響, 第119回日本循環器学会四国地方会, Dec. 2021.
171.	Yuichiroh Ohkushi, Kenya Kusunose, Yoshihito Saijyo, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心エコー検査によるがん治療関連心筋障害サーベイランスの有効性, 第119回日本循環器学会四国地方会, Dec. 2021.
172.	Yukako Honma, Yasunobu Hayabuchi, Takeshi Tobiume, Masataka Sata, 中島博 and 相庭武司 : S-ICD植え込みを施行したQT延長症候群の5歳男児例, 第25回日本小児心電学会学術集会, Nov. 2021.
173.	Daiju Fukuda, Pham Tran Phuong and Masataka Sata : Stimulator of interferon genesは血管の炎症と動脈硬化を促進する, 第53回日本動脈硬化学会総会・学術集会, Oct. 2021.
174.	Masataka Sata : 高血圧診療に無侵襲診断がどこまで必要か, 第53回日本動脈硬化学会総会・学術集会, Oct. 2021.
175.	Masataka Sata : 下肢虚血後の血管新生における自然免疫の役割, 第53回日本動脈硬化学会総会・学術集会, Oct. 2021.
176.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 循環器領域の AI 開発∼ Radiomics in Echocardiography ∼, 日本超音波医学会第48回関西地方学術集会, Oct. 2021.
177.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 人工知能(AI)による心エコー診断の進歩, 第69回日本心臓病学会学術集会, Sep. 2021.
178.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : Implementation of artificial intelligence assessment in echocardiography ACC-JCC Joint Symposium Artificial Intelligence Approach for Cardiovascular Imaging Diagnostics, 第69回日本心臓病学会学術集会, Sep. 2021.
179.	Yutaka Kawabata, Tetsuzo Wakatsuki, Koji Yamaguchi, Muneyuki Kadota, Takayuki Ise, Kenya Kusunose, Tomomi Matsuura, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : 冠動脈塞栓症を発症した2症例の臨床的検討, 第69回日本心臓病学会学術集会, Sep. 2021.
180.	Kenya Kusunose, Yuichiroh Ohkushi, Hirotsugu Yamada and Masataka Sata : 静脈血栓塞栓症における癌および経口抗凝固薬の予後に対する影響, 第69回日本心臓病学会学術集会, Sep. 2021.
181.	Takayuki Ise, Yutaka Kawabata, Tomonori Takahashi, Koji Yamaguchi, Daiju Fukuda, Tetsuzo Wakatsuki, Takaaki Samura, Eiki Fujimoto, Hiroki Hata and Masataka Sata : アクセス困難症例に対し，右鎖骨下動脈アプローチでTAVI施行した1例, 第27回日本心血管インターベンション治療学会(CVIT)中国四国地方会, Sep. 2021.
182.	Yutaka Kawabata, Tetsuzo Wakatsuki, Koji Yamaguchi, Tomonori Takahashi, Takayuki Ise, Daiju Fukuda and Masataka Sata : 回旋枝入口部線維製性プラークに対してOASを用いstentess PCIを施行で来た1例, 第27回日本心血管インターベンション治療学会(CVIT)中国四国地方会, Sep. 2021.
183.	Takayuki Ise, Yutaka Kawabata, Tomonori Takahashi, Koji Yamaguchi, Daiju Fukuda, Tetsuzo Wakatsuki and Masataka Sata : Withコロナに対した心臓カテーテルオンライン臨床実習システムの構築, 第27回日本心血管インターベンション治療学会(CVIT)中国四国地方会, Sep. 2021.
184.	Rei Mizobuchi, Hironori Tanaka, Naoya Tani, Kazuyoshi Noda, Takahiro Tanaka, Tetsu Tomonari, Tatsuya Taniguchi, Tomomi Matsuura, Masataka Sata and Tetsuji Takayama : 超音波観察を併用することで安全に治療した高度腎機能低下を合併した猪瀬型肝性脳症の1例, 第263回徳島医学会学術集会, Aug. 2021.
185.	Tomoya Yoshida, Hiromitsu Seno, Kazuhisa Matsumoto, Tomomi Matsuura, Yoshihito Saijyo, Muneyuki Kadota, Yutaka Kawabata, Kenya Kusunose, Takayuki Ise, Takeshi Soeki, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki, 多田恵曜 and Masataka Sata : ペースメーカー植え込み後に発覚した側頭葉てんかんによる発作性心静止の一例, 第263回徳島医学会学術集会, Aug. 2021.
186.	M Tserensonom, Shusuke Yagi, Takayuki Ise, Muneyuki Kadota, Yutaka Kawabata, Yoshihito Saijyo, Tomomi Matsuura, Kenya Kusunose, Koji Yamaguchi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 動脈硬化性疾患の高リスク患者において大動脈弁の石灰化と血清リポ蛋白との関連, 第263回徳島医学会学術集会, Aug. 2021.
187.	M Uugantsetseg, Daiju Fukuda and Masataka Sata : A selectiv mineralocorticoid receptor blocker, esaxerenone, attenuates vascular dystunction and atherosclerosis in apoliporotein E-deficient mice, 第263回徳島医学会学術集会, Aug. 2021.
188.	B Oyunbileg, Daiju Fukuda and Masataka Sata : Metabolic effects of a selective mineralocorticoid receptor blocker, esaxerenone, in obese mine, 第263回徳島医学会学術集会, Aug. 2021.
189.	Masataka Sata : 徳島県循環器病対策推進計画, 第263回徳島医学会学術集会, Aug. 2021.
190.	Kazuki Tezuka, Tomonori Takahashi, Yoshihito Saijyo, Yutaka Kawabata, Muneyuki Kadota, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Takaaki Samura, Hiroki Hata and Masataka Sata : ポスタ-セッション左冠動脈主幹部の急性冠症候群の2症例, 第263回徳島医学会学術集会(令和3年度夏期), Aug. 2021.
191.	Takayuki Ise, Muneyuki Kadota, Yutaka Kawabata, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Takaaki Samura, Eiki Fujimoto, Hiroki Hata and Masataka Sata : 合同シンポジウムカテ-テル大動脈弁置換術(TAVI)によって激変した大動脈弁狭窄症治療, 第263回徳島医学会学術集会(令和3年度夏期), Aug. 2021.
192.	Bavuu Oyunbileg, Daiju Fukuda and Masataka Sata : Metabolic effects of a selective mineralocorticoid receptor blocker, esaxerenone,in obese mice, 第11回日本脳血管・認知症学会総会, Aug. 2021.
193.	Munkhjargal Ungantsetseg, Daiju Fukuda and Masataka Sata : Esaxerenone attenuates vascular dysfunction and atherosclerosis in apolipoprotein E-deficient mice, 第11回日本脳血管・認知症学会総会, Aug. 2021.
194.	Takayuki Ise, 石井亜由美, 西川幸治, Muneyuki Kadota, 鈴木佳子, Hirokazu Ohminami, Shusuke Yagi and Masataka Sata : 大動脈狭窄症に対するTAVI後認知機能の変化, 第11回日本脳血管・認知症学会総会, Aug. 2021.
195.	Takayuki Ise, Yutaka Kawabata, Tomonori Takahashi, Koji Yamaguchi, Daiju Fukuda, Tetsuzo Wakatsuki, Takaaki Samura, Eiki Fujimoto, Hiroki Hata and Masataka Sata : TAVI術中に上行大動脈解離を合併し，PCIと自己拡張型TAVI弁留置によってbailoutできた症例, 第27回日本心血管インターベンション治療学会(CVIT)中国四国地方会, Aug. 2021.
196.	Takeshi Soeki, Daiju Fukuda, Tomomi Matsuura, Takeshi Tobiume, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Toll-Like Receptor 9 Is a Novel Therapeutic Target to Prevent Atrial Fibrillation, JHRS2021 第67回日本不整脈心電学会学術大会, Jul. 2021.
197.	山尾雅美, 山口夏美, 松本麻依, 平田有紀奈, 西尾進, Tomohiro Inui, Soichiroh Sasa, Mariko Aoyama, Hiroaki Inoue, Kazumasa Okumura, Hiroaki Toba, Takeshi Oya, Yoshimi Bando, Masataka Sata and Akira Tangoku : 硬化性腺症を背景に発生した悪性葉状腫瘍の1例, 第29回日本乳癌学会学術総会(ハイブリッド開催), Jul. 2021.
198.	Tomomi Matsuura, Takeshi Soeki, Kazuhisa Matsumoto, Takeshi Tobiume and Masataka Sata : Efficacy and Clinical Significance of Additional Left Atrial Posterior Wall Isolation in Patients with Persistent Atrial Fibrillation, 第67回日本不整脈心電学会学術大会, Jul. 2021.
199.	Hirokazu Ohminami, Ayano Kitamura, Miku Yamaguchi, Masaki Takikawa, Kohta Ohnishi, Masashi Masuda, Hisami Okumura, Takayuki Ise, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Masataka Sata and Yutaka Taketani : 心不全マウスを用いた心リハ評価系の確立, 第27回日本心臓リハビテーション学会, Jun. 2021.
200.	西川幸治, Takayuki Ise, 石井亜由美, 鈴木佳子, 大南博和, Muneyuki Kadota, Shusuke Yagi, 加藤真介 and Masataka Sata : AVI患者におけるADLスコア(FIM)の変化, 第27回日本心臓リハビリテーション学会学術集会, Jun. 2021.
201.	石井亜由美, Takayuki Ise, 西川幸治, 鈴木佳子, 大南博和, Muneyuki Kadota, Shusuke Yagi, 加藤真介 and Masataka Sata : 外来心臓リハビリテーション通院に関する患者の意識調査, 第 27 回日本心臓リハビリテーション学会学術集会, Jun. 2021.
202.	西川幸治, Takayuki Ise, 石井亜由美, 鈴木佳子, 大南博和, Muneyuki Kadota, Shusuke Yagi, 加藤真介 and Masataka Sata : TAVI患者におけるADLスコア(FIM)の変化, 第 27 回日本心臓リハビリテーション学会学術集会, Jun. 2021.
203.	Seno Hiromitsu, Koji Yamaguchi, Kenya Kusunose, Hirotsugu Yamada, Tetsuzo Wakatsuki, Takeshi Soeki, Masataka Sata, 佐村高明, 秦広樹 and 大豆本圭 : 広範な心嚢腔内進展を認めた心臓腫瘍の一例, 第116回第118回日本循環器学会中国・四国合同地方会, Jun. 2021.
204.	Akihiro Tani, Shusuke Yagi, Muneyuki Kadota, Yutaka Kawabata, Tomomi Matsuura, Kenya Kusunose, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 肺動脈性肺高血圧症に対する静注プロスタグランジン投与で高心拍出を呈した症例, 第116回第118回日本循環器学会中国・四国合同地方会, Jun. 2021.
205.	藤本鋭貴, 佐村高明, 菅野幹雄, 北市隆, Muneyuki Kadota, Yutaka Kawabata, Takayuki Ise, Masataka Sata and 秦広樹 : 右鎖骨下動脈アプローチを行った TAVI の1例, 第116回第118回日本循環器学会中国・四国合同地方会, Jun. 2021.
206.	Eiki Fujimoto, Takaaki Samura, Mikio Sugano, Takashi Kitaichi, Muneyuki Kadota, Yutaka Kawabata, Takayuki Ise, Masataka Sata and Hiroki Hata : 一般演題弁膜症2 右鎖骨下動脈アプローチを行ったTAVIの1例, 日本循環器学会, Jun. 2021.
207.	sutou kumiko, Daiju Fukuda and Masataka Sata : マクロファージのDNA分解機構が動脈硬化に与える影響, 第116回第118回日本循環器学会中国・四国合同地方会, Jun. 2021.
208.	Yuichiroh Ohkushi, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : ループ利尿薬使用下における心保護薬併用療法の有用性, 第116回第118回日本循環器学会中国・四国合同地方会, Jun. 2021.
209.	Susumu Nishio, Hirotsugu Yamada, Kenya Kusunose, 阿部美保, 林修司, 平田有紀奈, 山尾雅美, Takeshi Soeki and Masataka Sata : 徳島大学病院超音波センターの教育プログラム, May 2021.
210.	Kenya Kusunose, Miharu Arase, Yukina Hirata, Susumu Nishio, 山尾雅美, Hirotsugu Yamada, 阿部美保, Takeshi Soeki and Masataka Sata : 強皮症における6分間歩行負荷により評価した左室拡張能の臨床的意義, 第94回日本超音波医学会学術集会, May 2021.
211.	Hiromitsu Seno, Kazuhisa Matsumoto, Tomomi Matsuura, Takeshi Tobiume, Takeshi Soeki, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : ペースメーカー植込み後にj発覚した側頭葉てんかんによる発作性心静止の1例, 第124回日本内科学会四国地方会, May 2021.
212.	Kumiko Suto, Daiju Fukuda and Masataka Sata : Macrophage-specific DNase II Deletion Promotes Pro-inflammatory Activation of Macrophages and Atherogenesis, 第85回日本循環器学会学術集会, Mar. 2021.
213.	PP Tran, Daiju Fukuda, Kumiko Suto, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : DNA Damage Caused by Diabetes Induced Vascular Dysfunction : The Role of The Stimulator of Interferon Genes, 第85回日本循環器学会学術集会, Mar. 2021.
214.	PP Tran, Daiju Fukuda, Kumiko Suto, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Stimulator of Interferon Genes Plays a Pivotal Role in Vascular Inflammation and Atherosclerosis in Apolipoprotein E-deficient Mice, 第85回日本循環器学会学術集会, Mar. 2021.
215.	Hirotsugu Yamada, Kenya Kusunose, Yoshihito Saijyo, Y Okushi, M Fujiwara and Masataka Sata : Clinical Application of Strain Distribution by Speckle Tracking Echocardiography in Various Myocardial Disease, 第85回日本循環器学会学術集会, Mar. 2021.
216.	Koji Yamaguchi, Tetsuzo Wakatsuki, Yuichiroh Ohkushi, Kumiko Suto, 松本和久, Tomonori Takahashi, Muneyuki Kadota, Yutaka Kawabata, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Early and Chronic Phased Local Coagulative Responses Following Bioresorbable-polymer Drug-eluting Stent Implantation, 第85回日本循環器学会学術集会, Mar. 2021.
217.	Yutaka Kawabata, Tetsuzo Wakatsuki, Koji Yamaguchi, Daiju Fukuda, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, 添木武 and Masataka Sata : Relationship between Coronary Intraplaque Microluminal Structure and Epicardial Adipose Tissue and Plaque Formation -A Fresh Cadaveric Study-, 第85回日本循環器学会学術集会, Mar. 2021.
218.	Yukina Hirata, Kenya Kusunose, 辻拓将, 藤森康平, YAMAGUCHI Natsumi, Sae Morita, Susumu Nishio, Yuichiroh Ohkushi, Hiromitsu Seno, 高橋智紀, Takayuki Ise, 飛梅威, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Hirotsugu Yamada, 添木武, Tetsuzo Wakatsuki, 古徳純一 and Masataka Sata : Deep Learning for Detection of Elevated Pulmonary Artery Wedge Pressure Using Standard Chest X-Ray, 第85回日本循環器学会学術集会, Mar. 2021.
219.	Yuichiroh Ohkushi, Kenya Kusunose, 岡山佳弘, Hirotsugu Yamada and Masataka Sata : Prognostic Impact of Cancer on Venous Thromboembolism from Japanese Registry of All Cardiac and Vascular Datasets, 第85回日本循環器学会学術集会, Mar. 2021.
220.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : Utilization of Artificial Intelligence for Echocardiography and X-ray in the Real World, 第85回日本循環器学会学術集会, Mar. 2021.
221.	Daiju Fukuda and Masataka Sata : DNA Damage Response Associated with Vascular Aging Promotes Sterile Inflammation and Impairs Endothelial Function in Diabetes, 第85回日本循環器学会学術集会, Mar. 2021.
222.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : The Road to Automated Interpretation of Echocardiography with Artificial Intelligence, 第85回日本循環器学会学術集会, Mar. 2021.
223.	Shusuke Yagi and Masataka Sata : Angiogenetic Gene Therapy with Hepatocyte Growth Factor Plasmid in Patients with Chronic Limb-threatening Ischemia, 第85回日本循環器学会学術集会, Mar. 2021.
224.	阿部美保, Kenya Kusunose, Y Okushi, Zheng Robert, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Effects of Vitamin D Supplementation on Heart Failure Mortality from Japanese Registry of All Cardiac and Vascular Datasets, 第85回日本循環器学会学術集会, Mar. 2021.
225.	Masataka Sata : Anti-diabetic Treatments to Prevent Cardiovascular Events, 第85回日本循環器学会学術集会, Mar. 2021.
226.	Yutaka Kawabata, Tetsuzo Wakatsuki, Koji Yamaguchi, Daiju Fukuda, Hiroyuki Ito, Takayuki Ise, Kenya Kusunose, Tomomi Matsuura, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : 光干渉断層法で観察される冠動脈壁微小管腔構造と局所冠動脈周囲脂肪内炎症および冠動脈プラークの関連 -未固定遺体における検討-, Beyond Angiography Japan XXV, Mar. 2021.
227.	石井亜由美, Takayuki Ise, 西川幸治, 鈴木佳子, Hirokazu Ohminami, Muneyuki Kadota, Shusuke Yagi, 加藤真介 and Masataka Sata : 心臓リハビリテーションの日独比較 ∼ドイツ心リハ研修から∼, 第4回日本心臓リハビリテーション学会四国支部地方会, Mar. 2021.
228.	遠藤朱門, Shusuke Yagi, Takayuki Ise, Muneyuki Kadota, 石井亜由美, 西川幸治, 鈴木桂子, 大南博和, 加藤真介 and Masataka Sata : 若年健常人において，終末糖化産物は筋肉量・筋力の規定因子である, 第4回日本心臓リハビリテーション学会四国支部地方会, Mar. 2021.
229.	Takayuki Ise, Muneyuki Kadota, Shusuke Yagi, 石井亜由美, 西川幸治, 鈴木佳子, 大南博和, 加藤真介 and Masataka Sata : TAVI 実施症例の至適心臓リハビリテーションの考察, 第4回日本心臓リハビリテーション学会四国支部地方会, Mar. 2021.
230.	西川幸治, Takayuki Ise, 石井亜由美, 鈴木佳子, 大南博和, Muneyuki Kadota, Shusuke Yagi, Shinsuke Katoh and Masataka Sata : TAVI 施行前後の認知機能の変化について, 第4回日本心臓リハビリテーション学会四国支部地方会, Mar. 2021.
231.	Masataka Sata : 心臓脂肪と動脈硬化, 第38回日本肥満治療学会学術集会, Mar. 2021.
232.	Yukako Honma, Yasunobu Hayabuchi, Takeshi Tobiume, Masataka Sata and 中島博 : S-ICD植え込みを施行したQT延長症候群の5歳男児例, 第35回日本小児循環器学会近畿・中四国地方会, Mar. 2021.
233.	Takuya Yamada, Akihiro Tani, Muneyuki Kadota, Takayuki Ise, Yutaka Kawabata, Tomomi Matsuura, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 大動脈四尖弁に対してTAVIを施行した一症例, 第262回徳島医師学会学術集会, Mar. 2021.
234.	ムギー (名), Shusuke Yagi, Muneyuki Kadota, Yutaka Kawabata, 松本和久, Kenya Kusunose, Koji Yamaguchi, Takeshi Tobiume, Tomomi Matsuura, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 当院におけるイバブラジンの使用経験, 第262回徳島医師学会学術集会, Mar. 2021.
235.	高橋寛典, Kenya Kusunose, 西尾進, 平田有紀奈, 山口夏美, Masataka Sata, Hirotsugu Yamada, 高橋智紀, 瀬野弘光 and 大櫛祐一郎 : ESUSにおける新規発症心房細動と心エコー図指標との関連, 第85回日本循環器学会学術集会, Mar. 2021.
236.	平田有紀奈, Kenya Kusunose, 辻拓将, 藤森康平, 山口夏美, 森田沙瑛, 西尾進, 大櫛祐一郎, 瀬野弘光, 高橋智紀, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, 古徳純一 and Masataka Sata : ディープラーニングによる胸部X-pを用いた肺動脈圧上昇の検出, 第85回日本循環器学会学術集会, Mar. 2021.
237.	Muneyuki Kadota, Shusuke Yagi, Takayuki Ise, Yutaka Kawabata, Tomomi Matsuura, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Acute Hormonal Effect of the Angiotensin Receptor-Neprilysin Inhibitor in Patients with Chronic Heart Failure, 第85回日本循環器学会学術集会, Mar. 2021.
238.	Koji Yamaguchi, Tetsuzo Wakatsuki, Tomonori Takahashi, R Ueno, Yutaka Kawabata, Takayuki Ise, Takeshi Tobiume and Masataka Sata : Suppressed local coagulative response after newer-generation ultrathin strut SES implantation compared to older-generation SES implantation, 第29回日本心血管インターベンション治療学会, Feb. 2021.
239.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : AIが心エコー図法に与えるインパクト, 第31回日本心血管画像動態学会, Jan. 2021.
240.	Susumu Nishio, 森根裕二, Asami Yuasa, 松本力三, Yukina Hirata, 山尾雅美, Kenya Kusunose, Hirotsugu Yamada, 島田光生 and Masataka Sata : 下大静脈原発平滑筋肉腫の1例, 日本超音波医学会第93回学術集会, Dec. 2020.
241.	Kenya Kusunose, Akihiro Haga, Hirotsugu Yamada, Susumu Nishio, Yukina Hirata and Masataka Sata : 加速する循環器画像領域におけるAI研究の現在と未来, 日本超音波医学会第93回学術集会, Dec. 2020.
242.	Hiroshi Kawano, Yuya Yamashita, Nobuhito Naito, Seidai Satou, Muneyuki Kadota, Takayuki Ise, Shusuke Yagi, Masataka Sata, Hiroshi Nokihara and Yasuhiko Nishioka : 高安動脈炎による難治性皮膚潰瘍に対してべペルミノゲンペルプラスミド(ヒト肝細胞増殖因子プラスミドベクター)投与が奏効した1例, 第48回日本臨床免疫学会総会, Oct. 2020.
243.	松本力三, Susumu Nishio, Kei Daizumoto, Sae Morita, 湯浅麻美, Yukina Hirata, 山尾雅美, Takahiro Tanaka, Hiro-omi Kanayama and Masataka Sata : 多房性嚢胞状腎細胞癌の2症例, 日本超音波医学会第30回四国地方会学術集会, Oct. 2020.
244.	湯浅麻美, Susumu Nishio, Sae Morita, 松本力三, Yukina Hirata, 山尾雅美, Takahiro Tanaka, Yu Saitou, Mitsuo Shimada and Masataka Sata : 神経内分泌癌との鑑別が困難であった膵腺房細胞癌の1例, 日本超音波医学会第30回四国地方会学術集会, Oct. 2020.
245.	Hiromitsu Seno, Kenya Kusunose, Akihiro Tani, Yuichiroh Ohkushi, Tomonori Takahashi, Hirotsugu Yamada, Yukina Hirata, 山尾雅美, Susumu Nishio and Masataka Sata : 肥大型心筋症に心房性僧帽弁閉鎖不全症を合併し，重症心不全を呈した一例, 日本超音波医学会第30回四国地方会学術集会, Oct. 2020.
246.	Tomonori Takahashi, Kenya Kusunose, YAMAGUCHI Natsumi, Yukina Hirata, Susumu Nishio, Yuichiroh Ohkushi, Hiromitsu Seno, Shuji Hayashi, Hirotsugu Yamada and Masataka Sata : 経食道心臓超音波検査における左心耳内血栓評価にイソプロテレノール負荷が有用であった1例, 日本超音波医学会第30回四国地方会学術集会, Oct. 2020.
247.	Masataka Sata : Potential anti-inflammatory and anti-atherosclerotic effects of a direct oral anticoagulant, 第4回日本循環器学会基礎研究フォーラム, Sep. 2020.
248.	Hirotsugu Yamada, 大櫛祐一郎, Kenya Kusunose and Masataka Sata : 心エコー図検査を用いたCTRCD診断のピットフォール, 第3回日本腫瘍循環器学会学術集会, Sep. 2020.
249.	Yuichiroh Ohkushi, Kenya Kusunose, YAMAGUCHI Natsumi, Sae Morita, 平田有紀奈, 山尾雅美, Susumu Nishio, Tomonori Takahashi, Hirotsugu Yamada and Masataka Sata : 乳がん症例における化学療法開始後のトロポニンⅠ上昇の臨床的意義, 第3回日本腫瘍循環器学会学術集会, Sep. 2020.
250.	Masataka Sata : -, 第7回日本心血管脳卒中学会学術集会, Aug. 2020.
251.	Kenya Kusunose, Hirotsugu Yamada, 中谷敏 and Masataka Sata : Prospects for the Present and Future of Artificial Intelligence in Echocardiography, 第84回日本循環器学会学術集会, Aug. 2020.
252.	Shusuke Yagi and Masataka Sata : Modifying the Quality of Food Increases the Oral Caloric and Protein Intake in Patients with Heart Failure, 第84回日本循環器学会学術集会, Aug. 2020.
253.	泉侑希, Shunsuke Ishida, 長谷川結美, 武智研志, Mitsuhiro Goda, Yoshito Zamami, 桐野靖, 中村敏己, 寺岡和彦, Shusuke Yagi, Masataka Sata and Keisuke Ishizawa : 高齢者の薬物療法管理ツールを活用した薬剤業務の効率化, 第84回日本循環器学会学術集会, Jul. 2020.
254.	Koji Yamaguchi, Tetsuzo Wakatsuki, Yuichiroh Ohkushi, Kumiko Sutou, Kazuhisa Matsumoto, Tomonori Takahashi, Muneyuki Kadota, 上野理絵, Yutaka Kawabata, Tomomi Matsura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : The Effect of Lower Strut Thickness and Faster Polymer Resorption on Chronic Local Coagulative Response after Drug Eluting Stent Implantation, 第84回日本循環器学会学術集会, Jul. 2020.
255.	Gulinu Maimaituxun, Kenya Kusunose, Daiju Fukuda, Shusuke Yagi, Hirata Yukina, Hirotsugu Yamada, Takeshi Soeki, Masataka Sata and Michio Shimabukuro : Impact of Epicardial Adipose Tissue on Global Longitudinal Strain in Patients with Normal Left Ventricular Ejection Fraction, 第84回日本循環器学会学術集会, Jul. 2020.
256.	Ganbaatar Byambasuren, Daiju Fukuda, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : S1P2 Receptor Antagonist Attenuates Endothelial Dysfunction and Prevents Atherogenesis in Apolipoprotein-E-deficient Mice, 第84回日本循環器学会学術集会, Jul. 2020.
257.	Suto Kumiko, Daiju Fukuda, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Pemafibrate, a Novel Selective Peroxisome Proliferator-activated Receptor-α Modulator, Attenuates Vascular Inflammation and Endothelial Dysfunction in Diabetic Mice, 第84回日本循環器学会学術集会, Jul. 2020.
258.	Phuong Tran Pham, Daiju Fukuda and Masataka Sata : Stimulator of Interferon Genes Plays A Crucial Role in Atherogenesis via Macrophages Activation in Apolipoprotein E-Deficient Mice, 第84回日本循環器学会学術集会, Jul. 2020.
259.	西川幸治, Takayuki Ise, 石井亜由美, 鈴木佳子, Hirokazu Ohminami, Muneyuki Kadota, Shusuke Yagi, Shinsuke Katoh and Masataka Sata : TAVI後の認知機能低下に関連する因子の検討, 第26回日本心臓リハビリテーション学会学術集会, Jul. 2020.
260.	Muneyuki Kadota, Shusuke Yagi, Takayuki Ise, 石井亜由美, 西川幸治, 鈴木佳子, Hirokazu Ohminami, Shinsuke Katoh and Masataka Sata : イハブラジン導入前後の運動耐容能の推移を観察した虚血性心筋症の一例, 第26回日本心臓リハビリテーション学会学術集会, Jul. 2020.
261.	石井亜由美, Takayuki Ise, 西川幸治, Yukako Honma, 鈴木佳子, Hirokazu Ohminami, Muneyuki Kadota, Takeshi Tobiume, Shusuke Yagi, Yasunobu Hayabuchi, Shinsuke Katoh and Masataka Sata : 心配停止をきたしQT延長症候群と診断されS-ICD植込みとなった5歳児に対する心リハの経験, 第26回日本心臓リハビリテーション学会学術集会, Jul. 2020.
262.	Kenya Kusunose, Akihiro Haga, Muneyuki Kadota, 石井亜由美, Takayuki Ise, Shusuke Yagi, Hirotsugu Yamada and Masataka Sata : 心エコーへのAI応用について, 第26回日本心臓リハビリテーション学会学術集会, Jul. 2020.
263.	石井亜由美, Takayuki Ise, 西川幸治, Yukako Honma, 鈴木佳子, Hirokazu Ohminami, Muneyuki Kadota, Shusuke Yagi, Yasunobu Hayabuchi, Shinsuke Katoh and Masataka Sata : 小児に関する心臓リハビリテーションの取り組みと症例から学んだこと, 第26回日本心臓リハビリテーション学会学術集会, Jul. 2020.
264.	田中敦史, 田口功, 寺川宏樹, 石坂信和, 神崎裕美子, 冨山博史, Masataka Sata, 瀬在明, 江口和男, 加藤徹, 豊田茂, 石橋亮一, 石津智子, 植田真一郎, 前村浩二, 東幸仁, Hirotsugu Yamada, 大石充, 室原豊明, 尾山純一 and 野出孝一 : 無症候性高尿酸血症におけるフェブキソスタットの頸動脈内膜中膜複合体, 第52回日本動脈硬化学会総会学術集会, Jul. 2020.
265.	田中敦史, 田口功, 寺川宏樹, 石坂信和, 神崎裕美子, 冨山博史, Masataka Sata, 瀬在明, 江口和男, 加藤徹, 豊田茂, 石橋亮一, 苅尾七臣, 石津智子, 植田真一郎, 前村浩二, 東幸仁, Hirotsugu Yamada, 大石充, 横手幸太郎, 室原豊明, 尾山純一 and 野出孝一 : 無症候性高尿酸血症におけるフェブキソスタットの頸動脈内膜中膜複合体厚に対する効果の検, 第52回日本動脈硬化学会総会学術集会, Jul. 2020.
266.	Masataka Sata : 心血管イベント抑制に向けた脂質異常症対策, Patient-Centered Treatment Seminar, Feb. 2020.
267.	Masataka Sata : 心血管イベント抑制に向けた脂質異常症対策―動脈硬化の新知見とω-3不飽和脂肪酸の薬理作用―, TAKEDA CVM FORUM in SEINO, Feb. 2020.
268.	Masataka Sata : ''異所性脂肪``から考える動脈硬化の成因と糖尿病治療, 循環器の立場からみた心腎連関糖尿病治療を考える会, Feb. 2020.
269.	Masataka Sata : 循環器内科医から見た糖尿病治療とSGLT2阻害薬, 第291回四日市循環器懇話会―2月度例会―, Feb. 2020.
270.	Masataka Sata : 動脈硬化進展における血液凝固因子の役割―最新のエビデンスと動脈硬化研究からの考察―, New trends in antithrombotic therapy for patients with AF-CAD基礎メカニズムパート, Feb. 2020.
271.	Kazuhisa Matsumoto, Takeshi Tobiume, Tomomi Matsuura, Takeshi Soeki and Masataka Sata : 断端処理後リードの先端露出に対して鎖骨骨膜固定法が有用であった1例, 第12回植込みデバイス関連冬季大会, Feb. 2020.
272.	髙橋智子, Kazuhisa Matsumoto, Tomomi Matsuura, Takeshi Tobiume, Takeshi Soeki and Masataka Sata : S-ICDにpolytetrafluoroethyleneを被覆したこと，肥満により胸骨リードの挿入が浅くなったことでshock impedanceが著名に上昇した1例, 第12回植込みデバイス関連冬季大会, Feb. 2020.
273.	Masataka Sata : 動脈硬化進展における血液凝固因子の役割―最新のエビデンスと動脈硬化研究からの考察―, 心臓病治療を考える会in阿南市, Feb. 2020.
274.	Masataka Sata : 心血管イベント抑制に向けた脂質異常症対策―動脈硬化の新知見とω-飽和脂肪酸の薬理作用―, TAKEDA CVM Forum in GIFU, Feb. 2020.
275.	Masataka Sata : 異所性脂肪からみる動脈硬化の新知見―生活習慣病で血管と脂肪で生じる慢性炎症―, 第5回Niigata肝と代謝性炎症研究会, Feb. 2020.
276.	Masataka Sata : 動脈硬化進展における血液凝固因子の役割―最新のエビデンスと動脈硬化研究からの考察―, Hiroshima Circulation Conference, Jan. 2020.
277.	Masataka Sata : 循環器領域の最近の進歩―当科の取り組みと四国中央市との連携―, 令和2年度第3回四国中央医療セミナー, Jan. 2020.
278.	Masataka Sata : 心臓発作予防のため必要なこと, 社会医療法人平成記念会主催第159回県民公開学術研修セミナー講演会, Jan. 2020.
279.	Shusuke Yagi and Masataka Sata : 見た目の老化と筋力低下は冠動脈疾患の危険因子である, 脳心血管抗加齢研究会2019(第16回学術大会), Dec. 2019.
280.	Daiju Fukuda and Masataka Sata : 血管の炎症と動脈硬化における核酸受容体の役割, 脳心血管抗加齢研究会2019(第16回学術大会), Dec. 2019.
281.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 平田有紀奈, 鳥居裕太, 大櫛祐一郎, 高橋智紀, 山田なお and Masataka Sata : Isolated Post-capillaryとCombined Pre- and Post-capillary PHの予後予測指標の検討, 関西心エコーリサーチクラブ, Dec. 2019.
282.	Yukako Honma, Yasunobu Hayabuchi, Mutsuki Nakano, Shoji Kagami, Takeshi Tobiume, Takeshi Soeki, Masataka Sata, Ayumi Sasaki, Yukiko Kinoshita, Kazuhiro Mori and 中島博 : Bystander CPR からの救命の連鎖が奏効したQT延長症候群の1幼児例, 第153回日本小児科学会徳島地方会, Dec. 2019.
283.	毛利咲恵, 鶴尾美穂, 坂東佐知子, 添木武, 松本直也, Tomoyuki Yuasa, Akio Kuroda, Masataka Sata, Masahiro Abe, 寺澤敏秀 and Munehide Matsuhisa : 発熱，高血糖，低K血症を契機に一時的にBrugada型心電図を呈した糖尿病の1例, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
284.	Muneyuki Kadota, Kenya Kusunose, Takayuki Ise, Tomonori Takahashi, 藤本裕太, Yuichiroh Ohkushi, Kumiko Sutou, Kazuhisa Matsumoto, 上野理絵, Yutaka Kawabata, nao Yamada, Tomomi Matsuura, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : ドブダミン負荷下での血行動態評価を行った潜在性閉塞性肥大型心筋症2症例の検討, 第115回日本循環器学会四国地方会, Dec. 2019.
285.	Koji Yamaguchi, Tetsuzo Wakatsuki, Kazuhisa Matsumoto, Tomonori Takahashi, 上野理絵, Yutaka Kawabata, Tomomi Matsuura, Kenya Kusunose, Takeshi Tobiume, Takayuki Ise, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : クライオバルーンアブレーション後の肺静脈狭窄に対するDrug coated balloonの使用経験, 第115回日本循環器学会四国地方会, Dec. 2019.
286.	Koji Yamaguchi, Tetsuzo Wakatsuki, Kazuhisa Matsumoto, Tomonori Takahashi, 上野理絵, Yutaka Kawabata, Tomomi Matsuura, Kenya Kusunose, Takayuki Ise, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : 新規病変に対するDrug coated balloonの効果―局所血管反応と臨床成績について―, 第115回日本循環器学会四国地方会, Dec. 2019.
287.	Masataka Sata : 心血管イベント抑制に向けた脂質異常症対策, 高中性脂肪血症におけるω3脂肪酸製剤の役割, Dec. 2019.
288.	Masataka Sata : 心血管イベント抑制へ向けた高血圧治療―非ステロイド性新規MRブロッカーへの期待―, 高血圧Web Seminar徳島, Dec. 2019.
289.	Masataka Sata : 脂質異常症の最新動向―映像で見る動脈硬化の新知見と異所性脂肪―, 延岡医学会学術講演会, Nov. 2019.
290.	Masataka Sata : 心血管イベント抑制へ向けた高血圧治療―非ステロイド性新規MRブロッカーへの期待―, 大崎地区学術講演会∼高齢者のトータルケア心腎連関を考える∼, Nov. 2019.
291.	Masataka Sata : 動脈硬化進展における血液凝固因子の役割―最新のエビデンスと動脈硬化研究からの考察―, 高知抗血栓療法カンファレンス, Nov. 2019.
292.	Masataka Sata : 心血管イベント抑制に向けた脂質異常症対策, n-3 FUFA Forum in Kyoto ω3脂肪酸製剤の役割, Nov. 2019.
293.	Masataka Sata : SGLT2阻害剤, ARIA2019，Meet The Professor2 PCI患者のための，私の一押しの心血管イベント抑制剤2019, Nov. 2019.
294.	Masataka Sata : SGLT2阻害薬の今後の展望∼心・腎にどのような影響を及ぼすのか∼, 海部郡医師会学術講演会, Nov. 2019.
295.	Masataka Sata : 動脈硬化進展における血液凝固因子の役割―最新のエビデンスと動脈硬化研究からの考察―, PCI & 抗血栓療法セミナー, Nov. 2019.
296.	Masataka Sata : 心血管イベント抑制に向けた高血圧治療―動脈硬化の新知見と高血圧ガイドライン2019―, 熊本市内科医会学術講演会, Nov. 2019.
297.	Masataka Sata : 脂質異常症治療の最新の動向―映像で見る動脈硬化の新知見と異所性脂肪―, 第14回二日市循環器臨床カンファレンス, Nov. 2019.
298.	Masataka Sata : 生活習慣病を甘くみない―あなたと大切な家族を突然死と介護から守るために―, 鳴門市医師会第2回市民公開講座元気に生きるために, Nov. 2019.
299.	Masataka Sata : 冠動脈疾患における脂質低下療法，心房細動を合併した際の抗凝固療法, LA Summit in Tokushima, Nov. 2019.
300.	Takeshi Tobiume, Tomomi Matsuura, Kazuhisa Matsumoto, Sachiko Bandoh, 大河啓介, Takeshi Soeki and Masataka Sata : 房室ブロックの予防に順行性速伝導路と順行性遅伝導路のマッピングが有用であった順行性速伝導路の下方偏位を伴う遅速型房室結節リエントリー性頻拍の1 例, カテーテルアブレーション関連秋季大会2019, Nov. 2019.
301.	林昌晃, Takeshi Soeki, 玉上大暉, 野田康裕, 森西啓介, Kazuhisa Matsumoto, Sachiko Bandoh, Tomomi Matsuura, Takeshi Tobiume, Yoshiaki Ohnishi and Masataka Sata : 心房細動アブレーション時の鎮静不安定化に影響を及ぼす背景因子の検討, カテーテルアブレーション関連秋季大会2019, Nov. 2019.
302.	髙橋智子, Tomomi Matsuura, Kazuhisa Matsumoto, Sachiko Bandoh, Takeshi Tobiume, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : クライオバルーンアブレーション後にきたした高度肺静脈狭窄に対してDrugcoated balloon を用いて治療を行った1 例, カテーテルアブレーション関連秋季大会2019, Nov. 2019.
303.	Kazuhisa Matsumoto, Takeshi Tobiume, Sachiko Bandoh, Tomomi Matsuura, Takeshi Soeki and Masataka Sata : Crista terminalis を横断する伝導によりpseudo conduction を呈し，同部位への通電でcomplete isthmus block を確認し得た心房粗動の1 例, カテーテルアブレーション関連秋季大会2019, Nov. 2019.
304.	Masataka Sata : 心血管イベント抑制を目指した糖尿病治療戦略―GLP-1受容体作動薬の大規模臨床試験とESCガイドラインより―, Cardiology GLP-1 scientific update meeting 2019, Nov. 2019.
305.	Masataka Sata : インスリン抵抗性と動脈硬化における慢性炎症と自然免疫, 第40回日本肥満学会・第37回日本肥満症治療学会シンポジウム1合併症からみた生活習慣病上流因子としての肥満症:領域横断的肥満症WG連携企画①, Nov. 2019.
306.	Masataka Sata : 心血管イベント抑制に向けた脂質異常症対策, ロトリガ全国Web講演会, Oct. 2019.
307.	Masataka Sata : ``異所性脂肪''から考える動脈硬化の成因と糖尿病治療, SGLT2阻害薬Up to Date in 安曇野・大北, Oct. 2019.
308.	Masataka Sata : 心血管イベント抑制に向けて残余リスクを考える, 第19回神奈川けいれん・脳疾患治療研究会, Oct. 2019.
309.	Masataka Sata : 心血管イベント抑制に向けた高血圧治療―非ステロイド性新規MRブロッカーへの期待―, 第58回全国自治体病院学会ランチョンセミナー4, Oct. 2019.
310.	Masataka Sata : 脂質異常症治療の最新の動向―映像で見る動脈硬化の新知見と異所性脂肪―, 桜橋CVD SUMMIT 2019, Oct. 2019.
311.	松本力三, Susumu Nishio, Asami Yuasa, Sae Morita, Yukina Hirata, Yuta Torii, 山尾雅美, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 医原性仮性動脈瘤による正中神経麻痺の診断に超音波検査が有用であった1 例, 日本超音波医学会第29回四国地方会学術集会, Oct. 2019.
312.	Yukina Hirata, Susumu Nishio, Kenya Kusunose, Takaharu Kudoh, Akira Takahashi, Mai Matsumoto, Asami Yuasa, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 含水法で明瞭に描出できた口腔内癌の1 例, 日本超音波医学会第29回四国地方会学術集会, Oct. 2019.
313.	Natsumi Yamaguchi, Susumu Nishio, Kenya Kusunose, Yukina Hirata, Yuta Torii, 山尾雅美, 山尾雅美, Yuichiroh Ohkushi, nao Yamada, Hirotsugu Yamada and Masataka Sata : 当院における心室中部型たこつぼ心筋症の発症頻度と臨床的特徴, 日本超音波医学会第29回四国地方会学術集会, Oct. 2019.
314.	Yuichiroh Ohkushi, Kenya Kusunose, 松本力三, Yukina Hirata, Yuta Torii, 山尾雅美, Susumu Nishio, nao Yamada, Hirotsugu Yamada and Masataka Sata : 経胸壁心エコー上で結節様に観察されたThebesian 弁の一例, 日本超音波医学会第29回四国地方会学術集会, Oct. 2019.
315.	Masataka Sata : 動脈硬化抑制に向けた直接経口抗凝固薬の可能性, 第60日本脈管学会総会シンポジウム1動脈硬化に対する薬物療法の新展開, Oct. 2019.
316.	Masataka Sata : 脂質異常症の最新動向―映像で見る動脈硬化の新知見と異所性脂肪―, Clinical Cardiology Seminar, Oct. 2019.
317.	Yuta Torii, Kenya Kusunose, Hirotsugu Yamada, Natsumi Yamaguchi, Sae Morita, Yukina Hirata, Susumu Nishio, Yuichiroh Ohkushi, Tomonori Takahashi, nao Yamada and Masataka Sata : 心不全入院患者における左室拡張能評価と心血管イベントの関連:2009 年・2016 年拡張能ガイドラインの比較, 第23回日本心不全学会学術集会, Oct. 2019.
318.	Masataka Sata : ``異所性脂肪''から考える動脈硬化の成因と糖尿病治療, Reiwa Heart Seminar 2019 ∼高血圧と糖尿病を考える∼, Oct. 2019.
319.	Masataka Sata : 循環器専門医から見た2型糖尿病治療戦略∼大血管合併症予防の観点から∼, 徳島生活習慣病予防フォーラム2019∼Lipie & Diabetes Strategy∼, Sep. 2019.
320.	Masataka Sata : 『生活習慣病を甘くみない!』―あなたと大切な家族を突然死から守るために―, 四国こどもとおとなの医療センター市民公開講座こどもとおとな―みんなそろって健康に―, Sep. 2019.
321.	Ganbaatar Byambasuren, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki and Masataka Sata : S1P2 antagonist attenuates endothelial dysfunction and inhibits atherogenesis in apolipoprotein-E-deficient Mice, 日本性機能学会第30回学術集会, Sep. 2019.
322.	Pham Tran Phuong, Daiju Fukuda, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Rivaroxaban,a direct inhibitor of FXa,attenuated diabetes-induced endothelial dysfunction in wild-type mice, 日本性機能学会第30回学術集会, Sep. 2019.
323.	Arief Rahadian, Daiju Fukuda, Hotima Salim, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : SGLT2 inhibitor,Canagliflozin,Ameliorate Endothelial Dysfunction and Atherosclerosis in Diabetic ApoE-/- Mice, 日本性機能学会第30回学術集会, Sep. 2019.
324.	Aini Kunduziayi, Daiju Fukuda, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Vildagliptin,a DPP-4 Inhibitor,prevents endothelial dysfunction in nondiabetic apolipoprotein E-deficient mice, 日本性機能学会第30回学術集会, Sep. 2019.
325.	Yutaka Kawabata, Tetsuzo Wakatsuki, Koji Yamaguchi, Hiroyuki Ito, Ueno Rie, Takayuki Ise, Todoroki Takashi, Takeshi Tobiume and Masataka Sata : Relationship between coronary intraplaque microluminal structures and local inflammation in adjacent epicardial adipose tissue - A fresh cadaveric study, 第28回日本心血管インターベンション治療学会, Sep. 2019.
326.	Shusuke Yagi, Ken-ichi Aihara, Sumiko Yoshida, Yasumasa Ikeda, Masashi Akaike and Masataka Sata : 心血管病における性機能障害と男性ホルモンの心血管保護作用, 日本性機能学会第30回学術集会,シンポジウム, Sep. 2019.
327.	Koji Yamaguchi, Tetsuzo Wakatsuki, Tomonori Takahashi, 上野理絵, Yutaka Kawabata, Takayuki Ise, Takeshi Tobiume and Masataka Sata : アブレーション後に生じた肺静脈狭窄症に対するdrug coated balloonの使用経験, 第28回日本心血管インターベンション治療学会, Sep. 2019.
328.	Masataka Sata : 映像で見る動脈硬化の新知見とイメージングへの応用∼SGLT2阻害薬の話題も含めて∼, かわぐち心臓・呼吸器研究会, Sep. 2019.
329.	梶川正人, 丸橋達也, 日高貴之, 中野由紀子, 栗栖智, 大原康樹, 廣高史, 平山篤志, 椎名一紀, 冨山博史, Shusuke Yagi, 天野里江, Hirotsugu Yamada and Masataka Sata : 2型糖尿病患者におけるサキサグリプチンの血管内皮機能に及ぼす効果, 第67回日本心臓病学会学術集会, Sep. 2019.
330.	Koji Yamaguchi, Tetsuzo Wakatsuki, Yutaka Kawabata, nao Yamada, Kenya Kusunose, Takayuki Ise, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Optical coherence omographyにより器質化血栓の存在が疑われた肺癌術後急性冠症候群の1例, 第67回日本心臓病学会学術集会, Sep. 2019.
331.	Kenya Kusunose, Akihiro Haga, Hirotsugu Yamada, 中谷敏 and Masataka Sata : 心エコー図法における人工知能技術活用の今(シンポジウム19 AIでどこまで心臓病診療は進むか?), 第67回日本心臓病学会学術集会, Sep. 2019.
332.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 運動誘発性肺高血圧の臨床的意義と未来(シンポジウム14 負荷心エコーの展望), 第67回日本心臓病学会学術集会, Sep. 2019.
333.	Natsumi Yamaguchi, Kenya Kusunose, Akihiro Haga, Sae Morita, Yukina Hirata, Yuta Torii, 西尾進, nao Yamada, 阿部美保, Daiju Fukuda, Hirotsugu Yamada and Masataka Sata : 深層学習を用いた左室駆出率の推定:心エコー図法による検討(優秀演題メディカルスタッフ), 第67回日本心臓病学会学術集会, Sep. 2019.
334.	Yukina Hirata, Kenya Kusunose, Natsumi Yamaguchi, Sae Morita, Yuta Torii, Susumu Nishio, nao Yamada, 阿部美保, Hirotsugu Yamada and Masataka Sata : 心外膜下脂肪厚と性差および年齢との関連(優秀演題メディカルスタッフ), 第67回日本心臓病学会学術集会, Sep. 2019.
335.	nao Yamada, 小島友子, Hirotsugu Yamada, Kenya Kusunose, Susumu Nishio, Shuji Hayashi, 藤原美佳, Yoshihito Saijoh, Yukina Hirata, Yuta Torii and Masataka Sata : 高血圧心疾患における左室拡張期電気機械的カップリングの非侵襲的評価, 第67回日本心臓病学会学術集会, Sep. 2019.
336.	Masataka Sata : 動脈硬化進展における血液凝固因子の役割―最新のエビデンスと動脈硬化研究からの考察―, Masters Summit on Cardiology, Sep. 2019.
337.	Koji Yamaguchi, Tetsuzo Wakatsuki, Tomonori Takahashi, 上野理絵, Yutaka Kawabata, Takayuki Ise, Takeshi Tobiume and Masataka Sata : 腎不全合併虚血肢患者に対するminimum-contrast下肢血管形成術の取り組みについて, 第26回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2019.
338.	Yutaka Kawabata, Tetsuzo Wakatsuki, Koji Yamaguchi, Takayuki Ise, Tomonori Takahashi, 上野理絵, Takeshi Tobiume and Masataka Sata : 単冠動脈症合併重症大動脈弁狭窄症に対してTAVIを施行した1例, 第26回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2019.
339.	Masataka Sata : 動脈硬化の新知見とイメージングへの応用, 第12回大分心血管研究会, Sep. 2019.
340.	Masataka Sata : 脂質異常症の最新動向―映像で見る動脈硬化の新知見と異所性脂肪―, Lipid Biology Forum, Sep. 2019.
341.	Masataka Sata : 脂質異常症の最新動向―映像で見る動脈硬化の新知見と異所性脂肪―, 中河内生活習慣病フォーラム, Aug. 2019.
342.	Masataka Sata : 脂質異常症治療の最新の動向―映像でみる動脈硬化の新知見と異所性脂肪―, Hiroaki Kawanami記念東葛循環器セミナー, Aug. 2019.
343.	木田貴弘, Takeshi Tobiume, 松本和久, 坂東左知子, Tomomi Matsuura, Takeshi Soeki, 志村拓哉, 髙橋智子, 谷彰浩, 藤本裕太, 大櫛祐一郎, 數藤久美子, 髙橋智紀, 上野理絵, 門田宗之, 川端豊, Mika Bando, 山田なお, Hiroyuki Ito, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 房室ブロックの進行に伴い明らかになり，恒久的ペースメーカー植込み術後のファーフィールドR波センシングへの関与が疑われた束枝心室間副伝導路の1例, 第259回徳島医学会学術集会, Aug. 2019.
344.	井口裕貴, Takeshi Tobiume, 松本和久, 坂東左知子, Tomomi Matsuura, Takeshi Soeki, 志村拓哉, 髙橋智子, 谷彰浩, 藤本裕太, 大櫛祐一郎, 數藤久美子, 髙橋智紀, 上野理絵, 門田宗之, 川端豊, Mika Bando, 山田なお, Hiroyuki Ito, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 房室ブロックの予防に順行性速伝導路と順行性遅伝導路のマッピングが有用であった順行性速伝導路の下方偏位を伴う遅速型房室結節リエントリー性頻拍の1例, 第259回徳島医学会学術集会, Aug. 2019.
345.	Naoto Uyama, 松下知樹, 新井悠太, Hideki Otsuka, Youichi Otomi, Masafumi Harada, Shusuke Yagi and Masataka Sata : 当院における慢性血栓塞栓性肺高血圧症 5症例の臨床像について, 第259回徳島医学会学術集会, Aug. 2019.
346.	Masataka Sata : ``異所性脂肪''から考える動脈硬化の成因と糖尿病治療, 循環器疾患と糖尿病講演会in三次, Jul. 2019.
347.	Masataka Sata : 心血管イベント抑制に向けた脂質異常症対策―動脈硬化の新知見とω-3不飽和脂肪酸の薬理作用―, 所沢市循環器セミナー, Jul. 2019.
348.	Kazuhisa Matsumoto, Takeshi Soeki, Tomomi Matsuura, Takeshi Tobiume and Masataka Sata : Vidagliptin reduces inducibility of atrial fibrillation in hypertensive rats complicated with diabetes mellitus, 第66回日本不整脈心電学会学術大会, Jul. 2019.
349.	Masataka Sata : SGLT2阻害薬の今後の展望∼心・腎にどのような影響を及ぼすのか∼, 第16回徳島心臓リハビリテーション研究会, Jul. 2019.
350.	Masataka Sata : 動脈硬化進展における血液凝固因子の役割―最新のエビデンスと動脈硬化研究からの考察―, 血栓塞栓症の診断と治療について考える会, Jul. 2019.
351.	Daiju Fukuda and Masataka Sata : 血管の炎症と動脈硬化発症における核酸受容体の役割, 第40回日本炎症・再生医学会, Jul. 2019.
352.	石井亜由美, 西川幸治, Takayuki Ise, Takayuki Ise, Yoshiko Suzuki, 高川由利子, Shusuke Yagi, Shinsuke Katoh and Masataka Sata : 大動脈弁狭窄症に対するTAVI施行患者の認知機能の変化について, 第25回日本心臓リハビリテーション学会学術集会, Jul. 2019.
353.	Masataka Sata, 石井亜由美, 西川幸治, Shusuke Yagi, Takayuki Ise and Yuka Ueda : ``異所性脂肪''から考える動脈硬化の成因と心臓リハビリテーションの効果, 第25回日本心臓リハビリテーション学会学術集会指定講演,日本循環器学会・日本心臓リハビリテーション学会ジョイントセッション, Jul. 2019.
354.	西川幸治, 石井亜由美, Takayuki Ise, Yoshiko Suzuki, 高川由利子, Shusuke Yagi, Shinsuke Katoh and Masataka Sata : 継続的な活動量の記録は半年後の運動習慣の獲得につながるか, 第25回日本心臓リハビリテーション学会学術集会, Jul. 2019.
355.	Masataka Sata : 動脈硬化の病態における心外膜脂肪の役割, 第52回日本動脈硬化学会総会・学術集会シンポジウム17糖尿病・メタボリックシンドロームと心血管疾患病態治療学の最前線, Jul. 2019.
356.	Masataka Sata : 炎症の評価はガイドラインに反映されるか, 第52回日本動脈硬化学会総会・学術集会シンポジウム15動脈硬化性疾患予防ガイドライン次回改定に向けた課題と提言, Jul. 2019.
357.	Masataka Sata : 脂質異常症治療の最新の動向―映像でみる動脈硬化の新知見と異所性脂肪―, 埼玉西部地区脂質異常症治療セミナー, Jul. 2019.
358.	Masataka Sata : 動脈硬化進展における血液凝固因子の役割∼最新エビデンスと動脈硬化研究からの考察∼, 湖北Thrombosisカンファレンス特別講演, Jul. 2019.
359.	Masataka Sata : ``異所性脂肪''から考える動脈硬化の成因と糖尿病治療, Diabetes Update in Fukui特別講演, Jul. 2019.
360.	Masataka Sata : 心血管イベント抑制へ向けた高血圧治療―非ステロイド性新規MRブロッカーへの期待―, 第138回日本循環器学会北陸地方会ランチョンセミナー特別講演, Jun. 2019.
361.	Masataka Sata : SGLT2阻害薬の今後の展望∼心・腎にどのような影響を及ぼすのか∼, 日本医師会生涯教育講座循環器疾患と合併症, Jun. 2019.
362.	Masataka Sata : 心血管イベント抑制に向けた脂質異常症対策, n-3 PUFA Forum in Shikoku 高中性脂肪血症におけるω3脂肪酸製剤の役割, Jun. 2019.
363.	Gulinu Maimaituxun, Daiju Fukuda, Shusuke Yagi, Yukina Hirata, Takashi Iwase, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata and Michio Shimabukuro : Gender specific impact of epicardial adipose tissue thickness on coronary artery disease, 第19回日本抗加齢医学会総会, Jun. 2019.
364.	Masataka Sata : 映像で見る動脈硬化の新知見とイメージングへの応用―心臓脂肪とVasa Vasorum―, 第22回北野動脈硬化症セミナー, Jun. 2019.
365.	Masataka Sata : ''異所性脂肪''から考える動脈硬化の成因と糖尿病治療, 八幡遠賀中間第4回糖尿病と心血管疾患を考える会, Jun. 2019.
366.	Gulinu Maimaituxun, Michio Shimabukuro, Daiju Fukuda, Hirofumi Izaki, 平田陽一郎, 益崎裕章, Hiro-omi Kanayama and Masataka Sata : A link of adiponectin expression to kidney adipose tissue volume in human, 第4回J-ISCP(国際心血管薬物療法学会日本部会)年次学術集会, Jun. 2019.
367.	Takeshi Soeki, Daiju Fukuda, Tomomi Matsuura, 植松悦子 and Masataka Sata : 抗凝固薬の新しい可能性, 第4回J-ISCP(国際心血管薬物療法学会日本部会)年次学術集会会長企画セッション―心血管薬物治療の新たな可能性―, Jun. 2019.
368.	森田沙瑛, 西尾進, Kenya Kusunose, Takeshi Soeki, 松本和久, 山口夏美, 平田有紀奈, 鳥居裕太, 西條良仁, Hirotsugu Yamada and Masataka Sata : 右室容量負荷の原因を経胸壁心エコー図検査で診断し得なかった1例, 第114回日本循環器学会中国・四国合同地方会, Jun. 2019.
369.	數藤久美子, Kenya Kusunose, Tomomi Matsuura, 山田なお, 松本和久, 上野理絵, 川端豊, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 進行性心不全を呈す抗ミトコンドリア抗体陽性筋炎の症例, 第114回日本循環器学会中国・四国合同地方会, Jun. 2019.
370.	山田なお, Hirotsugu Yamada, Kenya Kusunose, 大櫛祐一郎, 髙橋智紀, 林修司, 阿部美保, Mika Bando, 西條良仁, 鳥居裕太, 平田有紀奈, 西尾進 and Masataka Sata : 肥大型心筋症に心房機能性僧帽弁閉鎖不全症を合併し，重症心不全を呈した一例, 第114回日本循環器学会中国・四国合同地方会, Jun. 2019.
371.	谷彰浩, Kenya Kusunose, 松本和久, Tomomi Matsuura, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 拡張期僧帽弁逆流の治療適応判断に心房心室同時ペーシングが有効であった1例, 第114回日本循環器学会中国・四国合同地方会, Jun. 2019.
372.	志村拓哉, Takayuki Ise, 川端豊, 藤本裕太, 松本和久, 上野理絵, 山田なお, Hiroyuki Ito, Tomomi Matsuura, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Hirotsugu Kurobe, Eiki Fujimoto and Masataka Sata : 先天性二尖弁に対するTAVIの2例, 第114回日本循環器学会中国・四国合同地方会, Jun. 2019.
373.	大池由夏, Takeshi Tobiume, 松本和久, 山田なお, 坂東左知子, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Tetsuzo Wakatsuki, Takeshi Soeki, Hirotsugu Yamada and Masataka Sata : His束より上方レベルの心房刺激でのみ誘発可能であった房室結節リエントリー性頻拍の1例, 第114回日本循環器学会中国・四国合同地方会, Jun. 2019.
374.	松本和久, Tomomi Matsuura, Takeshi Tobiume, Takeshi Soeki and Masataka Sata : 心臓電気生理検査中に4種類の頻拍が出現し治療に難渋した一例, 第114回日本循環器学会中国・四国合同地方会, Jun. 2019.
375.	中村昌史, 川端豊, Takayuki Ise, 藤本裕太, 原田貴文, 松本和久, 西條良仁, 上野理絵, 山田なお, Hiroyuki Ito, 轟貴史, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 経食道心エコーガイド下の経皮的腫瘍生検により早期に診断し得た心臓原発血管肉腫の一例, 第114回日本循環器学会中国・四国合同地方会, Jun. 2019.
376.	松本力三, 鳥居裕太, Tetsuzo Wakatsuki, 西尾進, 湯浅麻美, 平田有紀奈, 山尾雅美, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 右大腿動静脈瘻修復術後に繰り返し生じた深部静脈血栓症の1例, 第114回日本循環器学会中国・四国合同地方会, Jun. 2019.
377.	山尾雅美, 西尾進, 山口夏美, 平田有紀奈, 松本和久, 西條良仁, 阿部美保, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 脳梗塞の原因精査の心エコー図検査で右室内異常構造物を認めた卵巣癌の1例, 第114回日本循環器学会中国・四国合同地方会, Jun. 2019.
378.	平田有紀奈, Kenya Kusunose, Kumiko Kagawa, 山口夏美, 森田沙瑛, 鳥居裕太, 山尾雅美, 西尾進, 山田なお, Tomomi Matsuura, 阿部美保, Hirotsugu Yamada and Masataka Sata : 悪性リンパ腫の診断および経過観察に心エコー図検査が有用であった1例, 第114回日本循環器学会中国・四国合同地方会, Jun. 2019.
379.	鳥居裕太, Hirotsugu Yamada, Kenya Kusunose, 山田なお, 大櫛祐一郎, 西尾進, 平田有紀奈, 森田沙瑛, 山口夏美 and Masataka Sata : 左室拡張機能評価を用いた心房細動合併心不全の予後予測:新旧ガイドライン(2009年，2016年)の比較, 第114回日本循環器学会中国・四国合同地方会, Jun. 2019.
380.	坂東左知子, 坂元裕一郎, Takeshi Soeki, 山口遼, 吉本大祐, 鈴木孝彦, 中川博 and Masataka Sata : 心房細動アブレーション後の心房性不整脈検出における，14日間リードレスパッチ・ホルター心電図の有用性, 第114回日本循環器学会中国・四国合同地方会, Jun. 2019.
381.	Masataka Sata : 循環器専門医から見た2型糖尿病治療戦略 ∼大血管合併症予防の観点から∼, 糖尿病Webシンポジウム, Jun. 2019.
382.	Masataka Sata : 動脈硬化って何?, 第114回日本循環器学会中国四国合同地方会市民公開講座―心臓発作を行ないために―, Jun. 2019.
383.	Masataka Sata : 心血管イベント抑制に向けた脂質異常症対策―動脈硬化の新知見とω-3不飽和脂肪酸の薬理作用―, 丹波市循環器セミナー, May 2019.
384.	Masataka Sata : 脂質異常症の最新動向―映像で見る動脈硬化の新知見と異所性脂肪―, 積極的脂質性低下療法について考える会∼the lower, the betterの意義とは何か?∼, May 2019.
385.	Masataka Sata : 心血管イベント抑制へ向けた高血圧治療―非ステロイド性新規MRブロッカーへの期待―, 板野郡医師会学術講演会, May 2019.
386.	Susumu Nishio, Kenya Kusunose, Yukina Hirata, Yoshihito Saijoh, nao Yamada, Yuta Torii, 山尾雅美, Takeshi Soeki, Hirotsugu Yamada and Masataka Sata : 右心機能評価, 日本超音波医学会第92回学術集会パネルディスカッション循環器2, May 2019.
387.	Hirotsugu Yamada, Kenya Kusunose, Yoshihito Saijoh, nao Yamada, Yuta Torii, Yukina Hirata, 山尾雅美, Susumu Nishio, Takeshi Soeki and Masataka Sata : ASE/EACVI の心腔計測ガイドライン2015 の概要, 日本超音波医学会第92回学術集会パネルディスカッション循環器1, May 2019.
388.	Hirotsugu Yamada, Yoshihito Saijoh, Kenya Kusunose, nao Yamada, Yuta Torii, Yukina Hirata, 山尾雅美, Susumu Nishio, Takeshi Soeki and Masataka Sata : 「がん治療関連心筋障害(CTRCD)」の診療における心エコー図検査の有用性, 日本超音波医学会第92回学術集会シンポジウム循環器7, May 2019.
389.	Gulinu Maimaituxun, Daiju Fukuda, Shusuke Yagi, Tsukasa Iwase, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata and Michio Shimabukuro : Type 2 diabetes but not apicardial adipose tissue thickness is a predictor for coronary artery diseases in women, 第62回日本糖尿病学会年次学術集会, May 2019.
390.	阿部美保, Kenya Kusunose, Hirotsugu Yamada, 山田なお, Zheng Robert, 西條良仁, 西尾進, 平田有紀奈, 鳥居裕太 and Masataka Sata : 血清IgG4 値と心エコー図検査指標との関連性, 日本超音波医学会第92回学術集会, May 2019.
391.	Masataka Sata : 心血管イベント抑制に向けた脂質異常症対策, ロトリガ全国Web講演会, May 2019.
392.	Masataka Sata : 心房細動を合併した冠動脈疾患患者の抗血栓療法―エビデンスから考える最新の動向―, インターネット講演会虚血性心疾患合併心房細動治療Webセミナーin徳島, May 2019.
393.	Masataka Sata : 心血管イベント抑制に向けた脂質異常症対策―動脈硬化の新知見とω-3不飽和脂肪酸の薬理作用―, 小松島市医師会学術講演会, May 2019.
394.	Masataka Sata : 動脈硬化進展における血液凝固因子の役割―最新のエビデンスと動脈硬化研究からの考察―, 急性冠症候群を考える会 in Yokohama, May 2019.
395.	Masataka Sata : 心血管イベント抑制へ向けた高血圧治療 ―非ステロイド性新規MRブロッカーへの期待―, 今治市医師会医学講演会, May 2019.
396.	Masataka Sata : 心血管イベント抑制へ向けた高血圧治療 ―非ステロイド性新規MRブロッカーへの期待―, 美馬市医師会学術講演会, May 2019.
397.	西尾進, Kenya Kusunose, 高橋寛典, Hiroshi Kagusa, 平田有紀奈, 森田沙瑛, 山口夏美, 鳥居裕太, 山尾雅美, Zheng Robert, 西條良仁, 山田なお, 林修司, 阿部美保, 武市脩, Hirotsugu Yamada and Masataka Sata : 急性脳梗塞患者の病型分類におけるB型ナトリウム利尿ペプチドと心エコー図指標の臨床的意義, 日本心エコー図学会第30回学術集会, May 2019.
398.	平田有紀奈, Kenya Kusunose, 西尾進, 原田修, 宮里尚美, 原國督, 森田沙瑛, 西尾進, 鳥居裕太, 山尾雅美, Hirotsugu Yamada and Masataka Sata : 超音波検査を用いた心外膜下脂肪厚の測定精度の検討, 日本心エコー図学会第30回学術集会, May 2019.
399.	森田沙瑛, Kenya Kusunose, 平田有紀奈, 鳥居裕太, 天野理江, 西條良仁, 山田なお, 西尾進, 山尾雅美, 阿部美保, Takayuki Ise, Hirotsugu Yamada and Masataka Sata : 全身性強皮症における運動誘発性肺高血圧症の高リスク群の同定, 日本心エコー図学会第30回学術集会, May 2019.
400.	Kenya Kusunose, Hirotsugu Yamada, 西尾進 and Masataka Sata : 疣腫を視るー感染性心内膜炎のエコー診断, 日本心エコー図学会第30回学術集会, May 2019.
401.	Kenya Kusunose, Hirotsugu Yamada, 西尾進 and Masataka Sata : 心房細動と左房機能解析, 日本心エコー図学会第30回学術集会, May 2019.
402.	Gulinu Maimaituxun, Kenya Kusunose, Hirotsugu Yamada, Daiju Fukuda, Shusuke Yagi, Yukina Hirata, T Iwase, Takeshi Soeki, Masataka Sata and Michio Shimabukuro : Impact of epicardial adipose tissue thickness on left ventricular diastolic dysfunction in human, 第92回日本内分泌学会学術総会, May 2019.
403.	Gulinu Maimaituxun, Daiju Fukuda, Shusuke Yagi, Yukina Hirata, T Iwase, S Takao, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masafumi Harada, Masataka Sata and Michio Shimabukuro : Kidney fat and its impact on coronary artery disease, 第4回日本血管不全学会学術集会・総会, Apr. 2019.
404.	Gulinu Maimaituxun, Daiju Fukuda, Shusuke Yagi, Yukina Hirata, T Iwase, S Takao, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masafumi Harada, Masataka Sata and Michio Shimabukuro : Peri-renal fat volume is negatively associated with the adiponectin expression in human, 第4回日本血管不全学会学術集会・総会, Apr. 2019.
405.	石井亜由美, 西川幸治, Takayuki Ise, Yoshiko Suzuki, Shusuke Yagi, 高川由利子, Shinsuke Katoh and Masataka Sata : 外来心臓リハビリテーションにより外出への不安感が軽減し運動耐容能の向上を認めた症例, 日本心臓リハビリテーション学会第3回四国支部地方会, Apr. 2019.
406.	石井亜由美, 西川幸治, Takayuki Ise, Yoshiko Suzuki, 高川由利子, Shusuke Yagi, Shinsuke Katoh and Masataka Sata : Wearable ICD装着患者に対する心リハの経験, 日本心臓リハビリテーション学会第3回四国支部地方会, Apr. 2019.
407.	平田有紀奈, 西尾進, 山口夏美, 森田沙瑛, 鳥居裕太, 山尾雅美, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 心外膜下脂肪厚とBody mass indexとの関連, 超音波検査技術, Vol.44, No.Suppl, S165, Apr. 2019.
408.	Pham Tran Phuong, Daiju Fukuda, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Rivaroxaban, A Direct Inhibitor of FXa, Attenuated Diabetes-induced Endothelial Dysfunction by Inhibiting FXa-protease Activated Receptor 2 Signaling, 第83回日本循環器学会学術集会, Mar. 2019.
409.	Hiroyuki Ito, Tetsuzo Wakatsuki, Koji Yamaguchi, Daiju Fukuda, 川端豊, 轟貴史, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Microluminal structures of coronary plaque and vasa vasorums affect coronary inflammation: A fresh cadaveric studys, 第83回日本循環器学会学術集会, Mar. 2019.
410.	野出孝一, 田中敦史, 大屋祐輔, 岸拓弥, 冨山博史, Masataka Sata, 三浦克之 and 東條美奈子 : Annual report of action in the JCS prevention committee and future perspectives, 第83回日本循環器学会学術集会, Mar. 2019.
411.	Takeshi Soeki, Tomomi Matsuura, Daiju Fukuda, 松本和久, Takeshi Tobiume, Kenya Kusunose, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : The Factor Xa Inhibitor, Edoxaban, Prevents Cardiac Remodeling in Rats with Myocardial Infarction, 第83回日本循環器学会学術集会, Mar. 2019.
412.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : Stress Echocardiography for Pulmonary Hypertension, 第83回日本循環器学会学術集会, Mar. 2019.
413.	川端豊, Tetsuzo Wakatsuki, Koji Yamaguchi, Hiroyuki Ito, Daiju Fukuda, 轟貴史, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Coronary intraplaque microluminal structure are associated with the quality and quantity of epicardial adipose tissue -A fresh cadaveric stury-, 第83回日本循環器学会学術集会, Mar. 2019.
414.	平田有紀奈, Kenya Kusunose, Hirotsugu Yamada, 森田沙瑛, 鳥居裕太, 西尾進, ゼングロバート, 西條良仁, Shusuke Yagi, Takeshi Soeki and Masataka Sata : マラソン完走後の左房リザーバーストレイン反応を予測する指標の検討, 第83回日本循環器学会学術集会, Mar. 2019.
415.	Arief Rahadian, Daiju Fukuda, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Canagliflozin, a Sglt-2 Inhibitor, Prevents Endothelial Dysfunction and Atherosclerosis in Diabetic Apolipoprotein E-deficient Mice, 第83回日本循環器学会学術集会, Mar. 2019.
416.	Byambasuren Ganbaatar, Daiju Fukuda, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Empagliflozin Attenuates Endothelial Dysfunction and Atherogenesis by Inhibiting Inflammation in the Vasculature and Adipose Tissue in Diabetic Apolipoprotein E-deficient Mice, 第83回日本循環器学会学術集会, Mar. 2019.
417.	Aini Kunduziayi, Daiju Fukuda, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Vildagliptin, a DPP-4 Inhibitor, Prevents Atherogenesis Targeting Multiple Cell-types in Non-diabetic Apolipoprotein E-deficient Mice, 第83回日本循環器学会学術集会, Mar. 2019.
418.	Kenya Kusunose, 鳥居裕太, Hirotsugu Yamada and Masataka Sata : Clinical Role of Cardiovascular Imaging for IgG4-related Cardiovascular Disease, 第83回日本循環器学会学術集会, Mar. 2019.
419.	森田沙瑛, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 平田有紀奈, 鳥居裕太, 西條良仁, 阿部美保 and Masataka Sata : 強皮症における6分間歩行距離の規定因子:新エコー図法を用いた検討, 第83回日本循環器学会学術集会, Mar. 2019.
420.	平田有紀奈, Kenya Kusunose, Hirotsugu Yamada, 森田沙瑛, 鳥居裕太, 西尾進, 山口夏美, Zengu Robahto, 西條良仁, Shusuke Yagi, Takeshi Soeki and Masataka Sata : カーフスリーブは下腿浮腫を軽減するか:表在エコー検査による検討, 第83回日本循環器学会学術集会, Mar. 2019.
421.	藤本裕太, Kenya Kusunose, 西條良仁, Zheng Robert, 原田貴文, 松本和久, 上野理絵, 川端豊, 山田なお, Hiroyuki Ito, 轟貴史, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Hirotsugu Kurobe and Masataka Sata : Staphylococcus による感染性内膜炎の一例, 第113回日本循環器学会四国合同地方会, Dec. 2018.
422.	Zheng Robert, Takayuki Ise, 川端豊, Shusuke Yagi, 西條良仁, 上野理絵, Mika Bando, Hiroyuki Ito, 轟貴史, Tomomi Matsuura, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Hirotsugu Kurobe, Eiki Fujimoto, Tetsuya Kitagawa and Masataka Sata : Single coronary 合併重症ASに対してTAVIを施行し救命し得た1例, 第113回日本循環器学会四国合同地方会, Dec. 2018.
423.	Masataka Sata : Debate:炎症抑える次の一手は何か?【EPA】, 第4回ARIA 本音で徹底討論何でもARIA 日本のOpinion leader のDebete を聴こう!, Nov. 2018.
424.	Masataka Sata : DOAC(Vascular Protection), 第4回ARIA Meet the Professo∼これぞ教授の究極プレゼン!12人の現役教授が5分で語る心血管イベント抑制薬∼ 第2部, Nov. 2018.
425.	西條良仁, Hirotsugu Yamada, Kenya Kusunose and Masataka Sata : アントラサイクリン系抗がん剤による左室心筋障害の局在性とがん治療関連心機能障害発生の検討, 第1回日本腫瘍循環器学会学術集会, Nov. 2018.
426.	Kenya Kusunose, Hirotsugu Yamada, 西條良仁 and Masataka Sata : Vascular endothelial growth factor 阻害薬の眼内投与後に急性冠症候群を発症した 4 症例, 第1回日本腫瘍循環器学会学術集会, Nov. 2018.
427.	Hirotsugu Yamada, Mika Bando, Kenya Kusunose, 西條良仁 and Masataka Sata : 腫瘍循環器診療における超音波検査の役割，腫瘍循環器外来と超音波センターの連携, 第1回日本腫瘍循環器学会学術集会, Nov. 2018.
428.	Hirotsugu Yamada, 平田有紀奈, Mika Bando, Kenya Kusunose, 西條良仁, 西尾進, Takeshi Soeki and Masataka Sata : 心外膜下脂肪厚の超音波計測とその臨床的意義, 第45回日本超音波医学会関西地方会, Oct. 2018.
429.	Kenya Kusunose, Yuta Torii, Takayuki Ise, Hirotsugu Yamada and Masataka Sata : Incremental Prognostic Value of Diastolic Dysfunction by updated recommendation, 第22回日本心不全学会学術集会(東京), Oct. 2018.
430.	工藤明宏, 待井典剛, 小野利夫, 大城義人, 高橋隆, 種田嘉信, 比嘉盛丈, Shusuke Yagi, 仲地健, 小林淳, 及川雅啓, Hirotsugu Yamada, 竹石恭知, Masataka Sata and Michio Shimabukuro : 時効型インスリン療法中の2型糖尿病患者におけるタバグリフロジンの血糖日内変動に及ぼす効果, 第39回日本肥満学会(神戸), Oct. 2018.
431.	Yutaka Kawabata, Tetsuzo Wakatsuki, Koji Yamaguchi, Hiroyuki Itou, Kenya Kusunose, Tomomi Matsuura, Takafumi Todoroki, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : 未固定遺体において光干渉断層法で観察される冠動脈壁微小管腔構造と局所周囲脂肪炎症との関連, 第66回日本心臓病学会学術集会, Sep. 2018.
432.	Hiroyuki Ito, Tetsuzo Wakatsuki, Koji Yamaguchi, Daiju Fukuda, Yutaka Kawabata, Takayuki Ise, Kenya Kusunose, Tomomi Matsuura, Takafumi Todoroki, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : 未固定遺体における冠動脈壁小管腔構造と局所心臓周囲脂肪内炎症との関連, 第66回日本心臓病学会学術集会, Sep. 2018.
433.	Yukina Hirata, Hirotsugu Yamada, Kenya Kusunose, Susumu Nishio, Hrada Osamu, Miyasato Naomi, Hrakuni Atsusi, Ito Nobuhiko, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Echocardiographic Evaluation of Epicardial Adipose Tissue Thickness in Patients with Coronary Artery Disease: A Multicenter Study, 第66回日本心臓病学会学術集会, Sep. 2018.
434.	Yuta Torii, Kenya Kusunose, Susumu Nishio, 松本力三, Yukina Hirata, 天野里江, Yoshihito Saijoh, Mika Bando, Hirotsugu Yamada and Masataka Sata : 深部静脈血栓症に対する各種DOACsの治療成績∼下肢静脈エコー検査を用いた検討∼, 第66回日本心臓病学会学術集会, Sep. 2018.
435.	Susumu Nishio, Kenya Kusunose, Hiroshi Kagusa, Yukina Hirata, Yuta Torii, 天野里江, 山尾雅美, Yoshihito Saijoh, Mika Bando, Hirotsugu Yamada and Masataka Sata : 急性期脳卒中患者におけるB型ナトリウム利尿ペプチドの臨床的意義, 第66回日本心臓病学会学術集会, Sep. 2018.
436.	Koji Yamaguchi, Tetsuzo Wakatsuki, Yoshihito Saijoh, 上野理絵, Yutaka Kawabata, Mika Bando, Hiroyuki Ito, Takafumi Todoroki, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : 第三世代薬剤溶出性ステント留置後における局所凝固反応塗装ステント長の関連性, 第66回日本心臓病学会学術集会, Sep. 2018.
437.	Yukina Hirata, Kenya Kusunose, Hirotsugu Yamada, Yuta Torii, Susumu Nishio, Yoshihito Saijoh, Mika Bando, Takayuki Ise, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 過度に蓄積した心外膜下脂肪は薬剤溶出型ステント留置後の再狭窄を予測するマーカーとなる, 第66回日本心臓病学会学術集会, Sep. 2018.
438.	Daiju Fukuda, Koji Yamaguchi, Kenya Kusunose, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki, Takeshi Soeki and Masataka Sata : 活性型血液凝固第X因子が冠動脈硬化に与える影響, 第66回日本心臓病学会学術集会, Sep. 2018.
439.	Takafumi Todoroki, Tetsuzo Wakatsuki, Koji Yamaguchi, Kumiko Sutou, Takafumi Harada, 上野理絵, Yoshihito Saijoh, Yutaka Kawabata, Hiroyuki Itou, Takayuki Ise, Takeshi Tobiume and Masataka Sata : ステント遠位部狭窄病変の関与が疑われた2枝同時発症の超遅発性ステント血栓症の1例, 第25回日本心血管インターベーション治療学会(CVIT)中国・四国地方会, Sep. 2018.
440.	Yutaka Kawabata, Tetsuzo Wakatsuki, Koji Yamaguchi, Hiroyuki Itou, 上野理絵, Takayuki Ise, Takafumi Todoroki, Takeshi Tobiume and Masataka Sata : 光干渉断層法で観察される冠動脈壁微小管腔構造と局所周囲脂肪炎症との関連-未固定遺体における検討-, 第25回日本心血管インターベーション治療学会(CVIT)中国・四国地方会, Sep. 2018.
441.	Masataka Sata : ``異所性脂肪''から考える動脈硬化の成因と糖尿病治療, 第50回日本動脈硬化学会総会・学術集会ランチョンセミナー3, Jul. 2018.
442.	Masataka Sata : 脂質異常症治療の最新の動向-映像でみる動脈硬化の新知見と異所性脂肪-, 第5回日本心血管脳卒中学会学術集会,ランチョンセミナー3, Jun. 2018.
443.	Masataka Sata : 脂質異常症治療の最新の動向-映像でみる動脈硬化の新知見と異所性脂肪-, 第112回日本循環器学会中国・四国合同地方会ランチョンセミナー4:, Jun. 2018.
444.	Hiroyuki Ito, Takeshi Soeki, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : AVNRTアブレーション治療後に発生したJunctional Tachycardiaの1例, 第112回日本循環器学会中国・四国合同地方会, Jun. 2018.
445.	Takafumi Todoroki, Tetsuzo Wakatsuki, Koji Yamaguchi, Seno Hiromitsu, Kumiko Sutou, Yoshihito Saijoh, Yutaka Kawabata, 上野理絵, Hiroyuki Ito, Tomomi Matsuura, Kenya Kusunose, Takayuki Ise, Takeshi Tobiume, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : EES留置3年後，術前に抗血小板剤中止しペパリン置換したにもかかわらず2枝同時ステント閉塞を起こした1例, 第112回日本循環器学会中国・四国合同地方会, Jun. 2018.
446.	(名) Shimizu, Hiromitsu Seno, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Tetsuzo Wakatsuki, Takeshi Soeki, Takashi Iwase, Hirotsugu Kurobe, Tetsuya Kitagawa and Masataka Sata : 一年の経過で急速に進行したCalcified Amorphous Tumor(CAT)に対し腫瘍摘出手術を行った一例, 第112回日本循環器学会中国・四国合同地方会, Jun. 2018.
447.	Zheng Robert, Kumiko Sutou, Kenya Kusunose, Tomomi Matsuura, Hiromitsu Seno, Yoshihito Saijoh, 上野理絵, Yutaka Kawabata, Mika Bando, ito hironori, Takafumi Todoroki, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 薬物治療が著効したSLE関連心筋炎の一例, 第112回日本循環器学会中国・四国合同地方会, Jun. 2018.
448.	Yoshihito Saijoh, Kenya Kusunose, Hirotsugu Yamada, Susumu Nishio, Hiromitsu Seno, Kumiko Sutou, Yutaka Kawabata, 上野理絵, Hiroyuki Itou, Takafumi Todoroki, Tomomi Matsuura, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : アトラサイクリン系抗癌剤による心筋障害の局在性および化学療法関連心筋障害との関連の検討, 第112回日本循環器学会中国・四国合同地方会, Jun. 2018.
449.	Masataka Sata : 臨床教室における研究の楽しさ，リサーチ最前線, 第112回日本循環器学会中国・四国合同地方会, Jun. 2018.
450.	松本力三, Susumu Nishio, Yuta Torii, Asami Yuasa, Yukina Hirata, 天野里江, 山尾雅美, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 糖尿病性腎症の各病期における超音波像の比較, Japanese Journal of Medical Ultrasound Technology, Vol.43, No.Suppl., S131, Jun. 2018.
451.	Asami Yuasa, Susumu Nishio, Yukina Hirata, Yuta Torii, 天野里江, 松本真依, 松本力三, 山尾雅美, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 頸動脈プラーク潰瘍形成と神経学的症状の有無について, Japanese Journal of Medical Ultrasound Technology, Vol.43, No.Suppl., S189, Jun. 2018.
452.	平田有紀奈, Susumu Nishio, 原田修, 宮里尚美, 原國督, Kenya Kusunose, 伊藤敦彦, Hirotsugu Yamada and Masataka Sata : 心外膜下脂肪厚計測の有用性の証明多施設共同研究, Japanese Journal of Medical Ultrasound Technology, Vol.43, No.Suppl., S143, Jun. 2018.
453.	Yuta Torii, Susumu Nishio, 天野里江, Asami Yuasa, 松本力三, 平田有紀奈, 山尾雅美, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 右腎原発悪性リンパ腫の1例, Japanese Journal of Medical Ultrasound Technology, Vol.43, No.Suppl., S233, Jun. 2018.
454.	Yukina Hirata, Susumu Nishio, Yuta Torii, 天野里江, 山尾雅美, Yoshihito Saijoh, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 糖尿病患者の冠動脈有意狭窄予測における心外膜下脂肪厚計測の有用性, Japanese Journal of Medical Ultrasound Technology, Vol.43, No.3, 231-238, Jun. 2018.
455.	Susumu Nishio, Kenya Kusunose, 平田有紀奈, 鳥居裕太, 天野里江, 山尾雅美, Hiroyuki Ito, Takayuki Ise, Koji Yamaguchi, Tetsuzo Wakatsuki, Hirotsugu Yamada and Masataka Sata : 左上肢の脱力で脳卒中センターへ搬送された急性冠症候群の1例, Japanese Journal of Medical Ultrasound Technology, Vol.43, No.3, 363, Jun. 2018.
456.	Masataka Sata : 心血管イベント抑制に向けた脂質異常症対策-動脈硬化の新知見とω3不飽和脂肪酸の薬理作用-, 第18回日本抗加齢医学会総会,モーニングセミナー, May 2018.
457.	Masataka Sata : 心血管イベント抑制に向けた脂質異常症対策-動脈硬化の新知見とω3不飽和脂肪酸の薬理作用-, 第18回日本NO学会合同学術集会ランチョンセミナー, May 2018.
458.	松本力三, 鳥居裕太, 西尾進, 平田有紀奈, 天野里江, 徳永尚樹, Akishige Ikegame, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 深部静脈血栓症のスクリーニング検査におけるTATおよびD-dimerの検討, The Japanese Journal of Phlebology, Vol.29, No.2, 290, May 2018.
459.	天野理江, Kenya Kusunose, Kumiko Sutou, Hirotsugu Yamada and Masataka Sata : ステロイドおよび免疫抑制剤治療により改善がえられたSLE関連心筋炎の1症例, 日本心エコー図学会第29回学術集会, Apr. 2018.
460.	Yoshihito Saijoh, Hirotsugu Yamada, Kenya Kusunose, Mika Bando, Hiromitsu Seno, Susumu Nishio, Yuta Torii, Yukina Hirata, 天野理江, 山尾雅美, Takeshi Soeki and Masataka Sata : 化学療法関連心機能障害(CTRCD)に対し内科的加療が奏功した乳癌患者の一例, 日本心エコー図学会第29回学術集会, Apr. 2018.
461.	Mika Bando, Junya Kuwahata, Kenya Kusunose, Yoshihito Saijoh, Susumu Nishio, Yukina Hirata, Yuta Torii, Masataka Sata and Hirotsugu Yamada : サルコイドーシスにおける左室global longitudinal strainの臨床的意義, 日本心エコー図学会第29回学術集会, Apr. 2018.
462.	平田有紀奈, Kenya Kusunose, Hirotsugu Yamada, 阿部美保, Mika Bando, 西條良仁, 瀬野弘光, 西尾進, 鳥居裕太 and Masataka Sata : 自家末梢血幹細胞移植併用大量化学療法により長期生存が得られた心アミロイドーシスの1例, 日本心エコー図学会第29回学術集会, Apr. 2018.
463.	Yuta Torii, Kenya Kusunose, Hiromitsu Seno, Yoshihito Saijoh, Mika Bando, Susumu Nishio, Yukina Hirata, Masataka Sata and Hirotsugu Yamada : 2009年・2016年のASE左室拡張不全ガイドラインを用いた心不全患者の再入院予測, 日本心エコー図学会第29回学術集会, Apr. 2018.
464.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 心房細動による左室機能障害, 日本心エコー図学会第29回学術集会, Apr. 2018.
465.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 僧帽弁逆流症におけるストレインイメージングの臨床的有用性, 日本心エコー図学会第29回学術集会, Apr. 2018.
466.	Masataka Sata : 血管不全における血管周囲脂肪組織の役割, 第3回日本血管不全学会学術集会, Apr. 2018.
467.	Sae Morita, Susumu Nishio, (名) Hayashi, Kenya Kusunose, (名) Matsumoto, Yukina Hirata, Yuta Torii, (名) Amano, 山尾雅美, Yoshihito Saijoh, Hirotsugu Yamada and Masataka Sata : SphygmoCor-XCELの使用経験∼HEM-9000AIとの比較∼, 第3回日本血管不全学会学術集会, Apr. 2018.
468.	Yukina Hirata, Hirotsugu Yamada, Kenya Kusunose, Mika Bando, Yoshihito Saijoh, Hiromitsu Seno, Susumu Nishio, Yuta Torii and Masataka Sata : メタボリックシンドローム関連疾患のマネージメントにおける超音波検査の役割各種脂肪組織厚とメタボリックシンドロームとの関連超音波検査を用いた検討, Japanese Journal of Medical Ultrasonics, Vol.45, No.Suppl., S197, Apr. 2018.
469.	Hirotsugu Yamada, Mika Bando, Kenya Kusunose, Yoshihito Saijoh, Yukina Hirata, Yuta Torii, 天野里江, 山尾雅美, Susumu Nishio and Masataka Sata : Point-of-care USのプロトコルを考えるホーカス・ポーカス FOCUSだけではないPOCUSの心エコー検査, Japanese Journal of Medical Ultrasonics, Vol.45, No.Suppl., S200, Apr. 2018.
470.	Yoshihito Saijoh, Kenya Kusunose, Mika Bando, Hiromitsu Seno, Susumu Nishio, Yukina Hirata, Yuta Torii, 天野里江, Hirotsugu Yamada and Masataka Sata : Onco-Cardiologyにおける心血管超音波検査の活用法アントラサイクリン系抗癌剤による化学療法関連心筋障害の局在性評価, Japanese Journal of Medical Ultrasonics, Vol.45, No.Suppl., S258, Apr. 2018.
471.	Yuta Torii, Hirotsugu Yamada, Susumu Nishio, 松本力三, Yukina Hirata, 天野里江, Yoshihito Saijoh, Mika Bando, Kenya Kusunose and Masataka Sata : Onco-Cardiologyにおける心血管超音波検査の活用法担癌患者における癌種別の深部静脈血栓症有所見率とDダイマー値の検討, Japanese Journal of Medical Ultrasonics, Vol.45, No.Suppl., S260, Apr. 2018.
472.	Hirotsugu Yamada, Yoshihito Saijoh, Kenya Kusunose, Mika Bando, Yuta Torii, Yukina Hirata, 天野里江, 山尾雅美, Susumu Nishio and Masataka Sata : 心臓超音波検査の最新技術:本当に必要なの? 今はなくても困らない，でも，あったら便利, Japanese Journal of Medical Ultrasonics, Vol.45, No.Suppl., S267, Apr. 2018.
473.	Mika Bando, Hirotsugu Yamada, Kenya Kusunose, Yoshihito Saijoh, Masataka Sata and 和宏西上 : ERで求められる心血管超音波検査胸痛疾患での救急エコー心血管エコー検査による原因と血行動態の評価, Japanese Journal of Medical Ultrasonics, Vol.45, No.Suppl., S274, Apr. 2018.
474.	Kenya Kusunose, Yoshihito Saijoh, Hirotsugu Yamada and Masataka Sata : 負荷心臓超音波検査の活かし方・落とし穴(症例ベース) 症例から学ぶ負荷心臓超音波検査のピットフォール, Japanese Journal of Medical Ultrasonics, Vol.45, No.Suppl., S280, Apr. 2018.
475.	Mika Bando, Hirotsugu Yamada, Kenya Kusunose, Yoshihito Saijoh, Susumu Nishio, Masataka Sata and 西上和宏 : 深部静脈血栓症診療にエコーをどう活かすか深部静脈血栓症診療に超音波検査をどう活かすか他のモダリティーとの役割分担, Japanese Journal of Medical Ultrasonics, Vol.45, No.Suppl., S448, Apr. 2018.
476.	Hirotsugu Yamada, Mika Bando, Yuta Torii, Yukina Hirata, 天野里江, 山尾雅美, Susumu Nishio and Masataka Sata : 血管エコー技の伝承教育システムを考える「創生期」から「成長期」に入った血管エコー検査, Japanese Journal of Medical Ultrasonics, Vol.45, No.Suppl., S523, Apr. 2018.
477.	Yuta Torii, Susumu Nishio, 松本力三, Yukina Hirata, 天野里江, Yoshihito Saijoh, Hiromitsu Seno, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 深部静脈血栓症に対する直接経口抗凝固薬の治療効果下肢静脈エコー検査による検討, Japanese Journal of Medical Ultrasonics, Vol.45, No.Suppl., S600, Apr. 2018.
478.	天野里江, Yuta Torii, Susumu Nishio, Yukina Hirata, 松本力三, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 浅側頭動脈にMonckeberg型の石灰化を認めた巨細胞性動脈炎の3症例, Japanese Journal of Medical Ultrasonics, Vol.45, No.Suppl., S766, Apr. 2018.
479.	Susumu Nishio, Kenya Kusunose, Yukina Hirata, Yukina Fujita, Yuta Torii, 天野里江, 山尾雅美, Yoshihito Saijoh, Hirotsugu Yamada and Masataka Sata : 最新の心エコー装置および装置非依存性strain解析ソフトを用いたGLS計測の装置間差, Japanese Journal of Medical Ultrasonics, Vol.45, No.Suppl., S809, Apr. 2018.
480.	Kenya Kusunose, Yoshihito Saijoh, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Right Ventricular Function Predicts Beneficial Effects of Cardiac Rehabilitation in Patients with Chronic Heart Failure, 第82回日本循環器学会, Mar. 2018.
481.	Yuta Torii, Kenya Kusunose, Hirotsugu Yamada, Hiromitsu Seno, Yoshihito Saijoh, Susumu Nishio, hirata yukina and Masataka Sata : Association of Left Ventricular Diastolic Function using American Society of Echocardiography Recommendation with Readmission in Patients with Heart Failure, 第82回日本循環器学会, Mar. 2018.
482.	akira hirono, Kenya Kusunose, 蔭山徳人, 藤永裕之 and Masataka Sata : Development and validation of Optimal Cut-off value in inter-armsystolic Blood pressue Difference for prediction of Cardiovascular Events, 第82回日本循環器学会, Mar. 2018.
483.	Yoshihito Saijoh, Kenya Kusunose, Hirotsugu Yamada, Susumu Nishio, Yukina Hirata, Yuta Torii, Kumiko Sutou, 上野理絵, Yutaka Kawabata, Hiroyuki Itou, Takafumi Todoroki, Tomomi Matsuura, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Anthracyclines induce early changes in localized left ventricular dysfunction., 第82回日本循環器学会, Mar. 2018.
484.	Takeshi Soeki, Tomomi Matsuura, Daiju Fukuda, Takeshi Tobiume, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : C-type natriuretic peptide improves left ventricular diastolic dysfunction in HFpEF model rats., 第82回日本循環器学会, Mar. 2018.
485.	BYAMBASUREN GANBAATAR, Daiju Fukuda, Hotimah Masdan Salim, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Ticagrelor, a P2Y12 Antagonist,Attenuates Endothelial Dysfunction and Inhibits Atherogenesis in Apolipoprotein-E-deficient Mice., 第82回日本循環器学会, Mar. 2018.
486.	Yutaka Kawabata, Takeshi Soeki, Takayuki Ise, Tomomi Matsuura, Yoshihito Saijoh, Takeshi Tobiume, Shusuke Yagi, Koji Yamaguchi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Effects of L-/N-type Calcium Channel Blocker on Proteinuria and Angiotensin -renin Feedback in Hypertensive Patients, 第82回日本循環器学会, Mar. 2018.
487.	Takayuki Ise, Shusuke Yagi, Yutaka Kawabata, Seno Hiromitsu, Kumiko Sutou, Yoshihito Saijoh, Rie Ueno, Hiroyuki Ito, Takafumi Todoroki, Tomomi Matsuura, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Acute Hemodynamic Effect of Handgrip Stress in Patients with Chronic Heart Failure., 第82回日本循環器学会, Mar. 2018.
488.	Shusuke Yagi and Masataka Sata : Inhibition of Endothelin-1 Actions Improved Systemic Sclerosis-related Vasculopathy through Anti-oxidant Effects Leading to Increased Nitric Oxide Bioavailability., 第82回日本循環器学会, Mar. 2018.
489.	Daiju Fukuda and Masataka Sata : The Mechanism by Which Lifestyle-related Diseases Cause Atherosclerosis;The Role of Innate Immune System., 第82回日本循環器学会, Mar. 2018.
490.	Daiju Fukuda, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Inhibition of Thrombin Signaling by Dabigatran, a Direct Thrombin Inhibitor,Attenuates Endothelial Dysfunction in Diabetic Mice., 第82回日本循環器学会, Mar. 2018.
491.	Yukina Hirata, Kenya Kusunose, Hirotsugu Yamada, Yuta Torii, Susumu Nishio, Hiromitsu Seno, Tomomi Matsuura, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Impact of Marathon Running on Left Atrial function in healthy trained volunteers, 第82回日本循環器学会, Mar. 2018.
492.	Yuta Torii, Kenya Kusunose, Hirotsugu Yamada, Hiromitsu Seno, Yoshihito Saijoh, Susumu Nishio, Yukina Hirata and Masataka Sata : 退院前の推定左室充満圧および収縮期肺動脈圧は心不全患者の再入院と関連する, 第82回日本循環器学会, Mar. 2018.
493.	Akira Hirono, Kenya Kusunose, 蔭山徳人, 藤永裕之 and Masataka Sata : Efficacy and Safety of Alirocumab (150mg Q4W) in Japanese Hypercholesterolemic Patients on No statin or Lowest Dose Statin., 第82回日本循環器学会, Mar. 2018.
494.	Koji Yamaguchi, Tetsuzo Wakatsuki, Yutaka Kawabata, Hiroyuki Itou, Takafumi Todoroki, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Differential Response of Local Coagulation after Coronary Angioplasty with Paclitaxel., 第82回日本循環器学会, Mar. 2018.
495.	Hiroyuki Ito, Kenya Kusunose, Hirotsugu Yamada, Hiromitsu Seno, Yoshihito Saijoh, Susumu Nishio, Yukina Hirata and Masataka Sata : Association of Left Ventricular Diastolic Function using American Society of Echocardiography Recommendation with Readmission in Patients with Heart Failure., 第82回日本循環器学会, Mar. 2018.
496.	Tetsuzo Wakatsuki, Koji Yamaguchi, Daiju Fukuda, Yutaka Kawabata, 轟貴史, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Growth of vasa vasorum is associated with local inflammation around coronary plaque in fresh cadavers., 第82回日本循環器学会, Mar. 2018.
497.	Hiroyuki Ito, Tetsuzo Wakatsuki, Koji Yamaguchi, Daiju Fukuda, Yutaka Kawabata, 轟貴史, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Growth of Vasa Vasorum is Associated with Local Inflammation around Coronary Plaque in Fresh Cadavers(和訳中), 日本循環器学会学術集会抄録集, PJ007-3, Mar. 2018.
498.	Koji Yamaguchi, Tetsuzo Wakatsuki, Yutaka Kawabata, Hiroyuki Ito, 轟貴史, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Differential Response of Local Coagulation after Coronary Angioplasty with Paclitaxel(和訳中), 日本循環器学会学術集会抄録集, PJ022-1, Mar. 2018.
499.	Yutaka Kawabata, Takeshi Soeki, Takayuki Ise, Tomomi Matsuura, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Koji Yamaguchi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Effects of L-/N-type Calcium Channel Blocker on Proteinuria and Angiotensin II-renin Feedback in Hypertensive Patients(和訳中), 日本循環器学会学術集会抄録集, PJ067-4, Mar. 2018.
500.	Yuta Torii, Kenya Kusunose, Hirotsugu Yamada, Hiromitsu Seno, Yoshihito Saijoh, Susumu Nishio, Yukina Hirata and Masataka Sata : 退院前の推定左室充満圧および収縮期肺動脈圧は心不全患者の再入院と関連する, 日本循環器学会学術集会抄録集, CP17-2, Mar. 2018.
501.	Gulinu Maimaituxun, Michio Shimabukuro, Daiju Fukuda, Shusuke Yagi, Yukina Hirata, Takashi Iwase, Shoichiro Takao, Tomomi Matsuura, Takayuki Ise, Tetsuzo Wakatsuki, Masafumi Harada and Masataka Sata : The impact of epicardial adipose tissue thickness on left ventricular diastolic dysfunction in patients with preserved ejection fraction, 日本老年医学会四国地方会, Feb. 2018.
502.	Arief Rahadian, Daiju Fukuda, Salimc Masdan Hotimah, Michio Shimabukuro and Masataka Sata : Canagliflozin Attenuates Endothelial Dysfunctin and Atherosclerosis in Diabetic, 日本老年医学会四国地方会, Feb. 2018.
503.	KUNDUZIAYI AINI, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Combination of vildagliptin,a DPP-4 Inhibitor, and metformin have additive beneficial effects on endothelial function and atherogenesis in non-diabetic apolipoprotein-E deficient mice, 日本老年医学会四国地方会, Feb. 2018.
504.	Shusuke Yagi, Takayuki Ise, Yutaka Kawabata, Hiroyuki Ito, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 経カテーテル大動脈弁植込み術を施した超高齢大動脈弁狭窄症の1例, 日本老年医学会四国地方会, Feb. 2018.
505.	Shusuke Yagi, 西山誠一, 和田敏裕, 板垣達三, 植淵昌毅, 竹治尚志 and Masataka Sata : 当院におけるマムシ咬傷の検討, 第256回徳島医学会学術集会, Feb. 2018.
506.	Shusuke Yagi, 西山誠一, 和田敏裕, 植淵昌毅, 竹治尚志 and Masataka Sata : 当院における蜂刺傷症の検討, 第256回徳島医学会学術集会, Feb. 2018.
507.	平田有紀奈, 西尾進, 原田修, 宮里尚美, 原國督, Kenya Kusunose, 伊藤敦彦, Hirotsugu Yamada and Masataka Sata : 外膜下脂肪厚計測の有用性の証明~多施設共同研究~, 超音波検査技術, Vol.43, No.Suppl, S143, 2018.
508.	Ganbaatar Byambasuren, Daiju Fukuda, Salim Masdan Hotimah, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Ticagrelor, a P2Y12 antagonist, prevents endothelial dysfunction and the development of atherosclerosis in apolipoprotein-E deficient mice, 脳心血管抗加齢研究会2017, Dec. 2017.
509.	Aini Kunduziayi, Daiju Fukuda, Salim Masdan Hotimah, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Atheroprotective effects of Linagliptin, a DPP-4 inhibitor, in normoglycemic ApoE/mice, 脳心血管抗加齢研究会2017, Dec. 2017.
510.	Daiju Fukuda and Masataka Sata : 自己DNA断片を介した自然免疫機構が心血管代謝性疾患の発症を促進する, 脳心血管抗加齢研究会2017, Dec. 2017.
511.	Ganbaatar Byambasuren, Daiju Fukuda, Salim Masdan Hotimah, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Ticagrelor, a P2Y12 Antagonist, Attenuates Vascular Dysfunction and Inhibits Atherogenesis in Apolipoprotein-E-deficient Mice, CVMW2017, Dec. 2017.
512.	Aini Kunduziayi, Daiju Fukuda, Salim Masdan Hotimah, Shusuke Yagi, Takeshi Soeki and Masataka Sata : DPP-4 inhibitor, linagliptin, ameliorates endothelial dysfunction and the development of atherosclerosis in apolipoprotein-E deficient mice, CVMW2017, Dec. 2017.
513.	Akira Takashima, Daiju Fukuda, 田中君枝, 東邦康智, Yoichiro Hirata, Shusuke Yagi, Takeshi Soeki and Masataka Sata : ω3系不飽和脂肪酸の抗動脈硬化作用, CVMW2017, Dec. 2017.
514.	Daiju Fukuda, Salim Masdan Hotimah, Shusuke Yagi, Takeshi Soeki and Masataka Sata : 直接的トロンビン阻害薬であるダビガトランは糖尿病性血管内皮機能障害を改善する, CVMW2017, Dec. 2017.
515.	志村拓哉, 西條良仁, Koji Yamaguchi, Kenya Kusunose, Hirotsugu Yamada, 瀬野弘光, 數藤久美子, 上野理絵, 川端豊, 伊藤浩敬, 轟貴史, Tomomi Matsuura, Takayuki Ise, Takeshi Tobiume, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 下肢静脈血栓症の誘因となる下肢血流障害の検討-下肢静脈造影での検討-, 第111回日本循環器学会四国地方会, Dec. 2017.
516.	豊田直人, 轟貴史, Takeshi Soeki, 瀬野弘光, 數藤久美子, 西條良仁, 上野理絵, 川端豊, 伊藤浩敬, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 診断から40年後に治療しえた著明なBroad Kent束を有するWPW症候群の一例, 第111回日本循環器学会四国地方会, Dec. 2017.
517.	中野睦基, 川端豊, Takeshi Soeki, Tomomi Matsuura, Takeshi Tobiume, 瀬野弘光, 數藤久美子, 西條良仁, 上野理絵, 伊藤浩敬, 轟貴史, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 嚥下性失神に対して高級性ペースメーカー植え込み術が有効であった1例, 第111回日本循環器学会四国地方会, Dec. 2017.
518.	矢野哲弘, Tomomi Matsuura, 數藤久美子, 瀬野弘光, 西條良仁, 上野理絵, 川端豊, 伊藤浩敬, 轟貴史, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心房細動アブレーション後の医原性心房中隔欠損残存により右心不全症状をきたした一例, 第111回日本循環器学会四国地方会, Dec. 2017.
519.	Tatsuya Maruhashi, Junko Soga, Noritaka Fujimura, Naomi Idei, Shinsuke Mikami, Yumiko Iwamoto, Akimichi Iwamoto, Masato Kajikawa, Takeshi Matsumoto, Nozomu Oda, Shinji Kishimoto, Shogo Matsui, Haruki Hashimoto, Yoshiki Aibara, Farina Binti Mohamad Yusoff, Takayuki Hidaka, Yasuki Kihara, Kazuaki Chayama, Kensuke Noma, Ayumu Nakashima, Chikara Goto, Hirofumi Tomiyama, Bonpei Takase, Takahide Kohro, Toru Suzuki, Tomoko Ishizu, Shinichiro Ueda, Tsutomu Yamazaki, Tomoo Furumoto, Kazuomi Kario, Teruo Inoue, Shinji Koba, Kentaro Watanabe, Yasuhiko Takemoto, Takuzo Hano, Masataka Sata, Yutaka Ishibashi, Koichi Node, Koji Maemura, Yusuke Ohya, Taiji Furukawa, Hiroshi Ito, Hisao Ikeda, Akira Yamashina and Yukihito Higashi : Endothelial Function Is Impaired in Patients Receiving Antihypertensive Drug Treatment Regardless of Blood Pressure Level: FMD-J Study (Flow-Mediated Dilation Japan)., Hypertension, Vol.70, No.4, 790-797, Oct. 2017. (Summary) Hypertension is associated with endothelial dysfunction. Blood pressure significantly correlates with endothelial function in antihypertensive drug-naive subjects. The purpose of this study was to determine whether treatment status affects the relationship between blood pressure and endothelial function. We measured flow-mediated vasodilation (FMD) in 2297 subjects, including 1822 antihypertensive drug-naive subjects and 475 treated hypertensive patients. FMD significantly decreased in relation to increase in systolic blood pressure (8.2±3.1% in subjects with systolic blood pressure of <120 mm Hg, 7.5±2.8% for 120-129 mm Hg, 7.1±2.8% for 130-139 mm Hg, and 6.7±2.6% for ≥140 mm Hg; <0.001). Systolic blood pressure was independently associated with FMD in untreated subjects. In contrast, there was no significant relationship between systolic blood pressure and FMD in treated hypertensive patients (4.6±3.1% in treated hypertensives with systolic blood pressure of <120 mm Hg, 4.8±2.7% for 120-129 mm Hg, 4.9±2.8% for 130-139 mm Hg, and 4.5±2.3% for ≥140 mm Hg; =0.77). Propensity score matching analysis revealed that the prevalence of endothelial dysfunction defined as FMD of less than the division point for the lowest tertile, and the middle tertile of FMD was significantly higher in treated hypertensive patients than in untreated subjects in all systolic blood pressure categories. Endothelial function assessed by FMD was impaired regardless of the level of blood pressure achieved by antihypertensive drug treatment in hypertensive patients. (Keyword) Adult / Aged / Antihypertensive Agents / blood pressure / Blood Pressure Determination / Endothelium, Vascular / female / Humans / hypertension / Japan / male / Medication Therapy Management / Middle Aged / Vasodilation (Link to Publication Site) ● Publication site (DOI): 10.1161/HYPERTENSIONAHA.117.09612 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28808069 ● Summary page in Scopus @ Elsevier: 2-s2.0-85030614940 (DOI: 10.1161/HYPERTENSIONAHA.117.09612, PubMed: 28808069, Elsevier: Scopus)
520.	Susumu Nishio, Kenya Kusunose, Hirotsugu Yamada, Yukina Hirata, Yuta Torii, 天野里江, 山尾雅美, Seno Hiromitsu, Yoshihito Saijoh and Masataka Sata : 心エコー図検査の精度管理∼自施設内における検査間誤差∼, 第65回日本心臓病学会学術集会, Sep. 2017.
521.	Yutaka Kawabata, Tetsuzo Wakatsuki, Koji Yamaguchi, Hiroyuki Itou, Daiju Fukuda, Takayuki Ise, Kenya Kusunose, Tomomi Matsuura, 轟貴史, Akira Hirono, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : 未固定遺体における管脈プラーク性状と局所周囲脂肪内炎症物質との関連, 第65回日本心臓病学会学術集会, Sep. 2017.
522.	amano rie, Hirotsugu Yamada, Kenya Kusunose, Susumu Nishio, 平田有紀奈, Yuta Torii, Seno Hiromitsu, Yoshihito Saijoh and Masataka Sata : 頸動脈内膜中膜複合体厚にDPP4阻害薬シタグリプチンが及ぼす影響―アログリプチンからの切り替え試験, 第65回日本心臓病学会学術集会:大阪, Sep. 2017.
523.	Koji Yamaguchi, Tetsuzo Wakatsuki, 川端豊, 伊藤浩敬, 轟貴史, Tomomi Matsuura, Kenya Kusunose, Takeshi Tobiume, Takayuki Ise, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Biodegradable polymer SESの慢性期局所血管反応の検討-Durable polymer SESとの比較-, 第65回日本心臓病学会学術集会, Sep. 2017.
524.	Yoshihito Saijoh, Kenya Kusunose, Hirotsugu Yamada, Seno Hiromitsu, Susumu Nishio, Hiroyuki Itou, Takafumi Todoroki, Takayuki Ise, Tomomi Matsuura, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Tetsuzo Wakatsuki and Masataka Sata : 経食道心エコー図検査の再検によりvegetationを同定しえた感染性心内膜炎の一例, 第65回日本心臓病学会学術集会, Sep. 2017.
525.	Takafumi Todoroki, Shusuke Yagi, Kenya Kusunose, Takayuki Ise, Yoshihito Saijoh, Seno Hiromitsu, Akira Hirono, Tomomi Matsuura, Daiju Fukuda, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 膠原病患者での肺動脈楔入圧と左室拡張期末期圧の関係, 第65回日本心臓病学会学術集会, Sep. 2017.
526.	Masataka Sata : 心臓周囲脂肪から読み解く心不全合併糖尿病治療: SGLT2阻害薬の役割, 第65回日本心臓病学会学術集会, Sep. 2017.
527.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 肺高血圧症に対する6分間ホ高付加心エコー図検査の実際, 第65回日本心臓病学会学術集会, Sep. 2017.
528.	Yukina Hirata, Kenya Kusunose, Hirotsugu Yamada, Junya Kuwahata, Yuta Torii, 天野里江, Susumu Nishio, Hiromitsu Seno, Yoshihito Saijoh, Hiromitsu Seno, Shusuke Yagi, Takeshi Soeki and Masataka Sata : フルマラソンが心房機能に与える影響について∼，心エコー図検査を用いた検討∼, 第65回日本心臓病学会学術集会, Sep. 2017.
529.	Yuta Torii, Susumu Nishio, Kenya Kusunose, Yoshihito Saijoh, Hiromitsu Seno, 松本力三, Yukina Hirata, 天野里江, Hirotsugu Yamada and Masataka Sata : 治療効果判定に超音波検査が有用であったIgG4関連動脈周囲炎の1例, 第65回日本心臓病学会学術集会, Sep. 2017.
530.	Junya Kuwahata, Hirotsugu Yamada, 林修司, Kenya Kusunose, Yoshihito Saijoh, Hiromitsu Seno, Susumu Nishio, Yukina Hirata, Yuta Torii, Sae Morita and Masataka Sata : 左室・左房容積計測における Automated adaptive analytics algorithm を用いた3次元心エコー法と従来法との比較, 第65回日本心臓病学会学術集会, Sep. 2017.
531.	Tetsuzo Wakatsuki, Koji Yamaguchi, Daiju Fukuda, Yutaka Kawabata, Hiroyuki Itou, Takayuki Ise, Kenya Kusunose, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : 微小管腔構造を認める冠動脈壁の組織性状の評価-未固定遺体における検討-, 第65回日本心臓病学会学術集会, Sep. 2017.
532.	Hiromitsu Seno, Kenya Kusunose, Yoshihito Saijoh, Hirotsugu Yamada, Yukina Hirata, Yuta Torii, 天野里江, 山尾雅美, Susumu Nishio and Masataka Sata : 心臓リハビリテーションによる運動耐容能改善度の規定因子:心エコー図検査を用いた検討, 第65回日本心臓病学会学術集会, Sep. 2017.
533.	Kenya Kusunose, Hirotsugu Yamada, Susumu Nishio, Yuta Torii, Yukina Hirata, Hiromitsu Seno, Yoshihito Saijoh, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Preload Stress Echocardiography Predicts Outcomes in Patients with Pre-served Ejection Fraction and Low Gradient Aortic Stenosis, 第65回日本心臓病学会学術集会, Sep. 2017.
534.	Koji Yamaguchi, Tetsuzo Wakatsuki, Yutaka Kawabata, Hiroyuki Itou, 轟貴史, Takayuki Ise, Takeshi Tobiume and Masataka Sata : OPTIMOカテーテル使用後に生じた巨大血管解離の1例, 第24回日本心血管インターベーション治療学会中国・四国地方会, Sep. 2017.
535.	轟貴史, Tetsuzo Wakatsuki, Koji Yamaguchi, Yutaka Kawabata, Hiroyuki Itou, Takayuki Ise, Akira Hirono, Takeshi Tobiume and Masataka Sata : 局所的な右腎動脈狭窄を認め血管内超音波を併用し経皮的腎動脈形成術を施行した繊維筋性異形成症の1症例, 第24回日本心血管インターベーション治療学会中国・四国地方会, Sep. 2017.
536.	Yutaka Kawabata, Tetsuzo Wakatsuki, Koji Yamaguchi, Hiroyuki Itou, Takayuki Ise, 轟貴史, Takeshi Tobiume and Masataka Sata : SES留置遠隔期に再狭窄とPSSを同時に認めた病変に対するDCB治療の効果の検討-局所凝固反応の観点から-, 第24回日本心血管インターベーション治療学会中国・四国地方会, Sep. 2017.
537.	荒瀬美晴, Takeshi Tobiume, Hiroyuki Itou, Tomomi Matsuura, Takeshi Soeki, Hiromitsu Seno, Yoshihito Saijoh, Yutaka Kawabata, 轟貴史, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 薬物療法の継続が困難で頻脈誘発性心筋症を生じたが，カテーテルアブレーションにて合併症なく根治に成功した洞房リエントリー性頻拍の1例, 第255回徳島医学会学術集会, Aug. 2017.
538.	Masataka Sata : 動脈硬化の病態における慢性炎症の役割とその分子基盤, 第38回日本炎症・再生医学会, Jul. 2017.
539.	Hiroyuki Ito, Tetsuzo Wakatsuki, Koji Yamaguchi, Yutaka Kawabata, Akira Hirono, Takafumi Todoroki, Takayuki Ise, Takeshi Tobiume and Masataka Sata : The relationship between coronary plaque characteristics and local inflammation in adjacent epicardial adipose tissue in fresh cadaveric models, 第26回日本心血管インターベンション治療学会学術集会:京都, Jul. 2017.
540.	Yutaka Kawabata, Tetsuzo Wakatsuki, Koji Yamaguchi, 伊藤浩敬, Takayuki Ise, Akira Hirono, Takafumi Todoroki, Takeshi Tobiume and Masataka Sata : A first assessment of coronary plaque characteristics, adjacent epivascular adipose tissue, and histopathological findings in fresh cadaveric model-a case report-, 第26回日本心血管インターベンション治療学会学術集会:京都, Jul. 2017.
541.	Daiju Fukuda and Masataka Sata : The thrombin signaling in endothelial dysfunction in diabetes, 第49回日本動脈硬化学会総会・学術集会, Jul. 2017.
542.	瀬野弘光, Takeshi Soeki, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 計算負荷試験で誘発された心室性期外収縮の一例, 第110回日本循環器学会中国・四国合同地方会, Jun. 2017.
543.	Hiroyuki Itou, Takeshi Tobiume, Takeshi Soeki, Yuichiroh Ohkushi, Hiromitsu Seno, Yoshihito Saijoh, Yutaka Kawabata, 轟貴史, Akira Hirono, Tomomi Matsuura, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 左鎖骨下への植え込み型除細動器植え替え後に生じたTwiddler症候群の1例, 第110回日本循環器学会中国・四国合同地方会, Jun. 2017.
544.	川端豊, Takayuki Ise, Koji Yamaguchi, Tetsuzo Wakatsuki, Kenya Kusunose, Tomomi Matsuura, Shusuke Yagi, Takeshi Tobiume, Hirotsugu Yamada, Takeshi Soeki, 川谷洋平, 荒瀬裕己, Hirotsugu Kurobe, Eiki Fujimoto, Tetsuya Kitagawa and Masataka Sata : 肺癌術前にバルーン大動脈弁形成術を施行し良好な開大が得られた重症大動脈弁狭窄症の一例, 第110回日本循環器学会中国・四国地方会, Jun. 2017.
545.	Yoshihito Saijoh, Hirotsugu Yamada, Kenya Kusunose, Susumu Nishio, Yuichiroh Ohkushi, Hiromitsu Seno, Tomoya Hara, Yutaka Kawabata, Hiroyuki Itou, 轟貴史, Akira Hirono, Tomomi Matsuura, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki, Hirotsugu Kurobe, Shunsuke Watanabe and Masataka Sata : 著名な心内膜肥厚を認めた acromegalic cardiomyopathy の一例, 第110回日本循環器学会中国・四国地方会, Jun. 2017.
546.	Daiju Fukuda and Masataka Sata : 多価不飽和脂肪酸と動脈硬化性疾患, 第3回J-ISCP学術集会, Jun. 2017.
547.	Hirotsugu Yamada, Kenya Kusunose and Masataka Sata : Preload Stress Echocardiography を用いた運動耐用能の評価, 日本超音波医学会第90回学術集会, May 2017.
548.	Hirotsugu Yamada, Kenya Kusunose, 西條良仁 and Masataka Sata : 僧帽弁閉鎖不全症-重症度評価の落とし穴, 日本超音波医学会第90回学術集会, May 2017.
549.	Hirotsugu Yamada, Kenya Kusunose, 西尾進 and Masataka Sata : 技師に求める心エコー図検査の報告書, 日本超音波医学会第90回学術集会, May 2017.
550.	Hirotsugu Yamada, Kenya Kusunose and Masataka Sata : ポケットエコーを用いたFocused Cardiac Ultrasound(FoCUS), 日本超音波医学会第90回学術集会, May 2017.
551.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 症例から学ぶTR-PG計測のピットフォール, 日本超音波医学会第90回学術集会, May 2017.
552.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 肺高血圧症に対する負荷心エコーの積極活用, 日本超音波医学会第90回学術集会, May 2017.
553.	Kenya Kusunose, Hirotsugu Yamada, 林修司, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 経食道心エコー図の再検査によりVegetationを同定しえた感染性心内膜炎の1例, 日本内科学会第116回四国地方会, May 2017.
554.	Ganbaatar Byambasuren, Daiju Fukuda, Salim Masdan Hotimah, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Ticagrelor, a P2Y21 inhibitor, attenuated vascular dysfunction and inhibited atherogenesis in apolipoprotein-E-deficient mice, 第17回日本NO学会学術集会, May 2017.
555.	Kunduziayi Aini, Daiju Fukuda, Salim Masdan Hotimah, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Dipeptidyl peptidase-4 inhibitor, linagliptin, ameliorates endothelial dysfunction and the development of atherosclerosis in normoglycemic apolipoprotein-E deficient mice, 第17回日本NO学会学術集会, May 2017.
556.	Ganbaatar Byambasuren, Daiju Fukuda, Salim Masdan Hotimah, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Canagliflozin, a novel selective SGLT2 inhibitor, ameliorated endothelial dysfunction and atherogenesis in diabetic mice, 第17回日本NO学会学術集会, May 2017.
557.	Daiju Fukuda, Salim Masdan Hotimah, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Dabigatran, a direct thrombin inhibitor, attenuates endothelial dysfunction in diabetic mice, 第17回日本NO学会学術集会, May 2017.
558.	Gulinu Maimaituxun, Michio Shimabukuro, Yukina Hirata, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Masafumi Harada and Masataka Sata : Epicardial adipose tissue thickness in left anterior descending artery predictict coronary atherosclerosis, 第17回日本NO学会学術集会, May 2017.
559.	天野里江, Hirotsugu Yamada, 山尾雅美, 平田有紀奈, 宮崎達志, 足立克仁 and Masataka Sata : デュシェンヌ型筋ジストロフィー(DMD)保因者における心筋ストレインの検討, 日本心エコー図学会第28回学術集会, Apr. 2017.
560.	瀬野弘光, Hirotsugu Yamada, 大櫛祐一郎, 西條良仁, Kenya Kusunose, 平田有紀奈, 天野里江, 鳥居裕太, 山尾雅美, 西尾進, 林修司 and Masataka Sata : 肺動脈内に可動性に富む腫瘍を認めた原発性肺動脈血管内膜肉腫の1例, 日本心エコー図学会第28回学術集会, Apr. 2017.
561.	鳥居裕太, Kenya Kusunose, Hirotsugu Yamada, 大櫛祐一郎, 瀬野弘光, 西條良仁, 西尾進, 平田有紀奈, 天野里江 and Masataka Sata : 心疾患既往のない患者における非心臓手術前の心エコー図検査が術後生存率に与える影響, 日本心エコー図学会第28回学術集会, Apr. 2017.
562.	大櫛祐一郎, Kenya Kusunose, 瀬野弘光, 西條良仁, Hirotsugu Yamada, 西尾進, 鳥居裕太, 天野里江, 山尾雅美, Takeshi Soeki and Masataka Sata : 左房圧上昇評価における新しいASEガイドラインによる評価法と従来の包括的評価法との比較, 日本心エコー図学会第28回学術集会, Apr. 2017.
563.	西條良仁, Hirotsugu Yamada, Kenya Kusunose, 大櫛祐一郎, 瀬野弘光, 平田有紀奈, 鳥居裕太, 山尾雅美, 西尾進, Takeshi Soeki and Masataka Sata : 心房収縮期僧帽弁口血流速度の前負荷増大に対する反応性を用いた左房圧上昇の予測, 日本心エコー図学会第28回学術集会, Apr. 2017.
564.	西尾進, Kenya Kusunose, 桑畑絢也, 平田有紀奈, 鳥居裕太, 天野里江, 山尾雅美, 大櫛祐一郎, 瀬野弘光, 西條良仁, Hirotsugu Yamada and Masataka Sata : 糖尿病と左室global longitudinal strainおよび血管内皮機能との関連, 日本心エコー図学会第28回学術集会, Apr. 2017.
565.	平田有紀奈, Hirotsugu Yamada, Kenya Kusunose, 清水陸登, 桑畑絢也, 鳥居裕太, 天野里江, 山尾雅美, 西尾進, 大櫛祐一郎, 瀬野弘光, 西條良仁 and Masataka Sata : 低CHADS₂スコア患者の左心耳機能・形態と血栓形成リスクとの関連, 日本心エコー図学会第28回学術集会, Apr. 2017.
566.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 西條良仁, 瀬野弘光, 大櫛祐一郎, 平田有紀奈, 鳥居裕太, 山尾雅美, 阿部美保 and Masataka Sata : 下肢陽圧負荷心エコー図法で算出したprojected AVAiを用いた低圧較差高度大動脈弁狭窄のリスク層別化, 日本心エコー図学会第28回学術集会, Apr. 2017.
567.	Kenya Kusunose, 林修司, 西尾進, Hirotsugu Yamada and Masataka Sata : ストレイン法による左房機能評価, 日本心エコー図学会第28回学術集会, Apr. 2017.
568.	Kenya Kusunose, Hirotsugu Yamada, 西尾進 and Masataka Sata : 心不全と肺高血圧症, 日本心エコー図学会第28回学術集会, Apr. 2017.
569.	Hirotsugu Yamada, Kenya Kusunose, 天野里江, 西條良仁, 瀬野弘光, 西尾進, 平田有紀奈, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Effect of Sitagliptin on Left Ventricular Function in Patients with Type 2 Diabetes: A Subanalysis of the PROLOGUE Study, 第81回日本循環器学会学術集会, Mar. 2017.
570.	鳥居裕太, Hirotsugu Yamada, Kenya Kusunose, 大櫛祐一郎, 瀬野弘光, 西條良仁, 西尾進, 天野里江, 松本力三 and Masataka Sata : Comparison of the Effect on Deep Vein Thrombosis between Rivaroxaban and Edoxaban, 第81回日本循環器学会学術集会, Mar. 2017.
571.	西條良仁, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 瀬野弘光, 大櫛祐一郎, 高木恵理, 上野理絵, 原知也, 川端豊, 斎藤友子, 伊藤浩敬, 轟貴史, Tomomi Matsuura, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Impact of Left Atrial Ischemia on Left Atrial Reservoir Function in Patients with Old Myocardial Infarction, 第81回日本循環器学会学術集会, Mar. 2017.
572.	平田有紀奈, Kenya Kusunose, Hirotsugu Yamada, 清水陸登, 鳥居裕太, 西尾進, 瀬野弘光, 西條良仁, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Quantitative Classification of Left Atrial Appendage is Superior to Visual Classification for Risk Stratification of Stroke in Atrial Fibrillation, 第81回日本循環器学会学術集会, Mar. 2017.
573.	轟貴史, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takayuki Ise, Tomomi Matsuura, Takeshi Tobiume, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Serum Level of Lipoprotein (a) is a Risk Factor for Aortic Valve Sclerosis in Women, 第81回日本循環器学会学術集会, Mar. 2017.
574.	大櫛祐一郎, Hirotsugu Yamada, Kenya Kusunose, 西條良仁, 瀬野弘光, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Accuracy of Diagnosis of Elevated Left Atrial Pressure Using Recommendation for the Evaluation of Left Ventricular Diastolic Function by Echocardiograph, 第81回日本循環器学会学術集会, Mar. 2017.
575.	Hirotsugu Yamada and Masataka Sata : Role of Echocardiography in Diagnosis and Treatment of Infectious Endocarditis, 第81回日本循環器学会学術集会, Mar. 2017.
576.	Takayuki Ise, Shusuke Yagi, 瀬野弘光, 西條良仁, 高木恵理, 上野理絵, 原知也, 伊藤浩敬, Tomomi Matsuura, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Nocturnal Hypoxemia Predicts Cardiac Events in Patients with Cardiac Risk Factors, 第81回日本循環器学会学術集会, Mar. 2017.
577.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 平田有紀奈, 瀬野弘光, 西條良仁, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Right Ventricular Myocardial Strain during Preload Augmentation is Associated with Exercise Capacity in Patients with Chronic Heart Failure, 第81回日本循環器学会学術集会, Mar. 2017.
578.	Maimaituxun Gulinu, Michio Shimabukuro, Koji Yamaguchi, Shusuke Yagi, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Local Epicardial Adipose Tissue Thickness and Its Impact on Coronary Atherosclerosis, 第81回日本循環器学会学術集会, Mar. 2017.
579.	Shusuke Yagi and Masataka Sata : n-3 Polyunsaturated Fatty Acids: A Promising Target for the Prevention of Cardiovascular Events, 第81回日本循環器学会学術集会, Mar. 2017.
580.	鳥居裕太, Kenya Kusunose, Hirotsugu Yamada, 大櫛祐一郎, 瀬野弘光, 西條良仁, 西尾進, 天野里江, 平田有紀奈 and Masataka Sata : Perioperative Echocardiography before Major Elective Noncardiac Surgery Improves Postoperative Mortality Patients without Known Cardiovascular Disease, 第81回日本循環器学会学術集会, Mar. 2017.
581.	伊藤浩敬, Tetsuzo Wakatsuki, Koji Yamaguchi, Daiju Fukuda, 川端豊, 轟貴史, Tomomi Matsuura, Kenya Kusunose, Takayuki Ise, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Lipid-rich Coronary Plaque is Associated with Local Inflammation in Adjacent Epicardial Adipose Tissue in Fresh Cadaveric Models, 第81回日本循環器学会学術集会, Mar. 2017.
582.	Tetsuzo Wakatsuki, Koji Yamaguchi, 伊藤浩敬, Daiju Fukuda, 川端豊, 轟貴史, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : The Tissue Characteristics of Coronary Plaque with Microluminal Structures Identified by OCT Associated with Local Inflammatory Response in Fresh Cadavers, 第81回日本循環器学会学術集会, Mar. 2017.
583.	Koji Yamaguchi, Tetsuzo Wakatsuki, 伊藤浩敬, 川端豊, 轟貴史, Tomomi Matsuura, Kenya Kusunose, Takayuki Ise, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Comparison of Local Coagulative Response after Coronary Angioplasty - First Generation DES vs Second Generation-DES vs Drug Coated Balloon -, 第81回日本循環器学会学術集会, Mar. 2017.
584.	瀬野弘光, Kenya Kusunose, Hirotsugu Yamada, 西條良仁, 西尾進, 平田有紀奈, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Comparison of Right Ventricular Global Longitudinal Strain between Vender-dependent and Vender-independent Two-dimensional Speckle Tracking Software, 第81回日本循環器学会学術集会, Mar. 2017.
585.	冨山博史, 山科章, 前村浩二, 木庭新治, 山崎力, Masataka Sata, 石津智子, 伊藤浩, 竹本恭彦, 東幸仁, 鈴木亨, 大屋祐輔, 植田真一郎, 苅尾七臣, 古川泰司, 高瀬凡平, 井上晃男, 野出孝一, 松本知沙 and 石橋豊 : Endothelial Function and the Progression of Preclinical Vascular Damages Under Antihypertensive Medication: The Results of FMD-J Multi-Center Prospective Study, 第81回日本循環器学会学術集会, Mar. 2017.
586.	谷口実佑, Takeshi Soeki, Tomomi Matsuura, 佐藤裕紀, Takeshi Tobiume, 原知也, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Activated Factor X Signaling Pathway via Protease-Activated Receptor-2 is a Novel Therapeutic Target to Prevent Atrial Fibrillation, 第81回日本循環器学会学術集会, Mar. 2017.
587.	上田浩之, 瀬野弘光, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Tetsuzo Wakatsuki, Takeshi Soeki, Jun Higashijima and Masataka Sata : ベバシズマブ併用化学療法中に深部静脈血栓症および肺塞栓症を来した大腸癌の1例-血栓素因の検討も含めて, 第254回徳島医学会学術集会, Feb. 2017.
588.	西山美月, Takeshi Tobiume, Tomomi Matsuura, Takeshi Soeki and Masataka Sata : 左鎖骨下への植込み型除細動器植え替え後に生じたTwiddler症候群の1例, 第254回徳島医学会学術集会, Feb. 2017.
589.	山本清成, 轟貴史, 大櫛祐一郎, 上野理恵, Takayuki Ise, 瀬野弘光, 西條良仁, 高木恵理, 原知也, 川端豊, 斎藤友子, 伊藤浩敬, Tomomi Matsuura, Takeshi Tobiume, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masataka Sata, 門田友里, Masato Nishimura and Minoru Irahara : PET/CTにて診断できた心サルコイドーシスの1例, 第254回徳島医学会学術集会, Feb. 2017.
590.	笠井明成, 原知也, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, 足立克仁 and Masataka Sata : 著明な刺激伝導系異常を呈したBecker型筋ジストロフィーの1例, 第254回徳島医学会学術集会(平成28年度冬期), Feb. 2017.
591.	Maimaituxun Gulinu, Michio Shimabukuro, Daiju Fukuda, Shusuke Yagi, Yukina Hirata, Takashi Iwase, Shoichiro Takao, Tomomi Matsuura, Takayuki Ise, Tetsuzo Wakatsuki, Masafumi Harada and Masataka Sata : The impact of epicardial adipose tissue thickness on left ventricular diastolic dysfunction in patients with preserved ejection fraction., Feb. 2017.
592.	Masataka Sata : 臨床医が知っておくべき糖尿病の基礎心臓周囲脂肪組織とその意義, 第51回糖尿病学の進歩, Feb. 2017.
593.	西川幸治, 石井亜由美, Takayuki Ise, Shusuke Yagi, 高川由利子, Shinsuke Katoh and Masataka Sata : 心臓リハビリテーション導入後の活動範囲の回復に関わる因子の検討, 日本心臓リハビリテーション学会第1回四国支部地方会, Jan. 2017.
594.	石井亜由美, 西川幸治, Takayuki Ise, Shusuke Yagi, 高川由利子, Shinsuke Katoh and Masataka Sata : 術後の廃用性筋力低下が予測された高齢開心術後患者に対しB-SESを使用した経験, 日本心臓リハビリテーション学会第1回四国支部地方会, Jan. 2017.
595.	Yohsuke Tamba, Jiro Takeo, Masahiro Bando, Mayu Sebe, Yuki Yamasaki, Daiju Fukuda, Yuko Miyahara, Yumiko Miyatake, Naoya Suemasa, Masashi Kuroda, Saeko Masumoto, Nagakatsu Harada, Rie Tsutsumi, Masataka Sata and Hiroshi Sakaue : 魚油由来長鎖モノエン脂肪酸は抗動脈硬化作用を有する, 第21回病態栄養学会年次学術集会, Jan. 2017.
596.	Maimaituxun Gulinu, Michio Shimabukuro, 平田有紀奈, Takashi Iwase, Shoichiro Takao, Tomomi Matsuura, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, 田端実, 森本喜久, 赤坂武, 田中正史, 高梨秀一郎 and Masataka Sata : 心臓バイパス手術症例におけるリスク要因の定量的解析:古典的および非古典的リスクの性差, 脳心血管抗加齢研究会2016, Dec. 2016.
597.	Gulinu Maimaituxun, Michio Shimabukuro, 平田有紀奈, Takashi Iwase, 高尾正一郎, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, 原田雅史 and Masataka Sata : 局所心臓周囲脂肪厚の臨床的意義:冠動脈疾患での検討, 脳心血管抗加齢研究会2016, Dec. 2016.
598.	K Tanaka and Masataka Sata : Microangiopathy in diabetes; Analysis of adventitial vasa vasorum using mouse models., 第24回日本血管生物医学会学術集会, Dec. 2016.
599.	鈴木聖也, Hirotsugu Yamada, 高木恵理, 高川由利子, Tomomi Matsuura, Takayuki Ise, 平田有紀奈, Kenya Kusunose, 西條良仁, 瀬野弘光, 大櫛祐一郎, 西尾進, 山尾雅美, 鳥居裕太, Shusuke Yagi, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 経食道心エコー検査により原因が究明された高齢発症の右心不全の1例, 第109回日本循環器学会四国地方会, Dec. 2016.
600.	高木恵理, Shusuke Yagi, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata and 高川由利子 : 右心不全の精査の過程で偶発的に見つかった冠静脈洞閉鎖および重複上大静脈の一例, 第109回日本循環器学会四国地方会, Dec. 2016.
601.	上田浩之, 瀬野弘光, Tomomi Matsuura, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Tetsuzo Wakatsuki, Takeshi Soeki, 東島潤 and Masataka Sata : Bevacizumab併用化学療法中に深部静脈血栓症および肺塞栓症を発症した1例, 第109回日本循環器学会四国地方会, Dec. 2016.
602.	行重佐和香, Kenya Kusunose, 瀬野弘光, 西條良仁, Takayuki Ise, Shusuke Yagi, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 成人期に心不全症状を契機に発見された左室緻密化障害の一例, 第109回日本循環器学会四国地方会, Dec. 2016.
603.	ロバートゼング, 西條良仁, Kenya Kusunose, Hirotsugu Yamada, 轟貴史, 西尾進, 瀬野弘光, 高木恵理, 上野理絵, 原知也, 川端豊, 齋藤友子, 伊藤浩敬, Tomomi Matsuura, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 左上肢脱力を主訴に来院されたが心エコー図法を契機に急性冠症候群と診断しえた一例, 第109回日本循環器学会四国地方会, Dec. 2016.
604.	Shusuke Yagi, 加地伸介, 田代善彦 and Masataka Sata : 自宅の庭で受傷したマムシ咬傷の2例, 日本内科学会第115回四国地方会, Nov. 2016.
605.	岡本恵暢, 原知也, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 重症心不全を呈したBecker型筋ジストロフィーの1家系, 日本内科学会第115回四国地方会, Nov. 2016.
606.	本間友佳子, Yasunobu Hayabuchi, 小野朱美, Shoji Kagami, 井上美紀, Kazuhiro Mori, Masataka Sata, Takeshi Soeki, Takeshi Tobiume and Tomomi Matsuura : Left venous valve由来部位の異常自動能が示唆された右房後中隔起源の心房頻拍・頻拍誘発性心筋症の1女児例, 第21回日本小児心電学会学術集会, Nov. 2016.
607.	Kenya Kusunose, Hirotsugu Yamada, 西條良仁, 瀬野弘光, 大櫛祐一郎, 西尾進, 鳥居裕太, 平田有紀奈, Takayuki Ise, Shusuke Yagi and Masataka Sata : 肺高血圧症に対する運動負荷心エコー図法, 第53回日本臨床生理学会総会, Oct. 2016.
608.	Tomomi Matsuura, Takeshi Soeki, Takeshi Tobiume and Masataka Sata : 右房低位中隔部に電気的不連続性を認めた通常型心房粗動の1例, カテーテルアブレーション関連秋季大会2016, Oct. 2016.
609.	東邦康智, Masataka Sata and 小室一成 : The Regulatory Mechanism of Inflammation in the Heart through the Heart-Brain Interaction and Its Role in Pressure Overload-Induced Cardiac Hypertrophy, 第37回日本高血圧学会総会, Oct. 2016.
610.	西尾進, Yu Saitou, 鳥居裕太, 平田有紀奈, 山尾雅美, 松本力三, Seiji Iwamoto, Shoichiro Takao, Hirotsugu Yamada and Masataka Sata : 巨大肝嚢胞の2切除例, 日本超音波医学会第26回四国地方会学術集会, Oct. 2016.
611.	鳥居裕太, 西尾進, 松本力三, 平田有紀奈, 山尾雅美, 郷司剛志, Shoichiro Takao, Seiji Iwamoto, Hirotsugu Yamada and Masataka Sata : 当院における腎細胞癌膵転移6症例の超音波所見, 日本超音波医学会第26回四国地方会学術集会, Oct. 2016.
612.	鈴川理乃, Hirotsugu Yamada, 平田有紀奈, 西尾進, 山尾雅美, 天野里江, 鳥居裕太, 西條良仁, Kenya Kusunose and Masataka Sata : 異なる体位変換により左室流出路狭窄が重症化したS字状中隔の2症例, 日本超音波医学会第26回四国地方会学術集会, Oct. 2016.
613.	木村優希, Hirotsugu Yamada, 松浦一義, Kenya Kusunose, 西條良仁, 西尾進, 山尾雅美, 天野里江, 平田有紀奈 and Masataka Sata : 僧帽弁口血流速波形の偽正常化パターンと心房機能低下パターンの鑑別, 日本超音波医学会第26回四国地方会学術集会, Oct. 2016.
614.	衣川尚知, Hirotsugu Yamada, 西尾進, 山尾雅美, 鳥居裕太, 天野里江, 西條良仁, 林修司, Kenya Kusunose and Masataka Sata : 酵素補充療法に対する反応性が異なる心ファブリー病の2例, 日本超音波医学会第26回四国地方会学術集会, Oct. 2016.
615.	西條良仁, Kenya Kusunose, Hirotsugu Yamada, 瀬尾弘光, 天野里江, 山尾雅美, 西尾進, Hirotsugu Kurobe, 渡邉俊介 and Masataka Sata : Acromegalic cardiomyopathyの一例, 日本超音波医学会第26回四国地方会学術集会, Oct. 2016.
616.	瀬尾弘光, Hirotsugu Yamada, Kenya Kusunose, 西條良仁, 平田有紀奈, 鳥居裕太, 天野里江, 山尾雅美, 西尾進 and Masataka Sata : 肺動脈内に可動性に富む巨大血栓を認めた慢性血栓閉塞性肺動脈高血圧症の一例, 日本超音波医学会第26回四国地方会学術集会, Oct. 2016.
617.	大櫛祐一郎, Kenya Kusunose, 西條良仁, Hirotsugu Yamada, 西尾進, 鳥居裕太, 天野里江, 山尾雅美, Takeshi Soeki and Masataka Sata : 運動負荷心エコー図検査で肺高血圧症を診断しえた一例, 日本超音波医学会第26回四国地方会学術集会, Oct. 2016.
618.	Masahiro Bando, 竹尾仁良, Daiju Fukuda, 宮原裕子, 楊志宏, 西本幸子, 齋藤沙緒理, 川上真智子, 上吉原絢, 丹波洋介, Masataka Sata and Hiroshi Sakaue : 長鎖モノエン脂肪酸を含む魚油による抗動脈硬化作用, 第37回日本肥満学会, Oct. 2016.
619.	, Michio Shimabukuro and Masataka Sata : Impact of Epicardial Fat in Patients Underwent Coronary Artery Bypass Graft Surgery, 第37回日本肥満学会, Oct. 2016.
620.	Daiju Fukuda and Masataka Sata : 遊離核酸断片による血管の炎症と動脈硬化症発症機序の解明, 第39回日本高血圧学会総会, Sep. 2016.
621.	Michio Shimabukuro and Masataka Sata : 異所性脂肪・心臓周囲脂肪と心臓血管病バイオマーカー, 第64回日本心臓病学会学術集会, Sep. 2016.
622.	Shusuke Yagi, Takayuki Ise, 西川幸治, 石井亜由美, Kenya Kusunose, Koji Yamaguchi, Tomomi Matsuura, Takeshi Tobiume, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 心不全患者に対するAdaptive servo-ventilation装着下6分間歩行における運動耐容能改善効果, 第64回日本心臓病学会学術集会, Sep. 2016.
623.	鈴川理乃, Hirotsugu Yamada, Kenya Kusunose, 西條良仁, 瀬野弘光, 衣川尚知, 平田有紀奈, 天野里江, 鳥居裕太, 山尾雅美, 西尾進, Tomomi Matsuura, Takeshi Tobiume, Takeshi Soeki and Masataka Sata : 持続性心房細動の肺静脈隔離術後における左房機能の回復と再発との関連, 第64回日本心臓病学会学術集会, Sep. 2016.
624.	衣川尚知, 齋藤憲, 西尾進, 平田有紀奈, 天野里江, 山尾雅美, 鳥居裕太, 林修司, 阿部美保, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 心電図P波の電気軸から肺高血圧症の診断は可能か∼心エコー法による検討∼, 第64回日本心臓病学会学術集会, Sep. 2016.
625.	Hirotsugu Yamada, Kenya Kusunose, 西條良仁, 瀬野弘光, 西尾進, 山尾雅美, 天野里江, 鳥居裕太, 平田有紀奈, 田中秀和, 松本賢亮, 大北裕 and Masataka Sata : 表在エコー検査と心エコー検査のコラボレーションにより感染性心内膜炎が迅速に診断できた僧帽弁逸脱症の1例, 第64回日本心臓病学会学術集会, Sep. 2016.
626.	鳥居裕太, Kenya Kusunose, 西尾進, 平田有紀奈, 天野里江, 山尾雅美, 林修司, 阿部美保, Hirotsugu Yamada and Masataka Sata : 非心臓手術前の心エコー検査は，入院期間および死亡率に影響を与えない, 第64回日本心臓病学会学術集会, Sep. 2016.
627.	瀬野弘光, Kenya Kusunose, Hirotsugu Yamada, 西條良仁, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心血管イベント発症高リスク患者における非侵襲的血管機能検査の有用性, 第64回日本心臓病学会学術集会, Sep. 2016.
628.	Takeshi Soeki, 高橋甲介, Tomomi Matsuura, Kenya Kusunose, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : 心筋虚血再灌流障害に対する新たな治療薬としてのC型ナトリウム利尿ペプチドの可能性, 第64回日本心臓病学会学術集会, Sep. 2016.
629.	西尾進, Hirotsugu Yamada, Kenya Kusunose, 真鍋泰毅, 平田有紀奈, 鳥居裕太, 天野里江, 山尾雅美 and Masataka Sata : 心拍出量の増加が血流依存性血管拡張反応に及ぼす影響(若年健常者における検討), 第64回日本心臓病学会学術集会, Sep. 2016.
630.	西條良仁, Kenya Kusunose, Hirotsugu Yamada, 瀬野弘光, 西尾進, Takayuki Ise, Shusuke Yagi, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 下肢陽圧負荷心エコー検査により将来の左房圧上昇を予測できるか, 第64回日本心臓病学会学術集会, Sep. 2016.
631.	伊藤浩敬, Tetsuzo Wakatsuki, Koji Yamaguchi, Takayuki Ise, 川端豊, 上野理絵, 齋藤友子, 轟貴史, Tetsuzo Wakatsuki and Masataka Sata : SES留置後超遠隔期に初めて認めたPSSを伴う再狭窄病変に対してDCB治療を施行し局所凝固反応の推移を観察した一例, 第23回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2016.
632.	Takayuki Ise, Tetsuzo Wakatsuki, Koji Yamaguchi, 上野理絵, 川端豊, 齋藤友子, 伊藤浩敬, Takeshi Tobiume and Masataka Sata : PTSMA施行2日後に遅発性完全房室ブロックを認めた1例, 第23回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2016.
633.	西川幸治, 石井亜由美, Takayuki Ise, 高川由利子, 門田宗之, Shusuke Yagi, Takashi Iwase, Shinsuke Katoh and Masataka Sata : 退院時6MWDと入院期身体活動量の関係-MIとHFの比較, 第22回日本心臓リハビリテーション学会学術集会, Jul. 2016.
634.	石井亜由美, 西川幸治, Takayuki Ise, 高川由利子, 門田宗之, Shusuke Yagi, Takashi Iwase, Shinsuke Katoh and Masataka Sata : 心臓リハビリテーション患者におけるセルフエフィカシーの検討, 第22回日本心臓リハビリテーション学会学術集会, Jul. 2016.
635.	Shusuke Yagi, Takayuki Ise, 高川由利子, 西川幸治, 石井亜由美 and Masataka Sata : SGLT2阻害薬併用心臓リハビリテーションにより運動耐容能が改善した糖尿病合併慢性心不全の1例, 第22回日本心臓リハビリテーション学会学術集会, Jul. 2016.
636.	高川由利子, Shusuke Yagi, Takayuki Ise, 門田宗之 and Masataka Sata : 心臓リハビリテーションによる内臓・皮下脂肪量と骨格筋量に対する影響, 第22回日本心臓リハビリテーション学会学術集会, Jul. 2016.
637.	Masataka Sata : PDF5阻害薬の心血管系に及ぼす影響, 第16回日本Men's Health医学会第7回テストステロン研究会, Jul. 2016.
638.	H Ito, Tetsuzo Wakatsuki, Koji Yamaguchi, R Ueno, Y Saito, T Todoroki, Takayuki Ise, Takeshi Tobiume and Masataka Sata : A case of trapped floppy rotawire at the distal portion of wrapped left anterior descending coronary artery, 第25回日本心血管インターベンション治療学会, Jul. 2016.
639.	Koji Yamaguchi, Tetsuzo Wakatsuki, R Ueno, H Ito, Y Saito, T Todoroki, Takayuki Ise, Takeshi Tobiume and Masataka Sata : Suppressive Local Vascular Response after Paclitaxel Eluting Balloon Compared to Paclitaxel Eluting Stent, 第25回日本心血管インターベンション治療学会, Jul. 2016.
640.	玉井利奈, Hirotsugu Yamada, Mika Bando, 天野里江, 鳥居裕太, 平田有紀奈, 西尾進, Kenya Kusunose and Masataka Sata : 脂質低下療法に伴う頸動脈プラーク性状変化の定量化:頸動脈超音波画像のiPlaque解析を用いた検討, 第3回日本心血管脳卒中学会学術集会, Jun. 2016.
641.	原知也, Daiju Fukuda, 田中君枝, 東邦康智, 平田陽一郎, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : 活性型第X凝固因子によるマクロファージ活性化を介した新しい動脈硬化進展機序の検討, 第2回日本心血管脳卒中学会学術集会, Jun. 2016.
642.	原知也, Hirotsugu Yamada, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 重症心不全を呈したBecker型筋ジストロフィーの1剖検例, 第108回日本循環器学会中国・四国合同地方会, Jun. 2016.
643.	原知也, Takeshi Tobiume, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心房細動アブレーション後に麻痺性胃拡張を来した一例, 第108回日本循環器学会中国・四国合同地方会, Jun. 2016.
644.	山上圭, 西條良仁, Kenya Kusunose, Hirotsugu Yamada, 瀬野弘光, 原知也, 上野理絵, 門田宗之, 齋藤友子, 山﨑宙, 坂東左知子, 伊藤浩敬, 轟貴史, Tomomi Matsuura, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 生体腎移植後における腎静脈-外腸骨静脈間の血流動態変化が一因と考えられた深部静脈血栓症の一例, 第108回日本循環器学会中国・四国合同地方会, Jun. 2016.
645.	Takayuki Ise, Shusuke Yagi, 門田宗之, 瀬野弘光, 西條良仁, 上野理絵, 原知也, 齋藤友子, 山﨑宙, 坂東左知子, 伊藤浩敬, 轟貴史, Tomomi Matsuura, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 循環器病棟入院患者における睡眠時無呼吸，夜間低酸素血症の合併 ∼連続パルスオキシメータを用いた解析∼, 第108回日本循環器学会中国・四国合同地方会, Jun. 2016.
646.	本間友佳子, Kazuhiro Mori, Keisuke Fujioka, 佐々木亜由美, 寺田知正, 永井隆, 井上美紀, Yasunobu Hayabuchi, 小野朱美, Shoji Kagami, Masataka Sata, Takeshi Soeki, Takeshi Tobiume and Tomomi Matsuura : 持続する全身倦怠感を主訴とした異所性心房頻拍に伴う頻拍誘発性心筋症の1女児例, 第146回日本小児科学会徳島地方会, Jun. 2016.
647.	山尾雅美, 西尾進, 平田有紀奈, 鳥居裕太, Seiji Iwamoto, Naoki Muguruma, Hirotsugu Yamada, Masataka Sata, 藤崎由紀子 and 渡辺滋夫 : 膵臓原発性悪性リンパ腫の1例, 日本超音波医学会第89回学術集会, May 2016.
648.	松浦一義, Hirotsugu Yamada, Kenya Kusunose, 鈴川理乃, 平田有紀奈, 山尾雅美, 西尾進, Masashi Akaike and Masataka Sata : 医学生の心エコー実習におけるシミュレーター教育の効果, 日本超音波医学会第89回学術集会, May 2016.
649.	鳥居裕太, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 平田有紀奈, 天野里江, 山尾雅美, 林修司 and Masataka Sata : 心房細動が三尖弁輪収縮期移動距離に及ぼす影響, 日本超音波医学会第89回学術集会, May 2016.
650.	Kenya Kusunose, Hirotsugu Yamada, 鳥居裕太, 西尾進, 天野里江, 山尾雅美, 瀬野弘光, 西條良仁, 林修司 and Masataka Sata : 左室ストレイン値の不均衡を用いた頻脈性不整脈患者における左室収縮能改善の予測, 日本超音波医学会第89回学術集会, May 2016.
651.	西條良仁, Hirotsugu Yamada, Kenya Kusunose, 林修司, 鳥居裕太, 天野里江, 山尾雅美, 西尾進, Takeshi Soeki and Masataka Sata : ハンドグリップ負荷心エコー検査が有用であった心房細動合併慢性心不全の1例, 日本超音波医学会第89回学術集会, May 2016.
652.	Hirotsugu Yamada, Kenya Kusunose, 西條良仁, 瀬野弘光, 西尾進, 天野里江, 鳥居裕太, 平田有紀奈, 鈴川理乃 and Masataka Sata : 運動負荷誘発性肺高血圧症の診断基準:肺動脈圧上昇のみで診断してよいか?, 日本超音波医学会第89回学術集会, May 2016.
653.	Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 弁膜症における運動負荷心エコー図検査を用いた右心機能評価, 日本超音波医学会第89回学術集会, May 2016.
654.	Hirotsugu Yamada, Kenya Kusunose, 西條良仁, 瀬野弘光, 西尾進, 山尾雅美, 鳥居裕太, 平田有紀奈 and Masataka Sata : 心房細動のE/A 上昇は左房収縮低下か?左室拡張末期圧上昇か?, 日本超音波医学会第89回学術集会, May 2016.
655.	Hirotsugu Yamada, Kenya Kusunose, 西條良仁, 瀬野弘光 and Masataka Sata : 循環器系のpoint-of-care 超音波-超音波専門医の視点から, 日本超音波医学会第89回学術集会, May 2016.
656.	Shusuke Yagi, 西條良仁, 高川由利子, Masashi Akaike, Masataka Sata, Takeshi Kondo, Sumiko Yoshida, Itsuro Endo and Ken-ichi Aihara : 左副腎に腫瘤を認めた両側性特発性アルドステロン症の1例, 日本内科学会第114回四国地方会, May 2016.
657.	Tomomi Matsuura, Takeshi Soeki, Takeshi Tobiume, 上野理絵, 坂東左知子, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masataka Sata, Yasunobu Hayabuchi and 小野朱美 : 心房中隔起源の持続性心房頻拍により頻脈誘発性心筋症をきたした小児の1例, 日本内科学会第114回四国地方会, May 2016.
658.	伊藤浩敬, Tetsuzo Wakatsuki, Koji Yamaguchi, Takayuki Ise, 上野理絵, 齋藤友子, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : シロリムス溶出ステント留置7年後に初めて造影剤ステント周囲滲み出し像を認めその後も増大を呈した1例, 日本内科学会第114回四国地方会, May 2016.
659.	瀬野弘光, Hirotsugu Yamada, Kenya Kusunose, 西條良仁, Masataka Sata, 西尾進, 山尾雅美, 鳥居裕太, 天野里江 and 平田有紀奈 : 心サルコイドーシスの診断に2Dspeckle tracingが有用であった1例, 日本内科学会第114回四国地方会, May 2016.
660.	瀬野弘光, Hirotsugu Yamada, Kenya Kusunose, 西條良仁, Masataka Sata, 西尾進, 山尾雅美, 鳥居裕太, 天野里江 and 平田有紀奈 : 左室内脂肪腫性過誤腫の1例, 日本内科学会第114回四国地方会, May 2016.
661.	西條良仁, Hirotsugu Yamada, Kenya Kusunose, 瀬野弘光, Takayuki Ise, Shusuke Yagi, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : ペースメーカー植込み術後に等容拡張期の異常な左室中部流入血流を認めた1例, 日本内科学会第114回四国地方会, May 2016.
662.	西條良仁, Hirotsugu Yamada, Kenya Kusunose, 瀬野弘光, Takayuki Ise, Shusuke Yagi, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : ハンドグリップ負荷心エコー検査が心房細動合併心不全の治療評価に有用であった1例, 日本内科学会第114回四国地方会, May 2016.
663.	山崎宙, 西條良仁, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Tetsuzo Wakatsuki, Masataka Sata, Hajime Kinoshita, Hirotsugu Kurobe and Tetsuya Kitagawa : 左冠動脈入口部の高度狭窄により狭心症症状を繰り返した1例, 日本内科学会第114回四国地方会, May 2016.
664.	村上貴寛, Shusuke Yagi, 齋藤友子, Koji Yamaguchi, Takayuki Ise, Kenya Kusunose, Tetsuzo Wakatsuki, Masataka Sata, 高島啓 and 倉橋清衛 : Kallmann症候群を合併した若年重症虚血性心疾患の1例, 日本内科学会第114回四国地方会, May 2016.
665.	本田壮一, 小原聡彦, Katsuhiko Yoshimoto and Masataka Sata : FREED試験に参加する意義を考える, 第114回日本内科学会四国地方会, May 2016.
666.	鳥居裕太, 西尾進, 平田有紀奈, 天野里江, 山尾雅美, 高松直子, Kenya Kusunose, Kohhei Nakajima, Junichiro Satomi, Hirotsugu Yamada, Shinji Nagahiro and Masataka Sata : 若年女性の再発性脳梗塞の原因と考えられた頸動脈分岐部膜様構造物の1例, 第57回日本神経学会学術大会, May 2016.
667.	新井理沙, Hirotsugu Yamada, Kenya Kusunose, 林修司, 西條良仁, 瀬野弘光, 西尾進, 山尾雅美, 天野里江, 鳥居裕太, 平田有紀奈, Masataka Sata and 春藤譲治 : 座位で顕性化した左室流出路狭窄の1例, 日本心エコー図学会第27回学術集会, Apr. 2016.
668.	鳥居裕太, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 平田有紀奈, 天野里江, 山尾雅美, 林修司, 阿部美保 and Masataka Sata : 左室内脂肪腫性過誤腫の1例, 日本心エコー図学会第27回学術集会, Apr. 2016.
669.	天野里江, Kenya Kusunose, 林修司, 西尾進, 平田有紀奈, 鳥居裕太, 山尾雅美, 瀬野弘光, 西條良仁, 阿部美保, Hirotsugu Yamada and Masataka Sata : 部分肺静脈還流異常を合併した上位静脈洞型心房中隔欠損症の1例, 日本心エコー図学会第27回学術集会, Apr. 2016.
670.	瀬野弘光, Hirotsugu Yamada, Kenya Kusunose, 西條良仁, 平田有紀奈, 天野里江, 鳥居裕太, 山尾雅美, 西尾進, 林修司 and Masataka Sata : 経食道心エコー検査を用いたCHADS2スコア定値例における左心耳機能の検討, 日本心エコー図学会第27回学術集会, Apr. 2016.
671.	西尾進, Hirotsugu Yamada, Kenya Kusunose, 鈴川理乃, 平田有紀奈, 鳥居裕太, 天野里江, 山尾雅美, 瀬野弘光, 西條良仁 and Masataka Sata : 降圧治療が心臓および血管に与える影響, 日本心エコー図学会第27回学術集会, Apr. 2016.
672.	Kenya Kusunose, Hirotsugu Yamada, 瀬野弘光, 西條良仁, 平田有紀奈, 西尾進 and Masataka Sata : 膠原病患者における6分間歩行距離悪化予測因子の検討, 日本心エコー図学会第27回学術集会, Apr. 2016.
673.	平田有紀奈, Hirotsugu Yamada, Kenya Kusunose, 西條良仁, 瀬野弘光, 西尾進, 山尾雅美, 天野里江, 鳥居裕太 and Masataka Sata : 虚血性心疾患における心筋バイアビリティーと心外膜脂肪厚の関係, 日本心エコー図学会第27回学術集会, Apr. 2016.
674.	Kenya Kusunose, Hirotsugu Yamada, 瀬野弘光, 西條良仁, 平田有紀奈, 西尾進 and Masataka Sata : 下肢陽圧負荷心エコー法で評価した拡張期リザーブと運動耐容能との関連, 日本心エコー図学会第27回学術集会, Apr. 2016.
675.	Kenya Kusunose, Hirotsugu Yamada, 瀬野弘光, 西條良仁, 林修司, 西尾進, 山尾雅美, 天野里江, 鳥居裕太, 平田有紀奈, Takeshi Soeki and Masataka Sata : 弁膜症・肺高血圧症で使いこなす, 日本心エコー図学会第27回学術集会, Apr. 2016.
676.	Hirotsugu Yamada, Kenya Kusunose, 西條良仁, 瀬野弘光, 林修司, 西尾進, 山尾雅美, 天野里江, 鳥居裕太, 平田有紀奈, Takeshi Soeki and Masataka Sata : 肺高血圧症に対する負荷心エコー検査, 日本心エコー図学会第27回学術集会, Apr. 2016.
677.	Masataka Sata : 血管不全研究会から血管不全学会へ, 第1回日本血管不全学会学術集会, Apr. 2016.
678.	Kenya Kusunose, 佐藤光代, Hirotsugu Yamada, Daiju Fukuda, Shusuke Yagi, Michio Shimabukuro and Masataka Sata : 心血管イベント発症高リスク患者における非侵襲的血管機能検査の予後予測能, 第1回日本血管不全学会学術集会, Apr. 2016.
679.	H Tomiyama, T Kohro, Y Higashi, B Takase, T Suzuki, T Ishizu, S Ueda, T Yamazaki, T Furumoto, K Kario, T Inoue, S Koba, Y Takemoto, T Hano, Masataka Sata, Y Ishibashi, K Node, K Maemura, Y Ohya, T Furukawa and H Itoh : Reliability of Endothelial Function Assessment Using a Semi-automated Device across Multiple Institutions and Establishment of Normal/Reference Values., 第80回日本循環器学会学術集会, Mar. 2016.
680.	Shusuke Yagi, Ken-ichi Aihara, Daiju Fukuda, A Takashima, Mika Bando, T Hara, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Takeshi Tobiume, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Masashi Akaike and Masataka Sata : Reduced Ratio of Eicosapentaenoic Acid and Docosahexaenoic Acid to Arachidonic Acid is Associated with Early Onset of Acute Coronary Syndrome., 第80回日本循環器学会学術集会, Mar. 2016.
681.	Koji Yamaguchi, Tetsuzo Wakatsuki, T Hara, M Kadota, R Ueno, Mika Bando, H Yamazaki, Y Saito, S Bando, Tomomi Matsuura, Kenya Kusunose, Takayuki Ise, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Local Vascular Response after Paclitaxel Eluting Balloon Angioplasty Compared to Drug Eluting Stent Implantation in Stable Angina Patients., 第80回日本循環器学会学術集会, Mar. 2016.
682.	S Bando, Takeshi Soeki, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Plasma Myeloperoxidase Activity is Associated with Atrial Substrate Remodeling in Patients with Atrial Fibrillation., 第80回日本循環器学会学術集会, Mar. 2016.
683.	HM Salim, Daiju Fukuda, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Linagliptin, a Dipeptidyl Peptidase-4 Inhibitor, Ameliorates Endothelial Dysfunction and Atherogenesis in Normoglycemic Apolipoprotein-E Deficient Mice through GLP-1 Dependent Manner., 第80回日本循環器学会学術集会, Mar. 2016.
684.	Michio Shimabukuro, Hirotsugu Yamada, Hirotsugu Kurobe, Y Hirata, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki, Tetsuya Kitagawa and Masataka Sata : Ezetimibe Reduces Epicardial Fat and Improves Cardiac Performance in Swine Fed a High-fat Diet: A Pathophysiological Role of Oxidized Cholesterols., 第80回日本循環器学会学術集会, Mar. 2016.
685.	Tomomi Matsuura, Takeshi Soeki, Y Morimoto, S Bando, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Epicardial Adipose Tissue Produce Proinflammatory Cytokines and Influence the Pathogenesis of Atrial Fibrillation., 第80回日本循環器学会学術集会, Mar. 2016.
686.	Michio Shimabukuro, HM Salim, T Hara, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Antagonism of Protease-activated Receptor 2 (PAR-2) Recovers Endothelial Dysfunction in Diabetic Mice., 第80回日本循環器学会学術集会, Mar. 2016.
687.	Y Hirata, Kenya Kusunose, Hirotsugu Yamada, Y Torii, S Nishio, Mika Bando, S Hayashi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Structural Remodeling of Left Atrial Appendage in Patients with Atrial Fibrillation., 第80回日本循環器学会学術集会, Mar. 2016.
688.	Daiju Fukuda, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Deletion of Toll-Like Receptor 9 Prevented Atherosclerosis Induced by Angiotensin II., 第80回日本循環器学会学術集会, Mar. 2016.
689.	T Hara, Daiju Fukuda, K Tanaka, Y Higashikuni, Y Hirata, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Critical Role in Bone Marrow Protease-Activated Receptor-2 in the Pathogenesis of Vascular Inflammation and Atherosclerosis in ApoE-Deficient Mice., 第80回日本循環器学会学術集会, Mar. 2016.
690.	K Tanaka and Masataka Sata : Vasa Vasorum and Atherosclerosis; Analysis Using Murine Models of Vascular Diseases., 第80回日本循環器学会学術集会, Mar. 2016.
691.	Daiju Fukuda, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Cell-Free DNA/Toll-like Receptor 9 Axis Plays a Pivotal Role in Metabolic Disorder-induced Chronic Inflammation, Leading to Atherogenesis and Insulin Resistance., 第80回日本循環器学会学術集会, Mar. 2016.
692.	Shusuke Yagi, Ken-ichi Aihara, Masashi Akaike, T Hara, Takayuki Ise, Daiju Fukuda, Michio Shimabukuro and Masataka Sata : Modulation of Tissue Thrombin Action is a Novel Therapeutic Approach for Prevention of Polyvascular Disease., 第80回日本循環器学会学術集会, Mar. 2016.
693.	Kenya Kusunose, Hirotsugu Yamada, S Nishio, Y Hirata, H Seno, Y Saijo, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki, B Griffin and Masataka Sata : Echocardiographic Characteristics of Right Ventricular Size and Function are Associated with Cardiac Events in Sleep Apnea Syndrome., 第80回日本循環器学会学術集会, Mar. 2016.
694.	加藤悠人, Takeshi Tobiume, 小島義裕, 川端豊, Toshiyuki Niki, 岡村暢大, Yoshio Taketani, 坂東左知子, Tomomi Matsuura, Takeshi Soeki and Masataka Sata : His束近傍に起源を認めるATP感受性心房頻拍7例に関する検討, 第252回徳島医学会学術集会(平成27年度冬期), Feb. 2016.
695.	近藤大祐, Shusuke Yagi, Takayuki Ise, Koji Yamaguchi, Tetsuzo Wakatsuki, Kenya Kusunose, Tomomi Matsuura, Takeshi Tobiume, Hirotsugu Yamada, Takeshi Soeki, Daiju Fukuda, Masashi Akaike, Michio Shimabukuro and Masataka Sata : 急性冠症候群発症時のイコサペント酸とドコサヘキサエン酸の血中濃度低下は慢性期冠動脈ステント内再狭窄の予測因子である, 第45回日本心脈管作動物質学会, Feb. 2016.
696.	高島啓, Daiju Fukuda, 田中君枝, 東邦康智, 平田陽一郎, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : ω3系不飽和脂肪酸の脂質ラフト構造変化を介した抗動脈硬化作用の解明, 第45回日本心脈管作動物質学会, Feb. 2016.
697.	Salim Masdan Hotimah, Daiju Fukuda, 東邦康智, 田中君枝, 平田陽一郎, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Dipeptidyl peptidase-4 inhibitor, linagliptin, ameliorates endothelial dysfunction and atherogenesis in apolipoprotein-E deficient mice through GLP-1 dependent and independent manners., 第45回日本心脈管作動物質学会, Feb. 2016.
698.	坂東左知子, Takeshi Soeki, Kenji Kangawa and Masataka Sata : 非心不全担癌患者におけるBNPの動態, 第45回日本心脈管作動物質学会, Feb. 2016.
699.	西本幸子, Daiju Fukuda, 東邦康智, 田中君枝, 平田陽一郎, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata : 動脈硬化におけるマクロファージTLR9の役割, 第45回日本心脈管作動物質学会, Feb. 2016.
700.	原知也, Daiju Fukuda, 田中君枝, 東邦康智, 平田陽一郎, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : プロテアーゼ活性化受容体2によるマクロファージ活性化を介した新しい動脈硬化進展機序の検討, 第45回日本心脈管作動物質学会, Feb. 2016.
701.	上田雄大, Michio Shimabukuro, Maimaituxun Gulinu, Salim Masdan Hotimah, 坂東左知子, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Takashi Iwase, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masafumi Harada and Masataka Sata : 冠症候群発症例における心臓周囲脂肪および腹部脂肪分布の検討, 第45回日本心脈管作動物質学会, Feb. 2016.
702.	Maimaituxun Gulinu, Michio Shimabukuro, Salim Masdan Hotimah, Tomomi Matsuura, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, 田端実, 森本喜久, 赤坂武, 田中正史, 高梨秀一郎 and Masataka Sata : 冠動脈疾患と心臓周囲脂肪量:男女差の検討, 第45回日本心脈管作動物質学会, Feb. 2016.
703.	六車隆太郎, Daiju Fukuda, Michio Shimabukuro, 東邦康智, 田中君枝, 平田陽一郎, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : TLR9の活性化は虚血肢における炎症を増強し血流改善を遅延させる, 第45回日本心脈管作動物質学会, Feb. 2016.
704.	原知也, Daiju Fukuda, 田中君枝, 東邦康智, 平田陽一郎, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : FXa - PAR-2経路は血管の慢性炎症を惹起し動脈硬化を促進する, CVMW 2015, Dec. 2015.
705.	橋本怜, Michio Shimabukuro, Salim Masdan Hotimah, 原知也, Daiju Fukuda, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue and Masataka Sata : 糖尿病性血管障害におけるPAR2シグナルの関与, CVMW 2015, Dec. 2015.
706.	G Maimaituxun, Michio Shimabukuro, HM Salim, Tomomi Matsuura, Shusuke Yagi, D Fukuda, Hirotsugu Yamada, Takeshi Soeki, M Tabata, Y Morimoto, T Akasaka, M Tanaka, S Takanashi and Masataka Sata : EATV is determinant for coronary atherosclerosis in men, but not in women: Analysis from patients underwent coronary artery bypass surgery., CVMW 2015, Dec. 2015.
707.	HM Salim, Daiju Fukuda, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : Dipeptidyl peptidase-4 inhibitor, linagliptin, ameliorates endothelial dysfunction and the development of atherosclerosis in normoglycemic apolipoprotein-E deficient mice., CVMW 2015, Dec. 2015.
708.	西本幸子, Daiju Fukuda, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata : 動脈硬化発症におけるマクロファージToll-like receptor 9の役割, CVMW 2015, Dec. 2015.
709.	Daiju Fukuda, 西本幸子, 東邦康智, 田中君枝, 平田陽一郎, Shusuke Yagi, Takeshi Soeki, Michio Shimabukuro and Masataka Sata : 自己遊離核酸断片の認識を介した血管の炎症と動脈硬化発症メカニズム, CVMW 2015, Dec. 2015.
710.	Shusuke Yagi, 小島圭二, 阿部俊夫 and Masataka Sata : 下肢静脈瘤内血栓が塞栓源と考えられた急性肺血栓塞栓症の1例, 日本内科学会第113回四国地方会, Dec. 2015.
711.	上野理絵, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : 当院で出産まで管理しえた心室頻拍合併妊娠の2症例, 日本内科学会第113回四国地方会, Dec. 2015.
712.	長瀬襟加, 鳥居裕太, 西尾進, 平田有紀奈, 山尾雅美, Seiji Iwamoto, Hirotsugu Yamada, Naoki Muguruma and Masataka Sata : 好酸球性胆管炎の1例, 日本超音波検査学会第19回中国・四国第23回合同地方会学術集会, Nov. 2015.
713.	天野里江, 西尾進, 山尾雅美, 鳥居裕太, 平田有紀奈, Mika Bando, 林修司, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 内科的治療に苦渋した右心不全の1例, 日本超音波検査学会第19回中国・四国第23回合同地方会学術集会, Nov. 2015.
714.	西川幸治, 石井亜由美, Takayuki Ise, 高川由利子, 門田宗之, Shusuke Yagi, Takashi Iwase, Shinsuke Katoh and Masataka Sata : 心疾患患者における身体活動量と運動耐容能の関係, 第107回日本循環器学会四国地方会, Nov. 2015.
715.	Takayuki Ise, 西條良仁, Hirokazu Miki, Kumiko Kagawa, 瀬野弘光, 上野理絵, 原知也, 齋藤友子, Mika Bando, 坂東左知子, 伊藤浩敬, Tomomi Matsuura, Koji Yamaguchi, Takeshi Tobiume, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masahiro Abe and Masataka Sata : auto-PBSCT とBortezomibの併用が著効した高度心機能障害を伴う原発性心アミロイドーシスの1例, 第107回日本循環器学会四国地方会, Nov. 2015.
716.	門田宗之, Takayuki Ise, Kenya Kusunose, 瀬野弘光, 上野理絵, 原知也, 齋藤友子, 高島啓, Mika Bando, 山﨑宙, 坂東左知子, 伊藤浩敬, 飛梅威, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, 黒部裕嗣, 北川哲也 and Masataka Sata : 静脈洞型心房中隔欠損を合併した高齢難治性心不全に対し修復術が奏功した一例, 第107回日本循環器学会四国地方会, Nov. 2015.
717.	石井亜由美, 西川幸治, Takayuki Ise, 高川由利子, 門田宗之, Shusuke Yagi, Takashi Iwase, 加藤真介 and Masataka Sata : 心疾患患者の生活習慣是正に対するセルフエフィカシーと不安・抑うつとの関係, 第107回日本循環器学会四国地方会, Nov. 2015.
718.	坂東左知子, Takeshi Soeki, Tomomi Matsuura, 飛梅威, 瀬野弘光, 西條良仁, 門田宗之, 原知也, 上野理絵, 齋藤友子, Mika Bando, 山﨑宙, 伊藤浩敬, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 心室瘤を形成した心サルコイドーシス患者の薬剤抵抗性VT storm に対しアブレーションを行った一例, 第107回日本循環器学会四国地方会, Nov. 2015.
719.	西尾進, 鳥居裕太, Kenya Kusunose, 平田有紀奈, 天野里江, 山尾雅美, 山﨑宙, Mika Bando, 高尾正一郎, Hirotsugu Yamada and Masataka Sata : 運動負荷ABIおよび下肢動脈エコー検査が診断に有用であった膝窩動脈捕捉症候群の1症例, 第107回日本循環器学会四国地方会, Nov. 2015.
720.	西條良仁, Mika Bando, Kenya Kusunose, 門田宗之, Takayuki Ise, Hirotsugu Yamada, 西尾進, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : ハンドグリップ負荷による心臓カテーテル検査および心エコー検査が治療評価に有用であった2例, 第107回日本循環器学会四国地方会, Nov. 2015.
721.	伊藤浩敬, 高島啓, Shusuke Yagi, 瀬野弘光, 門田宗之, 原知也, 上野理絵, 齋藤友子, 山﨑宙, Mika Bando, 坂東左知子, Tomomi Matsuura, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, 飛梅威, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 重症筋無力症に対する免疫抑制療法中に生じた化膿性心膜炎の一例, 第107回日本循環器学会四国地方会, Nov. 2015.
722.	西條良仁, 齋藤友子, Hirotsugu Yamada, Kenya Kusunose, Mika Bando, 瀬野弘光, 門田宗之, 原知也, 上野理絵, 山﨑宙, 坂東左知子, 伊藤浩敬, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 遅延造影MRI検査が診断の契機となった心アミロイドーシスの1例, 第107回日本循環器学会四国地方会, Nov. 2015.
723.	山下雄也, Takayuki Ise, Mika Bando, 原知也, 高島啓, 山﨑宙, 齋藤友子, 坂東左知子, Kenya Kusunose, 飛梅威, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, 木下肇, 藤本鋭貴, 北川哲也 and Masataka Sata : 60歳代で発見され外科治療が奏功した大動脈縮窄症の1例, 第107回日本循環器学会四国地方会, Nov. 2015.
724.	近藤大祐, Shusuke Yagi, Takayuki Ise, Koji Yamaguchi, Tetsuzo Wakatsuki, Kenya Kusunose, Tomomi Matsuura, 飛梅威, Hirotsugu Yamada, Takeshi Soeki, Daiju Fukuda, 赤池雅史, 島袋充生 and Masataka Sata : 急性冠症候群患者におけるスタチンのω3不飽和脂肪酸濃度へ影響, 第107回日本循環器学会四国地方会, Nov. 2015.
725.	加藤悠人, 飛梅威, 坂東左知子, Tomomi Matsuura, Takeshi Soeki, 瀬野弘光, 上野理絵, 門田宗之, 原知也, 齋藤友子, 高島啓, 山﨑宙, Mika Bando, 伊藤浩敬, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : His束近傍に起源を認めるATP感受性心房頻拍7例に関する検討, 第107回日本循環器学会四国地方会, Nov. 2015.
726.	西尾進, 鳥居祐太, 平田有紀奈, 天野里江, 山尾雅美, Mika Bando, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 頚動脈模様構造物が脳梗塞の原因と考えられた若年女性の1例, 第56回日本脈管学会総会, Oct. 2015.
727.	鳥居祐太, 西尾進, 平田有紀奈, 天野里江, 山尾雅美, 山﨑宙, Mika Bando, 高尾正一郎, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 解剖学的異常を認めない膝窩動脈補捉症候群の1症例, 第56回日本脈管学会総会, Oct. 2015.
728.	M Kadota, Takayuki Ise, Shusuke Yagi, Kenya Kusunose, Hajime Kinoshita, Hirotsugu Kurobe, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Successful Surgical Repair of Aged Sinus Venous Connection : A Case Report, 第19回日本心不全学会学術集会, Oct. 2015.
729.	坂東左知子, Takeshi Tobiume, Takeshi Soeki, Tomomi Matsuura and Masataka Sata : 僧房弁輪後壁での通電にて治療に成功したLeft variant型房室結節リエントリー性頻拍の1例, カテーテルアブレーション関連秋季大会2015, Oct. 2015.
730.	Takeshi Tobiume, Yoshio Taketani, 小島義裕, 川端豊, Toshiyuki Niki, 岡村暢大, 坂東左知子, Tomomi Matsuura, Takeshi Soeki and Masataka Sata : 下壁誘導でtall R・V1でqrS patternを認めた右室流出路中隔起源心室性期外収縮の1例, カテーテルアブレーション関連秋季大会2015, Oct. 2015.
731.	島村宗尚, 中神啓徳, 郡山弘, Masataka Sata and 森下竜一 : 脳血管傷害後のリモデリング課程の解析-頭蓋外血管との比較-, 第38回日本高血圧学会総会, Oct. 2015.
732.	Masataka Sata : 動脈硬化の新知見とイメージングへの応用∼心血管イベント抑制に向けた生活習慣病対策∼, 第38回日本高血圧学会総会, Oct. 2015.
733.	西尾進, 鳥居裕太, 平田有紀奈, 山尾雅美, Shin-ichiro Yamada, Seiji Iwamoto, Hirotsugu Yamada, Naoki Muguruma, Mitsuo Shimada and Masataka Sata : 正常肝に発症した巨大肝細胞癌の1例, 日本超音波医学会第25回四国地方会学術集会, Oct. 2015.
734.	鈴川理乃, Hirotsugu Yamada, 西尾進, 鳥居裕太, 天野里江, 山尾雅美, Kenya Kusunose, 林修司, Takeshi Soeki and Masataka Sata : 高齢で心アミロイドーシスを発症した肥大型心筋症の一例, 日本超音波医学会第25回四国地方会学術集会, Oct. 2015.
735.	西條良仁, Hirotsugu Yamada, Kenya Kusunose, 林修司, Mika Bando, 天野里江, 西尾進, 山尾雅美, Takeshi Soeki and Masataka Sata : 等容拡張期に異常な左室中部流入血流を認めたペースメーカー植込み術後の1例, 日本超音波医学会第25回四国地方会学術集会, Oct. 2015.
736.	平田有紀奈, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 瀬野弘光, 山崎宙, Mika Bando, 林修司 and Masataka Sata : 僧帽弁置換術後早期に発症した人工弁血栓症の1例, 日本超音波医学会第25回四国地方会学術集会, Oct. 2015.
737.	瀬野弘光, Mika Bando, Hirotsugu Yamada, Kenya Kusunose, 西條良仁, 林修司, 平田有紀奈, 天野里江, 西尾進 and Masataka Sata : CHADS2スコアが低値の左心耳機能低下例についての検討, 日本超音波医学会第25回四国地方会学術集会, Oct. 2015.
738.	Michio Shimabukuro, 益崎裕章 and Masataka Sata : 異所性脂肪を標的とした生活習慣病の予防と治療, 第36回日本肥満学会, Oct. 2015.
739.	Takayuki Ise, Tetsuzo Wakatsuki, Koji Yamaguchi, Mika Bando, 門田宗之, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : PTSMA術後に左室流出路狭窄の急性増悪を認めたHOCMの1例, ストラクチャークラブ・ジャパンライブデモンストレーション2015, Sep. 2015.
740.	山尾雅美, 西尾進, 平田有紀奈, Misako Nakagawa, 森本雅美, Hirokazu Takechi, Yukiko Tadokoro, Hirotsugu Yamada, Masataka Sata and Akira Tangoku : 超音波検査による乳癌化学療法の効果予測, 第35回日本乳腺甲状腺超音波医学会, Sep. 2015.
741.	長野広実, Takeshi Soeki, 坂東左知子, Tomomi Matsuura, Takeshi Tobiume, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : 心房細動発症の予測因子-心電学的側面と心エコー学的側面からの検討-, 第63回日本心臓病学会学術集会, Sep. 2015.
742.	堀家由貴, Hirotsugu Yamada, Kenya Kusunose, Mika Bando, 鳥居裕太, 平田有紀奈, 山尾雅美, 西尾進 and Masataka Sata : 心不全に対する薬物療法を行ったDuchenne型筋ジストロフィーの予後, 第63回日本心臓病学会学術集会, Sep. 2015.
743.	坂東左知子, Takeshi Soeki, 飛梅威, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 薬剤抵抗性のPurkinje起源心室頻拍に対し，人工呼吸管理・PCPS装着下にカテーテルアブレーション治療を施行し，社会復帰に成功した若年例の一例, 第63回日本心臓病学会学術集会, Sep. 2015.
744.	瀬野弘光, Hirotsugu Yamada, Kenya Kusunose, Mika Bando, 西條良仁, 西尾進, 山尾雅美, 鳥居裕太, 平田有紀奈, Takayuki Ise, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 6分間歩行負荷心エコー検査を用いた運動負荷誘発性肺高血圧症例の検出とその特徴, 第63回日本心臓病学会学術集会, Sep. 2015.
745.	平田有紀奈, Hirotsugu Yamada, 西尾進, 鳥居裕太, 天野里江, 山尾雅美, Mika Bando, 林修司, Kenya Kusunose, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki, 島袋充生 and Masataka Sata : 冠動脈疾患の非侵襲的診断における心臓周囲脂肪厚の付加的価値, 第63回日本心臓病学会学術集会, Sep. 2015.
746.	Takayuki Ise, Kenya Kusunose, Tomomi Matsuura, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 急性心筋梗塞後にBeckerⅠ型とⅢ型の心破裂をきたし，救命しえた一例, 第63回日本心臓病学会学術集会, Sep. 2015.
747.	西尾進, Hirotsugu Yamada, 平田有紀奈, 西條良仁, 高川由利子, Mika Bando, 林修司, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Tetsuzo Wakatsuki and Masataka Sata : 冠攣縮性狭心症における心臓周囲脂肪厚の検討, 第63回日本心臓病学会学術集会, Sep. 2015.
748.	Mika Bando, Takayuki Ise, Hirotsugu Yamada, Kenya Kusunose, 西尾進, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 収縮期雑音を契機に発見された成人単純型大動脈縮窄症の1例, 第63回日本心臓病学会学術集会, Sep. 2015.
749.	齋藤友子, Tetsuzo Wakatsuki, Koji Yamaguchi, 上野理絵, 山﨑宙, Takayuki Ise, Takeshi Tobiume and Masataka Sata : 心臓カテーテル検査後に生じた橈骨仮性動脈瘤2例の検討, 第22回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2015.
750.	Koji Yamaguchi, Tetsuzo Wakatsuki, 上野理絵, 齋藤友子, 山﨑宙, Takayuki Ise, Takeshi Tobiume and Masataka Sata : 総腸骨動脈閉塞病変に対して留置したstentが大動脈中枢側へ伸展した1例, 第22回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2015.
751.	Takayuki Ise, Tetsuzo Wakatsuki, Koji Yamaguchi, 上野理絵, 斎藤友子, 髙島啓, 山崎宙, Takeshi Tobiume and Masataka Sata : PTSMA後に左室流出路狭窄の一過性急性増悪を認めた閉塞性肥大型心筋症の1例, 第22回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2015.
752.	山﨑宙, Tetsuzo Wakatsuki, Koji Yamaguchi, 上野理絵, 齋藤友子, Takayuki Ise, Takeshi Tobiume and Masataka Sata : 広範前壁心筋梗塞発症早期に左室内血栓を生じた2例の検討, 第22回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2015.
753.	長野広実, Takeshi Soeki, 坂東左知子, Tomomi Matsuura, 飛梅威, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, 島袋充生 and Masataka Sata : 心房細動発症の予測因子-心電学的側面と心エコー学的側面からの検討-, 第63回日本心臓病学会学術集会, Sep. 2015.
754.	山田亮, 原知也, Shusuke Yagi, Jun Higashijima, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Mitsuo Shimada and Masataka Sata : 下肢静脈血栓症を伴わない下大静脈限局型血栓症の1例, 第251回徳島医学会学術集会(平成27年度夏期), Aug. 2015.
755.	本田壮一, 白川光雄, 小原聡彦, 伊藤祐司, 井内貴彦, Hiroyuki Azuma, 安部あかね, Hiroyashu Bando, Takeshi Soeki and Masataka Sata : ワルファリン・コントロール良好にもかかわらず出血を合併した心房細動の2症例, 第251回徳島医学会学術集会(平成27年度夏期), Aug. 2015.
756.	H Yamazaki, Tetsuzo Wakatsuki, K Yamaguchi, Y Saito, A Takashima, Takayuki Ise, Takeshi Tobiume and Masataka Sata : A Case of Preoperative VLST due to Multiple Inter-strut Hollow despite Heparin Replacement therapy, and OCT-guided PCI, 第24回日本心血管インターベンション治療学会, Jul. 2015.
757.	Koji Yamaguchi, Tetsuzo Wakatsuki, A Takashima, H Yamazaki, Y Saito, Takayuki Ise, Takeshi Tobiume and Masataka Sata : Suppressive Local Coagulative and Inflammatory Response after Implantation of Biolimus-Eluting Stents, 第24回日本心血管インターベンション治療学会, Jul. 2015.
758.	Takeshi Tobiume, S Bando, Tomomi Matsuura, Takeshi Soeki and Masataka Sata : Efficacy of CATHPAX AF for the reduction of radiation exposure during ablation of atrial fibrillation., 第30回日本不整脈学会・第32回日本心電学会, Jul. 2015.
759.	S Bando, Takeshi Soeki, Tomomi Matsuura, Takeshi Tobiume and Masataka Sata : Successful catheter ablation of VT/VF triggered by PVC in acute phase of myocardial infarction., 第30回日本不整脈学会・第32回日本心電学会, Jul. 2015.
760.	石井亜由美, 西川幸治, Takayuki Ise, 高川由利子, Shusuke Yagi, Takashi Iwase, Shinsuke Katoh and Masataka Sata : 当院での小児に対する心臓リハビリテーションの経験, 第21回日本心臓リハビリテーション学会, Jul. 2015.
761.	西川幸治, 石井亜由美, Takayuki Ise, 高川由利子, Shusuke Yagi, Takashi Iwase, Shinsuke Katoh and Masataka Sata : 治療抵抗性の収縮性新膜炎に心臓リハビリテーションが有効であった一症例, 第21回日本心臓リハビリテーション学会, Jul. 2015.
762.	Shusuke Yagi, Takayuki Ise, 西川幸治, 石井亜由美, 高川由利子, Takashi Iwase, Masashi Akaike, Shinsuke Katoh and Masataka Sata : 重症心不全患者におけるAdaptive servo-ventilation装着による運動耐容能改善効果, 第21回日本心臓リハビリテーション学会, Jul. 2015.
763.	田中君枝 and Masataka Sata : 動脈硬化病変におけるvasa vasorumの役割:動脈硬化モデルマウスを用いた検討, 第47回日本動脈硬化学会, Jul. 2015.
764.	高島啓, 門田宗之, Koji Yamaguchi, 原知也, 齋藤友子, Mika Bando, 坂東左知子, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, 飛梅威, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : IgA腎症の加療中に若年で発症した急性冠症候群の一例, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
765.	西尾進, 鳥居裕太, 平田有紀奈, 天野里江, 山尾雅美, Mika Bando, 林修司, 阿部美保, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 左室流出路に棍棒状可動性腫瘤を認めた一例, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
766.	山﨑宙, Koji Yamaguchi, 原知也, 高島啓, Mika Bando, 齋藤友子, 坂東左知子, Tomomi Matsuura, Kenya Kusunose, Takayuki Ise, 飛梅威, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 右心不全を来した収縮性心膜炎合併心膜嚢胞の一例, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
767.	山﨑宙, Shusuke Yagi, 鳥居裕太, 天野里江, 西尾進, 原知也, 齋藤友子, 高島啓, Mika Bando, 坂東左知子, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, 飛梅威, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, 島袋充生, 赤池雅史 and Masataka Sata : 深部静脈血栓症に対するエドキサバンの凝固因子に与える影響, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
768.	山﨑宙, Shusuke Yagi, 原知也, 高島啓, Mika Bando, 齋藤友子, 坂東左知子, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, 飛梅威, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 家族性アミロイドポリニューロパチーを合併した心肥大の一例, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
769.	坂東左知子, Takeshi Soeki, 原知也, 齋藤友子, Mika Bando, 山﨑宙, 高島啓, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, 飛梅威, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki, 坂東正章 and Masataka Sata : Brugada症候群に閉塞性肥大型心筋症を併発した一例, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
770.	Shusuke Yagi, 山﨑宙, Kenya Kusunose, Takayuki Ise, 飛梅威, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, 赤池雅史 and Masataka Sata : 肺アスペルギルス症に合併した肺動静脈血栓症の1例, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
771.	山尾雅美, Hirotsugu Yamada, 西尾進, 平田有紀奈, 鳥居裕太, 天野里江, Mika Bando, Kenya Kusunose, 林修司, 三代裕一郎 and Masataka Sata : 連続性雑音を契機に発見された無症候性バルサルバ洞動脈瘤破裂の一例, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
772.	瀬野弘光, Mika Bando, Kenya Kusunose, Hirotsugu Yamada, 高川由利子, 林修司, 齋藤友子, 山﨑宙, 高島啓, 坂東左知子, Tomomi Matsuura, Takayuki Ise, 飛梅威, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki, 平田有紀奈, 西尾進, 島袋充生 and Masataka Sata : CHADS2スコア低値例における左心耳機能の検討, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
773.	飛梅威, 坂東左知子, Tomomi Matsuura, Takeshi Soeki, 今田久美子, 松本和久, 齋藤友子, 原知也, 高島啓, 山﨑宙, Mika Bando, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, 赤池雅史 and Masataka Sata : 心房細動カテーテルアブレーションにおける放射線防護キャビンの放射線被爆低減効果について, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
774.	Kenya Kusunose, Hirotsugu Yamada, ブライアングリフィン, Mika Bando, 西條良仁, 西尾進, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 睡眠時呼吸障害患者の右室機能評価は予後予測において有用である, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
775.	上野理絵, Mika Bando, Hirotsugu Yamada, Kenya Kusunose, 高川由利子, 瀬野弘光, 門田宗之, 原知也, 齋藤友子, 山﨑宙, 高島啓, 坂東左知子, Tomomi Matsuura, Takayuki Ise, 飛梅威, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki, 島袋充生 and Masataka Sata : 間質性肺炎合併膠原病性肺高血圧症にボセンタンが奏功した1例, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
776.	平田有紀奈, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 山尾雅美, 天野里江, 鳥居裕太, 鈴川理乃, 高川由利子, Mika Bando, 林修司, 阿部美保, 坂東左知子, Tomomi Matsuura, 飛梅威, Takeshi Soeki and Masataka Sata : 心房細動に対する肺静脈隔離術後における洞調律維持の予測∼心エコー検査を用いた検討∼, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
777.	鈴木智子, Kenya Kusunose, Hirotsugu Yamada, Mika Bando, 西條良仁, 西尾進, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : IGg4関連疾患に伴う巨大冠動脈瘤および冠動脈周囲偽腫瘍を認めた1例, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
778.	Kenya Kusunose, Hirotsugu Yamada, Mika Bando, 西條良仁, 西尾進, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 膠原病に伴う肺高血圧症の悪化予測:6分間歩行負荷心エコー図検査を用いた検討, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
779.	Hajime Kinoshita, Hirotsugu Kurobe, 伊勢孝之, 今田久美子, Tamotsu Kanbara, Eiki Fujimoto, Takashi Kitaichi, Masataka Sata and Tetsuya Kitagawa : 左室自由壁破裂修復術後に生じた左室仮性心室瘤に対する1手術例, 第106回日本循環器学会中国・四国合同地方会, Jun. 2015.
780.	原知也, Daiju Fukuda, 田中君枝, 東邦康智, 平田陽一郎, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : 活性型第X凝固因子によるマクロファージ活性化を介した新しい動脈硬化進展機序の検討, 第2回日本心血管脳卒中学会学術集会, Jun. 2015.
781.	山﨑宙, Tetsuzo Wakatsuki, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Masataka Sata, 鹿草宏, Junichiro Satomi and Shinji Nagahiro : 広範前壁心筋梗塞発症早期に左心室内血栓を生じた2例, 第2回日本心血管脳卒中学会学術集, Jun. 2015.
782.	坂東左知子, Tomomi Matsuura, Takeshi Soeki, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 感染性心内膜炎から多発性脳塞栓発症により死亡に至った一例, 第2回日本心血管脳卒中学会学術集会, Jun. 2015.
783.	Yuishin Izumi, 塚本愛, 澤村正典, Nobuaki Yamamoto, 織田雅也, Hirohisa Ogawa, Toshitaka Kawarai, Masataka Sata, 宇高不可思 and Ryuji Kaji : たこつぼ型心筋症を合併した筋萎縮性側索硬化症の2例, 第2回日本心血管脳卒中学会学術集会, Jun. 2015.
784.	本田壮一, 白川光雄, 小原聡彦, 橋本崇代, Junichiro Satomi, Teruyoshi Kageji, Masataka Sata and Shinji Nagahiro : 心筋梗塞・脳卒中の医療連携-ドクターヘリで搬送した2症例からの考察-, 第2回日本心血管脳卒中学会学術集会, Jun. 2015.
785.	Masataka Sata : 動脈硬化の進展と破綻に関する最近の知見, 第2回日本心血管脳卒中学会学術集会, Jun. 2015.
786.	飛梅威, 坂東左知子, Tomomi Matsuura, Takeshi Soeki, 今田久美子, 松本和久, 原知也, 齋藤友子, 高島啓, 山﨑宙, Mika Bando, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, 赤池雅史 and Masataka Sata : 心房細動カテーテルアブレーションにおける放射線防護キャビンの放射線被爆低減効果に関する検討, 第2回日本心血管脳卒中学会学術集会, Jun. 2015.
787.	天野里江, Hirotsugu Yamada, Kenya Kusunose, Mika Bando, 西尾進, 山尾雅美, 鳥居裕太, 平田有紀奈 and Masataka Sata : 高度僧帽弁輪石灰化による多発性脳梗塞の1例, 第2回日本心血管脳卒中学会学術集会, Jun. 2015.
788.	平田有紀奈, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 山尾雅美, Mika Bando, Tomomi Matsuura, 飛梅威, Takeshi Soeki and Masataka Sata : 心房細動に対する肺静脈隔離術後における洞調律維持の予測:経胸壁および3次元経食道心エコー検査を用いた検討, 第2回日本心血管脳卒中学会学術集会, Jun. 2015.
789.	山下雄也, Mika Bando, Kenya Kusunose, 宮本亮介, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 片麻痺および間代性痙攣でStroke Care Unit入室後に高度心機能低下をきたした1例, 第2回日本心血管脳卒中学会学術集会, Jun. 2015.
790.	鈴川理乃, 西尾進, Hirotsugu Yamada, Junko Hotsuchi, 平田有紀奈, 山﨑宙, Kenya Kusunose and Masataka Sata : 透析シャント造設後に失神を繰り返した鎖骨下動脈盗血症候群の一例, 第2回日本心血管脳卒中学会学術集会, Jun. 2015.
791.	Mika Bando, Hirotsugu Yamada, Kenya Kusunose, 平田有紀奈, 天野里江, 西尾進, 高川由利子, 林修司, 永廣信治 and Masataka Sata : CHADS2スコア低値症例における左心耳機能の検討, 第2回日本心血管脳卒中学会学術集会, Jun. 2015.
792.	Shinji Nagahiro, Junichiro Satomi, Kazuyuki Kuwayama, Yoshiteru Tada, 曽我部周, 山口泉, 吉岡正太郎 and Masataka Sata : 当院SCUにおける心疾患を合併した脳卒中症例, 第2回日本心血管脳卒中学会学術集会, Jun. 2015.
793.	Kazuyuki Kuwayama, 羽星辰哉, Kenji Yagi, Junichiro Satomi, Shinji Nagahiro, Mika Bando, Hirotsugu Yamada and Masataka Sata : くも膜下出血に続発したタコつぼ型心筋症(Neurogenic stress cardiomyopathy)の検討, 第2回日本心血管脳卒中学会学術集会, Jun. 2015.
794.	Shu Sogabe, Yoshiteru Tada, Junichiro Satomi, Kazuyuki Kuwayama, 吉岡正太郎, 山口泉, Shinji Nagahiro, Nobuaki Yamamoto, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 当院における院内発症脳卒中症例の検討, 第2回日本心血管脳卒中学会学術集会, Jun. 2015.
795.	原知也, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : アトピー性皮膚炎から感染性心内膜炎を来した1例, 日本内科学会第112回四国地方会, Jun. 2015.
796.	Hirotsugu Yamada, Mika Bando and Masataka Sata : 頚動脈plaque性状診断における脳神経超音波の信頼性-各種モダリティーとの比較から-超音波後方散乱信号を用いた頸動脈プラークの性状診断とその臨床応用, 第34回日本脳神経超音波学会総会, Jun. 2015.
797.	鳥居裕太, 西尾進, Kenya Kusunose, 玉井佑里恵, Mika Bando, Hirotsugu Yamada and Masataka Sata : 各種抗凝固薬における深部静脈血栓退縮効果の検討, 日本超音波医学会第88回学術集会, May 2015.
798.	西條良仁, Hirotsugu Yamada, 林修司, Kenya Kusunose, Mika Bando, 高川由利子, 西尾進, 天野里江 and Masataka Sata : 前負荷増大に対する心反応性に及ぼす左房機能の影響:陳旧性心筋梗塞例における下肢陽圧負荷を用いた検討, 日本超音波医学会第88回学術集会, May 2015.
799.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 鳥居裕太, 天野里江, 林修司, Takeshi Soeki and Masataka Sata : Automated Function Imaging の左室壁運動定量評価は心エコー初心者の判断の補助となる, 日本超音波医学会第88回学術集会, May 2015.
800.	Kenya Kusunose, Hirotsugu Yamada, 西條良仁, Mika Bando, 林修司, 山尾雅美, 鳥居裕太, Takeshi Soeki and Masataka Sata : 運動負荷後の右心機能指標は弁膜症の予後と関連する招待講演, 日本超音波医学会第88回学術集会, May 2015.
801.	Hirotsugu Yamada, Kenya Kusunose, Mika Bando, 林修司, 西尾進, 山尾雅美, 天野里江, 鳥居裕太, Takeshi Soeki and Masataka Sata : 左室の壁運動(e')と血流(E)の不整合は左室拡張末期圧の上昇を反映する．, 日本超音波医学会第88回学術集会, May 2015.
802.	Hirotsugu Yamada, Kenya Kusunose, 林修司, Mika Bando, 西條良仁, 西尾進, 山尾雅美, 鳥居裕太, 平田有紀奈, Takeshi Soeki and Masataka Sata : 心エコー・ドプラ法による左室拡張末期圧の推定は，心房細動でも可能か?, 日本超音波医学会第88回学術集会, May 2015.
803.	鳥居裕太, 西尾進, 鈴川理乃, 平田有紀奈, 天野里江, 山尾雅美, Mika Bando, Hajime Kinoshita, Shoichiro Takao, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 感染症心内膜炎が契機となった右脛骨腓骨動脈感染性動脈瘤の1例, 第40回日本超音波検査学会学術集会, May 2015.
804.	K Node, J Oyama, T Ishizu, M Nanasato, K Kodama, Y Bandoh, H Kamiya, K Kitagawa, S Ueda, H Tomiyama, Masataka Sata, K Maemura, Munehide Matsuhisa, T Inoue, Y Higashi, Hirotsugu Yamada, M Ishihara, A Yamashina, N Kashihara, Y Sato and T Murohara : The Study to Evaluate the Effects of DPP-4 Inhibitor on Atherosclerosis in Patients with Diabetes Mellitus: PROLOGUE Study., 第79回日本循環器学会学術集会, Apr. 2015.
805.	N Sawada, Hirotsugu Yamada, Kenya Kusunose, Takashi Iwase, Mika Bando, Y Saijo, Y Takagawa, S Nishio, Y Hirata and Masataka Sata : Dynamic Features of Cross-sectional Area of Right Ventricular Outflow Tract in a Cardiac Cycle: A Multi-modality Study., 第79回日本循環器学会学術集会, Apr. 2015.
806.	Michio Shimabukuro, Y Hasegawa, H Masuzaki and Masataka Sata : Subclinical Vascular Disease Burden in Japanese Residents: Region- and Sex-specific Differences through LDL- and Non-HLD Cholesterol., 第79回日本循環器学会学術集会, Apr. 2015.
807.	Koji Yamaguchi, Tetsuzo Wakatsuki, T Hara, Y Takagawa, Mika Bando, A Takashima, H Yamazaki, S Bando, Tomomi Matsuura, Kenya Kusunose, Takayuki Ise, Takeshi Tobiume, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Differential Local Vascular Responses after Implantation of Biolimus-Eluting and Everolimus-Eluting Stents Compared with Sirolimus-Eluting and Bare Metal Stents., 第79回日本循環器学会学術集会, Apr. 2015.
808.	T Hara, Daiju Fukuda, K Tanaka, Y Higashikuni, Y Hirata, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Inhibition of Activated Factor X Attenuates Neointima Formation after Wire-Mediated Vascular Injury., 第79回日本循環器学会学術集会, Apr. 2015.
809.	T Hara, Daiju Fukuda, K Tanaka, Y Higashikuni, Y Hirata, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Inhibition of Activated Factor X Attenuates Vascular Inflammation and Atherosclerosis in ApoE-deficient Mice., 第79回日本循環器学会学術集会, Apr. 2015.
810.	Y Higashikuni, Daiju Fukuda, Masataka Sata and I Komuro : The Inducible Nuclear Protein IB Plays a Pivotal Role in Transition from Adaptive to Maladaptive Cardiac Hypertrophy during Pressure Overload., 第79回日本循環器学会学術集会, Apr. 2015.
811.	Michio Shimabukuro, Daiju Fukuda, H Sato, S Nishimoto, T Hara, A Takashima, Y Hirata, Hirotsugu Kurobe, Shusuke Yagi, Takeshi Soeki, Hirofumi Izaki, Hiroshi Sakaue, Tetsuya Kitagawa, Hiro-omi Kanayama and Masataka Sata : Depot- and Gender-Specific Regulation of the Innate Immune System in Adipose Tissues: A Study from Human Biopsy Samples., 第79回日本循環器学会学術集会, Apr. 2015.
812.	Takeshi Soeki, Tomomi Matsuura, S Bando, Takeshi Tobiume, T Hara, A Takashima, Mika Bando, H Yamazaki, Y Saito, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Antiarrhythmic and Antiapoptotic Effects of C-type Natriuretic Peptide in Rats with Myocardial Ischemia/Reperfusion., 第79回日本循環器学会学術集会, Apr. 2015.
813.	Y Higashikuni, Masataka Sata and I Komuro : The Role of the Central Nervous System in Heart Disease., 第79回日本循環器学会学術集会, Apr. 2015.
814.	天野里江, Hirotsugu Yamada, 西尾進, 阿部美保, Kenya Kusunose, Mika Bando, 山尾雅美, 鳥居裕太, 平田有紀奈 and Masataka Sata : 肺動脈弁を往来する転移性心臓腫瘍の1例, 第26回日本心エコー図学会学術集会, Mar. 2015.
815.	Mika Bando, Hirotsugu Yamada, 高川由利子, 西條良仁, Kenya Kusunose, 林修司, 西尾進, 平田有紀奈, 鳥居裕太, 天野里江, 山尾雅美 and Masataka Sata : キアリ網に捕捉された右房内血栓の1例, 第26回日本心エコー図学会学術集会, Mar. 2015.
816.	山尾雅美, Hirotsugu Yamada, 西尾進, 平田有紀奈, 鳥居裕太, 天野里江, 高川由利子, Mika Bando, Kenya Kusunose, 林修司, 三代裕一郎 and Masataka Sata : 連続性雑音を契機に発見された無症候性大動脈―右房トンネルの一例, 第26回日本心エコー図学会学術集会, Mar. 2015.
817.	西尾進, Hirotsugu Yamada, 平田有紀奈, 鳥居裕太, 天野里江, 山尾雅美, 高川由利子, Mika Bando, 林修司, Kenya Kusunose, Koji Yamaguchi, Tetsuzo Wakatsuki and Masataka Sata : 冠攣縮性狭心症における心臓周囲脂肪厚の意義∼超音波検査を用いた検討∼, 第26回日本心エコー図学会学術集会, Mar. 2015.
818.	平田有紀奈, Hirotsugu Yamada, 西尾進, 鈴川理乃, 堀家由貴, 玉井祐里恵, 鳥居裕太, 天野里江, 山尾雅美, 高川由利子, Mika Bando, 林修司, Kenya Kusunose and Masataka Sata : 体位変換によって出現する左室流出路狭窄の1例, 第26回日本心エコー図学会学術集会, Mar. 2015.
819.	Kenya Kusunose, Hirotsugu Yamada, ブライアングリフィン, 西尾進, Mika Bando, 平田有紀奈, 西條良仁, 天野里江, 鳥居裕太, 山尾雅美 and Masataka Sata : 左室駆出率の保たれた睡眠時呼吸障害患者における右室機能と予後との関連, 第26回日本心エコー図学会学術集会, Mar. 2015.
820.	Kenya Kusunose, Hirotsugu Yamada, Mika Bando, 高川由利子, 西尾進, 天野里江, 平田有紀奈 and Masataka Sata : A Case of IgG4-related Disease with Multiple Coronary Aneurysms and Pseudo-tumors, 第26回日本心エコー図学会学術集会, Mar. 2015.
821.	Hirotsugu Yamada, Kenya Kusunose, Mika Bando, 西尾進, 天野里江, 平田有紀奈, Masataka Sata, 平野豊, 谷口貢, 土肥薫 and 山田典一 : 肺高血圧症に対する運動負荷心エコー法:運動負荷右心カテーテル法によるバリデーション, 第26回日本心エコー図学会学術集会, Mar. 2015.
822.	Masataka Sata : 心腎連関と動脈硬化, 第5回日本腎臓リハビリテーション学会, Mar. 2015.
823.	武井美貴子, Takeshi Tobiume, 坂東左知子, Tomomi Matsuura, Takeshi Soeki and Masataka Sata : 生理的ペーシングへのモード変更が心不全の改善に有効であった房室ブロックの1例, 第7回植込みデバイス関連冬季大会, Feb. 2015.
824.	Daiju Fukuda, 原知也, Michio Shimabukuro and Masataka Sata : 活性型血液凝固第X因子が血管の炎症と動脈硬化に与える影響, 第44回日本心脈管作動物質学会, Feb. 2015.
825.	原知也, Daiju Fukuda, 田中君江, 東邦康智, 平田陽一郎, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : 活性型第X凝固因子によるマクロファージ活性化を介した新しい動脈硬化進展機序の検討, 第44回日本心脈管作動物質学会, Feb. 2015.
826.	松本康平, Kenya Kusunose, 松本和久, 高川由利子, Mika Bando, Junko Hotsuchi, Tomomi Matsuura, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 動脈周囲炎をきたしたIgG4関連疾患の1例, 第250回徳島医学会学術集会(平成26年度冬期), Feb. 2015.
827.	鈴木智子, 山崎宙, 近藤彰, 高川由利子, Mika Bando, Junko Hotsuchi, Tomomi Matsuura, Kenya Kusunose, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 活動性を評価するにあたりPET-CTが特に有効であった心サルコイドーシスの1例, 第250回徳島医学会学術集会(平成26年度冬期), Feb. 2015.
828.	武井美貴子, Takeshi Tobiume, 坂東左知子, Tomomi Matsuura, Takeshi Soeki, 今田久美子, 松本和久, 高川由利子, 原知也, 高島啓, 齋藤友子, 山崎宙, Mika Bando, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 生理的ペーシングへのモード変更が心不全の改善に有効であった房室ブロックの1例, 第250回徳島医学会学術集会(平成26年度冬期), Feb. 2015.
829.	鈴川理之, Takakazu Kinugawa, Mai Matsumoto, Yuki Horike, Yurie Tamai, Susumu Nishio, Yukina Hirata, Hirotsugu Yamada, Kenya Kusunose, Masataka Sata and Ken Saito : 前負荷増大に対する右心系の反応性ー下肢陽圧負荷を用いた若年健常者における検討, 徳島県臨床検査技師会誌, 23, Dec. 2014. (Keyword) 下肢陽圧試験 / 前負荷増大 / 心筋ストレイン値
830.	今田久美子, Takayuki Ise, Shusuke Yagi, 高木恵理, 松本和久, 高川由利子, 原知也, 高島啓, 齋藤友子, Mika Bando, 山﨑宙, 坂東左知子, Tomomi Matsuura, Takeshi Tobiume, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 慢性血栓塞栓性肺高血圧症にリオシグアトを使用した1症例, 第105回日本循環器学会四国地方会, Dec. 2014.
831.	Takayuki Ise, Takashi Iwase, 高木恵理, 今田久美子, 松本和久, 高川由利子, 原知也, 齋藤友子, 高島啓, 山﨑宙, Mika Bando, 坂東左知子, Tomomi Matsuura, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心臓MRIガドリニウム遅延造影で検出できなかった心臓サルコイドーシス再燃の一例, 第105回日本循環器学会四国地方会, Dec. 2014.
832.	石井亜由美, 西川幸治, Takayuki Ise, 高川由利子, Shusuke Yagi, Takashi Iwase, Hajime Kinoshita, Miho Sakata, Yasunobu Hayabuchi, Masashi Akaike, Shinsuke Katoh, Tetsuya Kitagawa and Masataka Sata : 単心室症患児の開心術後に心臓リハビリテーションを有効に施行し得た一例, 第105回日本循環器学会四国地方会, Dec. 2014.
833.	堀家由貴, Hirotsugu Yamada, 玉井佑里恵, 平田有紀奈, 鳥居祐太, 天野里江, 西尾進, 山尾雅美, 高川由利子, Mika Bando, 林修司, Kenya Kusunose, 宮崎達志, 足立克仁, Masataka Sata and Ken Saito : 左室収縮不全に対する薬物療法によってDuchenne型筋ジストロフィーの予後は改善したか, 第105回日本循環器学会四国地方会, Dec. 2014.
834.	平田有紀奈, Hirotsugu Yamada, 西尾進, 堀家由貴, 玉井佑里恵, 鳥居祐太, 天野里江, 山尾雅美, 高川由利子, Mika Bando, 林修司, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 頸動脈プラークスコア，心臓周囲脂肪厚と冠動脈硬化の関連:超音波検査を用いた検討, 第105回日本循環器学会四国地方会, Dec. 2014.
835.	高島啓, Tetsuzo Wakatsuki, Koji Yamaguchi, 松本和久, 今田久美子, 高木恵理, 高川由利子, 原知也, 齋藤友子, 山﨑宙, Mika Bando, 坂東左知子, Tomomi Matsuura, Takayuki Ise, Takeshi Tobiume, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : 冠動脈完全閉塞性病変の治療後慢性期に形成された二重血行路をOCTで観察し得た一例, 第105回日本循環器学会四国地方会, Dec. 2014.
836.	Shusuke Yagi, 鳥居祐太, Takayuki Ise, Koji Yamaguchi, Takeshi Tobiume, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Masashi Akaike and Masataka Sata : 突然の片側性下肢腫脹を呈した変形性関節症の2例, 第105回日本循環器学会四国地方会, Dec. 2014.
837.	Kenya Kusunose, Hirotsugu Yamada, ポポヴィッチゾラン, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 無症候性僧帽弁逆流症と大動脈弁逆流症の自然経過, 第105回日本循環器学会四国地方会, Dec. 2014.
838.	坂東左知子, Takeshi Soeki, 今田久美子, 松本和久, 原知也, 高島啓, 山﨑宙, Mika Bando, 齋藤友子, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 右室流出路心外膜起源が疑われた突発性心室期外収縮の一例, 第105回日本循環器学会四国地方会, Dec. 2014.
839.	稲垣太造, Shusuke Yagi, Takayuki Ise, Koji Yamaguchi, Takeshi Tobiume, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Masashi Akaike and Masataka Sata : 治療抵抗性本態性高血圧に対する利尿剤の効果-インダパミドが効果的であった2例の検討-, 第105回日本循環器学会四国地方会, Dec. 2014.
840.	富永真由, Takayuki Ise, Mika Bando, 今田久美子, 松本和久, 高川由利子, 原知也, 齋藤友子, 高島啓, 山﨑宙, 坂東左知子, Tomomi Matsuura, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, 坂東正章 and Masataka Sata : 超選択的コントラストエコーを併用し経皮的中隔心筋焼灼術を有効に施行し得た閉塞性肥大型心筋症の1例, 第105回日本循環器学会四国地方会, Dec. 2014.
841.	Takayuki Ise, Takashi Iwase, 高川由利子, Kenya Kusunose, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心臓サルコイドーシス再燃に対してメトトレキサートの併用が有効であった1例, 第111回日本内科学会四国地方会, Nov. 2014.
842.	Y Higashikuni, Daiju Fukuda, Masataka Sata and I Komuro : The inducible nuclear protein IB plays a pivotal role in the transition from adaptive to maladaptive cardiac hypertrophy during pressure overload., The 31st Annual Meeting of the International Society for Heart Research Japanese Section, Nov. 2014.
843.	東邦康智, Masataka Sata and 小室一成 : 心疾患における自然炎症の役割とその制御機構, 第18回日本心血管内分泌代謝学会学術総会, Nov. 2014.
844.	東邦康智, Masataka Sata and 小室一成 : The Regulatory Mechanism of Inflammation in the Heart through the Heart-Brain Interaction and Its Role in Pressure Overload-Induced Cardiac Hypertrophy, 第37回日本高血圧学会総会, Oct. 2014.
845.	Shusuke Yagi, Ken-ichi Aihara, Masashi Akaike, Takeshi Soeki and Masataka Sata : High Serum Parathyroid Hormone Is Associated with Incidence of Hypertension, 第37回日本高血圧学会総会, Oct. 2014.
846.	平田有紀奈, Hirotsugu Yamada, 西尾進, 堀家由貴, 玉井佑里恵, 鳥居裕太, 天野里江, 山尾雅美, Mika Bando, 林修司, Kenya Kusunose and Masataka Sata : 肺高血圧を伴う右肺動脈上行大動脈起始の1例, JSS四国第20回地方会学術集会, Oct. 2014.
847.	山尾雅美, 西尾進, 鳥居裕太, 平田有紀奈, 笹田倫子, Shoichiro Takao, Naoki Muguruma, Hirotsugu Yamada, Mitsuo Shimada and Masataka Sata : 内部に嚢胞性変化を伴った肝過形成結節の1例, 第24回日本超音波医学会四国地方会学術集会, Oct. 2014.
848.	鳥居裕太, 西尾進, 山尾雅美, 平田有紀奈, 笹田倫子, 松本早代, Shoichiro Takao, Naoki Muguruma, Hirotsugu Yamada and Masataka Sata : 胃壁内膿瘍穿通による肝膿瘍の1例, 第24回日本超音波医学会四国地方会学術集会, Oct. 2014.
849.	玉井佑里恵, 西尾進, 堀家由貴, 平田有紀奈, 鳥居裕太, Hajime Kinoshita, Tetsuya Kitagawa, Junko Hotsuchi, Hirotsugu Yamada and Masataka Sata : 短期間にバイパス閉塞をきたしたLeriche症候群の1例, 第24回日本超音波医学会四国地方会学術集会, Oct. 2014.
850.	堀家由貴, Hirotsugu Yamada, 玉井佑里恵, 平田有紀奈, 鳥居裕太, 天野里江, Mika Bando, 西尾進, 山尾雅美 and Masataka Sata : 僧帽弁置換術が奏功したBecker型筋ジストロフィーに基づく拡張型心筋症の一例, 第24回日本超音波医学会四国地方会学術集会, Oct. 2014.
851.	澤田直子, Hirotsugu Yamada, Kenya Kusunose, 林修司, Mika Bando, 西條良仁, 高川由利子, 西尾進, 天野里江 and Masataka Sata : 3次元心エコー図検査が有用で3次元心エコー法を用いた右室流出路の心周期における形態変化の検討:造影CT検査との比較, 第24回日本超音波医学会四国地方会学術集会, Oct. 2014.
852.	高川由利子, 林修司, Hirotsugu Yamada, Mika Bando, 天野里江, 西尾進, 山尾雅美, Tomomi Matsuura and Masataka Sata : ペースメーカー植込み術後より聴取された収縮期雑音の診断に3次元心エコー図検査が有用であった一例, 第24回日本超音波医学会四国地方会学術集会, Oct. 2014.
853.	原國督, Hirotsugu Yamada, 澤田直子, 高川由利子, Mika Bando, 西尾進, 天野里江, 鳥居裕太, 平田有紀奈 and Masataka Sata : カラードプラ法では重症度を過小評価した人工弁置換術後大動脈弁逆流(AR)の2例, 第24回日本超音波医学会四国地方会学術集会, Oct. 2014.
854.	Mika Bando, Hirotsugu Yamada, 髙川由利子, 林修司, 西尾進, 平田有紀奈, 天野里江, 鳥居裕太, 山尾雅美 and Masataka Sata : インフルエンザ感染による心膜炎を合併した右房内クモの巣血栓の1例, 第24回日本超音波医学会四国地方会学術集会, Oct. 2014.
855.	天野里江, Hirotsugu Yamada, Junko Hotsuchi, Mika Bando, 西尾進, 山尾雅美, 鳥居裕太, 平田有紀奈, 原國督 and Masataka Sata : IGg4 関連疾患に伴う巨大冠動脈瘤の1例, 第24回日本超音波医学会四国地方会学術集会, Oct. 2014.
856.	西條良仁, Hirotsugu Yamada, 林修司, Kenya Kusunose, Mika Bando, 澤田直子, 高川由利子, 西尾進, 天野里江 and Masataka Sata : 前負荷増大に対する心反応性に及ぼす左房機能の影響:陳旧性心筋梗塞例における下肢陽圧負荷を用いた検討, 第24回日本超音波医学会四国地方会学術集会, Oct. 2014.
857.	Tomomi Matsuura, Takeshi Soeki, 西條良仁, 齋藤友子, 高島啓, Mika Bando, 坂東左知子, Junko Hotsuchi, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 筋強直性ジストロフィーに伴い二次性心筋症と心房頻拍を呈し，カテーテルアブレーションを施行した一例, 第62回日本心臓病学会学術集会, Sep. 2014.
858.	平田有紀奈, Hirotsugu Yamada, 西尾進, Kenya Kusunose, 澤田直子, 高川由利子, 西條良仁, Mika Bando, Junko Hotsuchi, 林修司, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心エコー法で計測する前室間溝心外膜脂肪厚はCTで計測した心外膜脂肪容積を反映する, 第62回日本心臓病学会学術集会, Sep. 2014.
859.	Junko Hotsuchi, Hirotsugu Yamada, 西條良仁, Mika Bando, 高島啓, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 薬剤抵抗性起立性調節障害に対する携帯型下肢陽圧装置の効果, 第62回日本心臓病学会学術集会, Sep. 2014.
860.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, Zoran Popovic and Masataka Sata : 無症候性大動脈弁閉鎖不全症における運動負荷心エコー図法の有用性, 第62回日本心臓病学会学術集会, Sep. 2014.
861.	西尾進, Hirotsugu Yamada, Kenya Kusunose, 平田有紀奈, 西條良仁, Mika Bando, Junko Hotsuchi, 林修司, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : S字状中隔と各種血管検査指標との関連, 第62回日本心臓病学会学術集会, Sep. 2014.
862.	坂東左知子, Takeshi Soeki, Takeshi Tobiume, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : ATP 感受性リエントリー性心房頻拍の2症例, 第62回日本心臓病学会学術集会, Sep. 2014.
863.	原知也, Tetsuzo Wakatsuki, Koji Yamaguchi, Takayuki Ise, Takeshi Tobiume, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : 十分な術前ヘパリン置換にもかかわらず超遅発性ステント血栓症を発症した症例の検討-OCT による観察から-, 第62回日本心臓病学会学術集会, Sep. 2014.
864.	Mika Bando, Hirotsugu Yamada, 西尾進, 林修司, Junko Hotsuchi, 西條良仁, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心房細動症例におけるCHADS2 およびCHA2DS2-VASc スコアと左心耳血流速度の関連, 第62回日本心臓病学会学術集会, Sep. 2014.
865.	Takeshi Soeki, 坂東左知子, Tomomi Matsuura, Takeshi Tobiume, 高島啓, Mika Bando, Junko Hotsuchi, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : 心房細動におけるmicroRNAと心房リモデリングおよび予後との関係, 第62回日本心臓病学会学術集会, Sep. 2014.
866.	西條良仁, Hirotsugu Yamada, 西尾進, Mika Bando, Junko Hotsuchi, 林修司, 澤田直子, 高川由利子, 平田有紀奈, Koji Yamaguchi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 僧帽弁血流速波形の前負荷増大に対する反応性には左房機能が関与する, 第62回日本心臓病学会学術集会, Sep. 2014.
867.	Koji Yamaguchi, Tetsuzo Wakatsuki, Takayuki Ise, 高島啓, 齋藤友子, Takeshi Tobiume, Takashi Iwase and Masataka Sata : 第一世代薬剤溶出性ステントの超遅発性血栓症の2例-病歴・病変観察の観点から-, 第21回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2014.
868.	高島啓, Tetsuzo Wakatsuki, Koji Yamaguchi, 齋藤友子, 山﨑宙, Takayuki Ise, Takeshi Tobiume, Takashi Iwase and Masataka Sata : CTO治療後慢性期に形成された二重血行路をOCTで観察した一例, 第21回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2014.
869.	A Takashima, Daiju Fukuda, K Tanaka, Y Higashikuni, Y Hirata, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Combined administration of eicosapentaenoic acid and docosahexaenoic acid reduces atherosclerotic lesion in apolipoprotein E-deficient mice., ESC 2014, Aug. 2014.
870.	富永真由, Takayuki Ise, Mika Bando, 今田久美子, 松本和久, 高川由利子, 高木恵理, 西條良仁, 原知也, 齋藤友子, 高島啓, 山﨑宙, 坂東左知子, Tomomi Matsuura, Junko Hotsuchi, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, 坂東正章 and Masataka Sata : 超選択的コントラストエコーを併用し経皮的中隔心筋焼灼術を有効に施行し得た閉塞性肥大型心筋症の一例, 第249回徳島医学会学術集会(平成26年度夏期), Jul. 2014.
871.	亀田香奈子, Takayuki Ise, 西條良仁, 今田久美子, 松本和久, 高川由利子, 高木恵理, 原知也, 齋藤友子, 高島啓, 山﨑宙, Mika Bando, 坂東左知子, Tomomi Matsuura, Junko Hotsuchi, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, 近藤剛 and Masataka Sata : 原発性アルドステロン症患者に高度冠攣縮を合併し心筋梗塞を発症した1症例, 第249回徳島医学会学術集会(平成26年度夏期), Jul. 2014.
872.	A Takashima, Tetsuzo Wakatsuki, Koji Yamaguchi, K Ogasawara, Takeshi Tobiume, Takashi Iwase and Masataka Sata : Local coagulation response and angiographic peri-stent contrast staining up to five years after sirolimus-eluting stent implantation., 第23回日本心血管インターベンション治療学会, Jul. 2014.
873.	Koji Yamaguchi, Tetsuzo Wakatsuki, A Takashima, K Ogasawara, Takeshi Tobiume, Takashi Iwase and Masataka Sata : Differential Responses of Local Coagulation after Implantation of Second-Generation Drug-Eluting Stent Compared with First-Generation Drug-Eluting Stents., 第23回日本心血管インターベンション治療学会, Jul. 2014.
874.	S Bando, Takeshi Soeki, Takeshi Tobiume, Tomomi Matsuura and Masataka Sata : Radiofrequency ablation of idiopathic premature ventricular contraction originating from the anterior papillary muscle in the left ventricle., 第29回日本不整脈学会・第31回日本心電学会合同学術大会, Jul. 2014.
875.	Tomomi Matsuura, Takeshi Soeki, Takeshi Tobiume, S Bando and Masataka Sata : A case of myotonic dystrophy presenting with atrial tachycardia and heart failure., 第29回日本不整脈学会・第31回日本心電学会合同学術大会, Jul. 2014.
876.	Takeshi Soeki, S Bando, Tomomi Matsuura, Takeshi Tobiume and Masataka Sata : Electrophysiological correlation and prognostic impact of pentraxin 3 as a local inflammatory marker in atrial fibrillation., 第29回日本不整脈学会・第31回日本心電学会合同学術集会, Jul. 2014.
877.	西川幸治, 石井亜由美, 後藤強, Takayuki Ise, Shusuke Yagi, Takashi Iwase, Masashi Akaike, Shinsuke Katoh and Masataka Sata : 運動習慣の有無が運動耐用能および動脈機能の関係に及ぼす影響について, 第20回日本心臓リハビリテーション学会学術集会, Jul. 2014.
878.	石井亜由美, Shusuke Yagi, 西川幸治, 後藤強, Takayuki Ise, Takashi Iwase, Masashi Akaike, Shinsuke Katoh and Masataka Sata : 心臓リハビリテーション実施期間中の体重増加が運動耐容能におよぼす影響, 第20回日本心臓リハビリテーション学会学術集会, Jul. 2014.
879.	西條良仁, Takayuki Ise, Hirokazu Miki, Kumiko Kagawa, 原知也, 齋藤友子, 高島啓, Mika Bando, 坂東左知子, Tomomi Matsuura, Junko Hotsuchi, Koji Yamaguchi, Takeshi Tobiume, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, 奥村宇信, 藤永裕之 and Masataka Sata : 高度心機能障害を伴う原発性心アミロイドーシスに対しauto-PBSCTを施行し得た一例, 第104回日本循環器学会中国・四国合同地方会, Jul. 2014.
880.	澤田直子, 高川由利子, Junko Hotsuchi, 西條良仁, 高島啓, Mika Bando, 山崎宙, 坂東左知子, Tomomi Matsuura, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心エコー検査による大動脈弁逆流の重症度判定が困難であった大動脈弁位生体弁機能不全の一例, 第104回日本循環器学会中国・四国合同地方会, Jul. 2014.
881.	原知也, Shusuke Yagi, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 大動脈解離の急性期降圧療法における経皮吸収型β1遮断薬の使用経験, 第104回日本循環器学会中国・四国合同地方会, Jul. 2014.
882.	鳥居裕太, Hirotsugu Yamada, 西尾進, 平田有紀奈, 天野里江, 山尾雅美, 高川由利子, 西條良仁, Mika Bando, Junko Hotsuchi, 林修司, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 遺残坐骨動脈奇形に伴う浅大腿動脈閉塞の1例, 第104回日本循環器学会中国・四国合同地方会, Jul. 2014.
883.	坂東左知子, Takeshi Soeki, Takeshi Tobiume, Tomomi Matsuura, 今田久美子, 松本和久, 高木恵理, 西條良仁, 原知也, 齋藤友子, 高島啓, Mika Bando, 山崎宙, Takayuki Ise, Junko Hotsuchi, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : ATP感受性リエントリー性心房頻拍の一例, 第104回日本循環器学会中国・四国合同地方会, Jul. 2014.
884.	Tomomi Matsuura, Takeshi Soeki, 松本和久, 今田久美子, 西條良仁, 高木恵理, 原知也, 齋藤友子, 高島啓, Mika Bando, 山崎宙, 坂東左知子, Junko Hotsuchi, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 心房頻拍と心不全を契機に発覚した筋強直性ジストロフィーの一例, 第104回日本循環器学会中国・四国合同地方会, Jul. 2014.
885.	坂東左知子, Takeshi Soeki, Takeshi Tobiume, Tomomi Matsuura, 齋藤友子, 高島啓, Mika Bando, 山崎宙, Takayuki Ise, Junko Hotsuchi, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Miho Sakata, Yasunobu Hayabuchi, 井上美紀, Kazuhiro Mori, 木下学 and Masataka Sata : 薬剤抵抗性特発性心室頻拍に対し，PCPS下にアブレーション治療を施行し，社会復帰に成功した若年例の一例, 第104回日本循環器学会中国・四国合同地方会, Jul. 2014.
886.	松本和久, Tetsuzo Wakatsuki, 高島啓, Koji Yamaguchi, 西條良仁, 高木恵理, 原知也, 齋藤友子, 高川由利子, 山崎宙, Mika Bando, 坂東左知子, Tomomi Matsuura, Takayuki Ise, Junko Hotsuchi, Takeshi Tobiume, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : シロリムス溶出ステント留置7年後に初めて造影剤ステント周囲滲み出し像と局所凝固反応亢進を認めた一例, 第104回日本循環器学会中国・四国合同地方会, Jul. 2014.
887.	原知也, Tetsuzo Wakatsuki, Koji Yamaguchi, Takayuki Ise, Takeshi Tobiume, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : 十分な術前ヘパリン置換にもかかわらず超遅発性ステント血栓症を発症した症例-OCTによる観察からの検討-, 第104回日本循環器学会中国・四国合同地方会, Jul. 2014.
888.	今田久美子, Takayuki Ise, 原知也, Shusuke Yagi, Takashi Iwase, 西條良仁, 小笠原梢, 高島啓, Mika Bando, 坂東左知子, Tomomi Matsuura, Junko Hotsuchi, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 心不全を合併した頻脈性心房細動にランジオロールを有効に使用することができた2症例, 第104回日本循環器学会中国・四国合同地方会, Jul. 2014.
889.	高川由利子, Shusuke Yagi, Hirotsugu Yamada, 林修司, Junko Hotsuchi, Mika Bando, Koji Yamaguchi, Takayuki Ise, Takeshi Tobiume, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 母児ともに救命できた母児間輸血症候群と妊娠高血圧腎症に合併した急性心不全の一例, 第104回日本循環器学会中国・四国合同地方会, Jul. 2014.
890.	西尾進, Hirotsugu Yamada, 真鍋泰毅, 佐藤光代, 平岡葉月, 河野裕美, 平田有紀奈, 天野里江, 西條良仁, 高川由利子, Mika Bando, Junko Hotsuchi, 林修司, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 血流量の増加は%FMDを増大させる, 第104回日本循環器学会中国・四国合同地方会, Jul. 2014.
891.	原知也, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Vascular endothelial growth factor (VEGF)阻害薬の眼内投与中に急性冠症候群を発症した4症例の検討, 第104回日本循環器学会中国・四国合同地方会, Jul. 2014.
892.	Hirotsugu Yamada, Michio Shimabukuro and Masataka Sata : 非侵襲的検査としてのFMDの特徴と課題, 第46回日本動脈硬化学会総会・学術集会, Jul. 2014.
893.	Kyoko Nishi, Koichiro Kajiura, Shinya Watanabe and Masataka Sata : 顕在化した徳島大学病院における医療体制の歪みは是正できるか, 第64回日本病院学会(シンポジウム), Jul. 2014.
894.	東邦康智, Masataka Sata and 小室一成 : 圧負荷心肥大の病態生理におけるNLRP3インフラマソームを介した心脳連関の役割, 第35回日本炎症・再生医学会, Jul. 2014.
895.	鳥居裕太, 西尾進, 平田有紀奈, 天野里江, 山尾雅美, 玉井佑里恵, 堀家由貴, Mika Bando, Hirotsugu Yamada and Masataka Sata : 上肢に認めた先天性および後天性静脈瘤の2例, 第39回日本超音波検査学会学術集会, Jun. 2014.
896.	平田有紀奈, 西尾進, 堀家由貴, 玉井佑里恵, 鳥居裕太, 天野里江, 山尾雅美, Mika Bando, Junko Hotsuchi, 林修司, Hirotsugu Yamada and Masataka Sata : 心外膜脂肪の肥厚が診断の契機となった冠攣縮性狭心症の1例, 第39回日本超音波検査学会学術集会, Jun. 2014.
897.	齋藤友子, Takayuki Ise, Junko Hotsuchi, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Hisatsugu Goto and Masataka Sata : 左室収縮不全と間質性肺炎に伴う肺高血圧症を合併した皮膚筋炎の1例, 第110回日本内科学会四国地方会, Jun. 2014.
898.	坂東左知子, Takeshi Soeki, Takeshi Tobiume, Tomomi Matsuura, Koji Yamaguchi, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masataka Sata, 井野口卓 and 折野俊介 : 左室前乳頭筋起源の特発性心室性不整脈の1例, 第110回日本内科学会四国地方会, Jun. 2014.
899.	齋藤友子, Takayuki Ise, Junko Hotsuchi, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata and Hisatsugu Goto : 左室収縮不全と間質性肺炎に伴う肺高血圧症を合併した皮膚筋炎の1例, 第110回日本内科学会四国地方会, Jun. 2014.
900.	Tomomi Matsuura, Takeshi Soeki, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : 心房高頻度刺激を行った糖尿病モデルラットにおける直接レニン阻害薬の内皮機能障害抑制効果, 第1回日本心血管脳卒中学会学術集会, Jun. 2014.
901.	Mika Bando, Hirotsugu Yamada, 平尾麻衣子, 平田有紀奈, 西尾進, 高川由利子, 西條良仁, 林修司, Junko Hotsuchi, Junichiro Satomi, Shinji Nagahiro and Masataka Sata : 心房細動におけるCHADS2およびCHA2DS2-VAScスコアと左心耳血流速度の関連, 第1回日本心血管脳卒中学会学術集会, Jun. 2014.
902.	菅澤典子, 中山泰介, 宅見央子, 東口文治, 松本幸子, 粟飯原賢一, 島袋充生, Masataka Sata, Tetsuya Kitagawa and Hirotsugu Kurobe : へスペリジンと血管機能 ―ヘスペリジンは動脈硬化進行を予防するか―, 第68回日本栄養・食糧学会, May 2014.
903.	Masataka Sata : 徳島県における急性心筋梗塞地域連携パスの運用について, 第4回豊橋ライブデモンストレーションコース, May 2014.
904.	Hirotsugu Kurobe, 菅澤典子, 平田陽一郎, Michio Shimabukuro, 中山泰介, 吉田恭史, 松岡祐貴, Hajime Kinoshita, Masataka Sata and Tetsuya Kitagawa : エゼチミブ投与が動脈リモデリング・機能へ与える影響の検討, 第42回日本血管外科学会学術総会, May 2014.
905.	Michio Shimabukuro, Sachiko Matsumoto, Daiju Fukuda, Takeshi Soeki, 山川研, 益崎裕章 and Masataka Sata : アンジオテンシンⅡタイプ1受容体拮抗薬アジルサルタンは，KKAy糖尿病マウスの炎症シグナル，一酸化窒素合成酵素のリン酸化能を正常化することで血管内皮機能を改善する, 第14回日本NO学会学術集会, May 2014.
906.	Masataka Sata : PCI後のイベント再発予防に向けた新規凝固薬の可能性-最新のエビデンスと動脈硬化研究からの考察-, 第14回日本NO学会学術集会, May 2014.
907.	高松直子, 森敦子, Hiroyuki Nodera, Yoshimitsu Shimatani, Yuishin Izumi, 西尾進, 山尾雅美, 鳥居裕太, Hirotsugu Yamada and Masataka Sata : 筋萎縮性側索硬化症の診断における神経超音波検査の有用性, 第87回日本超音波医学会学術集会, May 2014.
908.	堀家由貴, Hirotsugu Yamada, 西尾進, Junko Hotsuchi, 林修司, 玉井佑里恵, 宮崎達志, 足立克人, Ken Saito and Masataka Sata : Duchenne 型筋ジストロフィーにおける左心機能の経年変化, 第87回日本超音波医学会学術集会, May 2014.
909.	Junko Hotsuchi, Hirotsugu Yamada, 木村恵理子, Mika Bando, 林修司, 西條良仁, 西尾進, Takeshi Soeki, Kazuhiro Mori and Masataka Sata : 収縮期雑音の原因が仮性腱索と考えられた1例:ヴィオリンハート, 第87回日本超音波医学会学術集会, May 2014.
910.	天野里江, Hirotsugu Yamada, Junko Hotsuchi, 林修司, Mika Bando, 西條良仁, 西尾進, 山尾雅美, Takeshi Soeki and Masataka Sata : 上行大動脈の拡大が機序の異なる体位変換性呼吸困難に関与したと思われる1例, 第87回日本超音波医学会学術集会, May 2014.
911.	山尾雅美, Hirotsugu Yamada, 西尾進, 平田有紀奈, 鳥居裕太, 天野里江, 高島啓, Junko Hotsuchi, Takeshi Soeki and Masataka Sata : 冠状静脈洞内に疣腫を認めた冠動静脈瘻の一例, 第87回日本超音波医学会学術集会, May 2014.
912.	平尾麻衣子, Hirotsugu Yamada, Junko Hotsuchi, 林修司, Mika Bando, 西尾進, 山尾雅美, 鳥居裕太, Takeshi Soeki and Masataka Sata : CHADS2およびCHA2DS2-VAScスコアの増加は左心耳血流速度の低下と関連する, 第87回日本超音波医学会学術集会, May 2014.
913.	西尾進, 鳥居裕太, Hirotsugu Yamada and Masataka Sata : 下肢静脈領域, 第87回日本超音波医学会学術集会, May 2014.
914.	鳥居裕太, 西尾進, 山尾雅美, 平田有紀奈, Junko Hotsuchi, Takayuki Ise, Shoichiro Takao, Naoki Muguruma, Hirotsugu Yamada and Masataka Sata : 門脈圧亢進症および門脈・左胃静脈内血栓による巨大脾動脈瘤の1症例, 第87回日本超音波医学会学術集会, May 2014.
915.	Hirotsugu Yamada, 西尾進, Junko Hotsuchi, Mika Bando, 西條良仁 and Masataka Sata : 循環器領域の救急超音波診断∼胸痛の鑑別∼, 第87回日本超音波医学会学術集会, May 2014.
916.	平田有紀奈, Hirotsugu Yamada, 西尾進, 山尾雅美, 鳥居裕太, Mika Bando, 林修司, Junko Hotsuchi, 西條良仁, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 頸動脈プラークスコアおよび心外膜脂肪厚により冠動脈狭窄が予測できるか?, 第25回日本心エコー図学会学術集会, Apr. 2014.
917.	Junko Hotsuchi, Hirotsugu Yamada, 西條良仁, Mika Bando, 林修司, 木村恵理子, 平田有紀奈, 天野里江, 鳥居裕太, 山尾雅美, 西尾進 and Masataka Sata : 膠原病例における6分間の歩行後右房-右室圧較差の経年的変化, 第25回日本心エコー図学会学術集会, Apr. 2014.
918.	秋山晋一郎, Hirotsugu Yamada, Junko Hotsuchi, 林修司, Mika Bando, 西條良仁, 西尾進, 平田有紀奈, 山尾雅美 and Masataka Sata : ルーチン検査における各種右室収縮期指標と三次元心エコー法により求めた右室駆出率との相関, 第25回日本心エコー図学会学術集会, Apr. 2014.
919.	Mika Bando, Hirotsugu Yamada, 西尾進, 天野里江, 平田有紀奈, 山尾雅美, 鳥居裕太, 林修司, Junko Hotsuchi, 西條良仁 and Masataka Sata : 頸動脈プラークの組織性状評価による冠動脈ステントの再狭窄の予測:iPlaqueを用いた検討, 第25回日本心エコー図学会学術集会, Apr. 2014.
920.	Hirotsugu Yamada, 西尾進 and Masataka Sata : 遠隔診断を病診連携に活かす, 第25回日本心エコー図学会学術集会, Apr. 2014.
921.	西尾進, Hirotsugu Yamada and Masataka Sata : 日常診療での心エコー図による右心機能評価;様々な指標の解釈と問題点, 第25回日本心エコー図学会学術集会, Apr. 2014.
922.	西尾進, Hirotsugu Yamada and Masataka Sata : 先天性心疾患:結局のところ，どういう異常なのか?, 第25回日本心エコー図学会学術集会, Apr. 2014.
923.	Hirotsugu Yamada, 西尾進 and Masataka Sata : ネットワーク時代の画像情報管理とTele-medicine, 第25回日本心エコー図学会学術集会, Apr. 2014.
924.	山尾雅美, 西尾進, Hirotsugu Yamada and Masataka Sata : 超音波センターで育成される "General sonographer'', 第25回日本心エコー図学会学術集会, Apr. 2014.
925.	Hirotsugu Yamada, 西尾進, Mika Bando, Junko Hotsuchi, 西條良仁, 山尾雅美, 天野里江, 鳥居裕太, 平田有紀奈 and Masataka Sata : 血管エコー検査と心エコー検査のコラボレーション, 第25回日本心エコー図学会学術集会, Apr. 2014.
926.	Mika Bando, Hirotsugu Yamada, 西尾進, 天野里江, 平田有紀奈, 山尾雅美, 鳥居裕太, 西條良仁, 林修司, Junko Hotsuchi, Takashi Iwase, Shoichiro Takao and Masataka Sata : 心サルコイドーシスの左室局所心筋におけるガドリニウム遅延造影と収縮期ストレイン, 第25回日本心エコー図学会学術集会, Apr. 2014.
927.	平田有紀奈, Hirotsugu Yamada, 西尾進, 鳥居裕太, 山尾雅美, Mika Bando, 林修司, Junko Hotsuchi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 冠動脈硬化と関連するのはSubepicardial Fat か，Pericardil Fat か, 第78回日本循環器学会学術集会, Mar. 2014.
928.	西尾進, Hirotsugu Yamada, 山尾雅美, 平田有紀奈, Kazuhiro Mori, 松岡優 and Masataka Sata : 心エコー検査による先天性心疾患スクリーニングの有用性:子育て支援イベントにおける12年間のまとめ, 第78回日本循環器学会学術集会, Mar. 2014.
929.	Y Higashikuni, Masataka Sata and I Komuro : NLRP3 inflammasome activation through the heart-brain interaction contributes to adaptive cardiac hypertrophy in response to pressure overload, 第78回日本循環器学会学術集会, Mar. 2014.
930.	Z Tian, K Miyata, H Tadume, E Horio, H Sakaguchi, H Hao, M Tabata, S Takanashi, Michio Shimabukuro, Masataka Sata, M Kawasuji and Y Oike : Periadventitial adipose tissue secreted-angiopoietin-like protein 2 (Angptl2) aggravates neointimal hyperplasia in endovascular wire injury model., 第78回日本循環器学会学術集会, Mar. 2014.
931.	Masayoshi Ishida, Michio Shimabukuro, Shusuke Yagi, Daiju Fukuda, Takeshi Soeki and Masataka Sata : Post-transcriptional regulation of endothelial NADPH oxidase 4 (NOX4) by miR-100: a human biopsy study in subcutaneous and visceral adipose tissue., 第78回日本循環器学会学術集会, Mar. 2014.
932.	Sachiko Matsumoto, Michio Shimabukuro, Daiju Fukuda, T Hara, Takeshi Soeki and Masataka Sata : Antagonism of protease-activated receptors rescues vascular endothelial function in KK-Ay mice: a novel mechanism of rivaroxaban, a factor Xa inhibitor., 第78回日本循環器学会学術集会, Mar. 2014.
933.	S Bando, Takeshi Soeki, T Matsuura, Takeshi Tobiume, T Hara, A Takashima, Mika Bando, K Ogasawara, Y Saito, Junko Hotsuchi, E Kimura, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Atrial late potentials and atrial substrate remodeling in patients with atrial fibrillation., 第78回日本循環器学会学術集会, Mar. 2014.
934.	Masayoshi Ishida, Michio Shimabukuro, Shusuke Yagi, Daiju Fukuda, Takeshi Soeki and Masataka Sata : Post-transcriptional regulation of adiponectin by microRNA 378 in white adipose tissue: a novel mechanism., 第78回日本循環器学会学術集会, Mar. 2014.
935.	S Bando, Takeshi Soeki, T Hara, A Takashima, Mika Bando, K Ogasawara, Y Saito, T Matsuura, Junko Hotsuchi, E Kimura, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro, Kenji Kangawa and Masataka Sata : Ghrelin ameliorates the progression of experimental autoimmune myocarditis., 第78回日本循環器学会学術集会, Mar. 2014.
936.	S Hayashi, Hirotsugu Yamada, S Nishio, Junko Hotsuchi, Mika Bando and Masataka Sata : Differentiation between hypertrophic cardiomyopathy and hypertensive heart disease using tricuspid annular motion velocity., 第78回日本循環器学会学術集会, Mar. 2014.
937.	Koji Yamaguchi, Tetsuzo Wakatsuki, T Hara, K Ogasawara, Mika Bando, A Takashima, S Bando, T Matsuura, Takayuki Ise, Junko Hotsuchi, Takeshi Tobiume, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Differential responses of local coagulation after implantation of biolimus-eluting and everolimus-eluting stents compared with sirolimus-eluting and bare metal stents., 第78回日本循環器学会学術集会, Mar. 2014.
938.	Mika Bando, Hirotsugu Yamada, S Nishio, Junko Hotsuchi, S Hayashi, E Kimura, Takayuki Ise, T Matsuura, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Parallel changes in sonographic characteristics of carotid and coronary plaques., 第78回日本循環器学会学術集会, Mar. 2014.
939.	Takayuki Ise, Shusuke Yagi, Takashi Iwase, Masashi Akaike, A Takashima, Mika Bando, S Bando, T Matsuura, Junko Hotsuchi, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Impact of cardiac rehabilitation on oxidized stress in patients with heart failure., 第78回日本循環器学会学術集会, Mar. 2014.
940.	T Matsuura, Takeshi Soeki, R Ota, T Hara, Y Saito, K Ogasawara, A Takashima, Mika Bando, S Bando, Junko Hotsuchi, E Kimura, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : Increased local production of c-type natriuretic peptide in patients with vasospastic angina., 第78回日本循環器学会学術集会, Mar. 2014.
941.	Takeshi Soeki, S Bando, T Matsuura, Takeshi Tobiume, T Hara, R Ota, A Takashima, Mika Bando, K Ogasawara, Y Saito, Takayuki Ise, Junko Hotsuchi, E Kimura, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Relationship between local production of microRNA-328 and atrial substrate remodeling in atrial fibrillation., 第78回日本循環器学会学術集会, Mar. 2014.
942.	Miho Sakata, Yasunobu Hayabuchi, Shoji Kagami, Takashi Kitaichi, Eiki Fujimoto, Tamotsu Kanbara, Hirotsugu Kurobe, Tetsuya Kitagawa, Takeshi Soeki, Takeshi Tobiume, 松浦朋美, 板東左知子 and Masataka Sata : 経皮的心肺補助装置(PCPS)装着下にカテーテルアブレーションを施行し，救命し得た心室頻拍1男児例, 第28回日本小児循環器学会近畿・中四国地方会, Mar. 2014.
943.	今田久美子, Shusuke Yagi, Koji Yamaguchi, Tetsuzo Wakatsuki, Takayuki Ise, 太田理絵, 門田宗之, 高島啓, 松浦朋美, Takeshi Tobiume, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : 心不全を合併した腎血管性高血圧に対する経皮的腎動脈形成術の有効性, 第248回徳島医学会学術集会, Feb. 2014.
944.	松本和久, 高島啓, Koji Yamaguchi, Tetsuzo Wakatsuki, 西條良仁, 高木恵理, 原知也, 齋藤友子, 小笠原梢, Mika Bando, 坂東左知子, 松浦朋美, Takayuki Ise, Junko Hotsuchi, 木村恵理子, Takeshi Tobiume, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : シロリムス溶出ステント留置7年後に初めて造影剤ステント周囲滲み出し像を認めた一例, 第248回徳島医学会学術集会, Feb. 2014.
945.	Shusuke Yagi, Ken-ichi Aihara, Masashi Akaike, Sachiko Matsumoto, Daiju Fukuda, 松浦朋美, Takayuki Ise, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Toshio Matsumoto and Masataka Sata : DPP-4阻害薬の血糖降下作用に対する有効性予測因子, 第248回徳島医学会学術集会, Feb. 2014.
946.	坂東左知子, Takeshi Soeki, Takeshi Tobiume, 松浦朋美, Masataka Sata, Miho Sakata, Yasunobu Hayabuchi, Shoji Kagami, 井上美紀, Kazuhiro Mori and 木下学 : 薬剤抵抗性の特発性心室頻拍に対しPCPS下にカテーテルアブレーション治療を施行し，社会復帰に成功した一例, 第248回徳島医学会学術集会, Feb. 2014.
947.	坂東左知子, Takeshi Soeki, Takeshi Tobiume, 松浦朋美, 西條良仁, 高木恵理, 原知也, 小笠原梢, Mika Bando, 齋藤友子, 高島啓, 發知淳子, 木村恵理子, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, 坂東正章 and Masataka Sata : Aorta-mitral continuityが起源の心房頻拍の一例, 第103回日本循環器学会四国地方会, Dec. 2013.
948.	發知淳子, Hirotsugu Yamada, 原知也, 太田理絵, 高島啓, Mika Bando, 小笠原梢, 坂東左知子, 松浦朋美, Takayuki Ise, 木村恵理子, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 下肢陽圧負荷の効果があった薬剤抵抗性起立性低血圧の2症例, 第103回日本循環器学会四国地方会, Dec. 2013.
949.	Shusuke Yagi, 三次実, 和田敏裕 and Masataka Sata : 野球ピッチャーに発症したPaget-Schroetter症候群の1例, 第103回日本循環器学会四国地方会, Dec. 2013.
950.	高島啓, Shusuke Yagi, 高木恵理, Hajime Kinoshita, Tamotsu Kanbara, 原知也, 太田理絵, Mika Bando, 坂東左知子, Takayuki Ise, 松浦朋美, 發知淳子, Takeshi Tobiume, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, 木村建彦, Tetsuya Kitagawa and Masataka Sata : 冠静脈洞に疣贅が認められた冠動静脈瘻を合併した感染性心内膜炎の一例, 第103回日本循環器学会四国地方会, Dec. 2013.
951.	生田奈央, 高島啓, 原知也, Takayuki Ise, Michio Shimabukuro, 西條良仁, 高木恵理, 太田理絵, 齋藤友子, Mika Bando, 坂東左知子, 松浦朋美, 發知淳子, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心身症として見過ごされてきた体位性起立頻脈症候群を的確に診断・治療し得た1例, 第103回日本循環器学会四国地方会, Dec. 2013.
952.	西條良仁, 松浦朋美, Takeshi Tobiume, Takeshi Soeki, 坂東左知子, 高木恵理, 太田理絵, 原知也, 小笠原梢, 齋藤友子, 高島啓, Mika Bando, 發知淳子, 木村恵理子, Takayuki Ise, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 上位共通路の存在が示唆され室房ブロックを伴っても持続する2種類の房室結節リエントリー性頻拍を認めた1例, 第103回日本循環器学会四国地方会, Dec. 2013.
953.	坂東左知子, Takeshi Tobiume, Takeshi Soeki, 松浦朋美, 西條良仁, 高木恵理, 原知也, 小笠原梢, Mika Bando, 齋藤友子, 高島啓, 發知淳子, 木村恵理子, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : AMI急性期のVT/VF stormに対しtriggered PVC ablation を施行した一例, 第103回日本循環器学会四国地方会, Dec. 2013.
954.	松浦朋美, Takeshi Tobiume, Takeshi Soeki, 坂東左知子, 高木恵理, 西條良仁, 太田理絵, 原知也, 齋藤友子, 小笠原梢, 高島啓, Mika Bando, Takayuki Ise, 發知淳子, 木村恵理子, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : ペースメーカー植込みの是非に検討を要した洞心不全症候群の一例, 第103回日本循環器学会四国地方会, Dec. 2013.
955.	玉井佑里恵, 西尾進, Mika Bando, 松浦朋美, 堀家由貴, 眞鍋泰毅, 友藤達陽, 平田有紀奈, 鳥居裕太, 天野里江, 山尾雅美, 林修司, 發知淳子, 木村恵理子, Hirotsugu Yamada and Masataka Sata : たこつぼ型心筋症の回復期に左室壁肥厚を認めた2例, 第103回日本循環器学会四国地方会, Dec. 2013.
956.	堀家由貴, Mika Bando, 太田理絵, 西尾進, 玉井佑里恵, 眞鍋泰毅, 友藤達陽, 平田有紀奈, 鳥居裕太, 天野里江, 山尾雅美, 林修司, 發知淳子, 木村恵理子, Hirotsugu Yamada and Masataka Sata : 複合先天性疾患術後の重症三尖弁閉鎖不全合併妊娠の1例, 第103回日本循環器学会四国地方会, Dec. 2013.
957.	鳥居裕太, 西尾進, Tamotsu Kanbara, 友藤達陽, 玉井佑里恵, 堀家由貴, 眞鍋泰毅, 平田有紀奈, 天野里江, 山尾雅美, Mika Bando, 林修司, 發知淳子, 木村恵理子, Hirotsugu Yamada and Masataka Sata : 左上肢Klippel Trenaunay Syndrome(KTS)に伴う血栓性静脈炎の1例, 第103回日本循環器学会四国地方会, Dec. 2013.
958.	石井亜由美, 西川幸治, Takayuki Ise, Shusuke Yagi, Takashi Iwase, 門田宗之, 西條良仁, 高島啓, 松浦朋美, 發知淳子, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, 中山泰介, Masashi Akaike, Shinsuke Katoh, Tetsuya Kitagawa and Masataka Sata : 人工呼吸管理中の心不全症例に心臓リハビリテーションが有効に施行しえた症例, 第103回日本循環器学会四国地方会, Dec. 2013.
959.	Takayuki Ise, Shusuke Yagi, Takashi Iwase, 西條良仁, 高木恵理, 太田理絵, 門田宗之, 原知也, 小笠原梢, 高島啓, Mika Bando, 坂東左知子, 松浦朋美, 發知淳子, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 当院でのAdaptive-Servo Ventilationが有効であった拡張障害心不全の症例検討, 第103回日本循環器学会四国地方会, Dec. 2013.
960.	木村恵理子, Hirotsugu Yamada, 西尾進, 發知淳子, 林修司, Mika Bando, 山尾雅美, 鳥居裕太, 平田有紀奈, 友藤達陽, 玉井佑里恵, 堀家由貴, Kazuhiro Mori and Masataka Sata : 仮性腱索が収縮器雑音の原因と考えられた1例, 第103回日本循環器学会四国地方会, Dec. 2013.
961.	小笠原梢, Takayuki Ise, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Fallot四徴症に対する根治術施行30年後に左心不全を合併した1例, 第109回日本内科学会四国地方会, Dec. 2013.
962.	玉置俊輔, 原知也, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 冠攣縮および器質的冠狭窄を合併したBuerger病の1例, 第109回日本内科学会四国地方会, Dec. 2013.
963.	Takayuki Ise, Takashi Iwase, Hirotsugu Yamada, Shusuke Yagi, Takeshi Tobiume, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Progression of a Case of Myocardial Damage Caused by Beckers Muscular Dystrophy., 第17回日本心不全学会学術集会, Nov. 2013.
964.	坂東左知子, Takeshi Soeki, Kenji Kangawa and Masataka Sata : 自己免疫性心筋炎におけるヘルパーT細胞制御を介したグレリンの治療効果, 第17回日本心血管内分泌代謝学会学術総会, Nov. 2013.
965.	東邦康智, Masataka Sata and 小室一成 : 自然免疫受容体を介した炎症反応が心臓の圧負荷に対する適応応答を誘導する, 第17回日本心血管内分泌代謝学会学術総会, Nov. 2013.
966.	畠中貴代子, 山下修司, 橋村慧, 加藤瞭典, Tamotsu Tanaka, 中山泰介, Hajime Kinoshita, 原知也, Takeshi Soeki, Masataka Sata, Tetsuya Kitagawa and Akira Tokumura : 心血管病変患者血漿でのリン脂質メディエーターLC-MS/MS 分析—バイオマーカーとしての有用性—, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, プログラム, Oct. 2013.
967.	Ryo Tabata, Hirotsugu Yamada, 西尾進, 井口明子, 三橋乃梨子, 小幡史明, Yuka Nishida, Keisuke Kawahito, Saaya Tada, 原田貴文, 梅谷一公, 伊藤潤, 中西嘉憲, 河南真吾, Shino Yuasa, Nobuhiko Shimizu, Harutaka Yamaguchi, Mitsuhiro Kohno, Masataka Sata, Kenji Tani and Hiroyashu Bando : 徳島大学病院超音波センターと徳島県立海部病院間の心エコーによる遠隔診断支援システムを運用して, 第13回日本プライマリ・ケア連合学会四国ブロック支部大会, Oct. 2013.
968.	長谷川吉正, Michio Shimabukuro, 比嘉盛丈, Yutaka Nakaya, 益崎裕章 and Masataka Sata : インスリン分泌能の性別・県別の比較:沖縄県，長野県，徳島県3951名の解析, 第34回肥満学会, Oct. 2013.
969.	西尾進, Hirotsugu Yamada and Masataka Sata : 脈管診療における血管診療技師(CVT)の役割∼四国の現状と展望∼, 第54回日本脈管学会総会, Oct. 2013.
970.	Masataka Sata : 冠動脈疾患の診断・治療・予防の進歩, 平成25年度日本内科学会生涯教育講演会Bセッション(第2回), Oct. 2013.
971.	西條良仁, Hirotsugu Yamada, 林修司, 西尾進, 發知淳子, Mika Bando, 鳥居裕太, 天野里江, Takeshi Soeki and Masataka Sata : 僧房弁位人工弁機能不全の診断に3次元経食道心エコー検査が有用であった1例, 第23回日本超音波医学会四国地方会学術集会, Oct. 2013.
972.	鳥居裕太, 西尾進, 山尾雅美, 平田有紀奈, 笹田倫子, Takayuki Ise, Shoichiro Takao, Naoki Muguruma, Hirotsugu Yamada and Masataka Sata : 巨大脾動脈瘤の1症例, 第23回日本超音波医学会四国地方会学術集会, Oct. 2013.
973.	平田有紀奈, 西尾進, 山尾雅美, 鳥居裕太, 笹田倫子, 大塚加奈子, Shoichiro Takao, Naoki Muguruma, Hirotsugu Yamada and Masataka Sata : 十二指腸壁内血腫の1例, 第23回日本超音波医学会四国地方会学術集会, Oct. 2013.
974.	山尾雅美, 西尾進, 鳥居裕太, 平田有紀奈, 藤岡啓介, Yumiko Kotani, Shoichiro Takao, Naoki Muguruma, Hirotsugu Yamada and Masataka Sata : カテーテル感染を契機に巨大脾腫をきたした一例, 第23回日本超音波医学会四国地方会学術集会, Oct. 2013.
975.	友藤達陽, 林修司, 西尾進, 發知淳子, 天野里江, Mika Bando, 鳥居裕太, 平田有紀奈, Hirotsugu Yamada and Masataka Sata : 心膜から右室への浸潤が経時的に観察できた胸腺癌の一例, 第23回日本超音波医学会四国地方会学術集会, Oct. 2013.
976.	Mika Bando, Hirotsugu Yamada, 發知淳子, 林修司, 西尾進, 平田有紀奈, 天野里江, 鳥居裕太, 山尾雅美 and Masataka Sata : 術前心エコー検査で診断された未破裂巨大Valsalva洞動脈瘤1例, 第23回日本超音波医学会四国地方会学術集会, Oct. 2013.
977.	眞鍋泰毅, Hirotsugu Yamada, 西尾進, Mika Bando, 平田有紀奈, 天野里江, 鳥居裕太, 發知淳子, 林修司 and Masataka Sata : 一過性の左室壁肥厚を認めたたこつぼ型心筋症の一例, 第23回日本超音波医学会四国地方会学術集会, Oct. 2013.
978.	太田理絵, 今田久美子, Shusuke Yagi, 坂東左知子, 松浦朋美, Takayuki Ise, 發知淳子, Yuka Ueda, Takeshi Tobiume, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 冠灌流域に合致しない心電図誘導にJ波を認めた急性冠症候群の一例, 第61回日本心臓病学会学術集会, Sep. 2013.
979.	太田理絵, 今田久美子, Shusuke Yagi, 坂東左知子, 松浦朋美, Takayuki Ise, 發知淳子, Yuka Ueda, Takeshi Tobiume, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 経皮的腎動脈形成術により難治性心不全が改善した両側腎動脈狭窄症の1例, 第61回日本心臓病学会学術集会, Sep. 2013.
980.	門田宗之, Takayuki Ise, Shusuke Yagi, Takashi Iwase, Masashi Akaike, 原知也, 太田理絵, Mika Bando, 高島啓, 坂東左知子, 松浦朋美, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 慢性心不全患者に対するトルバプタン投与における薬物血中濃度と利尿効果の検討, 第61回日本心臓病学会学術集会, Sep. 2013.
981.	Takayuki Ise, Takashi Iwase, Masashi Akaike, 西尾進, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Intramural Hematoma症例のUlcer Like Projection形成と拡大における穿通枝の重要性, 第61回日本心臓病学会学術集会, Sep. 2013.
982.	Takayuki Ise, Takashi Iwase, Hirotsugu Yamada, Mika Bando, 西尾進, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Becker型筋ジストロフィーによる心筋障害の経過を観察し得た1例, 第61回日本心臓病学会学術集会, Sep. 2013.
983.	Takashi Iwase, Shoichiro Takao, 太田理絵, Koji Yamaguchi, Masashi Akaike, Takayuki Ise, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masafumi Harada and Masataka Sata : 3ステラ非造影心臓MRI検査が左室内壁在血栓の検出ならびに治療方針決定に有用であった無症候性心筋虚血の1例, 第61回日本心臓病学会学術集会, Sep. 2013.
984.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, Takayuki Ise, Shusuke Yagi, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Yasuhiko Nishioka, Masafumi Harada and Masataka Sata : 左室収縮不全を伴う心サルコイドーシスと他の心疾患鑑別におけるガドリニウム遅延造影定量評価の有用性, 第61回日本心臓病学会学術集会, Sep. 2013.
985.	平田有紀奈, Hirotsugu Yamada, 西尾進, 真鍋泰毅, 友藤達陽, 天野里江, 鳥居裕太, 山尾雅美, Mika Bando, 林修司, Takayuki Ise, Koji Yamaguchi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 冠動脈硬化症と各種脂肪厚との関連∼超音波検査を用いた検討∼, 第61回日本心臓病学会学術集会, Sep. 2013.
986.	Koji Yamaguchi, Tetsuzo Wakatsuki, Mika Bando, 高島啓, Takayuki Ise, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Everolimus-eluting stent留置後における局所凝固反応とステント長の関連性, 第61回日本心臓病学会学術集会, Sep. 2013.
987.	安岡紗哉香, Hirotsugu Yamada, Mika Bando, 林修司, 西尾進, 天野里江, 平田有紀奈, 横倉航一, Takayuki Ise, Koji Yamaguchi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : たこつぼ型心筋症の予後と回復過程に関する検討, 第61回日本心臓病学会学術集会, Sep. 2013.
988.	林修司, Hirotsugu Yamada, 西尾進, Mika Bando, 平田有紀奈, Takayuki Ise, Koji Yamaguchi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 冠動脈疾患におけるAugmentation indexの臨床的有用性についての検討, 第61回日本心臓病学会学術集会, Sep. 2013.
989.	Tetsuzo Wakatsuki, Koji Yamaguchi, Takayuki Ise, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : OCTにてmicrochannel構造を認める冠動脈プラークの局所炎症性の評価, 第61回日本心臓病学会学術集会, Sep. 2013.
990.	Takeshi Soeki, 坂東左知子, 松浦朋美, 高島啓, Mika Bando, 發知淳子, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : 心房細動におけるPentraxin3と心房リモデリングおよび予後との関係, 第61回日本心臓病学会学術集会, Sep. 2013.
991.	坂東左知子, Takeshi Soeki, 植松悦子, 松浦朋美, Takayuki Ise, 發知淳子, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro, Kenji Kangawa and Masataka Sata : 自己免疫性心筋炎に対するグレリンの効果, 第61回日本心臓病学会学術集会, Sep. 2013.
992.	西尾進, Hirotsugu Yamada, 平田有紀奈, 鳥居裕太, 天野里江, 山尾雅美, 真鍋泰毅, 友藤達陽, Mika Bando, 林修司, Takayuki Ise, Koji Yamaguchi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 各種血管機能検査指標における性差の影響, 第61回日本心臓病学会学術集会, Sep. 2013.
993.	高島啓, Tetsuzo Wakatsuki, Koji Yamaguchi, 植田初江, 田端実, 小笠原梢, Takeshi Tobiume, Takashi Iwase, 高梨秀一郎 and Masataka Sata : 各種冠動脈ステント再狭窄病変の病理学的所見の比較 -冠動脈バイパス術症例での検討-, 第20回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2013.
994.	Koji Yamaguchi, Tetsuzo Wakatsuki, 高島啓, 小笠原梢, Takeshi Tobiume, Takashi Iwase and Masataka Sata : 各種冠動脈ステント留置後の慢性期局所凝固反応の比較, 第20回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2013.
995.	今田久美子, 太田理絵, Shusuke Yagi, Koji Yamaguchi, Tetsuzo Wakatsuki, Takashi Iwase, 西條良仁, 高木恵理, 門田宗之, 原知也, 齋藤友子, 高島啓, Mika Bando, 坂東左知子, 松浦朋美, Takayuki Ise, 發知淳子, Takeshi Tobiume, Hirotsugu Yamada, Takeshi Soeki, Masataka Sata and 春藤譲冶 : 経皮的腎動脈形成術により難治性心不全が改善したCardiac disturbance syndromeの1例, 第247回徳島医学会学術集会, Aug. 2013.
996.	生田奈央, 高島啓, 原知也, Takayuki Ise, 西條良仁, 高木恵理, 門田宗之, 太田理絵, 齋藤友子, Mika Bando, 坂東左知子, 松浦朋美, 發知淳子, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, Michio Shimabukuro, Daiju Fukuda and Masahito Tomotake : 心身症として見過ごされていた体位性起立頻脈症候群を的確に診断・治療し得た一例, 第247回徳島医学会学術集会, Aug. 2013.
997.	門田宗之, Takayuki Ise, Shusuke Yagi, Takashi Iwase, 太田理絵, 原知也, 高島啓, Mika Bando, 坂東左知子, 松浦朋美, 發知淳子, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata and Masashi Akaike : 慢性心不全における新規利尿薬tolvaptanの効果予測因子, 第247回徳島医学会学術集会, Aug. 2013.
998.	石井亜由美, 西川幸治, Shinsuke Katoh, Takayuki Ise, Shusuke Yagi, Takashi Iwase, Yuka Ueda, 門田宗之, 高島啓, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, 中川泰介, Tetsuya Kitagawa and Masashi Akaike : 人工呼吸管理中に心臓リハビリを有効に施行しえた開心術後の心不全症例, 第247回徳島医学会学術集会, Aug. 2013.
999.	西尾進, Hirotsugu Yamada, 山尾雅美, 平田有紀奈, Masataka Sata, Kazuhiro Mori and 松岡優 : 乳幼児に対する心エコー検査を用いた先天性心疾患のスクリーニング:子育て支援イベント12年間の成果, 第247回徳島医学会学術集会, Aug. 2013.
1000.	西條良仁, 松浦朋美, Takeshi Tobiume, Takeshi Soeki, 坂東左知子, 高木恵理, 太田理絵, 門田宗之, 原知也, 齋藤友子, 高島啓, Mika Bando, Takayuki Ise, 發知淳子, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masataka Sata and 三木延茂 : 室房ブロックを伴っても持続する2種類の房室結節リエントリー性頻拍を認め，上位共通路の存在が示唆された1例, 第247回徳島医学会学術集会, Aug. 2013.
1001.	太田理絵, Shusuke Yagi, Tetsuzo Wakatsuki, Takashi Iwase, 西條良仁, 高木恵理, 門田宗之, 原知也, 齋藤友子, 高島啓, Mika Bando, 坂東左知子, 松浦朋美, Takayuki Ise, 發知淳子, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Masataka Sata, 今田久美子 and Shoichiro Takao : 急性期の心電図でJ波を認めた急性心筋梗塞の一例, 第247回徳島医学会学術集会, Aug. 2013.
1002.	Ryo Tabata, 中西嘉憲, 河南真吾, Shino Yuasa, 清水伸彦, Harutaka Yamaguchi, Mitsuhiro Kohno, Kenji Tani, Hirotsugu Yamada, 西尾進, 井口明子, 小幡史明, Hiroyashu Bando and Masataka Sata : 徳島県立海部病院の徳島大学病院による遠隔診断支援システムについて, 第247回徳島医学会学術集会, Aug. 2013.
1003.	Masataka Sata : 冠動脈疾患と炎症 (シンポジウム4), 第45回日本動脈硬化学会総会・学術集会, Jul. 2013.
1004.	Masataka Sata : 冠動脈疾患の診断・治療・予防の進歩, 平成25年度日本内科学会生涯教育講演会Bセッション, Jul. 2013.
1005.	Toshiyuki Niki, Tetsuzo Wakatsuki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase and Masataka Sata : Effects of additional Eicosapentaenoic Acid on Inflammatory Cytokines and Coronary Plaque Component Assessed by Integrated Backscatter Intravascular Ultrasound., 第22回日本心血管インターベンション治療学会学術集会, Jul. 2013.
1006.	Koji Yamaguchi, Tetsuzo Wakatsuki, Toshiyuki Niki, Yoshio Taketani, Takashi Iwase and Masataka Sata : Local Coagulation Response after Sirolimus-eluting, Zotarolimus-eluting, and Bare-metal Stents Implantation., 第22回日本心血管インターベンション治療学会学術集会, Jul. 2013.
1007.	S Bando, Takeshi Soeki, T Matsuura, Yuka Ueda and Masataka Sata : A Case of Atrioventricular Reentrant Tachycardia with Cycle Length Alternance., 第28回日本不整脈学会学術大会, Jul. 2013.
1008.	T Matsuura, Takeshi Soeki, S Bando, Yuka Ueda and Masataka Sata : Effect of a Aliskiren on Atrial Endocardial Dysfunction in Rapidly Paced Rats., 第28回日本不整脈学会学術大会, Jul. 2013.
1009.	平田有紀奈, 西尾進, 小笠原梢, Toshiyuki Niki, Mika Bando, Junko Hotsuchi, 中川摩耶, 玉井利奈, 弘田大智, Hirotsugu Yamada and Masataka Sata : 右房内浮遊血栓から肺動脈塞栓を来し保存的加療が奏功した1例, 第38回日本超音波検査学会学術集会, Jun. 2013.
1010.	平田有紀奈, 西尾進, 山尾雅美, 鳥居裕太, 玉井利奈, 中川摩耶, Hirotsugu Yamada and Masataka Sata : 冠動脈疾患における前室間溝心外膜下脂肪厚の検討, 第38回日本超音波検査学会学術集会, Jun. 2013.
1011.	Hirotsugu Yamada, 西尾進 and Masataka Sata : 超音波検査士に望む, 第38回日本超音波検査学会学術集会, Jun. 2013.
1012.	Mika Bando, Hirotsugu Yamada, 發知淳子, Masataka Sata, 西尾進, 天野里恵, 平田有紀奈, Junichiro Satomi, Shinji Nagahiro and 玉井利奈 : 超音波Integrated backscatterカラーマッピング法を用いた頸動脈プラークの組織性状診断, 第32回日本脳神経超音波学会総会, Jun. 2013.
1013.	Shusuke Yagi, 發知淳子, Hirotsugu Yamada, Takashi Iwase, Takayuki Ise, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata and Takeshi Kondo : 高血圧・糖尿病・脂質異常症・脳心血管障害を合併した原発性副甲状腺機能亢進症の1例, 日本内科学会第108回四国地方会, Jun. 2013.
1014.	坂東左知子, Koji Yamaguchi, Takeshi Soeki, 太田理絵, 松浦朋美, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masataka Sata and 四宮秀美 : 恒久ペースメーカ植込み後に発見された無症候性内頚静脈血栓の1例, 日本内科学会第108回四国地方会, Jun. 2013.
1015.	太田理絵, Koji Yamaguchi, 發知淳子, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 41歳で初めて診断された肺動静脈瘻合併右肺動脈上行大動脈起始症の1例, 日本内科学会第108回四国地方会, Jun. 2013.
1016.	Jun Kishi, Maya Nakagawa, Hiroshi Kawano, 西尾進, 平田有紀菜, Hirotsugu Yamada, Masataka Sata and Yasuhiko Nishioka : 膠原病の関節炎における腋窩リンパ節の超音波性状に関する検討, 第86回日本超音波医学会学術集会, May 2013.
1017.	西尾進, Hirotsugu Yamada, Junko Hotsuchi, 平田有紀奈, 友藤達陽, Mika Bando, 林修司, Takeshi Soeki and Masataka Sata : イルベサルタンは腎末梢血管抵抗を改善する ∼腎血管エコー検査を用いた検討∼, 第86回日本超音波医学会学術集会, May 2013.
1018.	Junko Hotsuchi, Hirotsugu Yamada, 西尾進, 平田有紀奈, Mika Bando, 林修司, 冨田紀子, Takeshi Soeki and Masataka Sata : 膠原病関連運動誘発性肺高血圧における右室機能の評価, 第86回日本超音波医学会学術集会, May 2013.
1019.	友藤達陽, Hirotsugu Yamada, 西尾進, Mika Bando, Junko Hotsuchi, 林修司, 平田有紀奈, Takeshi Soeki, Takeshi Soeki and Masataka Sata : 心エコー法を用いた平均右房圧推定法の検証, 第86回日本超音波医学会学術集会, May 2013.
1020.	Mika Bando, Hirotsugu Yamada, 西尾進, 平田有紀奈, 林修司, Junko Hotsuchi, 冨田紀子, 松浦朋美, Takeshi Soeki and Masataka Sata : 左房還流型左上大静脈遺残を伴うunroofed coronary sinusの1例, 第86回日本超音波医学会学術集会, May 2013.
1021.	林修司, Hirotsugu Yamada, Junko Hotsuchi, Mika Bando, 西尾進, 山尾雅美, 鳥居祐太, 平田有紀奈, Takeshi Soeki and Masataka Sata : 僧帽弁輸運動速波形と推定中心血圧を用いた左室-動脈連関の臨床的評価, 第86回日本超音波医学会学術集会, May 2013.
1022.	西尾進, Hirotsugu Yamada and Masataka Sata : 大学病院・中核病院における技師の教育, 第86回日本超音波医学会学術集会, May 2013.
1023.	Hirotsugu Yamada, 西尾進 and Masataka Sata : スペックルトラッキング法を用いた右室機能の評価, 第86回日本超音波医学会学術集会, May 2013.
1024.	Hirotsugu Yamada, 西尾進, Mika Bando, Junko Hotsuchi, 林修司, 平田有紀奈 and Masataka Sata : 心:その息切れ・・・・年のせい?心不全?, 第86回日本超音波医学会学術集会, May 2013.
1025.	平田有紀奈, 西尾進, 友藤達陽, Mika Bando, 林修司, Junko Hotsuchi, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : 超音波検査で計側した各種脂肪組織厚と冠動脈硬化症との関連, 第86回日本超音波医学会学術集会, May 2013.
1026.	Ryo Tabata, Hirotsugu Yamada, 西尾進, 井口明子, 小幡史明, 發知淳子, 林修司, 中西嘉憲, 河南真吾, Shino Yuasa, Nobuhiko Shimizu, Harutaka Yamaguchi, Mitsuhiro Kohno, Masataka Sata, Kenji Tani and Hiroyashu Bando : リアルタイム心エコーによる遠隔診断支援システムを運用して, 第4回日本プライマリ・ケア連合学会学術大会, May 2013.
1027.	Ryo Tabata, Hirotsugu Yamada, 西尾進, 井口明子, 小幡史明, 發知淳子, 林修司, 中西嘉憲, 河南真吾, Shino Yuasa, Nobuhiko Shimizu, Harutaka Yamaguchi, Mitsuhiro Kohno, Masataka Sata, Hiroyashu Bando and Hiroyashu Bando : リアルタイム心エコーによる遠隔診断支援システムを運用して, 第4回日本プライマリ・ケア連合学会学術大会, May 2013.
1028.	Masataka Sata : PCI後のイベント再発予防に向けた新規抗凝固薬の可能性-最新のエビデンスと動脈硬化研究からの考察-, 第7回トランスカテーテルイメージングフォーラム TCIF 2013, May 2013.
1029.	平田有紀奈, 西尾進, Hirotsugu Yamada, Junko Hotsuchi, Mika Bando, 林修司, 冨田紀子, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 冠動脈狭窄と関連する脂肪組織はどれか?∼超音波検査を用いた検討∼, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1030.	西尾進, Hirotsugu Yamada, Junko Hotsuchi, 平田有紀奈, Mika Bando, 林修司, 冨田紀子, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 高血圧患者の腎末梢血管抵抗に対するイルベサルタンの効果, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1031.	原知也, 門田宗之, 川端豊, 太田理絵, 高島啓, Mika Bando, 坂東左知子, 松浦朋美, Yuka Ueda, 冨田紀子, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : スピロノラクトンを中心とした薬物療法で30年間経過を観察しえたが，病勢制御困難となり手術療法を要したアルドステロン産生腺腫の一例, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1032.	幸田舞子, Takayuki Ise, 川端豊, 門田宗之, 原知也, 太田理絵, Mika Bando, 坂東左知子, 松浦朋美, Toshiyuki Niki, Junko Hotsuchi, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, Hirotsugu Yamada, Masashi Akaike, 林友鴻, 長谷川拓也 and Masataka Sata : 経皮的中隔心筋焼灼術が奏功した閉塞性肥大型心筋症の1例, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1033.	太田理絵, Koji Yamaguchi, 門田宗之, 川端豊, 原知也, 高島啓, Mika Bando, 坂東左知子, 松浦朋美, Takayuki Ise, Toshiyuki Niki, Yuka Ueda, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 治療方針に苦慮したDIC・多臓器不全合併コレステロール血晶塞栓症の一例, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1034.	太田理絵, Koji Yamaguchi, 門田宗之, 川端豊, 原知也, 高島啓, Mika Bando, 坂東左知子, 松浦朋美, Takayuki Ise, Toshiyuki Niki, Yuka Ueda, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, 坂東正章 and Masataka Sata : 治療方法選択に難渋した肺動静脈瘻合併右肺動脈上行大動脈起始症の一例, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1035.	Mika Bando, Hirotsugu Yamada, Toshiyuki Niki, Koji Yamaguchi, Junko Hotsuchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心エコードプラ検査と心臓カテーテル検査で圧較差に乖離を認めた大動脈弁狭窄症の2例, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1036.	羽星辰哉, 門田宗之, Junko Hotsuchi, Yoshio Taketani, Tamotsu Kanbara, 川端豊, 原知也, 高島啓, Mika Bando, 坂東左知子, 松浦朋美, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Tetsuya Kitagawa and Masataka Sata : プロテインC欠損に心房細動および低左心機能を合併した左室・右房内血栓の一例, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1037.	門田宗之, Takayuki Ise, Shusuke Yagi, Takashi Iwase, 太田理絵, 小笠原梢, 川端豊, 原知也, Mika Bando, 坂東左知子, 松浦朋美, Junko Hotsuchi, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : トルバプタンが効果を示したEisenmenger症候群に伴う高度右心不全の一例, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1038.	高木恵理, 太田理絵, Toshiyuki Niki, 門田宗之, 川端豊, 原知也, 高島啓, Mika Bando, 坂東左知子, 松浦朋美, Takayuki Ise, Yuka Ueda, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 妊娠中に静脈血栓症を発症し診断されたATⅢ欠損症合併妊娠の一例, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1039.	山中森晶, 坂東左知子, Koji Yamaguchi, 西尾進, 太田理絵, Takeshi Soeki, 松浦朋美, 門田宗之, 川端豊, 原知也, 高島啓, Mika Bando, Takayuki Ise, Toshiyuki Niki, Junko Hotsuchi, Yuka Ueda, 冨田紀子, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, Hirotsugu Yamada, Tetsuzo Wakatsuki, 四宮秀美 and Masataka Sata : 永久ペースメーカー植え込み後に偶発的に見つかった内頸静脈血栓の一例, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1040.	高島啓, Michio Shimabukuro, 田端実, 植田初江, 植松悦子, 太田理絵, 門田宗之, 川端豊, 原知也, Mika Bando, 坂東左知子, 松浦朋美, Toshiyuki Niki, Takayuki Ise, Junko Hotsuchi, Yuka Ueda, 冨田紀子, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, 高梨秀一郎 and Masataka Sata : 冠動脈内ステント内再狭窄4症例の病理組織学的検討, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1041.	Takayuki Ise, Takashi Iwase, Hirotsugu Yamada, 川端豊, 門田宗之, Toshiyuki Niki, Mika Bando, 坂東左知子, 松浦朋美, Koji Yamaguchi, Shusuke Yagi, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 心病変の経過を観察し得たBecker型筋ジストロフィーによる心不全の1例, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1042.	坂東左知子, Takeshi Soeki, 門田宗之, 川端豊, 原知也, 高島啓, Mika Bando, 松浦朋美, Takayuki Ise, Toshiyuki Niki, Junko Hotsuchi, Yuka Ueda, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, Hirotsugu Yamada, Tetsuzo Wakatsuki, 石本武男 and Masataka Sata : AVN dual pathwayにより頻拍周期が一心拍ごとに変化下Orthodromic AVRTの一例, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1043.	松浦朋美, Takeshi Soeki, Takayuki Ise, Toshiyuki Niki, Junko Hotsuchi, Yuka Ueda, 冨田紀子, Koji Yamaguchi, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 通電により電動特性が変化した副伝導路の一例, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1044.	Junko Hotsuchi, Hirotsugu Yamada, 西尾進, Mika Bando, 林修司, 冨田紀子, 太田理絵, 門田宗之, 川端豊, 原知也, 高島啓, 坂東左知子, 松浦朋美, Takayuki Ise, Toshiyuki Niki, Yuka Ueda, Koji Yamaguchi, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 運動誘発性肺高血圧を有する膠原病例における右室機能の検討, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1045.	Takayuki Ise, Shusuke Yagi, Takashi Iwase, 門田宗之, Toshiyuki Niki, Mika Bando, 坂東左知子, 松浦朋美, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 慢性心不全におけるAdaptive-Servo Ventilationの血行動態に対する効果, 第102回日本循環器学会中国・四国合同地方会, May 2013.
1046.	Sumiko Yoshida, Ken-ichi Aihara, Yasumasa Ikeda, Matomo Sakari, Takahiro Matsumoto, Masashi Akaike, Masataka Sata and Toshio Matsumoto : アンドロゲン受容体は性差非依存的にVEGF受容体を介して虚血反応性血管新生を促進する, 第86回日本内分泌学会学術総会, Apr. 2013.
1047.	Junko Hotsuchi, Hirotsugu Yamada, Mika Bando, 林修司, 冨田紀子, 平田有紀奈, 西尾進 and Masataka Sata : 大動脈弁穿孔を伴った感染症心内膜炎の1例, 第24回日本心エコー図学会学術集会, Apr. 2013.
1048.	林修司, Hirotsugu Yamada, 西尾進, 冨田紀子, Junko Hotsuchi, Mika Bando, 玉井利奈, 中川摩耶, 弘田大智, 平田有紀奈 and Masataka Sata : 左房ストレイン解析における解析開始時間設定の重要性, 第24回日本心エコー図学会学術集会, Apr. 2013.
1049.	Mika Bando, Hirotsugu Yamada, 西尾進, 玉井利奈, 平田有紀奈 and Masataka Sata : 超音波後方散乱信号解析による頸動脈プラークの組織性状カラーマッピング法の臨床応用:急性冠症候群における検討, 第24回日本心エコー図学会学術集会, Apr. 2013.
1050.	平田有紀奈, 西尾進, 友藤達陽, 真鍋泰毅, 太田理絵, Mika Bando, 林修司, Junko Hotsuchi, Hirotsugu Yamada and Masataka Sata : 成人期に診断された右肺動脈上行大動脈起始の一例, 第24回日本心エコー図学会学術集会, Apr. 2013.
1051.	西尾進, Takeshi Soeki, 坂東左知子, 松浦朋美, 平田有紀奈, Mika Bando, Junko Hotsuchi, 林修司, 冨田紀子, Hirotsugu Yamada and Masataka Sata : 心房細動例の左心耳局所炎症と左心耳経食道心エコー図指標との関連, 第24回日本心エコー図学会学術集会, Apr. 2013.
1052.	Masataka Sata : 脂質異常症治療の最新の動向-映像でみる動脈硬化の新知見と異所性脂肪-, 第77回日本循環器学会学術集会, Mar. 2013.
1053.	Masataka Sata : 『Cardio Renal Syndromeの病態に迫る』-インドキシル硫酸を知って心腎連関を断つ-, 第77回日本循環器学会学術集会, Mar. 2013.
1054.	Masataka Sata : Impact of Hypertension on the Pathogenesis of Atherosclerosis., 第77回日本循環器学会学術集会, Mar. 2013.
1055.	Michio Shimabukuro and Masataka Sata : Ectopic Fat Depositions and Diabetic Vascular Disease., 第77回日本循環器学会学術集会, Mar. 2013.
1056.	T Matsuura, Takeshi Soeki, S Bando, T Hara, M Kadota, Y Kawabata, Mika Bando, J Hotchi, N Tomita, Yuka Ueda, Toshiyuki Niki, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : A Renin Inhibitor Prevents Atrial Endocardial Dysfunction in Rapidly Paced Rats with Streptozotocin-induced Diabetes., 第77回日本循環器学会学術集会, Mar. 2013.
1057.	Takayuki Ise, Shusuke Yagi, Masashi Akaike, Takashi Iwase, M Kadota, R Ota, Y Kawabata, T Hara, K Ogasawara, Mika Bando, S Bando, T Matsuura, Toshiyuki Niki, J Hotchi, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Adaptive Servo-Ventilation Improves Symptoms and Hemodynamics in Both Patients with Systolic and Diastolic Heart Failure., 第77回日本循環器学会学術集会, Mar. 2013.
1058.	T Nakayama, Hirotsugu Kurobe, H Sugasawa, Hajime Kinoshita, M Higashida, Y Matsuoka, Y Yoshida, Y Hirata, M Sakata, Yousuke Takahama, Masataka Sata, Toshiaki Tamaki, Tetsuya Kitagawa and Shuhei Tomita : Macrophage-specific HIF-1a-deficient Mice Suppress Vascular Remodeling., 第77回日本循環器学会学術集会, Mar. 2013.
1059.	Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki, Toshiyuki Niki, Yoshio Taketani, R Ota, M Kadota, Y Kawabata, T Hara, Mika Bando, S Bando, T Matsuura, Takayuki Ise, J Hotchi, Yuka Ueda, Takashi Iwase, N Tomita, Hirotsugu Yamada and Masataka Sata : Impact of Indoxyl Sulfate, a Uremic Toxin, on Non-Culprit Coronary Plaque Composition Assessed by Integrated Backscatter Intravascular Ultrasound., 第77回日本循環器学会学術集会, Mar. 2013.
1060.	Takayuki Ise, Takashi Iwase, Shoichiro Takao, M Kadota, Mika Bando, S Bando, T Matsuura, Toshiyuki Niki, J Hotchi, Shusuke Yagi, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masafumi Harada and Masataka Sata : Evaluation of Right Ventricular Hypertrophy by Cardiac Magnetic Resonance is Useful for Detecting Cardiac Amyloidosis., 第77回日本循環器学会学術集会, Mar. 2013.
1061.	K Tanaka, Y Hirata, Y Ouchi and Masataka Sata : Local Administration of Suramin Inhibits Angiogenesis in Adventitia and Arterial Lesion Progression in Apolipoprotein E-deficient Mice., 第77回日本循環器学会学術集会, Mar. 2013.
1062.	Koji Yamaguchi, Tetsuzo Wakatsuki, Toshiyuki Niki, Yoshio Taketani, R Ota, M Kadota, Y Kawabata, T Hara, Mika Bando, S Bando, T Matsuura, Takayuki Ise, J Hotchi, Yuka Ueda, Takashi Iwase, N Tomita, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Differential Responses of Local Coagulation after Implantation of Everolimus-Eluting Stent Compared with Early-Generation Drug-Eluting Stents., 第77回日本循環器学会学術集会, Mar. 2013.
1063.	Shusuke Yagi, Takayuki Ise, Hirotsugu Yamada, S Nishio, Yuka Ueda, Takashi Iwase, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Ratio of Eicosapentaenoic Acid to Arachidonic Acid is a Predictive Factor of Albuminuria and Endothelial Function in Patients with Dyslipidemia., 第77回日本循環器学会学術集会, Mar. 2013.
1064.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, Takayuki Ise, Toshiyuki Niki, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Ken-ichi Aihara, Tetsuzo Wakatsuki, Yasuhiko Nishioka, Masafumi Harada and Masataka Sata : Differentiation of Left Ventricular Systolic Dysfunction Related to Cardiac Sarcoidosis and Other Heart Diseases Using contrast-enhanced Cardiovascular Magnetic Resonance., 第77回日本循環器学会学術集会, Mar. 2013.
1065.	M Kadota, Takayuki Ise, Shusuke Yagi, Takashi Iwase, Masashi Akaike, R Ota, Y Kawabata, T Hara, K Ogasawara, Mika Bando, S Bando, T Matsuura, Toshiyuki Niki, J Hotchi, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Effects of Tolvaptan are Predicted by Vasopressin/Aldosterone Ratio and Urine Osmolality in Patients with Chronic Heart Failure., 第77回日本循環器学会学術集会, Mar. 2013.
1066.	Toshiyuki Niki, Tetsuzo Wakatsuki, Mika Bando, Koji Yamaguchi, Yoshio Taketani, R Ota, Y Kawabata, M Kadota, T Hara, Mika Bando, Takayuki Ise, T Matsuura, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Effects of Additional Eicosapentaenoic Acid Therapy on Inflammatory Cytokines and Atherosclerotic Plaque Component Assessed by Integrated Backscatter Ultrasound Systems., 第77回日本循環器学会学術集会, Mar. 2013.
1067.	Michio Shimabukuro, C Okawa, M Higashida, H Sato, Hirotsugu Kurobe, Shoichiro Takao, Y Hirata, T Nakayama, XF Lei, JR Kim-Kaneyama, Daiju Fukuda, Hirotsugu Yamada, M Sato, Tetsuya Kitagawa and Masataka Sata : Effects of Ezetimibe on Oxidized Cholesterol and Fatty-acid Components in Epicardial Fat and Myocardium: A Gas Chromatography-Mass Spectrometry Analysis., 第77回日本循環器学会学術集会, Mar. 2013.
1068.	Daiju Fukuda, Michio Shimabukuro, Shusuke Yagi, Takeshi Soeki and Masataka Sata : Genetic Ablation of TLR9 Improves Insulin Resistance through the Reduction of Hepatic SREBP-1c Expression., 第77回日本循環器学会学術集会, Mar. 2013.
1069.	Masayoshi Ishida, Michio Shimabukuro, Shusuke Yagi, Daiju Fukuda, Takeshi Soeki, H Sato, E Uematsu, Sachiko Matsumoto, Hiroshi Sakaue, Hirofumi Izaki, Hiro-omi Kanayama and Masataka Sata : MicroRNA-100 Regulates Adipocytokine Expression in Subcutaneous and Visceral Adipose Tissue: An Observation from Human Biopsy Study., 第77回日本循環器学会学術集会, Mar. 2013.
1070.	Takeshi Soeki, S Bando, T Matsuura, T Hara, R Ota, Y Kawabata, Mika Bando, J Hotchi, N Tomita, Yuka Ueda, Toshiyuki Niki, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Pentraxin 3 is a Local Inflammatory Marker in Atrial Fibrillation., 第77回日本循環器学会学術集会, Mar. 2013.
1071.	Mika Bando, Hirotsugu Yamada, S Nishio, N Tomita, J Hotchi, S Hayashi, K Ogasawara, A Takashima, S Bando, Takayuki Ise, Toshiyuki Niki, T Matsuura, Yuka Ueda, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Effect of Eicosapentaenoic Acid on the Stabilization of Vulnerability in Carotid Artery Plaque: Evaluation Using iPlaque® Software., 第77回日本循環器学会学術集会, Mar. 2013.
1072.	Y Higashikuni, R Nagai, Masataka Sata and I Komuro : Toll-Like Receptor 2-Mediated Inflammation is Critically Involved in Cardiac Adaptive Response to Pressure Overload., 第77回日本循環器学会学術集会, Mar. 2013.
1073.	S Bando, Daiju Fukuda, Takeshi Soeki, E Uematsu, H Sato, A Takashima, Mika Bando, T Matsuura, Toshiyuki Niki, Takayuki Ise, J Hotchi, Yuka Ueda, N Tomita, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Shusuke Yagi, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Relationship between NLRP3 Inflammasome Activation in Adipose Tissue and Atherosclerosis., 第77回日本循環器学会学術集会, Mar. 2013.
1074.	Y Higashikuni, R Nagai, Masataka Sata and I Komura : Eicosapentaenoic Acid Ameliorates Survival and Ventricular Remodeling after Myocardial Infarction by Reducing Inflammatory Responses in Mice., 第77回日本循環器学会学術集会, Mar. 2013.
1075.	Michio Shimabukuro, Y Hirata, M Tabata, M Dagvasumberel, Daiju Fukuda, Hirotsugu Kurobe, Takeshi Soeki, S Takanashi and Masataka Sata : Epicardial Adipose Tissue Volume as a Novel Determinant of Human Coronary Atherosclerosis: Role of Adipocytokine Imbalance., 第77回日本循環器学会学術集会, Mar. 2013.
1076.	Takeshi Soeki, Koji Yamaguchi, Toshiyuki Niki, R Ota, T Hara, M Kadota, Mika Bando, S Bando, T Matsuura, J Hotchi, N Tomita, Yuka Ueda, Takayuki Ise, Shusuke Yagi, Daiju Fukuda, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Cardiospecific microRNA Plasma Levels are Associated With Coronary Plaque Vulnerability., 第77回日本循環器学会学術集会, Mar. 2013.
1077.	Masataka Sata : EPAを用いた心血管イベント抑制-動脈硬化に関する新知見とn-3脂肪酸の多面的作用-, ECHO AWAJI 2013, Mar. 2013.
1078.	中山泰介, Shuhei Tomita, Hirotsugu Kurobe, 菅澤典子, Hajime Kinoshita, Mikio Sugano, Tamotsu Kanbara, Eiki Fujimoto, Takashi Kitaichi, Toshiaki Tamaki, Masataka Sata and Tetsuya Kitagawa : 小口径グラフト開存を目的とするマクロファージHIFと極性の動脈リモデリング基礎研究, 第43回日本心臓血管外科学会学術総会, Feb. 2013.
1079.	E Takagi, R Ota, Toshiyuki Niki, M Kadota, Y Kawabata, T Hara, A Takashima, Mika Bando, S Bando, T Matsuura, Takayuki Ise, J Hotchi, Yuka Ueda, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, Souichiro Nakayama, Kazuhisa Maeda and Minoru Irahara : 妊娠を契機にATⅢ欠損症と診断され，血栓管理の後に出産に至った一例, 第246回徳島医学会学術集会(平成24年度冬期), Feb. 2013.
1080.	T Haboshi, M Kadota, J Hotchi, Yoshio Taketani, T Matsuura, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, Hajime Kinoshita, Tamotsu Kanbara, Tetsuya Kitagawa, Hiroyuki Furumoto and Hisaya Takahashi : プロテインC欠損に心房細動および低左心機能を合併した左室・右房内血栓の一例, 第246回徳島医学会学術集会(平成24年度冬期), Feb. 2013.
1081.	S Sakamoto, M Kadota, Takayuki Ise, Takashi Iwase, S Bando, T Matsuura, Toshiyuki Niki, J Hotchi, N Tomita, Yuka Ueda, Koji Yamaguchi, Shusuke Yagi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, Masashi Akaike and M Takeuchi : 再熱と寛解を繰り返す特発性心膜炎に対しイブプロフェンが有効であった1例, 第246回徳島医学会学術集会(平成24年度冬期), Feb. 2013.
1082.	K Ota, Toshiyuki Niki, R Ota, Y Kawabata, M Kadota, T Hara, A Takashima, Mika Bando, S Bando, T Matsuura, Takayuki Ise, J Hotchi, Yuka Ueda, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata and J Shunto : 偶発的に発見された末梢動脈閉塞の二例, 第246回徳島医学会学術集会(平成24年度冬期), Feb. 2013.
1083.	M Koda, Masataka Sata, Takayuki Ise, Y Kawabata, Takashi Iwase, M Kadota, T Hara, R Ota, Mika Bando, S Bando, T Matsuura, Toshiyuki Niki, J Hotchi, N Tomita, Yuka Ueda, Koji Yamaguchi, Shusuke Yagi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, S Okazaki, 林友鴻 and T Hasegawa : 難治性の閉塞性肥大型心筋症に対して経皮的中隔心筋焼灼術が著効した1例, 第246回徳島医学会学術集会(平成24年度冬期), Feb. 2013.
1084.	J Hotchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Masataka Sata, Takeshi Kondo, Tomoharu Fukumori, Koji Fujita, Yuka Terasawa, Masayuki Inoue and H Sato : 原発性副甲状腺機能亢進症・高血圧・糖尿病・脂質異常症に合併した若年性多発性脳梗塞の一例, 第246回徳島医学会学術集会(平成24年度冬期), Feb. 2013.
1085.	R Ota, Koji Yamaguchi, M Kadota, Y Kawabata, T Hara, A Takashima, Mika Bando, S Bando, T Matsuura, Takayuki Ise, Toshiyuki Niki, J Hotchi, Yuka Ueda, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, Shoichiro Takao, Masafumi Harada and M Bando : 41歳まで無症状で経過した肺動静脈瘻合併右肺動脈上行大動脈起始症の一例, 第246回徳島医学会学術集会(平成24年度冬期), Feb. 2013.
1086.	Masataka Sata : 動脈硬化研究から見たErectile Dysfunction, 第23回日本性機能学会西部総会, Feb. 2013.
1087.	Masataka Sata : 映像でみる動脈硬化の新知見とω-3多価不飽和脂肪酸の多面的作用, 第13回日本内分泌学会関東甲信越支部学術集会, Dec. 2012.
1088.	Masataka Sata : 心筋梗塞発症に関する新知見とイメージングへの応用, 第26回日本冠疾患学会学術集会第16回再灌流療法フォーラム, Dec. 2012.
1089.	Mika Bando, Hirotsugu Yamada, S Nishio, R Tamai, Y Hirata, N Tomita, J Hotchi, S Hayashi, M Nakagawa, D Hirota, A Takashima, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : イコサペント酸エチルは頸動脈プラークの安定化に寄与する:iPlaque®を用いた検討, 第101回日本循環器学会四国地方会, Dec. 2012.
1090.	Yuka Ueda, Takayuki Ise, Takashi Iwase, K Maeda, K Nishikawa, M Kadota, T Hara, Y Kawabata, R Ota, Toshiyuki Niki, Koji Yamaguchi, Shusuke Yagi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Shinsuke Katoh, Natsuo Yasui and Masataka Sata : 心臓リハビリテーションにおける禁煙継続効果の検討, 第101回日本循環器学会四国地方会, Dec. 2012.
1091.	Y Kawabata, Takayuki Ise, T Matsuura, S Bando, Takashi Iwase, K Ogasawara, Mika Bando, Toshiyuki Niki, J Hotchi, N Tomita, Yuka Ueda, Koji Yamaguchi, Shusuke Yagi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 高度肥満を伴った拡張型心筋症の1例, 第101回日本循環器学会四国地方会, Dec. 2012.
1092.	R Ota, Toshiyuki Niki, Yoshio Taketani, M Kadota, Y Kawabata, T Hara, Mika Bando, S Bando, T Matsuura, Takayuki Ise, J Hotchi, Yuka Ueda, Koji Yamaguchi, Takashi Iwase, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : カテーテル的血栓吸引・血栓溶解療法が奏功し，心肺停止状態から救命できた院内発症急性肺血栓塞栓症の一例, 第101回日本循環器学会四国地方会, Dec. 2012.
1093.	M Nakagawa, Hirotsugu Yamada, S Nishio, N Tomita, J Hotchi, S Hayashi, Mika Bando, R Tamai, Y Hirata, D Hirota, S Yasuoka, K Yokokura, Toshiyuki Niki, Takayuki Ise, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心房細動例における拡張中期僧帽弁口血流速波高は左室充満圧を反映する, 第101回日本循環器学会四国地方会, Dec. 2012.
1094.	S Sakamoto, M Kadota, Takayuki Ise, Takashi Iwase, S Bando, T Matsuura, Toshiyuki Niki, J Hotchi, N Tomita, Yuka Ueda, Koji Yamaguchi, Shusuke Yagi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 再燃と寛解を繰り返す特発性心膜炎に対しイブプロフェンが有効であった1例, 第101回日本循環器学会四国地方会, Dec. 2012.
1095.	N Kobayashi, T Hara, Koji Yamaguchi, K Ogasawara, Mika Bando, S Bando, T Matsuura, J Hotchi, N Tomita, Takayuki Ise, Toshiyuki Niki, Yuka Ueda, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, M Bando and Masataka Sata : 多彩な血圧変動素因により顕著な夜間血圧を認めた一例, 第101回日本循環器学会四国地方会, Dec. 2012.
1096.	S Yasuoka, Hirotsugu Yamada, K Yokokura, Y Hirata, D Hirota, R Tamai, M Nakagawa, S Nishio, Mika Bando, J Hotchi, S Hayashi, N Tomita, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 当院におけるたこつぼ型心筋症の臨床的特徴, 第101回日本循環器学会四国地方会, Dec. 2012.
1097.	K Yokokura, Hirotsugu Yamada, S Yasuoka, Y Hirata, D Hirota, R Tamai, M Nakagawa, S Nishio, Mika Bando, J Hotchi, S Hayashi, N Tomita, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心エコー法を用いた平均右房圧推定法の検証, 第101回日本循環器学会四国地方会, Dec. 2012.
1098.	T Hara, Koji Yamaguchi, Takashi Iwase, M Kadota, K Ogasawara, Mika Bando, S Bando, T Matsuura, J Hotchi, N Tomita, Takayuki Ise, Toshiyuki Niki, Yuka Ueda, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, S Orino and Masataka Sata : Churg-Strauss症候群に合併した好酸球性心筋炎の一例, 第101回日本循環器学会四国地方会, Dec. 2012.
1099.	Masataka Sata : 『N型Ca拮抗薬のPleiotropic effect』-Ca拮抗薬のドラッグエフェクトを考える-, 第20回日本血管生物医学会学術集会, Dec. 2012.
1100.	K Tanaka and Masataka Sata : Angiogenesis in atherosclerosis., The 20th Annual Meeting of the Japanese Vascular Biology and Medicine Organization, Dec. 2012.
1101.	Masataka Sata : A Pleitropic effect of N-type Ca channel blocker Up-close to the drug effect of CCB., The 20th Annual Meeting of the Japanese Vascular Biology and Medicine Organization, Dec. 2012.
1102.	Mika Bando, Hirotsugu Yamada, S Nishio, R Tamai, Y Hirata, D Hirota, M Nakagawa, S Hayashi, N Tomita, J Hotchi, Toshiyuki Niki, Koji Yamaguchi, Daiju Fukuda, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Shinji Nagahiro and Masataka Sata : Effect of EPA of Carotid Artery Plaque Assessed by Integrated Backscatter Mapping : Development of imaging analytical software., 第20回日本血管生物医学会学術集会, Dec. 2012.
1103.	Koji Yamaguchi, Tetsuzo Wakatsuki, Toshiyuki Niki, Yoshio Taketani, H Oezuka, R Ota, Y Kawabata, T Hara, M Kadota, K Ogasawara, S Bando, T Matuura, J Hotchi, Takayuki Ise, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Telmisartan reduces local inflammatory response and coronary plaque vulnerability assessed by integrated backscatter intravascular ultrasound in hypertensive patients., 第20回日本血管生物医学会学術集会, Dec. 2012.
1104.	S Bando, Daiju Fukuda, Takeshi Soeki, E Uematsu, H Sato, Michio Shimabukuro and Masataka Sata : Relationship between NLRP3 inflammasome and atherosclerosis., 第20回日本血管生物医学会学術集会, Dec. 2012.
1105.	Masataka Sata : 動脈硬化の新知見とイメージングへの応用-心エコーでEpicardiol Adipose Tissue厚を測定する意義と高血圧治療-, 第7回東京エコーラボ, Dec. 2012.
1106.	Y Yokota, S Bando, Takeshi Soeki, M Kadota, T Matsuura, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masataka Sata, H Yoshida and T Ishimoto : AVN dual pathwayにより頻拍周期が1心拍ごとに変化したOrthodromic AVRTの1例, 第107回日本内科学会四国地方会, Dec. 2012.
1107.	M Miyauchi, T Matsuura, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心臓粗動を契機として右心不全を発症し，左房還流型PLSVCとunroofed CSの合併が判明した1例, 第107回日本内科学会四国地方会, Dec. 2012.
1108.	M Kadota, Takayuki Ise, Takashi Iwase, Masashi Akaike, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Tetsuzo Wakatsuki, Takeshi Soeki and Masataka Sata : Prediction of Responder and Influence for Cardio-Renal Interaction by Tolvaptan in Patients with Chronic Heart Failure., 第16回日本心不全学会学術集会, Nov. 2012.
1109.	Takayuki Ise, Shusuke Yagi, Masashi Akaike, Takashi Iwase, M Kadota, T Hara, Koji Yamaguchi, Yoshio Taketani, Tetsuzo Wakatsuki and Masataka Sata : Acute Hemodynamic Effects of Adaptive Servo-Ventilation in Patients with Chronic Heart Failure., 第16回日本心不全学会学術集会, Nov. 2012.
1110.	Masataka Sata : 慢性炎症と心不全, 第16回日本心不全学会学術集会, Nov. 2012.
1111.	Y Higashikuni, R Nagai and Masataka Sata : Toll-Like Receptor 2 is Critically Involved in Cardiac Adaptive to Pressure Overload., 第16回日本心不全学会学術集会, Nov. 2012.
1112.	Ryo Tabata, Hirotsugu Yamada, 西尾進, 井口明子, 小幡史明, 發知淳子, 林修司, 中西嘉憲, 河南真吾, Shino Yuasa, Nobuhiko Shimizu, Harutaka Yamaguchi, Mitsuhiro Kohno, Masataka Sata, Kenji Tani and Hiroyashu Bando : 徳島大学病院と徳島県立海部病院との心エコー遠隔診断支援システムについて, 第12回日本プライマリ・ケア連合学会四国支部学術集会, Nov. 2012.
1113.	Masataka Sata : 動脈硬化に関する新知見とイメージングへの応用, 第19回動脈硬化危険因子研究会, Nov. 2012.
1114.	Masataka Sata : 血管老化の機序から考える脂質異常症治療, Anti-aging Science 脳心血管抗加齢研究会, Nov. 2012.
1115.	Masataka Sata : 脂質異常症治療の最新の動向-映像でみる動脈硬化の新知見と異所性脂肪-, 第4回臨床動脈硬化研究会, Nov. 2012.
1116.	Masataka Sata : 糖尿病性大血管合併症予防に関する最新の動向-心腎連関に関する新概念と治療戦略-, The 12th Biennial International Endotoxin & Innate Immunity Society (IEIIS) Meeting 2012, Oct. 2012.
1117.	Y Higashikuni, R Nagai and Masataka Sata : Toll-Like Receptor 2 is Critically Involved in Cardiac Adaptive to Pressure Overload., The 29th Annual Meeting of the International Society for Heart Research Japanese Section, Oct. 2012.
1118.	Y Hirata, Y Nakagawa, S Nishio, D Hirota, R Tamai, Hirotsugu Yamada and Masataka Sata : 回腸Meckel憩室の1例, 第22回日本超音波医学会四国地方会学術集会，第11回四国地方会講習会, Oct. 2012.
1119.	R Tamai, Hirotsugu Yamada, S Nishio, Y Hirata, D Hirota, M Nakagawa, Mika Bando, S Hayashi, J Hotchi and Masataka Sata : 当施設における心サルコイドーシスに心エコー所見の検討, 第22回日本超音波医学会四国地方会学術集会，第11回四国地方会講習会, Oct. 2012.
1120.	S Hayashi, Hirotsugu Yamada, N Tomita, J Hotchi, Mika Bando, S Nishio, M Nakagawa, D Hirota, Y Hirata and Masataka Sata : 中心血圧と僧帽弁輪運動速波形を用いた健常者における左室・動脈連関についての検討, 第22回日本超音波医学会四国地方会学術集会，第11回四国地方会講習会, Oct. 2012.
1121.	J Hotchi, Hirotsugu Yamada, Mika Bando, S Hayashi, N Tomita, S Nishio, Y Hirata, D Hirota, Takeshi Soeki and Masataka Sata : 大動脈弁穿孔を伴った感染性心内膜炎の1例, 第22回日本超音波医学会四国地方会学術集会，第11回四国地方会講習会, Oct. 2012.
1122.	D Hirota, Hirotsugu Yamada, S Nishio, Y Hirata, R Tamai, M Nakagawa, S Hayashi, J Hotchi, Masataka Sata and Ken Saito : 当院で経験した大動脈二尖弁の特徴, 第22回日本超音波医学会四国地方会学術集会，第11回四国地方会講習会, Oct. 2012.
1123.	Mika Bando, Hirotsugu Yamada, Y Hirata, D Hirota, R Tamai, M Nakagawa, S Nishio, J Hotchi, N Tomita and Masataka Sata : 肝細胞癌化学療法中に発症した亜型たこつぼ型心筋症の1例, 第22回日本超音波医学会四国地方会学術集会，第11回四国地方会講習会, Oct. 2012.
1124.	M Nakagawa, S Nishio, R Tamai, D Hirota, Y Hirata, Takeshi Soeki, Hirotsugu Yamada and Masataka Sata : 診断と治療効果の判定に超音波検査が有用であった上肢バージャー病の1例, 第22回日本超音波医学会四国地方会学術集会，第11回四国地方会講習会, Oct. 2012.
1125.	中山泰介, Shuhei Tomita, Hirotsugu Kurobe, 菅澤典子, Hajime Kinoshita, Mikio Sugano, Tamotsu Kanbara, Eiki Fujimoto, Takashi Kitaichi, Toshiaki Tamaki, Masataka Sata, Yousuke Takahama and Tetsuya Kitagawa : 小口径グラフト開存性改善を目的とする血管リモデリングにおけるマクロファージの基礎研究, 第65回日本胸部外科学会定期学術集会, Oct. 2012.
1126.	Masataka Sata : 血管機能診断法, 第53回日本脈管学会総会, Oct. 2012.
1127.	H Sato, Y Hirata, Michio Shimabukuro, Daiju Fukuda, M Tabata, Hirotsugu Kurobe, S Takanashi, Tetsuya Kitagawa, Yutaka Nakaya and Masataka Sata : ヒト脂肪組織における炎症性シグナルとNLRP3インフラマソームの関与, 第33回日本肥満学会, Oct. 2012.
1128.	Masataka Sata : 冠動脈疾患診療の最新の動向, 第26回日本臨床内科医学会, Oct. 2012.
1129.	Masataka Sata : 糖尿病性大血管合併症の病態とイメージングへの応用, 第26回日本心臓血管内視鏡学会, Oct. 2012.
1130.	Masataka Sata : Metabolic Syndrome and Atherosclerosis., 第35回日本高血圧学会総会, Sep. 2012.
1131.	Toshiyuki Niki, Tetsuzo Wakatsuki, Mika Bando, 西尾進, 小笠原梢, 坂東左知子, Takayuki Ise, 發知淳子, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, 冨田紀子, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : スタチンへのEPA製剤追加による動脈硬化病変の組織性状変化に関する検討, 第60回日本心臓病学会学術集会, Sep. 2012.
1132.	Masataka Sata : 高脂血症から心臓を守る, 第60回日本心臓病学会学術集会, Sep. 2012.
1133.	Michio Shimabukuro, C Okawa, M Higashida, Hirotsugu Kurobe, H Sato, Shoichiro Takao, Y Hirata, 雷小峰, S Kaneyama, T Nakayama, Daiju Fukuda, Hirotsugu Yamada, M Sato, Tetsuya Kitagawa and Masataka Sata : エゼチミブ投与によるブタ心臓周囲脂肪ならびに心筋組織の酸化コレステロール，脂肪酸分画の変動:GC/MS法による検討, 第60回日本心臓病学会学術集会, Sep. 2012.
1134.	Y Hirata, T Hara, Hirotsugu Yamada, S Nishio, D Hirota, R Tamai, M Nakagawa, Mika Bando, J Hotchi, N Tomita, S Hayashi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心膜内膿瘍を合併した収縮性心膜炎の一例, 第60回日本心臓病学会学術集会, Sep. 2012.
1135.	S Bando, Takeshi Soeki, Takayuki Ise, Takashi Iwase, T Hara, M Kadota, Mika Bando, K Ogasawara, J Hotchi, N Tomita, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 心房周囲炎症と心囊液貯留により収縮性心膜炎の病態を呈した一例, 第60回日本心臓病学会学術集会, Sep. 2012.
1136.	J Hotchi, Hirotsugu Yamada, S Nishio, Mika Bando, S Hayashi, N Tomita, Y Hirata, D Hirota, R Tamai, M Nakagawa, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 安静時に肺高血圧を呈さない膠原病例における心エコー・ドプラ法を用いた右室機能不全の評価, 第60回日本心臓病学会学術集会, Sep. 2012.
1137.	Koji Yamaguchi, Tetsuzo Wakatsuki, Toshiyuki Niki, Yoshio Taketani, S Bando, Takayuki Ise, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : シロリムス溶出ステント留置後における局所血管反応の検討-局所バイオマーカーとperi-contrast stainingの観点から-, 第60回日本心臓病学会学術集会, Sep. 2012.
1138.	S Hayashi, Hirotsugu Yamada, N Tomita, J Hotchi, Mika Bando, S Nishio, R Tamai, M Nakagawa, D Hirota, Y Hirata, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 僧帽弁口血流速波系が偽正常化パターンを示す左室駆出率が保持された心不全(HFPEF)と左房機能不全の鑑別, 第60回日本心臓病学会学術集会, Sep. 2012.
1139.	Takayuki Ise, Takashi Iwase, K Nanjo, Shoichiro Takao, R Ota, S Bando, Toshiyuki Niki, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masafumi Harada and Masataka Sata : 心臓MRIを用いた左室肥大患者における右室壁厚の検討, 第60回日本心臓病学会学術集会, Sep. 2012.
1140.	Takeshi Soeki, Koji Yamaguchi, Toshiyuki Niki, K Ogasawara, Mika Bando, S Bando, T Matsuura, N Tomita, Yuka Ueda, Takayuki Ise, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : 血中micro RNAは冠動脈不安定プラークのバイオマーカーになりえるか?, 第60回日本心臓病学会学術集会, Sep. 2012.
1141.	S Bando, Takeshi Soeki, T Matsuura, Mika Bando, K Ogasawara, J Hotchi, N Tomita, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : NLRPインフラマソームと冠動脈硬化の関連について, 第60回日本心臓病学会学術集会, Sep. 2012.
1142.	H Sato, Michio Shimabukuro, Y Hirata, M Tabata, M Dagvasumberel, S Bando, Hirotsugu Kurobe, Daiju Fukuda, Takeshi Soeki, S Takanashi, Tetsuya Kitagawa, Yutaka Nakaya and Masataka Sata : 心臓周囲脂肪酸NLRP3インフラマゾームのヒト冠動脈硬化症における役割, 第60回日本心臓病学会学術集会, Sep. 2012.
1143.	Mika Bando, Hirotsugu Yamada, S Nishio, N Tomita, J Hotchi, R Tamai, M Nakagawa, D Hirota, Y Hirata, S Hayashi, K Ogasawara, Toshiyuki Niki, Koji Yamaguchi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 重症大動脈弁狭窄症を呈した成人大動脈一尖弁の2例, 第60回日本心臓病学会学術集会, Sep. 2012.
1144.	Tetsuzo Wakatsuki, Toshiyuki Niki, Koji Yamaguchi, Takayuki Ise, Takashi Iwase, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : OCTにてneovascularizationを認めた冠動脈プラークのIB-IVUSによる組織性状の評価, 第60回日本心臓病学会学術集会, Sep. 2012.
1145.	S Nishio, Hirotsugu Yamada, M Sato, H Hiraoka, Y Hirata, D Hirota, Mika Bando, S Hayashi, J Hotchi, N Tomita, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 糖尿病において左房容積係数と最も相関する非侵襲的血管検査指標は何か:左房-左室-血管連関についての検討, 第60回日本心臓病学会学術集会, Sep. 2012.
1146.	Toshiyuki Niki, Tetsuzo Wakatsuki, Mika Bando, S Nishio, K Ogasawara, S Bando, Takayuki Ise, J Hotchi, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, N Tomita, H Yamada, Takeshi Soeki and Masataka Sata : スタチンへのEPA製剤追加による動脈硬化病変の組織性状変化に関する検討, 第60回日本心臓病学会学術集会, Sep. 2012.
1147.	Masataka Sata : 動脈硬化の新知見とイメージングへの応用, 第22回東京高血圧研究会血管内皮障害と高血圧, Sep. 2012.
1148.	Masataka Sata : 動脈硬化と異所性脂肪, 第3回Molecular Cardiovascular Conference Ⅱ, Sep. 2012.
1149.	Taisuke Nakayama, Yuki Matsuoka, Hirotsugu Kurobe, Noriko Sugasawa, Yoichiro Hirata, Takaki Hori and Masataka Sata : Azelnidipine suppresses the progression of aortic aneurysm in wild mice model through anti-inflammatory effects, 第7回日独血管外科学会, Sep. 2012.
1150.	Ryo Tabata, Hirotsugu Yamada, 西尾進, 井口明子, 小幡史明, 發知淳子, 林修司, 中西嘉憲, 河南真吾, Shino Yuasa, Nobuhiko Shimizu, Harutaka Yamaguchi, Mitsuhiro Kohno, Masataka Sata, Kenji Tani and Hiroyashu Bando : リアルタイム心エコーによる遠隔診断支援システムについて, 第3回日本プライマリ・ケア連合学会学術大会, Sep. 2012.
1151.	Toshiyuki Niki, Tetsuzo Wakatsuki, K Ogasawara, Takayuki Ise, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase and Masataka Sata : Neovascularizationを認めた冠動脈プラークの組織性状の評価-OCTおよびIB-IVUS所見の比較検討-, 第19回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2012.
1152.	Masataka Sata : Renin angiotensin system and atherosclerosis., The International Vascular Biology Symposium in Nagoya 2012, Aug. 2012.
1153.	Y Yokota, M Kadota, Takayuki Ise, Takashi Iwase, T Hara, R Ota, Y Kawabata, K Ogasawara, Mika Bando, S Bando, T Matsuura, Toshiyuki Niki, J Hotchi, N Tomita, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, Masashi Akaike, Mariko Egawa and Yoshinori Mitamura : 眼病変の経過中に心室中隔の肥厚および完全房室ブロックで発症した心サルコイドーシスの一例, 第245回徳島医学会学術集会(平成24年度夏期), Jul. 2012.
1154.	N Kawano, Toshiyuki Niki, K Ogasawara, R Ota, M Kadota, Y Kawabata, T Hara, Takayuki Ise, T Matsuura, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, T Yamamoto, K Kawano, 角谷明佳, K Seto and Hiro-omi Kanayama : シスプラチン，エトポシド，ブレオマイシンの三剤化学療法併用中に急性心筋梗塞を発症した二例, 第245回徳島医学会学術集会(平成24年度夏期), Jul. 2012.
1155.	K Matsumoto, Toshiyuki Niki, K Ogasawara, R Ota, M Kadota, Y Kawabata, T Hara, Takayuki Ise, T Matsuura, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata and Y Sawa : プロテインC活性低下を背景とし，オートマチック車への変更を契機に肺血栓塞栓症を発症したタクシー運転手の一例, 第245回徳島医学会学術集会(平成24年度夏期), Jul. 2012.
1156.	N Kobayashi, T Hara, Koji Yamaguchi, M Kadota, R Ota, Y Kawabata, K Ogasawara, Mika Bando, S Bando, T Matsuura, J Hotchi, N Tomita, Takayuki Ise, Toshiyuki Niki, Yuka Ueda, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata and M Bando : 著名な自立神経障害を背景とした治療抵抗性夜間高血圧症の一例, 第245回徳島医学会学術集会(平成24年度夏期), Jul. 2012.
1157.	Masataka Sata : 動脈硬化病態生理におけるレニン・アンジオテンシン系の役割-新規ARBアジルサルタンへの期待-, 第21回日本心血管インターベンション治療学会学術集会, Jul. 2012.
1158.	Yuka Ueda, Takashi Iwase, Takayuki Ise, K Maeda, K Nishikawa, Mika Bando, K Ogasawara, S Bando, Toshiyuki Niki, J Hotchi, Koji Yamaguchi, N Tomita, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Shinsuke Katoh, Natsuo Yasui and Masataka Sata : 喫煙継続者における心臓リハビリテーションの効果の検討, 第18回心臓リハビリテーション学会, Jul. 2012.
1159.	K Maeda, Yuka Ueda, Takayuki Ise, Takashi Iwase, K Nishikawa, Mika Bando, K Ogasawara, S Bando, Toshiyuki Niki, J Hotchi, Koji Yamaguchi, N Tomita, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Shinsuke Katoh, Natsuo Yasui and Masataka Sata : 患者の気持ちを汲んだ患者教育の実際, 第18回心臓リハビリテーション学会, Jul. 2012.
1160.	A Takashima, Takayuki Ise, Yuka Ueda, K Maeda, K Nishikawa, K Ogasawara, Mika Bando, N Tomita, Toshiyuki Niki, J Hotchi, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Shinsuke Katoh, Masashi Akaike, Natsuo Yasui and Masataka Sata : 心臓リハビリテーションは酸化LDLを低下させる, 第18回心臓リハビリテーション学会, Jul. 2012.
1161.	Masataka Sata : 心血管イベント抑制のためにできること-PCIと薬物のハイブリッド療法-, 第21回日本心血管インターベンション治療学会学術集会・CVIT2012, Jul. 2012.
1162.	Toshiyuki Niki, Tetsuzo Wakatsuki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase and Masataka Sata : The Tissue characteristics of coronary plaque with microchannel structure in patients with coronary artery disease assessed by OCT and IB-IVUS, 第21回日本心血管インターベンション治療学会学術集会, Jul. 2012.
1163.	Koji Yamaguchi, Tetsuzo Wakatsuki, Toshiyuki Niki, Yoshio Taketani, Takashi Iwase and Masataka Sata : Local Coagulative Response after Zotarolimus-eluting, Sirolimus-eluting and Bare-metal Stents Implantation in the Chronic Phase., 第21回日本心血管インターベンション治療学会学術集会, Jul. 2012.
1164.	Masataka Sata : 心筋梗塞が発症する機序に関する新知見とイメージングへの応用, 第32回心筋梗塞研究会, Jul. 2012.
1165.	Masataka Sata : Adventitial angiogenesis plays an important role in the pathogenesis of atherosclerosis., 第33回日本炎症・再生医学会, Jul. 2012.
1166.	Y Nagai, Y Watanabe, T Suganami, Hirofumi Izaki, S Akira, K Miyake, Hiro-omi Kanayama, Michio Shimabukuro, Masataka Sata, T Sasaoka, Y Ogawa, K Tobe and K Takatsu : TLRファミリー分子RP105/MD-1は高脂肪食誘発性の肥満，脂肪組織炎症，インスリン抵抗性を制御する, 第33回日本炎症・再生医学会, Jul. 2012.
1167.	Masataka Sata : 脂質異常症治療の最新の動向-映像でみる動脈硬化の新知見と異所性脂肪-, 第12回日本NO学会学術集会, Jun. 2012.
1168.	S Bando, Takeshi Soeki, Takayuki Ise, Takashi Iwase, Mika Bando, K Ogasawara, J Hotchi, N Tomita, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Tetsuzo Wakatsuki, Mikio Sugano, Tamotsu Kanbara, Tetsuya Kitagawa and Masataka Sata : 心房周囲炎症と心囊液貯留により収縮性心膜炎の病態を呈した一例, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1169.	A Tachibana, Takayuki Ise, Takeshi Soeki, Takashi Iwase, R Ota, M Kadota, T Hara, Mika Bando, K Ogasawara, S Bando, Toshiyuki Niki, J Hotchi, N Tomita, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : CRT-Dが著効した重症拡張型心筋症の2症例, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1170.	S Nagasaka, Takayuki Ise, Takashi Iwase, R Ota, M Kadota, T Hara, Mika Bando, K Ogasawara, S Bando, Toshiyuki Niki, J Hotchi, N Tomita, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : マルチモダリティを用いて鑑別し得た冠動脈病変合併たこつぼ型心筋症の1症例, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1171.	Takayuki Ise, K Nanjo, Takashi Iwase, Shoichiro Takao, R Ota, M Kadota, T Hara, Mika Bando, K Ogasawara, S Bando, Toshiyuki Niki, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masafumi Harada and Masataka Sata : 左室肥大患者における右室壁厚の検討, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1172.	J Hotchi, S Taoka, Mika Bando, K Ogasawara, A Takashima, H Yamasaki, S Bando, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Yuka Ueda, N Tomita, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Y Saijo and Masataka Sata : 緊密な病診連携と詳細な副腎静脈サンプリングが迅速な根治術につながった原発性アルドステロン症の一例, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1173.	Takayuki Ise, Takashi Iwase, R Ota, M Kadota, T Hara, A Takashima, H Yamasaki, Mika Bando, K Ogasawara, S Bando, Toshiyuki Niki, J Hotchi, N Tomita, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Adaptive Servo-Ventilationが心不全治療に有効であった心アミロイドーシスの2症例, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1174.	K Maeda, Yuka Ueda, Takayuki Ise, Takashi Iwase, K Nishikawa, Mika Bando, K Ogasawara, S Bando, Toshiyuki Niki, J Hotchi, Koji Yamaguchi, N Tomita, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Shinsuke Katoh, Natsuo Yasui and Masataka Sata : チーム医療で取り組む重症心不全に対する心臓リハビリテーション, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1175.	S Taoka, Takayuki Ise, Takashi Iwase, R Ota, M Kadota, T Hara, K Ogasawara, Mika Bando, S Bando, Toshiyuki Niki, J Hotchi, N Tomita, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : テニスラケットによる打撲が誘引で深部静脈血栓・急性肺塞栓症を来した1症例, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1176.	K Ogasawara, Toshiyuki Niki, Mika Bando, S Bando, Takayuki Ise, J Hotchi, Yuka Ueda, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : 永久型下大静脈フィルター血栓閉塞に対し抗凝固療法を中心とした保存的加療が有効であった2症例, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1177.	Mika Bando, Hirotsugu Yamada, K Ogasawara, Toshiyuki Niki, N Tomita, J Hotchi, R Tamai, Y Hirata, D Hirota, S Nishio, S Bando, Takayuki Ise, Yuka Ueda, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, H Kawano and Yasuhiko Nishioka : 肺動脈血栓に対してフォンダパリヌクスが著効した静脈血栓塞栓症の一例, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1178.	S Nishio, Hirotsugu Yamada, R Tamai, Y Hirata, D Hirota, M Yamao, Kazuhiro Mori, Masataka Sata and S Matsuoka : 子育て支援イベントにおける先天性心疾患スクリーニング:10年間のまとめ, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1179.	R Tamai, Mika Bando, Hirotsugu Yamada, S Nishio, N Tomita, J Hotchi, S Hayashi, M Nakagawa, Y Hirata, D Hirota, K Ogasawara, H Yamasaki, S Bando, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 超音波後方散乱信号を用いたカラーマッピングシステムの脂質低下療法における臨床応用:case report, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1180.	Y Hirata, S Nishio, Hirotsugu Yamada, S Hayashi, J Hotchi, N Tomita, Mika Bando, D Hirota, R Tamai, M Nakagawa, H Hiraoka, M Sato and Masataka Sata : 心房-心室-血管連関において左房容積係数と最も相関する血管機能指標はどれか?, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1181.	Y Oguro, Toshiyuki Niki, K Ogasawara, Mika Bando, S Bando, Takayuki Ise, J Hotchi, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : マニュアル車からオートマチック車に変更後に左下肢深部静脈血栓症を生じたタクシー運転手の一例, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1182.	森住俊, J Hotchi, Hirotsugu Yamada, Mika Bando, H Yamasaki, K Ogasawara, K Takashima, S Bando, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, N Tomita, Yuka Ueda, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 完全房室ブロックを合併して恒久的ペースメーカー植込みを必要としたたこつぼ型心筋症の一症例, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1183.	N Kawano, Toshiyuki Niki, K Ogasawara, Mika Bando, S Bando, Takayuki Ise, J Hotchi, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, T Yamamoto, K Kawano, 角谷明佳 and Masataka Sata : シスプラチン，エトポシド，ブレオマイシンの三剤化学療法併用中に急性心筋梗塞を発症した二例, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1184.	Koji Yamaguchi, Tetsuzo Wakatsuki, Takeshi Soeki, Toshiyuki Niki, Yoshio Taketani, H Oezuka, K Ogasawara, Mika Bando, S Bando, J Hotchi, Yuka Ueda, N Sakamoto, Takayuki Ise, Takashi Iwase, Hirotsugu Yamada and Masataka Sata : テルミサルタンの冠動脈プラークに対する抗動脈硬化作用の検討, 第100回日本循環器学会中国・四国合同地方会, Jun. 2012.
1185.	Masataka Sata, Hirotsugu Yamada, 平田陽一郎, 中村和人, 岩田洋 and 松本邦夫 : 合成低分子化合物による内因性増殖因子発現誘導と循環器疾患の治療への応用, 第11回日本再生医療学会総会, Jun. 2012.
1186.	Kenji Otsuka, Tomoya Hara, Yuko Toyoda, Jun Kishi, Yoshinori Aono, Koji Yamaguchi, Masaki Hanibuchi, Masataka Sata and Yasuhiko Nishioka : 心筋炎を合併したChurg-Strauss症候群の1例, 第106回日本内科学会四国地方会, Jun. 2012.
1187.	弘田大智, 西尾進, Mika Bando, 冨田紀子, 發知淳子, 林修司, 中川摩耶, 平田有紀奈, Takashi Iwase, Hirotsugu Yamada, Ken Saito and Masataka Sata : 右室自由壁の著名な肥厚を認めた右室心筋脂肪浸潤の1例, 第37回日本超音波検査学会学術集会, Jun. 2012.
1188.	玉井利奈, 西尾進, Hirotsugu Yamada, Mika Bando, 平田有紀奈, 弘田大智, 中川摩耶, 林修司, 發知淳子, 冨田紀子 and Masataka Sata : 超音波後方散乱信号を用いた頸動脈プラーク性状変化の評価, 第37回日本超音波検査学会学術集会, Jun. 2012.
1189.	J Hotchi, Hirotsugu Yamada, M Nakagawa, S Nishio, R Tamai, Y Hirata, D Hirota, H Yamasaki, N Tomita and Masataka Sata : 透析シャント造設後に失神を繰り返した鎖骨下動脈盗血症候群の一例, 日本超音波医学会第85回学術集会, May 2012.
1190.	Y Hirata, S Hayashi, Hirotsugu Yamada, S Nishio, N Tomita, J Hotchi, D Hirota, R Tamai, M Nakagawa and Masataka Sata : 肺平滑筋肉腫の心筋内転移の診断，経過観察に経過観察に経過観察に傾胸壁心エコーが有用であった一例, 日本超音波医学会第85回学術集会, May 2012.
1191.	M Nakagawa, S Nishio, Hirotsugu Yamada, Misako Nakagawa, Hirokazu Takechi, Yukikiyo Kawakami, M Morimoto, Masataka Sata and Akira Tangoku : 超音波検査による乳癌術前化学療法の効果予測, 日本超音波医学会第85回学術集会, May 2012.
1192.	Mika Bando, Hirotsugu Yamada, S Nishio, R Tamai, Y Hirata, D Hirota, J Hotchi, N Tomita, Takeshi Soeki and Masataka Sata : 超音波integrated backscatterカラーマッピング法による頸動脈プラークの組織性状診断, 日本超音波医学会第85回学術集会, May 2012.
1193.	S Hayashi, Hirotsugu Yamada, N Tomita, J Hotchi, Mika Bando, S Nishio, R Tamai, D Hirota, Y Hirata and Masataka Sata : 僧帽弁輪運動速波刑を用いた左室駆出率が保持された心不全と心房機能不全の鑑別, 日本超音波医学会第85回学術集会, May 2012.
1194.	D Hirota, Hirotsugu Yamada, S Nishio, Y Hirata, M Nakgawa, Mika Bando, J Hotchi, N Tomita, Masataka Sata and Ken Saito : ボセンタン投与により肺動脈性肺高血圧症合併妊娠の転機が改善した一例, 日本超音波医学会第85回学術集会, May 2012.
1195.	S Nishio, Hirotsugu Yamada, M Yamao, Y Hirata, D Hirota, R Tamai, Masataka Sata, Kazuhiro Mori and S Matsuoka : 心エコー検査による小児心臓検診の有用性:子育て支援イベント10年間のまとめ, 日本超音波医学会第85回学術集会, May 2012.
1196.	M Nakagawa, S Nishio, Hirotsugu Yamada and Masataka Sata : 静脈エコーでどこまで診るか?:目的別にみた検査法の工夫, 日本超音波医学会第85回学術集会, May 2012.
1197.	H Sato, Y Hirata, Michio Shimabukuro, M Tabata, Hirotsugu Kurobe, M Higashida, Asuka Shiota, Hirofumi Izaki, Hiro-omi Kanayama, S Takanashi, Tetsuya Kitagawa, Yutaka Nakaya and Masataka Sata : 心臓周囲脂肪NLRP3インフラマゾームのヒト冠動脈硬化症における役割, 第55回日本糖尿病学会年次学術集会, May 2012.
1198.	Sumiko Yoshida, Ken-ichi Aihara, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : エイコサペントエン酸は酸化ストレス抑制を介して心臓リモデリングを抑制する, 日本高血圧学会第1回臨床高血圧フォーラム, May 2012. (Keyword) Eicosapentaenoic Acid(薬理学,治療的利用) 疾患モデル(動物) 心臓血管疾患(超音波診断,病理学,予防) 酸化ストレス BALB Cマウス心室リモデリング(予防) ヒトマウス動物男女
1199.	S Hayashi, M Sato, Hirotsugu Yamada, N Tomita, J Hotchi, Mika Bando, S Nishio, R Tamai, M Nakagawa, D Hirota, Y Hirata, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 僧帽弁輪運動速波形指標およびAugmentation Indenxの性差と相互連関についての検討, 第23回日本心エコー図学会学術集会, Apr. 2012.
1200.	N Tomita, Hirotsugu Yamada, S Nishio, J Hotchi, S Hayashi, Mika Bando, M Nakagawa, R Tamai, Y Hirata, D Hirota, Hiraoka H, M Sato, Yoshio Taketani, Takeshi Soeki and Masataka Sata : 大動脈弁硬化における性差の検討, 第23回日本心エコー図学会学術集会, Apr. 2012.
1201.	R Tamai, S Nishio, M Sato, H Hiraoka, Y Hirata, D Hirota, M Nakagawa, Mika Bando, S Hayashi, J Hotchi, N Tomita, Hirotsugu Yamada and Masataka Sata : 2型糖尿病患者の左室拡張能に影響を及ぼす非侵襲的血管機能指標は何か?, 第23回日本心エコー図学会学術集会, Apr. 2012.
1202.	Y Hirata, S Nishio, K Ogasawara, Toshiyuki Niki, Mika Bando, N Tomita, J Hotchi, S Hayashi, M Nakagawa, R Tamai, D Hirota, Yoshio Taketani, Hirotsugu Yamada and Masataka Sata : 右房内浮遊血栓から肺動脈塞栓を来したが，保存的加療が奏功した静脈血栓症の1例, 第23回日本心エコー図学会学術集会, Apr. 2012.
1203.	M Nakagawa, Hirotsugu Yamada, S Nishio, R Tamai, N Tomita, J Hotchi, S Hayashi, Mika Bando, Y Hirata, D Hirota and Masataka Sata : 左室駆出率が保持された心房細動におけるL波の意義, 第23回日本心エコー図学会学術集会, Apr. 2012.
1204.	Hirotsugu Yamada, Ryo Tabata, S Nishio, N Tomita, J Hotchi, S Hayashi, Mika Bando, R Tamai, M Nakagawa and Masataka Sata : 市販のビデオ会議システムを用いた心エコー検査の遠隔診断支援システムの構築, 第23回日本心エコー図学会学術集会, Apr. 2012.
1205.	D Hirota, S Nishio, Mika Bando, N Tomita, J Hotchi, S Hayashi, M Nakagawa, R Tamai, Y Hirata, Takashi Iwase, Yoshio Taketani, Hirotsugu Yamada, Ken Saito and Masataka Sata : 右室自由壁の著明な肥厚を認めた右室心筋脂肪浸潤の1例, 第23回日本心エコー図学会学術集会, Apr. 2012.
1206.	J Hotchi, Hirotsugu Yamada, Yoshio Taketani, S Nishio, N Tomita, S Hayashi, Mika Bando, R Tamai, D Hirota, Y Hirata, M Nakagawa and Masataka Sata : Six-minute stress echocardiography in patients with connective tissue disease., 第23回日本心エコー図学会学術集会, Apr. 2012.
1207.	Mika Bando, Hirotsugu Yamada, S Nishio, R Tamai, N Tomita, J Hotchi, S Hayashi, M Nakagawa, Y Hirata, D Hirota, Yoshio Taketani, Takeshi Soeki and Masataka Sata : Effect of statin therapy on carotid artery plaque assesed by integrated backscatter color mapping., 第23回日本心エコー図学会学術集会, Apr. 2012.
1208.	松岡祐貴, Hirotsugu Kurobe, 平田陽一郎, 菅澤典子, 東田真由子, 中山泰介, Masataka Sata and Tetsuya Kitagawa : 野生型マウス大動脈瘤モデルの確立とsmall aortic aneurysm拡大予防について, 第42回日本心臓血管外科学会学術総会, Apr. 2012.
1209.	中山泰介, Hirotsugu Kurobe, 菅澤典子, 東田真由子, 吉田恭史, Masataka Sata, Toshiaki Tamaki, Tetsuya Kitagawa and 冨田修平 : 小口径グラフト開存性改善を目的とするマクロファージHIF制御に関しての基礎研究, 第42回日本心臓血管外科学会学術総会, Apr. 2012.
1210.	Masataka Sata : Atherosclerosis and Epicardial Adipose Tissues., 第76回日本循環器学会学術集会, Mar. 2012.
1211.	Masataka Sata : Impact of Hyperglycemia on the Pathogenesis of Atherosclerosis., 第76回日本循環器学会学術集会, Mar. 2012.
1212.	弘田大智, 西尾進, Hirotsugu Yamada, 遠藤桂輔, 冨田紀子, 林修司, 平田有紀奈, 玉井利奈, 中川摩耶, Masataka Sata and Ken Saito : 陳旧性心筋梗塞におけるV1誘導のP波と左房負荷:心エコー・ドプラ法を用いた検討, The 76th Annual Scientific Meeting of the Japanese Circulation Society, Mar. 2012.
1213.	Tomita Noriko, Hirotsugu Yamada, Kenya Kusunose, Nishio Susumu, Hotchi Junko, Hayashi Shuji, Mika Bando, Bando Sachiko, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Clinical Efficacy of Beat-to-beat Variability of Diastolic Filling in Atrial Fibrillation., 第76回日本循環器学会学術集会, Mar. 2012.
1214.	Munkbaatar Dagvasumberel, Michio Shimabukuro, Nishiuchi Takeshi, Hirata Yoichiro, Takeshi Soeki, Masashi Akaike, Takashi Iwase, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Shusuke Yagi, Tomita Noriko, Hirotsugu Yamada, Tetsuzo Wakatsuki, Hirotsugu Kurobe, Tetsuya Kitagawa and Masataka Sata : Gender Disparities in Association of Epicardial Adipose Tissue Volume and Coronary Atherosclerosis., 第76回日本循環器学会学術集会, Mar. 2012.
1215.	Bando Sachiko, Takeshi Soeki, Ogasawara Kozue, Takashima Akira, Mika Bando, Yamazaki Hiromu, Hotchi Junko, Tomita Noriko, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Relationship between NLRP3 Inflammasome and Coronary Atherosclerosis., 第76回日本循環器学会学術集会, Mar. 2012.
1216.	Hotchi Junko, Hirotsugu Yamada, Kenya Kusunose, Nishio Susumu, Mika Bando, Tomita Noriko, Hayashi Shuji, Bando Sachiko, Toshiyuki Niki, Takayuki Ise, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Effect of Irbesartan on Left Ventricular Myocardial Function in Patients with Hypertension: Assessment by Two-dimensional Speckle Tracking Echocardiography., 第76回日本循環器学会学術集会, Mar. 2012.
1217.	Koji Yamaguchi, Tetsuzo Wakatsuki, Toshiyuki Niki, Yoshio Taketani, Bando Sachiko, Hotchi Junko, Tomita Noriko, Takayuki Ise, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : Angiographic Peri-stent Contrast Staining Leading to Local Persistent Hypercoagulability up to Five Years after Sirolimus-eluting Stent Implantation:Comparison with Bare-Metal Stent., 第76回日本循環器学会学術集会, Mar. 2012.
1218.	Higashikuni Yasutomi, Nagai Ryozo and Masataka Sata : The ATP-binding Cassette Transporter ABCG2 Protects against Pressure Overload-induced Cardiac Hypertrophy and Heart Failure via Regulation of Antioxidant Response., 第76回日本循環器学会学術集会, Mar. 2012.
1219.	Kimura Sahika, Yuka Ueda, Takayuki Ise, Takashi Iwase, Takashima Akira, Yamazaki Hiromu, Ogasawara Kozue, Bando Sachiko, Hayashi Shuji, Takeuchi Hidekazu, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, Tomita Noriko, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Cardiac Rehabilitation decreases Urinary Albumin Excretion in Patients with Cardiovascular Disease., 第76回日本循環器学会学術集会, Mar. 2012.
1220.	Hirotsugu Kurobe, Matsuoka Yuki, Higashida Mayuko, Sugasawa Noriko, Hirata Yoichiro, Yoshida Yasushi, Sato Hiromi, Nakayama Taisuke, Michio Shimabukuro, Masataka Sata and Tetsuya Kitagawa : The Selective Mineralocorticoid Receptor Antagonist, Eplerenone, is Protective in Vascular Remodeling by Anti-inflammatory Effects., 第76回日本循環器学会学術集会, Mar. 2012.
1221.	Taisuke Nakayama, Hirotsugu Kurobe, Noriko Sugasawa, Hajime Kinoshita, Mayuko Higashida, Yuuki Matsuoka, Mitsuru Takaku, Yasushi Yoshida, Yoichiro Hirata, Yousuke Takahama, Masataka Sata, Toshiaki Tamaki, Tetsuya Kitagawa and Shuhei Tomita : Role of Hypoxia-Inducible Factor1-alpha in Macrophage as an Aggravation Regulator in Development of Vascular Remodeling., 第76回日本循環器学会学術集会, Mar. 2012.
1222.	Takashima Akira, Takayuki Ise, Takashi Iwase, Yuka Ueda, Masashi Akaike, Yamazaki Hiromu, Mika Bando, Ogasawara Kozue, Bando Sachiko, Tomita Noriko, Takeuchi Hidekazu, Toshiyuki Niki, Hotchi Junko, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Effect of Cardiac Rehabilitation on Level of Oxidized LDL., 第76回日本循環器学会学術集会, Mar. 2012.
1223.	Hirotsugu Yamada, Tomita Noriko, Hayashi Shuji, Hotchi Junko, Nishio Susumu, Tamai Rina, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Prognostic Value of Preload Stress Echocardiographyin Patients with Mild Heart Failure., 第76回日本循環器学会学術集会, Mar. 2012.
1224.	Takeshi Soeki, Toshiyuki Niki, Koji Yamaguchi, 坂東左知子, Yuka Ueda, 冨田紀子, Takayuki Ise, Kenya Kusunose, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike, Michio Shimabukuro and Masataka Sata : Inflammatory Biomarkers as Predictors of Vulnerable Coronary Plaques., 第76回日本循環器学会学術集会，Symposium 3, Mar. 2012.
1225.	Hirotsugu Yamada, 西尾進, Mika Bando, 發知淳子, 林修司, 冨田紀子, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Carotid Ultrasound Imaging to Evaluate Atherosclerotic Diseases., 第76回日本循環器学会学術集会，KSC-JCS Joint Symposium-2, Mar. 2012.
1226.	立花綾香, Yuka Ueda, Takayuki Ise, 高島啓, 山崎宙, 小笠原梢, 坂東左知子, Toshiyuki Niki, 發知淳子, 冨田紀子, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, Masashi Akaike and 廣野明 : CRT-Dが著効した重症慢性心不全の1例, 第244回徳島医学会学術集会 (平成23年度冬期), Feb. 2012.
1227.	田岡志保, Yuka Ueda, Takayuki Ise, 高島啓, 山崎宙, 小笠原梢, 坂東左知子, Toshiyuki Niki, 發知淳子, 冨田紀子, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, Masashi Akaike and 井上洋行 : テニスラケットによる外傷が誘因で深部静脈血栓・急性肺塞栓症を来した一症例, 第244回徳島医学会学術集会 (平成23年度冬期), Feb. 2012.
1228.	森住俊, 發知淳子, Hirotsugu Yamada, 山崎宙, 小笠原梢, 高島啓, Mika Bando, 坂東左知子, 竹内秀和, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, 冨田紀子, Yuka Ueda, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, 久保克之, Katsuya Sasaki and 富田芳雄 : たこつぼ型心筋症に完全房室ブロックを合併した一症例, 第244回徳島医学会学術集会 (平成23年度冬期), Feb. 2012.
1229.	Mika Bando, Hirotsugu Yamada, 冨田紀子, 發知淳子, 小笠原梢, 高島啓, 山崎宙, 坂東左知子, Takayuki Ise, Toshiyuki Niki, Yuka Ueda, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masataka Sata, 西尾進, 林修司, 中川摩耶, 玉井利奈, 平田有紀奈 and 弘田大智 : 脂質低下療法による頸動脈プラーク安定化の評価:超音波integrated backscatterを用いたカラーマッピングシステムの臨床応用, 第244回徳島医学会学術集会 (平成23年度冬期), Feb. 2012.
1230.	Koji Yamaguchi, Tetsuzo Wakatsuki, Takeshi Soeki, Toshiyuki Niki, Yoshio Taketani, 小笠原梢, Mika Bando, 坂東左知子, 發知淳子, Yuka Ueda, 冨田紀子, 竹内秀和, Takayuki Ise, Takashi Iwase, Hirotsugu Yamada, Masataka Sata and 麻植塚浩康 : テルミサルタンの冠動脈プラークに対する抗動脈硬化作用の検討, 第244回徳島医学会学術集会 (平成23年度冬期), Feb. 2012.
1231.	Toshiyuki Niki, 小笠原梢, Mika Bando, 坂東左知子, 竹内秀和, Takayuki Ise, 發知淳子, Yuka Ueda, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, 冨田紀子, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, Emiko Nakataki, Masaji Nishimura and 上山祐二 : 低体温療法が著効し社会復帰をなし得たBrugada症候群の一例, 第244回徳島医学会学術集会 (平成23年度冬期), Feb. 2012.
1232.	太田理絵, Tetsuzo Wakatsuki, Takashi Iwase, Shoichiro Takao, Hirotsugu Yamada, Masashi Akaike, 坂東左知子, Toshiyuki Niki, Hayato Nose, 冨田紀子, Koji Yamaguchi, Yoshio Taketani, Takeshi Soeki, Yasuhiko Nishioka, Masafumi Harada and Masataka Sata : 肺，皮膚病変診断4年後に心病変が顕在化したサルコイドーシスの1例, 第22回日本心血管画像動態学会, Jan. 2012.
1233.	Toshiyuki Niki, Tetsuzo Wakatsuki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, 麻植塚浩康, 西尾進, 小笠原梢, Mika Bando, 坂東左知子, Takayuki Ise, 冨田紀子, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : 冠動脈プラークに対するスタチンへのEPA製剤add on 効果の検討-IB-IVUSおよびIB-頸動脈エコーの観点から-, 第22回日本心血管画像動態学会, Jan. 2012.
1234.	前田香代子, Yuka Ueda, Takayuki Ise, Takashi Iwase, 西川幸治, 高島啓, 小笠原梢, 山崎宙, 坂東左知子, Toshiyuki Niki, 發知淳子, Koji Yamaguchi, 冨田紀子, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Shinjiro Takata, Natsuo Yasui and Masataka Sata : 大学病院での心臓リハビリテーション立ち上げの問題点, 第99回日本循環器学会四国地方会, Dec. 2011.
1235.	Mika Bando, 林修司, Hirotsugu Yamada, 冨田紀子, 發知淳子, 西尾進, 玉井利奈, 平田有紀奈, 弘田大智, 小笠原梢, 高島啓, 山崎宙, 坂東左知子, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 平滑筋肉腫の心筋内転移の診断，経過観察に経胸壁心エコー法が有用であった一例, 第99回日本循環器学会四国地方会, Dec. 2011.
1236.	高島啓, Koji Yamaguchi, 原知也, 山崎宙, 小笠原梢, 坂東左知子, 發知淳子, 冨田紀子, 竹内秀和, Toshiyuki Niki, Takayuki Ise, Yuka Ueda, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Jun Hanaoka, Mitsuo Shimada and Masataka Sata : 真性多血症患者に発症した心原生脾梗塞の1例, 第99回日本循環器学会四国地方会, Dec. 2011.
1237.	田根なつ紀, Koji Yamaguchi, Yoshio Taketani, 高島啓, 山崎宙, 小笠原梢, 坂東左知子, Toshiyuki Niki, Takayuki Ise, 發知淳子, Takashi Iwase, 冨田紀子, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 重症下肢虚血病変に対して経皮的下肢動脈形成術が奏功し，予定されていた下肢切断手術を回避できた一症例, 第99回日本循環器学会四国地方会, Dec. 2011.
1238.	高橋直希, Toshiyuki Niki, 高島啓, 山崎宙, 小笠原梢, 坂東左知子, Takayuki Ise, 發知淳子, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, 冨田紀子, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, Emiko Nakataki, Masaji Nishimura and 上山祐二 : 低体温療法が著効し社会復帰をなし得たBrugada症候群の一例, 第99回日本循環器学会四国地方会, Dec. 2011.
1239.	藤岡啓介, 山崎宙, Takayuki Ise, Kenya Kusunose, 木村白陽花, 高島啓, 小笠原梢, 坂東左知子, 發知淳子, 冨田紀子, 竹内秀和, Yuka Ueda, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : ULPの発生から拡大，消失までを経時的に観察し得たacute aortic syndromeの一例, 第99回日本循環器学会四国地方会, Dec. 2011.
1240.	Naoki Sawada, Jiang Aihua, Takizawa Fumiko, Croce Kevin, Manika Andre, Tesmenitsky Yevgenia, Kang Tae Kyu, Bischoff Joyce, Kalwa Hermann, Michel Thomas, Kamei Yasutomi, Benjamin E. Laura, Masataka Sata, Mizutani Shuki, Ogawa Yoshihiro and Arany Zolt : Endothelial PGC-1alpha is highly responsive to metabolic stress and serves as a key determinant of angiogenic response, The 19th Annual Meeting of the Japanese Vascular Biology and Medicine Organization the 1st Asia-Pacific Vascular Meeting., Dec. 2011.
1241.	東田真由子, 西雄千佳, 松岡祐貴, 平田陽一郎, Hirotsugu Kurobe, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : 血管リモデリングにおけるHMGB1の果たす役割, Anti-aging Science アンチエイジングフェスタ 2011: 抗加齢医学の実践, Dec. 2011.
1242.	Masataka Sata : 血管老化の仕組みと予防法, Anti-aging Science アンチエイジングフェスタ 2011; 加齢医学の実態, Dec. 2011.
1243.	山田諭, Seiji Kishi, 柴田恵理子, Motokazu Matsuura, Kojiro Nagai, Hideharu Abe, Toshio Doi, 小笠原梢 and Masataka Sata : ヒトパルボウィルスB19による急性糸球体腎炎の1例, 第105回日本内科学会四国地方会, Nov. 2011.
1244.	坂東左知子, Hirotsugu Yamada, Takeshi Soeki, 木内誠, Hiroshi Kitahata, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Tetsuzo Wakatsuki and Masataka Sata : 全身麻酔により顕在性Brugada型心電図の1例, 第105回日本内科学会四国地方会, Nov. 2011.
1245.	山崎宙, Kenya Kusunose, Takayuki Ise, Yoshio Taketani, Tetsuzo Wakatsuki, Toshifumi Tezuka, Souji Kakiuchi, Yasuhiko Nishioka, Yoshimi Bando and Masataka Sata : 稀な画像所見を呈する肺アスペルギルス症により治療抵抗性心不全を認めた1症例, 第105回日本内科学会四国地方会, Nov. 2011.
1246.	坂東左知子, Takeshi Soeki, Takayuki Ise, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, 木村建彦, 西内健 and Masataka Sata : CRT-Dによって僧帽弁閉鎖不全症が劇的に改善した突発性拡張型心筋症の1例, 第105回日本内科学会四国地方会, Nov. 2011.
1247.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, Hayato Nose, Takayuki Ise, 小笠原梢, 山崎宙, 髙島啓, 坂東左知子, Toshiyuki Niki, Kenya Kusunose, 發知淳子, 冨田紀子, Yuka Ueda, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Yasuhiko Nishioka, Masafumi Harada and Masataka Sata : 心臓MRIによるサルコイドーシス心病変検出の有用性, 第31回日本サルコイドーシス/肉芽腫性疾患学会総会, Oct. 2011.
1248.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : エイコサペントエン酸の酸化ストレス抑制を介したアンジオテンシンII刺激による心血管リモデリング抑制効果の検討, 第34回日本高血圧学会総会, Oct. 2011.
1249.	木谷光宏, Takeshi Soeki, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Tetsuzo Wakatsuki, Masashi Akaike, 山本浩史, 折野俊介, 角谷昭佳, 坂東重信 and Masataka Sata : 高血圧患者におけるシルニジピンの酸化ストレスに対する作用, 第34回日本高血圧学会総会, Oct. 2011.
1250.	Masataka Sata : 高血圧:ACE-IとARBのどちらがfirst choiceか?■ARB, 第1回豊橋ライブデモンストレーションコース，エキスパートディベート, Oct. 2011.
1251.	安岡紗哉香, Kenya Kusunose, Hirotsugu Yamada, 發知淳子, 冨田紀子, 林修司, 西尾進, 中川摩耶, 平田有紀奈 and Masataka Sata : ボセンタン投与により肺動脈性肺高血圧症合併妊娠の転機が改善した一例, 第21回日本超音波医学会四国地方学術集会, Oct. 2011.
1252.	林修司, Hirotsugu Yamada, 西尾進, 玉井利奈, 中川摩耶, 弘田大智, 平田有紀奈, Takashi Iwase, Takeshi Soeki and Masataka Sata : 多発性肺平衡筋肉腫の心筋内転移の診断，経過観察に経胸壁心エコーが有用であった一例, 第21回日本超音波医学会四国地方学術集会, Oct. 2011.
1253.	發知淳子, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 冨田紀子, 林修司, 弘田大智, 玉井利奈, Takeshi Soeki and Masataka Sata : 保存的加療により潰瘍様突出像が消退した大動脈壁内血腫の一例, 第21回日本超音波医学会四国地方学術集会, Oct. 2011.
1254.	玉井利奈, Hirotsugu Yamada, 西尾進, 冨田紀子, 林修司, 發知淳子, 平田有紀奈, 弘田大智, Takeshi Soeki and Masataka Sata : 左心不全に合併した肺高血圧症における三尖弁輪運動速波形の特徴, 第21回日本超音波医学会四国地方学術集会, Oct. 2011.
1255.	冨田紀子, Hirotsugu Yamada, 西尾進, 林修司, 發知淳子, 中川摩耶, 平田有紀奈, 弘田大智, Takeshi Soeki and Masataka Sata : S字状中隔心の心エコー・ドプラ所見についての検討, 第21回日本超音波医学会四国地方会学術集会, Oct. 2011.
1256.	Masataka Sata : 心臓周囲脂肪組織と動脈硬化，心不全, 第15回日本心不全学会学術集会, Oct. 2011.
1257.	Takayuki Ise, Takashi Iwase, Kumiko Kagawa, Toshiyuki Niki, Kenya Kusunose, 冨田紀子, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masahiro Abe, Masashi Akaike and Masataka Sata : Successful Autologous Peripheral Blood Stem Cell Transplantation for Primary Cardiac Amyloidosis Patients with Heart Failure : three cases report., 第15回日本心不全学会学術集会, Oct. 2011.
1258.	山川研, 比嘉南夫, 旭朝弘, 比嘉盛丈, 大城義人, 植田真一郎, 益崎裕章, Masataka Sata and Michio Shimabukuro : エイコサペンタエン酸は高脂血症において脂肪酸構成を変化させ，血管内皮機能を改善する, 第32回日本肥満学会, Sep. 2011.
1259.	Asuka Shiota, Daiju Fukuda, 佐藤寛美, 東田真由子, 榎本操一郎, 平田陽一郎, Hirotsugu Kurobe and Masataka Sata : テルミサルタンは，beyond AT1R作用により動脈硬化抑制作用を示す, 第32回日本肥満学会, Sep. 2011.
1260.	佐藤寛美, 平田陽一郎, Michio Shimabukuro, Asuka Shiota, 田端実, Hirotsugu Kurobe, 東田真由子, Hirofumi Izaki, Hiro-omi Kanayama, 高梨秀一郎, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : 心臓周囲脂肪におけるインフラマゾームの病態的意義, 第32回日本肥満学会, Sep. 2011.
1261.	冨田紀子, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 林修司, 玉井利奈, 坂東左知子, 久岡白陽花, Yuka Ueda, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心房細動における僧帽弁口血流速拡張早期波の心拍変動性の臨床的意義, 第59回日本心臓病学会学術集会, Sep. 2011.
1262.	林修司, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 西尾進, 玉井利奈, 三木淳子, 坂東左知子, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 三尖弁輪運動速波形による肥大型心筋症と高血圧性心疾患の鑑別, 第59回日本心臓病学会学術集会, Sep. 2011.
1263.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, Hayato Nose, 久岡白陽花, Takayuki Ise, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Yasuhiko Nishioka, Masafumi Harada and Masataka Sata : サルコイドーシス心病変検出における心臓MRI検査の有用性, 第59回日本心臓病学会学術集会, Sep. 2011.
1264.	坂東左知子, Takeshi Soeki, Toshiyuki Niki, 久岡白陽花, 竹内秀和, 冨田紀子, Kenya Kusunose, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike, Kenji Kangawa and Masataka Sata : グレリンによる自律神経およびConnexin43発現調節を介した抗不整脈作用の検討, 第59回日本心臓病学会学術集会, Sep. 2011.
1265.	Hirotsugu Yamada, Kenya Kusunose, 西尾進, 冨田紀子, 玉井利奈, 清水拓, 林修司, 坂東左知子, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 膠原病における潜在性肺動脈性高血圧症の検出:運動負荷心エコー法の有用性, 第59回日本心臓病学会学術集会, Sep. 2011.
1266.	西尾進, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 林修司, 玉井利奈, 三木淳子, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 冠動脈硬化症を最も反映する非侵襲的血管検査法についての検討, 第59回日本心臓病学会学術集会, Sep. 2011.
1267.	玉井利奈, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 林修司, 冨田紀子, 坂東左知子, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 左心不全に合併した肺高血圧症における三尖弁輪運動速波形の特徴:HFPEFとHFREFの差異, 第59回日本心臓病学会学術集会, Sep. 2011.
1268.	Koji Yamaguchi, Tetsuzo Wakatsuki, Takeshi Soeki, Toshiyuki Niki, Yoshio Taketani, 麻植塚浩康, 坂東左知子, Yuka Ueda, 冨田紀子, 竹内秀和, Kenya Kusunose, Takashi Iwase, Hirotsugu Yamada and Masataka Sata : 冠動脈プラークに対するテルミサルタンの多面的効果の検討-Integrated backscatter IVUS観察と炎症性サイトカインによる観点から-, 第59回日本心臓病学会学術集会, Sep. 2011.
1269.	Takeshi Soeki, 坂東左知子, Toshiyuki Niki, 久岡白陽花, 竹内秀和, Kenya Kusunose, Yuka Ueda, 冨田紀子, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 心房細動における局所炎症反応に関する検討, 第59回日本心臓病学会学術集会, Sep. 2011.
1270.	Masataka Sata : EPAはいかに冠動脈疾患を抑制するか-エビデンスと動脈硬化研究からの考察-, 第59回日本心臓病学会学術集会, Sep. 2011.
1271.	Tetsuzo Wakatsuki, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, 麻植塚浩康, 西尾進, 坂東左知子, 冨田紀子, 竹内秀和, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : 冠動脈プラークに対するスタチンへのEPA製剤add on効果の検討 -Integrated backscatter IVUSおよび局所Biomaker観察の観点から-, 第59回日本心臓病学会学術集会, Sep. 2011.
1272.	Masataka Sata : 動脈硬化抑制に向けたRAA系阻害戦略-異所性脂肪とアルドステロン-, 第59回日本心臓病学会学術集会, Sep. 2011.
1273.	Toshiyuki Niki, Tetsuzo Wakatsuki, Koji Yamaguchi, Yoshio Taketani, Kenya Kusunose, 小笠原梢, 高島啓, 山崎宙, Takashi Iwase and Masataka Sata : OCTにてneovascularizationを認めた冠動脈プラークのIB-IVUSによる組織性状の評価, 第18回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2011.
1274.	Ken-ichi Aihara, Sumiko Yoshida, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, 久岡白陽花, 平田陽一郎, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Eicosapentaenoic acid-to-arachidonic acid ratio is inversely associated with albuminuria in individuals with cardiovascular risk factors, 第75回日本循環器学会総会・学術集会パシフィコ横浜, Aug. 2011.
1275.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Eicosapentaenoic acid protects against angiotensin II-induced cardiovascular remodeling via attenuation of oxidative stress., 第75回日本循環器学会総会・学術集会パシフィコ横浜, Aug. 2011.
1276.	C. Nishio, M. Higashida, Y. Hirata, Hirotsugu Kurobe, Masashi Akaike, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : GLP-1 Receptor Agonist Attenuates Vascular Remodeling after Endovascular Injury., 第75回日本循環器学会総会・学術集会, Aug. 2011.
1277.	M. Higashida, C. Nishio, Y. Hirata, Hirotsugu Kurobe, Masashi Akaike, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : HMGB1 Plays a Critical Role in Chronic Inflammation and Vascular Remodeling after Endovascular Injury., 第75回日本循環器学会総会・学術集会, Aug. 2011.
1278.	Masashi Akaike, Koichiro Tsuchiya, Yoshiki Kashiwada, Yoshihisa Takaishi, Toshiaki Tamaki, Takashi Iwase, Masataka Sata, Ken-ichi Aihara, Sumiko Yoshida, Toshio Matsumoto, 佐藤千穂, 西条伴香 and Hiroaki Yanagawa : 生活習慣病関連リスクファクターに及ぼすスダチ果皮加工品の効果 ∼探索的臨床試験による検討∼, 第243回徳島医学会学術集会公開シンポジウム, Jul. 2011.
1279.	Masashi Akaike, Koichiro Tsuchiya, Yoshiki Kashiwada, Yoshihisa Takaishi, Toshiaki Tamaki, Takashi Iwase, Masataka Sata, Ken-ichi Aihara, 吉田守実子, Toshio Matsumoto, 佐藤千穂, 西条伴香 and Hiroaki Yanagawa : 生活習慣病関連リスクファクターに及ぼすスダチ果皮加工品の効果-探索的臨床試験による検討-, 第243回徳島医学会学術集会, Jul. 2011.
1280.	高木恵理, 高島啓, Koji Yamaguchi, Yoshio Taketani, 坂東左知子, 冨田紀子, 竹内秀和, Toshiyuki Niki, Kenya Kusunose, Yuka Ueda, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masataka Sata, Atsushi Morimoto, Ichiro Hashimoto, Hideki Nakanishi, 和田美智子, 石本武男 and 田蒔正治 : 重症下肢虚血病変に対して経皮的下肢動脈血管形成術が奏功し，予定されていた下肢切手術を回避できた一症例, 第243回徳島医学会学術集会, Jul. 2011.
1281.	原知也, Takashi Iwase, 高島啓, 山崎宙, 小笠原梢, 坂東左知子, Takayuki Ise, Toshiyuki Niki, Kenya Kusunose, Yuka Ueda, 冨田紀子, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 心サルコイドーシス診断の手引きにおける各種診断モダリティーの検討, 第243回徳島医学会学術集会, Jul. 2011.
1282.	高島啓, Takeshi Soeki, Koji Yamaguchi, Yoshio Taketani, 坂東左知子, 林修司, 久岡白陽花, 冨田紀子, 竹内秀和, Toshiyuki Niki, Kenya Kusunose, Yuka Ueda, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 埋め込み型デバイスにより胸郭内インピーダンスの増悪と改善が観察できた拡張相肥大型心筋症の一例, 第243回徳島医学会学術集会, Jul. 2011.
1283.	Koji Yamaguchi, Tetsuzo Wakatsuki, Kenya Kusunose, Toshiyuki Niki, Yoshio Taketani and Masataka Sata : Different response of local persistent hypercoagulability after zotarolimus-eluting, paclitaxel-eluting, sirolimus-eluting and bare-metal stent implantaion., 第20回日本心血管インターベンション治療学会 CVIT 2011, Jul. 2011.
1284.	Toshiyuki Niki, Tetsuzo Wakatsuki, Koji Yamaguchi, Yoshio Taketani, Kenya Kusunose and Masataka Sata : Impact of statin therapy on local coagulative response after sirolimus-eluting stent implantation in late chronic phase., 第20回日本心血管インターベンション治療学会 CVIT 2011, Jul. 2011.
1285.	西川幸治, Yuka Ueda, 久岡白陽花, 前田香代子, Takashi Iwase, 坂東左知子, 林修司, 竹内秀和, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, 冨田紀子, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Shinjiro Takata, Natsuo Yasui and Masataka Sata : 当院心臓リハビリテーション参加者の運動能力について, 第17回日本心臓リハビリテーション学会学術集会, Jul. 2011.
1286.	前田香代子, Yuka Ueda, 久岡白陽花, Takashi Iwase, 西川幸治, 坂東左知子, 林修司, 竹内秀和, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, 冨田紀子, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Shinjiro Takata, Natsuo Yasui and Masataka Sata : 大学病院での心臓リハビリテーション立ち上げに携わって, 第17回日本心臓リハビリテーション学会学術集会, Jul. 2011.
1287.	久岡白陽花, Yuka Ueda, Takashi Iwase, 前田香代子, 西川幸治, 坂東左知子, 林修司, 竹内秀和, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, 冨田紀子, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Shinjiro Takata, Natsuo Yasui and Masataka Sata : 尿中アルブミン排泄量に及ぼす心臓リハビリテーションの効果, 第17回日本心臓リハビリテーション学会学術集会, Jul. 2011.
1288.	Ogawa Hiroko, Yonezawa Tomoko, Masataka Sata, Hirohata Satoshi, Oohashi Toshitaka, Kusachi Shozo, Koide Norio and Ninomiya Yoshifumi : The Role of 556 Chains of TypeIV Collagen In Restenosis After Angioplasty., 第43回日本動脈硬化学会総会・学術集会, Jul. 2011.
1289.	Higashida Mayuko, Hirata Yoichiro, Hirotsugu Kurobe, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : Toll-like receptor 9 plays a critical role in vascular remodeling., 第43回日本動脈硬化学会総会・学術集会, Jul. 2011.
1290.	Kim-Kaneyama Joo-ri, Takeda Naoki, Sasai Asami, Miyazaki Akira, Masataka Sata, Hirabayashi Takahiro, Shibanuma Motoko, Yamada Gen and Nose Kiyoshi : Hic-5 deficiency enhances mechanosensitive apoptosis and modulates vascular remodeling., 第43回日本動脈硬化学会総会・学術集会, Jul. 2011.
1291.	Masataka Sata : 虚血性心疾患の臨床-診断と治療，予防に関する最近の話題-, 日本内科学会中国支部第44回生涯教育講演会, 山口大学, May 2011.
1292.	玉井利奈, 西尾進, Hirotsugu Yamada, 遠藤桂輔, 栗坂彩美, 三木淳子, Kenya Kusunose, 林修司, 冨田紀子 and Masataka Sata : 下肢血管エコー検査における深部静脈血栓とD-dimer値, 第84回日本超音波医学会学術集会, May 2011.
1293.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 林修司, 玉井利奈, Takeshi Soeki, Masashi Akaike and Masataka Sata : TE-e'は左室拡張末期圧を反映する―下肢腸圧および硝酸薬負荷を用いた検討―, 第84回日本超音波医学会学術集会, May 2011.
1294.	林修司, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 多田津陽子, 西尾進, 玉井利奈, Takashi Iwase, Takeshi Soeki and Masataka Sata : 体位変換により右室内圧較差が変化をきたす右室二腔症の一例, 第84回日本超音波医学会学術集会, May 2011.
1295.	西尾進, Hirotsugu Yamada, Kenya Kusunose, 玉井利奈, 佐藤光代, 冨田紀子, 林修司, Takeshi Soeki, Masashi Akaike and Masataka Sata : 冠動脈硬化症を最も反映する非侵襲的血管検査指標は何か?, 第84回日本超音波医学会学術集会, May 2011.
1296.	Masataka Sata : メタボはなぜ心臓に悪い?, 第98回日本循環器学会中国・四国合同地方会，市民公開講座，あわぎんホール, May 2011.
1297.	竹内秀和, Tetsuzo Wakatsuki, 阪本紀子, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki and Masataka Sata : BNP relates to FT3 negatively in cardiac patients with normal FT3, which might be mediated by HDAC3., 第98回日本循環器学会中国・四国合同地方会, May 2011.
1298.	東田真由子, Hirotsugu Kurobe, 松岡裕貴, 平田陽一郎, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : 血管リモデリングにおけるHMGB1の果たす役割, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1299.	松岡祐貴, Hirotsugu Kurobe, 平田陽一郎, 菅澤典子, 東田真由子, 西雄千佳, Yasuhisa Kanematsu, Yayoi Fukuhara, 中山泰介, Mikio Sugano, Tatsuo Motoki, Tamotsu Kanbara, Takashi Kitaichi, Yutaka Nakaya, Shinji Nagahiro, Masataka Sata and Tetsuya Kitagawa : 野生型マウスでの大動脈瘤モデル作製とトランスレーショナルリサーチとしての活用, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1300.	清水拓, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 林修司, 玉井利奈, 河野裕美, 平岡葉月, 佐藤光代, Yoshio Taketani, Takeshi Soeki and Masataka Sata : 運動負荷心エコー法を用いた膠原病例における潜在性肺動脈性肺高血圧症の検出, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1301.	Munkhbaatar Dagvasumberel, Junji Ueno, Shoichiro Takao, 西内健, 平田陽一郎, 坂東左知子, 久岡白陽花, 林修司, 冨田紀子, 竹内秀和, Yuka Ueda, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Tetsuya Kitagawa and Masataka Sata : Increased epicardial adipose tissue and coronary atherosclerosis., 第98回日本循環器学会中国・四国合同地方会, May 2011.
1302.	山中森晶, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 林修司, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, 西尾進, 玉井利奈 and 三木淳子 : ストロークケアユニット(SCU)に救急搬送された心原性脳塞栓症例の特徴, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1303.	玉井利奈, 西尾進, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 林修司, 三木淳子, 坂東左知子, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 下肢静脈エコー検査におけるD-dimer値の意義, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1304.	西尾進, Hirotsugu Yamada, 玉井利奈, 平田陽一郎, Kenya Kusunose, 冨田紀子, 林修司, 三木淳子, 坂東左知子, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 頸動脈エコーによるプラークの超音波性状カラーイメージの試み, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1305.	前田香代子, Yuka Ueda, 久岡白陽花, Takashi Iwase, 西川幸治, 坂東左知子, 林修司, 竹内秀和, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, 冨田紀子, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Shinjiro Takata, Natsuo Yasui and Masataka Sata : 通院型心臓リハビリテーションの継続における開始3カ月目の重要性, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1306.	西川幸治, Yuka Ueda, 久岡白陽花, 前田香代子, Takashi Iwase, 坂東左知子, 林修司, 竹内秀和, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, 冨田紀子, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Shinjiro Takata, Natsuo Yasui and Masataka Sata : 心臓リハビリによる運動能力改善を阻害する因子の検討, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1307.	佐藤光代, Hirotsugu Yamada, 平岡葉月, 西尾進, 玉井利奈, Kenya Kusunose, 冨田紀子, 林修司, 三木淳子 and Masataka Sata : 動脈硬化指標としてのbaPWVとCAVIの比較, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1308.	太田理絵, Takashi Iwase, 久岡白陽花, Hirotsugu Yamada, Yasuhiko Nishioka, Shoichiro Takao, 坂東左知子, Hayato Nose, Kenya Kusunose, Toshiyuki Niki, 冨田紀子, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Saburo Sone and Masataka Sata : 心室固有調律が心病変診断のきっかけとなったサルコイドーシスの1例, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1309.	原知也, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 林修司, 玉井利奈, 坂東左知子, 久岡白陽花, Toshiyuki Niki, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 心サルコイドーシスにおける左室形態異常の多様性, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1310.	本田壮一, 川井尚臣, 白川光雄, 小原聡彦, Masashi Akaike and Masataka Sata : 急性冠症候群の医療連携―「海部プロジェクト」自験症例より―, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1311.	白川光雄, 本田壮一, 川井尚臣, 山口普史 and Masataka Sata : PT-INR小型測定装置を用い出血性イベントを診断・予防した4例, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1312.	小笠原梢, Toshiyuki Niki, Takeshi Soeki, 坂東左知子, 久岡白陽花, 竹内秀和, Kenya Kusunose, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, 冨田紀子, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 様々な要因によりtorsade de pointesを来した一例, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1313.	久岡白陽花, Yuka Ueda, Takashi Iwase, 前田香代子, 西川幸治, 坂東左知子, 林修司, 竹内秀和, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, 冨田紀子, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Shinjiro Takata, Natsuo Yasui and Masataka Sata : 尿中アルブミン排出量に及ぼす通院心臓リハビリテーションの効果, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1314.	Masataka Sata : 動脈硬化の新知見-Vasa VasorumとEpicardial Adipose Tissue-, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1315.	高島啓, Koji Yamaguchi, Takeshi Soeki, 坂東左知子, 林修司, 久岡白陽花, 冨田紀子, 竹内秀和, Toshiyuki Niki, Kenya Kusunose, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 埋め込み型デバイスにより胸郭内インピーダンスの憎悪と改善が観察できた拡張肥大型心筋症の一例, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1316.	冨田紀子, Hirotsugu Yamada, 西尾進, Kenya Kusunose, 林修司, 玉井利奈, 遠藤桂輔, 平岡葉月, 佐藤光代, 坂東左知子, 久岡白陽花, 竹内秀和, Yuka Ueda, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 超高齢者における大動脈弁硬化の進行に関与する因子についての検討, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1317.	林修司, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 西尾進, 玉井利奈, 三木淳子, 坂東左知子, 久岡白陽花, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : S字状中隔によるdynamic obstructionが胸痛の原因と考えられた高齢者の一例, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1318.	坂東左知子, Takeshi Soeki, 久岡白陽花, 冨田紀子, 竹内秀和, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 房室結節三重伝道路の存在が示唆された房室結節リエントリー性頻拍の1例, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1319.	高島啓, Koji Yamaguchi, 坂東左知子, 林修司, 久岡白陽花, 冨田紀子, 竹内秀和, Toshiyuki Niki, Kenya Kusunose, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Sumiko Yoshida, Toshio Matsumoto and Masataka Sata : 甲状腺機能亢進症と腰痛が発症の誘因と考えられた難治性冠攣縮性狭心症の1例, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1320.	Tatsuo Motoki, 平田陽一郎, Hirotsugu Kurobe, 菅澤典子, 中山泰介, Mikio Sugano, Tamotsu Kanbara, Takashi Kitaichi, Masataka Sata and Tetsuya Kitagawa : ピオグリタゾン投与による腹部大動脈瘤における坑動脈硬化作用の検討, 第98回日本循環器学会中国・四国合同地方会, May 2011.
1321.	外磯千智, Takashi Iwase, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, Masashi Akaike, Shoichiro Takao and Masafumi Harada : 心臓MRI検査で左室に広範なガドリニウム異常集積を認めたNoonan syndromeの1例, 第104回日本内科学会四国地方会, May 2011.
1322.	安積麻衣, Takashi Iwase, Toshiyuki Niki, Tetsuzo Wakatsuki, Masataka Sata, Masashi Akaike, Shoichiro Takao, Masafumi Harada, Yasuhiko Nishioka and Saburo Sone : 眼，肺，筋病変に続いて経過中に新病変の顕在化を認めたサルコイドーシスの一例, 第104回日本内科学会四国地方会, May 2011.
1323.	Ken-ichi Aihara, Sumiko Yoshida, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : フェノフィブラートはアンジオテンシンⅡ負荷による高血圧と心筋リモデリングを抑制する, 第84回日本内分泌学会学術総会, Apr. 2011.
1324.	Hirotsugu Kurobe, 平田陽一郎, 西雄千佳, 東田真由子, 松岡祐貴, Masashi Akaike, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : GLP-1 receptor agonist が血管リモデリングに与える影響の検討, 第84回日本内分泌学会学術総会, Apr. 2011.
1325.	Masashi Akaike, Ken-ichi Aihara, Yasumasa Ikeda, Shusuke Yagi, 石川カズ江, Sumiko Yoshida, Yuka Ueda, Takashi Iwase, Masataka Sata and Toshio Matsumoto : グルココルチコイド誘発性血管内皮細胞障害に対するアルドステロン受容体拮抗薬の効果, 第84回日本内分泌学会学術総会, Apr. 2011.
1326.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : エイコサペントエン酸は酸化ストレス抑制を介してアンジオテンシンⅡ刺激による心血管リモデリングを抑制する, 第84回日本内分泌学会学術総会, Apr. 2011.
1327.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : 虚血ストレスによる骨格筋アポトーシスおよび血管新生におけるアンドロゲン受容体の意義, 第84回日本内分泌学会学術総会, Apr. 2011.
1328.	Hirotsugu Kurobe, Ken-ichi Aihara, 平田陽一郎, 西矢昌子, 中山泰介, Tatsuo Motoki, Mikio Sugano, Tamotsu Kanbara, Takashi Kitaichi, Masashi Akaike, Masataka Sata, Tetsuya Kitagawa and Toshio Matsumoto : エゼチミブ投与による脂質代謝および血管機能改善効果の検討, 第84回日本内分泌学会学術総会, Apr. 2011.
1329.	冨田紀子, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 林修司, 玉井利奈, 遠藤桂輔, 河野裕美, 平岡葉月, 佐藤光代, Yoshio Taketani, Takeshi Soeki and Masataka Sata : 高齢者における大動脈弁硬化の進行に関与する因子についての検討, 第22回日本心エコー図学会学術集会, Apr. 2011.
1330.	林修司, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 玉井利奈, 冨田紀子, 遠藤桂輔, 河野裕美, 平岡葉月, 佐藤光代, Yoshio Taketani, Takeshi Soeki and Masataka Sata : 徐脈を呈する高齢者の左室弛緩能についての検討:僧帽弁口血流速パターンをどう解釈するか, 第22回日本心エコー図学会学術集会, Apr. 2011.
1331.	清水拓, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 林修司, 玉井利奈, 遠藤桂輔, 河野裕美, 平岡葉月, 佐藤光代, Yoshio Taketani, Takeshi Soeki and Masataka Sata : 運動負荷心エコー法を用いた膠原病例における潜在性肺動脈性肺高血圧症の検出, 第22回日本心エコー図学会学術集会, Apr. 2011.
1332.	Yoshio Taketani, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 冨田紀子, 林修司, 玉井利奈, 遠藤桂輔, 河野裕美, 平岡葉月, 佐藤光代, Takeshi Soeki and Masataka Sata : 三次元心エコー法により術前診断ができたペースメーカーリードの弁尖穿通による重症三尖弁逆流の一例, 第22回日本心エコー図学会学術集会, Apr. 2011.
1333.	玉井利奈, Hirotsugu Yamada, 西尾進, Kenya Kusunose, 冨田紀子, 林修司, 遠藤桂輔, 河野裕美, 平岡葉月, 佐藤光代, Yoshio Taketani, Takeshi Soeki and Masataka Sata : 心エコー検査で診断された肺高血圧症連続387例の基礎疾患と三尖弁輪運動速波形指標, 第22回日本心エコー図学会学術集会, Apr. 2011.
1334.	西尾進, Hirotsugu Yamada, 玉井利奈, 林修司, 遠藤桂輔, 清水拓, 高島弘光, 山中森晶, 不動祐司, 酒井芳紀 and Masataka Sata : モノクロタリン誘発性イヌ肺高血圧モデルにおけるMモード法およびスペックストラッキング法を用いた右室収縮能の検討, 第22回日本心エコー図学会学術集会, Apr. 2011.
1335.	高島啓, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 冨田紀子, 林修司, 遠藤桂輔, 玉井利奈, 河野裕美, 平岡葉月, 佐藤光代, Yoshio Taketani, Takeshi Soeki and Masataka Sata : リアルタイム3次元経食道心エコーガイド下に経皮的僧帽弁交連切開術を行った僧帽弁狭窄症の1例, 第22回日本心エコー図学会学術集会, Apr. 2011.
1336.	Hirotsugu Yamada, 遠藤桂輔, 西尾進, Kenya Kusunose, 冨田紀子, 林修司, 玉井利奈, 河野裕美, 平岡葉月, 佐藤光代, Yoshio Taketani, Takeshi Soeki and Masataka Sata : 陳旧性心筋梗塞症におけるV1誘導のP terminal forceの臨床的意義: 心エコー・ドプラ法を用いた検討, 第22回日本心エコー図学会学術集会, Apr. 2011.
1337.	Yasumasa Ikeda, Ken-ichi Aihara, Masashi Akaike, Sumiko Yoshida, Takashi Iwase, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Masataka Sata, Toshio Matsumoto and Toshiaki Tamaki : Heparin cofactor II enhances vascular endothelial cells function and angiogenesis, 第75回日本循環器学会総会・学術集会, Mar. 2011.
1338.	S. Bando, Takeshi Soeki, Toshiyuki Niki, Y. Hirata, N. Tomita, H. Takeuchi, Kenya Kusunose, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Plasma Brain Natriuretic Peptide (BNP) Level is Elevated in Patients with Cancer., 第75回日本循環器学会総会・学術集会, Mar. 2011.
1339.	Takeshi Soeki, Toshiyuki Niki, Koji Yamaguchi, S. Bando, Yuka Ueda, N. Tomita, Takayuki Ise, Kenya Kusunose, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike, Michio Shimabukuro and Masataka Sata : Inflammatory Biomarkers as Predictors of Vulnerable Coronary Plaques., 第76回日本循環器学会学術集会，Symposium 3, Mar. 2011.
1340.	C. Nishio, M. Higashida, Y. Hirata, Hirotsugu Kurobe, Masashi Akaike, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : GLP-1 Receptor Agonist Attenuates Vascular Remodeling after Endovascular Injury., 第75回日本循環器学会総会・学術集会, Mar. 2011.
1341.	M. Higashida, C. Nishio, Y. Hirata, Hirotsugu Kurobe, Masashi Akaike, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : HMGB1 Plays a Critical Role in Chronic Inflammation and Vascular Remodeling after Endovascular Injury., 第75回日本循環器学会総会・学術集会, Mar. 2011.
1342.	Y. Higashikuni, K. Nakamura, M. Takaoka, S. Enomoto, H. Iwata, M. Sahara, K. Tanaka, R. Nagai and Masataka Sata : The ATP-Binding Cassette Transporter ABCG2 Plays a Protective Role in Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure., 第75回日本循環器学会総会・学術集会, Mar. 2011.
1343.	Y. Higashikuni, K. Nakamura, M. Takaoka, S. Enomoto, H. Iwata, M. Sahara, K. Tanaka, R. Nagai and Masataka Sata : Combination Therapy of Aliskiren and Valsartan Exerts Synergistic Protective Effects against Ventricular Remodeling after Myocardial Infarction in Mice., 第75回日本循環器学会総会・学術集会, Mar. 2011.
1344.	S. Nishio, Hirotsugu Yamada, Kenya Kusunose, N. Tomita, S. Hayashi, K. Endo, R. Tamai, J. Miki, S. Bando, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Which Noninvasive Vascular Index is the Best Predictor of the Severity of Coronary Atherosclerosis?, 第75回日本循環器学会総会・学術集会, Mar. 2011.
1345.	S. Hayashi, Hirotsugu Yamada, S. Nishio, N. Tomita, Kenya Kusunose, K. Endo, R. Tamai, S. Bando, S. Hisaoka, H. Takeuchi, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Tricuspid Annular Motion Velocity in Left Ventricular Hypertrophy: Comparison between Hypertensive Heart Disease and Hypertrophic Cardiomyopathy., 第75回日本循環器学会総会・学術集会, Mar. 2011.
1346.	H. Takeuchi and Masataka Sata : Serum HDL-C, ApoA1 and ApoA2 have Negative Relation to BNP, Which Might Mean High ApoA2 Might Improve Heart Function., 第75回日本循環器学会総会・学術集会, Mar. 2011.
1347.	Toshiyuki Niki, Takeshi Soeki, S. Bando, Kenya Kusunose, S. Hisaoka, S. Hayashi, Yuka Ueda, S. Tomita, H. Takeuchi, Takashi Iwase, Yoshio Taketani, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Role of Circulating High-Mobility Group Box-1 (HMGB1) in Patients with Coronary Artery Disease., 第75回日本循環器学会総会・学術集会, Mar. 2011.
1348.	Kenya Kusunose, Hirotsugu Yamada, N. Tomita, S. Nishio, S. Bando, S. Hisaoka, S. Hayashi, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Clinical Efficacy of Beat-to-beat Variability of Diastolic Filling in Atrial Fibrillation., 第75回日本循環器学会総会・学術集会, Mar. 2011.
1349.	Koji Yamaguchi, Tetsuzo Wakatsuki, Toshiyuki Niki, Koji Yamaguchi, S. Bando, S. Hisaoka, S. Hayashi, Yuka Ueda, N. Tomita, H. Takeuchi, Kenya Kusunose, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Masashi Akaike and Masataka Sata : Local Persistent Coagulative Response to Zotarolimus-eluting, Sirolimus-eluting and Bare-metal Stents Implanted in Patients with Stable Angina., 第75回日本循環器学会総会・学術集会, Mar. 2011.
1350.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, S. Bando, S. Hisaoka, Toshiyuki Niki, Kenya Kusunose, N Tomita, Y. Hirata, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Ken-ichi Aihara, M. Harada and Masataka Sata : Diagnostic Utility of Cardiac Magnetic Resonance for Prediction of Cardiac Events in Patients with Hypertrophic Cardiomyopathy., 第75回日本循環器学会総会・学術集会, Mar. 2011.
1351.	Hirotsugu Yamada, Masataka Sata and T. Oki : Diagnosis of Heart Failure with Preserved Ejection Fraction by Doppler Echocardiography., 第75回日本循環器学会総会・学術集会, Mar. 2011.
1352.	Tetsuzo Wakatsuki, Koji Yamaguchi, Yoshio Taketani, Toshiyuki Niki, Kenya Kusunose, N. Tomita, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : Analysis of Tissue Characteristics of In-Stent Restenotic Lesion 5-Years after Coronary Stenting with Drug-Eluting Stent Using Integrated Backscatter Intravascular Ultrasound., 第75回日本循環器学会総会・学術集会, Mar. 2011.
1353.	Masataka Sata : Potential Role of Epicardial Adipose Tissue in the Pathogenesis of Coronary Atherosclerosis., 第75回日本循環器学会総会・学術集会, Mar. 2011.
1354.	Masataka Sata : Orally Administered Eicosapentaenoic Acid Reduces and Stabilizes Atherosclerotic Lesions., 第75回日本循環器学会総会・学術集会, Mar. 2011.
1355.	Masataka Sata : PCI専門医に求められる術後管理''生命予後改善にむけたPCIと薬物のハイブリッド療法, 第75回日本循環器学会総会・学術集会, Mar. 2011.
1356.	高柳友貴, Toshiyuki Niki, 坂東左知子, 久岡白陽花, 林修司, Yuka Ueda, 冨田紀子, 竹内秀和, Kenya Kusunose, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masataka Sata, 中山泰介, Tetsuya Kitagawa and 村野栄一 : ペースメーカーリードの弁尖穿通による重症三尖弁逆流症の一例, 第242回徳島医学会学術集会，平成22年度冬期, Feb. 2011.
1357.	坂東美佳, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, 竹内秀和, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masataka Sata, Hayato Nose, Hideki Otsuka and Masafumi Harada : 拡張型心筋症として診断・加療されていた心サルコイドーシスの一例, 第242回徳島医学会学術集会，平成22年度冬期, Feb. 2011.
1358.	末広英也, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 坂東左知子, 久岡白陽花, 林修司, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masataka Sata, Hayato Nose, Hideki Otsuka, Shoichiro Takao and Masafumi Harada : 心サルコイドーシスにおける左室形態異常の多様性, 第242回徳島医学会学術集会，平成22年度冬期, Feb. 2011.
1359.	太田理絵, 冨田紀子, Kenya Kusunose, 坂東左知子, 久岡白陽花, 林修司, 竹内秀和, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masataka Sata, 木村建彦, 西内健, Hirotsugu Kurobe and Tetsuya Kitagawa : 出産後の甲状腺機能亢進症が発見の契機となったLeft Main Coronary Trunk Compression Syndromeの一例, 第242回徳島医学会学術集会，平成22年度冬期, Feb. 2011.
1360.	髙島啓, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 坂東左知子, 久岡白陽花, 林修司, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masataka Sata, 竹崎彰夫, Hiroya Tada and Saburo Sone : コントラスト心エコー法で診断できたHepatopulmonary Syndromeの1例, 第242回徳島医学会学術集会，平成22年度冬期, Feb. 2011.
1361.	清水拓, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 玉井利奈, 遠藤桂輔, 佐藤光代, 河野裕美, Masashi Akaike and Masataka Sata : 運動負荷心エコー法を用いた膠原病例における潜在性肺動脈性高血圧症の検出, 第242回徳島医学会学術集会，平成22年度冬期, Feb. 2011.
1362.	Reiko Okahisa, Toshiko Tada, Chieko Fujii, Yasuko Matsushita and Masataka Sata : 高血圧予防をテーマにした市民公開講座参加者の保健行動について, 第242回徳島医学会学術集会，平成22年度冬期, Feb. 2011.
1363.	竹内秀和, 久岡白陽花, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Takeshi Soeki, Masashi Akaike and Masataka Sata : Fibrinogen relates to free triiodothyronin (FT3) negatively, which might be regulated via Hdac3., 第97回日本循環器学会四国地方会, Feb. 2011.
1364.	平田陽一郎, Tatsuo Motoki, Hirotsugu Kurobe, Masashi Akaike, 田端実, 高梨秀一郎, Tetsuya Kitagawa and Masataka Sata : 心臓周囲脂肪組織における炎症性サイトカインの発見と冠動脈病変の関連, 第40回日本心脈管作動物質学会, Feb. 2011.
1365.	東田真由子, 西雄千佳, 松岡祐貴, 平田陽一郎, Hirotsugu Kurobe, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : 血管モデリングにおけるHMGB1の果たす役割, 第40回日本心脈管作動物質学会, Feb. 2011.
1366.	Hirotsugu Yamada, 玉井利奈, 清水拓, 西尾進, Takashi Iwase, Kenya Kusunose, 遠藤桂輔, Masashi Akaike, Masataka Sata and Shusuke Yagi : 膠原病と肺高血圧, 肺高血圧症とエンドセリン学術講演会, Dec. 2010.
1367.	小笠原梢, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, 竹崎彰夫, 多田浩也, Saburo Sone and Masataka Sata : コントラスト心エコー法で診断できたHepatopulmonary Syndromeの1例, 第97回日本循環器学会四国地方会, Dec. 2010.
1368.	坂東左知子, Takeshi Soeki, Toshiyuki Niki, 久岡白陽花, 平田陽一郎, 冨田紀子, 竹内秀和, Kenya Kusunose, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takashi Iwase, Masashi Akaike and Masataka Sata : 二種類の上室性頻拍出が認められた例, 第97回日本循環器学会四国地方会, Dec. 2010.
1369.	高柳友貴, Toshiyuki Niki, Hirotsugu Yamada, Kenya Kusunose, Koji Yamaguchi, Takashi Iwase, 冨田紀子, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : ペースメーカーリードの弁尖穿通による重症三尖弁逆流症の1例, 第97回日本循環器学会四国地方会, Dec. 2010.
1370.	竹内秀和 and Masataka Sata : ApoA1 is strongly associated with ApoA2. And HDL-C has stronger relations to ApoA1 than ApoA2., 第97回日本循環器学会四国地方会, Dec. 2010.
1371.	竹内秀和, 平田陽一郎, 冨田紀子, Kenya Kusunose, Yoshio Taketani, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : HDL-C interacts to EPA positively,which might mean HDL-C regulates EPA via SREBP., 第97回日本循環器学会四国地方会, Dec. 2010.
1372.	竹内秀和 and Masataka Sata : Identifying putative AP2alpha binding site in human PTEN promoter by genome comparison., 第97回日本循環器学会四国地方会, Dec. 2010.
1373.	坂東美佳, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, 竹内秀和, 竹谷義雄, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 心サルコイドーシスの1例, 第97回日本循環器学会四国地方会, Dec. 2010.
1374.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : アンドロゲン受容体は虚血後骨格筋細胞のアポトーシスと血管新生を制御する, 第18回日本血管生物医学会学術集会, Dec. 2010.
1375.	平田陽一郎, Tatsuo Motoki, Hirotsugu Kurobe, Masashi Akaike, 田端実, 高梨秀一郎 and Masataka Sata : Macrophages shift toward inflammatory state in epicardial fat of patients with coronary artery disease., 第18回日本血管生物医学会学術集会, Dec. 2010.
1376.	西雄千佳, 東田真由子, 松岡裕貴, 平田陽一郎, Hirotsugu Kurobe, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : GLP-1 receptor agonist の血管リモデリングに与える影響の検討, 第18回日本血管生物医学会学術集会, Dec. 2010.
1377.	松岡裕貴, Hirotsugu Kurobe, 平田陽一郎, Hirotsugu Kurobe, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : 大動脈瘤モデルの作製とその評価系の確立, 第18回日本血管生物医学会学術集会, Dec. 2010.
1378.	東田真由子, 西雄千佳, 松岡裕貴, 平田陽一郎, Hirotsugu Kurobe, Yutaka Nakaya, Tetsuya Kitagawa and Masataka Sata : 血管リモデリングにおけるHMGB1の果たす役割, 第18回日本血管生物医学会学術集会, Dec. 2010.
1379.	Masataka Sata : Atherosclerosis, Angiogenesis and Sex hormones., 第18回日本血管生物医学会学術集会, Dec. 2010.
1380.	末広英也, Kenya Kusunose, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 心室中隔肥厚を認めた心サルコイドーシスの1例, 第103回日本内科学会四国地方会, Nov. 2010.
1381.	山崎宙, Koji Yamaguchi, Kenya Kusunose, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 趾間部のマダニ咬傷後に足趾血行不良から壊死に陥った1例, 第103回日本内科学会四国地方会, Nov. 2010.
1382.	玉井利奈, 遠藤桂輔, Hirotsugu Yamada, Masataka Sata, 西尾進, 河野裕美, 平岡葉月 and 佐藤光代 : 下肢陽圧負荷心エコー検査の臨床応用∼肥大型心筋症の2例∼, 第43回中国四国医学検査学会, Nov. 2010.
1383.	遠藤桂輔, 斉藤憲, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 西尾進, 林修司, Takeshi Soeki, Masashi Akaike and Masataka Sata : 高度僧帽弁輪石灰化による多発性脳梗塞の1例, 第20回日本超音波医学会四国地方会学術集会, Oct. 2010.
1384.	太田理恵, 冨田紀子, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 遠藤桂輔, 佐藤光代, Takeshi Soeki, Masashi Akaike and Masataka Sata : 産後の甲状腺機能亢進が診断の契機となったLeft Main Coronary Trunk Compression Syndromeの一例, 第20回日本超音波医学会四国地方会学術集会, Oct. 2010.
1385.	河野裕美, Hirotsugu Yamada, 佐藤光代, 西尾進, 冨田紀子, 遠藤桂輔, Kenya Kusunose, Takeshi Soeki, Masashi Akaike and Masataka Sata : Intramural hematoma(IMH)を呈したStanford B型大動脈解離の二例, 第20回日本超音波医学会四国地方会学術集会, Oct. 2010.
1386.	玉井利奈, Hirotsugu Yamada, 西尾進, 遠藤桂輔, Toshiyuki Niki, Kenya Kusunose, 冨田紀子, Takeshi Soeki, Masashi Akaike and Masataka Sata : 三次元心エコー法により術前診断ができたペースメーカーリードの弁尖穿通による重症三尖弁逆流の一例, 第20回日本超音波医学会四国地方会学術集会, Oct. 2010.
1387.	林修司, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 冨田紀子, 遠藤桂輔, 玉井利奈, Takeshi Soeki, Masashi Akaike and Masataka Sata : 徐脈の高齢者において僧帽弁口血流波形がE>Aを呈するメカニズムについての検討, 第20回日本超音波医学会四国地方会学術集会, Oct. 2010.
1388.	清水拓, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 玉井利奈, 遠藤桂輔, 佐藤光代, 河野裕美, Masashi Akaike and Masataka Sata : 運動負荷心エコー法を用いた膠原病例における潜在性肺動脈性肺高血圧症の検出, 第20回日本超音波医学会四国地方会学術集会, Oct. 2010.
1389.	末広英也, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 佐藤光代, 冨田紀子, 玉井利奈, 遠藤桂輔, Masashi Akaike and Masataka Sata : 心室中隔肥厚を認めた心サルコイドーシスの1例, 第20回日本超音波医学会四国地方会学術集会, Oct. 2010.
1390.	Masashi Akaike, Shusuke Yagi, Ken-ichi Aihara, 石川カズ江, Yasumasa Ikeda, Sumiko Yoshida, Yuka Ueda, Takashi Iwase, Toshio Matsumoto and Masataka Sata : ピタバスタチンによる血管内皮細胞での一酸化窒素合成酵素の発現亢進作用とその機序の検討, 第33回日本高血圧学会総会, 390, Oct. 2010. (Keyword) 血管内皮高血圧(薬物療法) Pitavastatin(治療的利用,薬理学) 内皮細胞 *Nitric Oxide Synthase Type III ヒト
1391.	市岡誠之, 菅波孝祥, 津田直人, 田中都, 白川伊吹, 平田陽一郎, 宮本恵宏, Masataka Sata, 亀井康富 and 小川佳宏 : 肥満の脂肪組織における新たな炎症関連遺伝子の探索, 第31回日本肥満学会, Oct. 2010.
1392.	Hirotsugu Yamada, 三代裕一郎, Kenya Kusunose, Toshiyuki Niki, 林修司, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 高齢者および壮年者における高圧利尿薬インダパミドの少量追加投与の有効性と安全性-連日投与と隔日投与の比較-, 第33回日本高血圧学会総会, Oct. 2010.
1393.	H. Takeuchi and Masataka Sata : Serum HDL-C is Positively Related to CVRR as an Index of ANS, which Relation is Attenuated by Rosuvastatin., 第14回日本心不全学会学術集会, Oct. 2010.
1394.	H. Takeuchi and Masataka Sata : CRP Positively Interacts with Microalbuminuria,which Represent CRP Might Regulate the Microalubuminuria,which Interaction is Weakly Attenuated by Carvedilol., 第14回日本心不全学会学術集会, Oct. 2010.
1395.	H. Takeuchi and Masataka Sata : CRP has Significant Relation to Pulse Wave Velocity(PWV)in the Cardiovascular Patients, But BNP haz No Significant Relation., 第14回日本心不全学会学術集会, Oct. 2010.
1396.	Koji Yamaguchi, Tetsuzo Wakatsuki, 坂東左知子, 久岡白陽花, Toshiyuki Niki, Kenya Kusunose, 冨田紀子, 竹内秀和, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike, Masataka Sata and 麻植塚浩康 : 冠動脈プラークに対する薬剤多面的効果の検討-Integrated backscatter IVUS観察による観点から-, 第58回日本心臓病学会学術集会, Sep. 2010.
1397.	Koji Yamaguchi, Tetsuzo Wakatsuki, Toshiyuki Niki, Kenya Kusunose, 竹谷善雄 and Masataka Sata : スタチンによる冠動脈ステント植え込み後edge部性状の短絡的変化の検討―IB-IVUSにて観察した二例―, 第17回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2010.
1398.	門田宗之, Tetsuzo Wakatsuki, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani and Masataka Sata : 繰り返す心不全と維持透析導入から離脱しえた腎動脈狭窄症の一例, 第17回日本心血管インターベンション治療学会中国・四国地方会, Sep. 2010.
1399.	Tetsuzo Wakatsuki, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : 薬剤溶出ステントによる冠動脈内皮機能障害の経年変化に関する検討, 第58回日本心臓病学会学術集会, Sep. 2010.
1400.	冨田紀子, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 林修司, 遠藤桂輔, 河野裕美, 平岡葉月, 佐藤光代, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : S字状中隔を呈する例の心エコー・ドプラ所見についての検討, 第58回日本心臓病学会学術集会, Sep. 2010.
1401.	坂東左知子, Takeshi Soeki, Toshiyuki Niki, 久岡白陽花, 竹内秀和, 平田陽一郎, 冨田紀子, Kenya Kusunose, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 脳性ナトリウム利尿ペプチド(BNP)と癌との関係について, 第58回日本心臓病学会学術集会, Sep. 2010.
1402.	竹内秀和 and Masataka Sata : Serum ApoA1 and ApoA2 Have Positive Relation to ANP, but ApoB Has no Relation., 第58回日本心臓病学会学術集会, Sep. 2010.
1403.	竹内秀和 and Masataka Sata : Serum ANP is Negatively Related to the CVRR as an Index of ANS, which Relation is Diminished by Rosuvastatin., 第58回日本心臓病学会学術集会, Sep. 2010.
1404.	Takeshi Soeki, Toshiyuki Niki, 坂東左知子, 久岡白陽花, 竹内秀和, Kenya Kusunose, 冨田紀子, 平田陽一郎, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike, Kenji Kangawa and Masataka Sata : グレリンの心臓自律神経への作用と心血管系における意義, 第58回日本心臓病学会学術集会, Sep. 2010.
1405.	林修司, Hirotsugu Yamada, 中田拓史, Kenya Kusunose, 西尾進, 冨田紀子, 玉井利奈, 遠藤桂輔, 河野裕美, 平岡葉月, 佐藤光代, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 僧帽弁口血流速波形用いた左室拡張能評価の限界:E>Aパターンを呈する高齢者での検討, 第58回日本心臓病学会学術集会, Sep. 2010.
1406.	遠藤桂輔, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 冨田紀子, 三木淳子, 林修司, 玉井利奈, 河野裕美, 平岡葉月, 佐藤光代, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Ken Saito and Masataka Sata : EPA/AA比は冠動脈疾患の重症度に相関する:徳島大学病院循環器内科データベースを用いた検討, 第58回日本心臓病学会学術集会, Sep. 2010.
1407.	Toshiyuki Niki, Tetsuzo Wakatsuki, Koji Yamaguchi, Kenya Kusunose, Yoshio Taketani, Takashi Iwase, 冨田紀子, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : 薬剤溶出ステント植え込み慢性期における冠動脈局所凝固異常に対するスタチンの効果, 第58回日本心臓病学会学術集会, Sep. 2010.
1408.	冨田紀子, Kenya Kusunose, 玉井利奈, 遠藤桂輔, 西尾進, 三木淳子, 林修司, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, 若槻哲三, Masashi Akaike and Masataka Sata : 出産後の甲状腺機能亢進症が発見の契機となったLeft Main Coronary Trunk Compression Syndromeの一例, 第58回日本心臓病学会学術集会, Sep. 2010.
1409.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 玉井利奈, 遠藤桂輔, 三木淳子, 坂東左知子, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 拡張型心筋症の左室内同期不全に対する前負荷増大の影響:3次元心エコー法を用いた検討, 第58回日本心臓病学会学術集会, Sep. 2010.
1410.	玉井利奈, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 冨田紀子, 三木淳子, 林修司, 遠藤桂輔, 河野裕美, 平岡葉月, 佐藤光代, Takashi Iwase, 添木武, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 下肢陽圧負荷心エコー法が臨床的に有用であった肥大型心筋症の2例, 第58回日本心臓病学会学術集会, Sep. 2010.
1411.	西尾進, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 林修司, 玉井利奈, 遠藤桂輔, 三木淳子, 竹崎彰夫, Hiroya Tada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Saburo Sone and Masataka Sata : コントラスト心エコー法で診断できたHepatopulmonary Syndoromeの1例, 第58回日本心臓病学会学術集会, Sep. 2010.
1412.	Hirata Yoichiro, Tatsuo Motoki, Hirotsugu Kurobe, Masashi Akaike, Tabata Minoru, Takanashi Shuichiro, Igarashi Takashi, Tetsuya Kitagawa and Masataka Sata : Macrophage Polarization in Epicardial Adipose Tissue Enhances Atherosclerosis of Human Coronary Arteries., The58th Annual Scientific Session of the Japanese College of Cardiology, Sep. 2010.
1413.	門田宗之, Kenya Kusunose, 竹谷善雄, 坂東左知子, 久岡白陽花, Toshiyuki Niki, 冨田紀子, 竹内秀和, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 繰り返す心不全と維持透析導入から離脱しえた腎動脈狭窄症の一例, 第241回徳島医学会学術集会(平成22年度夏期), Aug. 2010.
1414.	阿部容子, Takeshi Soeki, 仁木敏之, Kenya Kusunose, 平田陽一郎, 冨田紀子, 山口浩司, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masataka Sata, 坂東正章 and 清水渉 : KCNH2遺伝子にダブル異変を認めた先天性QT延長症候群の兄弟例, 第241回徳島医学会学術集会(平成22年度夏期), Aug. 2010.
1415.	山崎宙, Koji Yamaguchi, 坂東左知子, 久岡白陽花, Toshiyuki Niki, Kenya Kusunose, 冨田紀子, 竹内秀和, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, 福永豊 and Hideki Nakanishi : 趾間部のマダニ咬傷後に足趾血行不良から壊死に陥った1例, 第241回徳島医学会学術集会(平成22年度夏期), Aug. 2010.
1416.	Masataka Sata : 冠動脈疾患の病態解明と新しい診断治療技術の開発, 第241回徳島医学会学術集会(平成22年度夏期),教授就任記念講演, Aug. 2010.
1417.	Koji Yamaguchi, Tetsuzo Wakatsuki, Kenya Kusunose, Toshiyuki Niki, Yoshio Taketani and Masataka Sata : Two cases showing stabilization of coronary plaques in stent edge after statin therapy assessed by integrated backscatter intravascular ultrasound., 第19回日本心血管インターベンション治療学会, Aug. 2010.
1418.	Masataka Sata : Orally administered eicosapentaenoic acid reduces and stabilizes atherosclerotic lesions., 第42回日本動脈硬化学会総会・学術集会，シンポジウム, Jul. 2010.
1419.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : A role of androgen receptor in ischemia-induced tissue damage and angiogenesis in male, 第42回日本動脈硬化学会総会・学術集会長良川国際会議場, Jul. 2010.
1420.	太田理絵, Toshiyuki Niki, Takashi Iwase, 坂東左知子, 久岡白陽花, Kenya Kusunose, Yuka Ueda, 冨田紀子, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, Masafumi Harada and Shoichiro Takao : 軽微な臨床経過にもかかわらず心臓MRI検査にて異常所見を認めた急性心筋炎の1例, 第241回徳島医学会学術集会(平成22年度夏期), Jul. 2010.
1421.	S. Keneyama, Masataka Sata and A. Miyazaki : Hic-5 deficiency enhances mechanosensitive apoptosis and modulates vascular remodeling., 第42回日本動脈硬化学会総会・学術集会, Jul. 2010.
1422.	Y. Sumiko, Ken-ichi Aihara, T. Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : A role of androgen receptor in iscchemia-induced tissue damage and angiogenesis in male., 第42回日本動脈硬化学会総会・学術集会, Jul. 2010.
1423.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : アンドロゲンーアンドロゲン受容体系は下肢虚血における組織傷害防御と血管新生に必須である, 2010 年度(第 52 回)日本老年医学会学術集会神戸国際会議場・神戸商工会議所・神戸ポートピアホテル, Jun. 2010.
1424.	Hirotsugu Kurobe, 菅野幹雄, Tamotsu Kanbara, Kenya Kusunose, Hirohisa Ogawa, Tatsuo Motoki, Homare Yoshida, 中山泰介, Takashi Kitaichi, Keisuke Izumi, Masataka Sata and Tetsuya Kitagawa : 前屈位にて胸苦を自覚し発見された高齢者での巨大左房腫瘍の一例, 関西胸部学会学術集会, Jun. 2010.
1425.	Hirotsugu Kurobe, Tamotsu Kanbara, Koji Yamaguchi, Tatsuo Motoki, 菅野幹雄, 中山泰介, Takashi Kitaichi, Masataka Sata and Tetsuya Kitagawa : Parkes Weber症候群様所見を認めた1例, 第30回静脈学会総会, Jun. 2010.
1426.	Masataka Sata : EPAを用いた心血管イベント抑制-動脈硬化に関する新知見とn-3脂肪酸の多面的作用-, 北海道EPAシンポジウム, Jun. 2010.
1427.	小笠原梢, 仁木敏之, Kenya Kusunose, Koji Yamaguchi, Kunihiko Koshiba, 冨田紀子, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Takeshi Soeki, Masashi Akaike, Masataka Sata and Tetsuya Kitagawa : IgA腎症ともやもや病を合併した若年発症の感染性心内膜炎の一例, 第96回日本循環器学会中国・四国合同地方会, Jun. 2010.
1428.	岩河早保, Kenya Kusunose, Takashi Iwase, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, 冨田紀子, Yoshio Taketani, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike, Masataka Sata, 橋詰俊二, 木村建彦 and 西内健 : 出産後left main compression syndromeによる狭心症を発症した心内膜床欠損(不完全型)の1例, 第96回日本循環器学会中国・四国合同地方会, Jun. 2010.
1429.	坂東美佳, Koji Yamaguchi, Takashi Iwase, Kenya Kusunose, 仁木敏之, 冨田紀子, Kunihiko Koshiba, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 高度拡張不全による心不全症状の再燃を認めた心尖部肥大型心筋症の1例, 第96回日本循環器学会中国・四国合同地方会, Jun. 2010.
1430.	阿部容子, Takeshi Soeki, 仁木敏之, Kenya Kusunose, 平田陽一郎, 冨田紀子, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike, 坂東正章, 清水渉 and Masataka Sata : KCNH2遺伝子にダブル変異を認めた先天性QT延長症候群の1例, 第96回日本循環器学会中国・四国合同地方会, Jun. 2010.
1431.	Kenya Kusunose, Yoshio Taketani, 西尾進, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Takashi Iwase, 冨田紀子, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 右腎癌摘出後に心不全を繰り返した腎動脈狭窄症の一例, 第96回日本循環器学会中国・四国合同地方会, Jun. 2010.
1432.	仁木敏之, Takeshi Soeki, Kenya Kusunose, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Takashi Iwase, 冨田紀子, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 心電図異常が乏しいBrugada症候群の1例, 第96回日本循環器学会中国・四国合同地方会, Jun. 2010.
1433.	Masataka Sata : イベント抑制にむけた脂質異常症対策の新展開-動脈硬化の仕組みからの考察-, 日本医師会障害教育講座脂質異常症治療学術講演会，特別講演, Jun. 2010.
1434.	Masataka Sata : 動脈硬化と炎症，免疫，脂肪, 日本食品免疫学会第6回学術大会,シンポジウム, Jun. 2010.
1435.	Masataka Sata : 虚血性心疾患の臨床-診断と治療，予防に関する最近の話題-, 日本内科学会四国支部主催第42回生涯教育講演会, May 2010.
1436.	鹿草宏, 仁木敏之, Kenya Kusunose, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 急性大動脈解離の1例, 日本内科学会第102回四国地方会, May 2010.
1437.	原知也, 仁木敏之, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masataka Sata and 関啓 : 大動脈二尖弁における感染性心内膜炎に合併した大動脈弁輪周囲膿瘍の1例, 日本内科学会第102回四国地方会, May 2010.
1438.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 林修司, 河野裕美, 佐藤光代, Takeshi Soeki, Masashi Akaike and Masataka Sata : 虚血の診断に有用な指標は何か?, 日本超音波医学会第83回学術集会, May 2010.
1439.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 林修司, 河野裕美, 佐藤光代, Takeshi Soeki, Masashi Akaike and Masataka Sata : 卵円孔開存の診断におけるコントラストリアルタイム3次元経食道心エコー法の有用性, 日本超音波医学会第83回学術集会, May 2010.
1440.	Hirotsugu Yamada, Kenya Kusunose, 西尾進, Masataka Sata and 大木崇 : 肺静脈血流速波形の意義, 日本超音波医学会第83回学術集会, May 2010.
1441.	高島弘光, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 冨田紀子, 三村千尋, 佐藤光代, Takeshi Soeki, Masashi Akaike and Masataka Sata : 大動脈弁硬化における頸動脈の動脈硬化所見の検討, 日本超音波医学会第83回学術集会, May 2010.
1442.	Hirotsugu Yamada, Kenya Kusunose, 西尾進, 河野裕美, 佐藤光代, 冨田紀子, 林修司, Takeshi Soeki, Masashi Akaike and Masataka Sata : 下肢陽圧負荷時の僧帽弁口血流速波形の反応性を用いた軽症心不全患者の予後予測:''前負荷ストレス心エコー法''の臨床応用, 日本超音波医学会第83回学術集会, May 2010.
1443.	Masataka Sata : 糖尿病性大血管病抑制に向けたVascular Protection, 第53回日本糖尿病学会年次学術集会イブニングセミナー, May 2010.
1444.	Asuka Shiota, Yutaka Taketani, 田中輝実, Masataka Sata, Hironori Yamamoto and Eiji Takeda : -, 第64回日本栄養・食糧学会大会,徳島,平成22年5月21日~23日, May 2010.
1445.	Yoshio Taketani, Tetsuzo Wakatsuki, Hirotsugu Yamada, Koji Yamaguchi, 西尾進, Kenya Kusunose, 冨田紀子, 林修司, 仁木敏之, Kunihiko Koshiba, Takashi Iwase, Takeshi Soeki, Masashi Akaike and Masataka Sata : スタチンによる冠動脈プラーク性状の短期変化についてのIB-IVUSを用いた検討, 第21回日本心エコー図学会学術集会, May 2010.
1446.	林修司, Hirotsugu Yamada, 西尾進, Kenya Kusunose, 冨田紀子, 河野裕美, 平岡葉月, 佐藤光代, 三木淳子, 仁木敏之, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 3次元経食道心エコー(3D-TEE)法にて経過が観察できた巨大左心耳血栓の1例, 第21回日本心エコー図学会学術集会, May 2010.
1447.	遠藤桂輔, Hirotsugu Yamada, 西尾進, 冨田紀子, Kenya Kusunose, 林修司, 佐藤光代, 平岡葉月, 河野裕美, 三木淳子, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masataka Sata and Ken Saito : リアルタイム3次元経食道エコー法により観察しえた孤立性僧帽弁クレフトの1例, 第21回日本心エコー図学会学術集会, May 2010.
1448.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, Takashi Iwase, 冨田紀子, 林修司, 三木淳子, 遠藤桂輔, 河野裕美, 平岡葉月, 佐藤光代, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 心房のみの心アミロイドーシスにおける心筋局所ストレインとMRIガドリニウム遅延造影所見の比較, 第21回日本心エコー図学会学術集会, May 2010.
1449.	西尾進, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 林修司, 遠藤桂輔, 河野裕美, 平岡葉月, 佐藤光代, 三木淳子, Yoshio Taketani, Takeshi Soeki, Masashi Akaike and Masataka Sata : コントラスト心エコー法で診断した肝肺症候群の1例, 第21回日本心エコー図学会学術集会, May 2010.
1450.	西尾進, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 林修司, 三木淳子, 遠藤桂輔, 河野裕美, 平岡葉月, 佐藤光代, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 心房のみの心病変を認めた多発性筋炎の一例, 第21回日本心エコー図学会学術集会, May 2010.
1451.	中田拓史, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 冨田紀子, 林修司, 遠藤桂輔, 河野裕美, 平岡葉月, 佐藤光代, 三木淳子, Yoshio Taketani, Takeshi Soeki, Masashi Akaike and Masataka Sata : 僧帽弁口血流速波形がE>Aパターンを呈する高齢者の内訳, 第21回日本心エコー図学会学術集会, May 2010.
1452.	Ken-ichi Aihara, Sumiko Yoshida, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka, Toshio Matsumoto, Takashi Iwase, Masashi Akaike and Masataka Sata : ロスバスタチンによる心筋リモデリング抑制効果の検討, 第83回日本内分泌学会学術総会, Mar. 2010.
1453.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Accelerated cellular apoptosis and impaired angiogenesis after hindlimb ischemia in male mice lacking androgen receptor, 第74回日本循環器学会総会・学術集会国立京都国際会館, Mar. 2010.
1454.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 遠藤桂輔, 河野裕美, 佐藤光代, Takeshi Soeki, Masashi Akaike, Masataka Sata and 平岡葉月 : 心エコー・ドプラ指標により前負荷軽減に対する心反応性は予測できるか, 日本超音波医学会四国地方会, Dec. 2009.
1455.	西尾進, Hirotsugu Yamada, 遠藤桂輔, 佐藤光代, 平岡葉月, 河野裕美, 三木淳子, Kenya Kusunose, 冨田紀子, 多田津陽子, Takeshi Soeki and Masataka Sata : 卵円孔にトラップされた下肢静脈遊離血栓の1例∼3D経食道心エコー法による観察∼, 日本超音波医学会四国地方会, Dec. 2009.
1456.	遠藤桂輔, Ken Saito, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 多田津陽子, Takeshi Soeki, Masataka Sata, 西尾進, 佐藤光代, 平岡葉月, 河野裕美 and 三木淳子 : 心エコー図検査で偶然発見された乳頭状線維弾性腫の2例, 日本超音波医学会四国地方会, Dec. 2009.
1457.	Tatsuo Motoki, Tamotsu Kanbara, 菅野幹雄, Hirotsugu Kurobe, Homare Yoshida, Takashi Kitaichi, Koji Yamaguchi, Masataka Sata and Tetsuya Kitagawa : 副乳頭筋断裂により心不全を来たした1例, 第95回日本循環器学会四国地方会, Dec. 2009.
1458.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, 住友由佳, Toshio Matsumoto, Shusuke Yagi, Takashi Iwase, Masashi Akaike, Hirotsugu Yamada, Masataka Sata and 西尾進 : 副腎アンドロゲンDHEASの抗動脈硬化作用における性差の検討, 第32回日本高血圧学会学術集会, Oct. 2009.
1459.	Ken-ichi Aihara, Yuichi Fujinaka, Mizuho Kinouchi, Sumiko Yoshida, 鈴木麗子, 倉橋清衛, Itsuro Endo, Shusuke Yagi, Takashi Iwase, 平田陽一郎, Masashi Akaike, Masataka Sata and Toshio Matsumoto : 内臓脂肪蓄積制御に関わる因子の臨床的検討, 第32回日本高血圧学会総会, 196, Oct. 2009. (Keyword) LDL Cholesterol 危険因子 *腹腔内脂肪(X線診断) ヒト中年(45~64) 高齢者(65~79) 男女
1460.	Sumiko Yoshida, Ken-ichi Aihara, 伊勢孝之, 上田由佳, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Masashi Akaike, Masataka Sata and Toshio Matsumoto : 副腎アンドロゲンDHEASの抗動脈硬化作用における性差の検討, 第32回日本高血圧学会総会, Oct. 2009.
1461.	Masashi Akaike, Ken-ichi Aihara, Yasumasa Ikeda, 石川カズ江, Sumiko Yoshida, Yuka Ueda, Shusuke Yagi, Takashi Iwase, Toshio Matsumoto and Masataka Sata : ミネラルコルチコイド受容体を介したグルココルチコイド過剰による血管内皮細胞障害作用, 第32回日本高血圧学会総会, 244, Oct. 2009. (Keyword) Glucocorticoids 血管内皮細胞系 Mineralocorticoid Receptors 内皮細胞ヒト
1462.	Koji Yamaguchi, Tetsuzo Wakatsuki, 仁木敏之, Kenya Kusunose, Kunihiko Koshiba, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, 冨田紀子, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : シロリムス溶出性ステント留置後における局所凝固反応とステント長の関連性, 第57回日本心臓病学会学術集会, Sep. 2009.
1463.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, 足立克仁, Shusuke Yagi, 仁木敏之, Kenya Kusunose, Koji Yamaguchi, Kunihiko Koshiba, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masafumi Harada, Hiromu Nishitani and Masataka Sata : Duchenne型筋ジストロフィー女性キャリアにおける心病変早期検出の試み-心臓MRIによる検討-, 第57回日本心臓病学会学術集会, Sep. 2009.
1464.	西尾進, Kenya Kusunose, Hirotsugu Yamada, 冨田紀子, 遠藤桂輔, 千葉ちひろ, 平岡葉月, 佐藤光代, 鈴木麗子, Ken-ichi Aihara, Yuichi Fujinaka and Masataka Sata : 糖尿病の動脈硬化指標:%FMDを用いた検討, 第57回日本心臓病学会学術集会, Sep. 2009.
1465.	冨田紀子, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 遠藤桂輔, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 大動脈弁硬化の進行に関連する因子, 第57回日本心臓病学会学術集会, Sep. 2009.
1466.	Kunihiko Koshiba, Takeshi Soeki, 仁木敏之, Kenya Kusunose, 平田陽一郎, Koji Yamaguchi, 冨田紀子, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Th1/Th2バランスの改善を介したPravastatinの実験的自己免疫性心筋炎抑制効果, 第57回日本心臓病学会学術集会, Sep. 2009.
1467.	Tetsuzo Wakatsuki, Koji Yamaguchi, 仁木敏之, Kenya Kusunose, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, 冨田紀子, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : 薬剤溶出ステント植え込み後慢性期の冠動脈局所炎症と凝固異常遷延の関連性, 第57回日本心臓病学会学術集会, Sep. 2009.
1468.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 遠藤桂輔, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 心房細動におけるE/e'の計測法:dual Doppler法を用いた検討, 第57回日本心臓病学会学術集会, Sep. 2009.
1469.	西尾進, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 佐藤光代, 平岡葉月, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : ASD，PSに合併した右室転移性腫瘤の1例, 第57回日本心臓病学会学術集会, Sep. 2009.
1470.	Takeshi Soeki, 仁木敏之, Kunihiko Koshiba, Kenya Kusunose, 平田陽一郎, Koji Yamaguchi, Shusuke Yagi, 冨田紀子, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 血漿pentraxin3 (PTX3)濃度は冠動脈不安定プラークの指標となり得るか?, 第57回日本心臓病学会学術集会, Sep. 2009.
1471.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 遠藤桂輔, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 僧帽弁口血流と僧帽弁輪運動の開始時間の差は左室拡張末期圧を反映する:下肢陽圧負荷を用いた検討, 第57回日本心臓病学会学術集会, Sep. 2009.
1472.	近藤可菜, Shusuke Yagi, Masashi Akaike, Takashi Iwase, Kenya Kusunose, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, 冨田紀子, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 重症心不全患者に対するAdaptive-servo ventilator療法の効果, 第239回徳島医学会学術集会, Aug. 2009.
1473.	平田陽一郎, 仁木敏之, Koji Yamaguchi, Kenya Kusunose, Kunihiko Koshiba, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masataka Sata, Hirotsugu Kurobe, Tamotsu Kanbara, 筑後文雄, Tetsuya Kitagawa and 堀貴樹 : 冠動脈周囲脂肪組織におけるマクロファージ浸潤の動脈硬化病変形成に与える影響, 第239回徳島医学会学術集会, Aug. 2009.
1474.	Masataka Sata : 循環器疾患の予防と生活習慣, 第239回徳島医学会学術集会(平成21年度夏期), Aug. 2009.
1475.	Ken-ichi Aihara, Yuichi Fujinaka, Mizuho Kinouchi, Sumiko Yoshida, 倉橋清衛, Itsuro Endo, Yuka Ueda, 平田陽一郎, Shusuke Yagi, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Influence of lipid profile on endothelial function in subjects with cardiovascular risk factors, 第41回日本動脈硬化学会総会・学術集会, Jul. 2009.
1476.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka, Shusuke Yagi, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Regular use of rosuvastatin attenuates carotid atherosclerosis regardless of LDL cholesterol lowering effect, 第41回日本動脈硬化学会総会・学術集会, Jul. 2009.
1477.	Kenya Kusunose, Hirotsugu Yamada, 冨田紀子, Masataka Sata, 岸史, Toshio Doi, 西尾進, 遠藤桂輔, 平岡葉月, 佐藤光代 and 三木淳子 : ファブリー病の2家系, 第105回UCG談話会, Jul. 2009.
1478.	西尾進, Hirotsugu Yamada, Kenya Kusunose, 佐藤光代, 平岡葉月, 冨田紀子, 阿部美保 and Masataka Sata : 両心房粘液腫の1例, 第34回日本超音波検査学会, Jun. 2009.
1479.	平岡葉月, Hirotsugu Yamada, 西尾進, 佐藤光代, Kenya Kusunose, 冨田紀子, Masashi Akaike, Takashi Kitaichi, Tetsuya Kitagawa and Masataka Sata : 3D経食道心エコー法で診断できた僧帽弁位人工弁機能不全の一例, 第34回日本超音波検査学会, Jun. 2009.
1480.	佐藤光代, Kenya Kusunose, Hirotsugu Yamada, 冨田紀子, 西尾進, 平岡葉月 and Masataka Sata : 脳塞栓を契機に発見された左房腫瘍の1例, 第34回日本超音波検査学会, Jun. 2009.
1481.	仁木敏之, Tetsuzo Wakatsuki, Koji Yamaguchi, Kenya Kusunose, Kunihiko Koshiba, Shusuke Yagi, Yoshio Taketani, 冨田紀子, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : たこつぼ型心筋障害の亜型と考えられた左室mid-portion ballooningの二例, 第94回日本循環器学会中国・四国合同地方会, Jun. 2009.
1482.	Kenya Kusunose, Hirotsugu Yamada, 冨田紀子, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 心エコーによる心病変の経過観察が可能であった続発性(AA)アミロイドーシスの一例, 第94回日本循環器学会中国・四国合同地方会, Jun. 2009.
1483.	Kunihiko Koshiba, 仁木敏之, Kenya Kusunose, 平田陽一郎, Koji Yamaguchi, 冨田紀子, Yoshio Taketani, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Takeshi Soeki, Masashi Akaike and Masataka Sata : 多発性筋炎に伴う心障害の一例, 第94回日本循環器学会中国・四国合同地方会, Jun. 2009.
1484.	Hirotsugu Kurobe, Tamotsu Kanbara, Homare Yoshida, Tatsuo Motoki, 菅野幹雄, Takashi Kitaichi, Kenya Kusunose, Hirotsugu Yamada, Masataka Sata and Tetsuya Kitagawa : 塞栓症を契機に発見された乳頭状線維弾性腫の2例, 第94回日本循環器学会中国・四国合同地方会, Jun. 2009.
1485.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 平岡葉月, 佐藤光代, 多田津陽子, 冨田紀子, Takeshi Soeki, Masashi Akaike and Masataka Sata : 安静時post systolic shortening による虚血心筋の検出, 日本超音波医学会第82回学術集会, May 2009.
1486.	西尾進, Hirotsugu Yamada, Kenya Kusunose, 平岡葉月, 佐藤光代, 多田津陽子, 冨田紀子, Takeshi Soeki, Masashi Akaike and Masataka Sata : 下肢静脈血栓スクリーニング検査で発見されたベーカー嚢胞破裂の2症例, 日本超音波医学会第82回学術集会, May 2009.
1487.	倉橋清衛, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Yuichi Fujinaka, Shusuke Yagi, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : 一酸化炭素中毒にて急性心筋梗塞を発症した2型糖尿病の1例, 第100回日本内科学会四国地方会, May 2009.
1488.	Shusuke Yagi, Takashi Iwase, Masashi Akaike, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 重症心不全患者における酸素療法とAdaptive-servo ventilator療法の効果の比較検討, 日本内科学会第100回四国地方会, May 2009.
1489.	Masashi Akaike, Ken-ichi Aihara, Yasumasa Ikeda, 石川カズ江, 住友由佳, Sumiko Yoshida, Shusuke Yagi, Takashi Iwase, Toshio Matsumoto and Masataka Sata : グルココルチコイド誘発性血管内皮細胞障害におけるミネラルコルチコイド受容体の関与, 第82回日本内分泌学会学術総会, Vol.85, No.1, 373, Apr. 2009. (Keyword) Glucocorticoids(毒性・副作用) 血管内皮培養細胞 Mineralocorticoid Receptors(薬理学) 内皮細胞ヒト
1490.	Sumiko Yoshida, Ken-ichi Aihara, 西尾進, 倉橋清衛, Itsuro Endo, Yuichi Fujinaka, Takayuki Ise, 住友由佳, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Masashi Akaike, Masataka Sata and Toshio Matsumoto : 副腎アンドロゲンDHEASは血管内皮機能非依存的に頸動脈硬化を抑制する, 第82回日本内分泌学会学術総会, Vol.85, No.1, 366, Apr. 2009. (Keyword) 頸動脈疾患血管内皮動脈硬化症 Dehydroepiandrosterone Sulfate(薬理学) ヒト男女
1491.	佐藤光代, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 平岡葉月, 冨田紀子, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 経食道心エコー検査により治療経過が観察できた高安動脈炎に伴う肺動脈狭窄症の一例, 第20回日本心エコー図学会学術集会, Apr. 2009.
1492.	平岡葉月, Hirotsugu Yamada, 西尾進, 佐藤光代, 高松直子, Kenya Kusunose, 冨田紀子, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 心エコーによる心病変の経過観察が可能であった続発性(AA)アミロイドーシスの一例, 第20回日本心エコー図学会学術集会, Apr. 2009.
1493.	高松直子, Hirotsugu Yamada, 西尾進, 佐藤光代, 平岡葉月, Kenya Kusunose, 冨田紀子, Yuishin Izumi, Ryuji Kaji and Masataka Sata : 麦角系アルカロイド剤を服用しているパーキンソン病患者の心エコー所見, 第20回日本心エコー図学会学術集会, Apr. 2009.
1494.	西尾進, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 平岡葉月, 佐藤光代, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 三尖弁輪運動速波形を用いた二次性肺高血圧の評価, 第20回日本心エコー図学会学術集会, Apr. 2009.
1495.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 平岡葉月, 佐藤光代, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : Post systolic shortening(PSS)による心筋虚血の検出, 第20回日本心エコー図学会学術集会, Apr. 2009.
1496.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 平岡葉月, 佐藤光代, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 僧帽弁口血流と僧帽弁輪運動の不整合は左室拡張能の評価に有用か:dual Doppler systemを用いた検討, 第20回日本心エコー図学会学術集会, Apr. 2009.
1497.	Ken-ichi Aihara, Sumiko Yoshida, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka, Toshio Matsumoto, Takashi Iwase, Masashi Akaike and Masataka Sata : ロスバスタチンによる心筋リモデリング抑制効果の検討, 第83回日本内分泌学会学術総会国立京都国際会館, Mar. 2009.
1498.	Ken-ichi Aihara, Sumiko Yoshida, Takayuki Ise, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Kurahashi Kiyoe, Itsuro Endo, Yuichi Fujinaka, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Increased serum triglyceride but not LDL cholesterol is associated with left ventricular diastolic dysfunction., 第73回日本循環器学会総会・学術集会, Mar. 2009.
1499.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, 住友由佳, Shusuke Yagi, Takashi Iwase, 倉橋清衛, Itsuro Endo, Yuichi Fujinaka, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Dehydroepiandrosterone sulfate is an antivascular remodeling factor, 第73回日本循環器学会総会・学術集会, Mar. 2009.
1500.	住友由佳, Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Shusuke Yagi, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Heparin Cofactor II-deficient Mice Exert Exacerbation of Angiotensin II-induced Cardiac Remodeling through Enhancement of NADPH oxidase - TGF- 1 Pathway, 第73回日本循環器学会総会・学術集会, Mar. 2009.
1501.	Masashi Akaike, Ken-ichi Aihara, Yasumasa Ikeda, 石川カズ江, Sumiko Yoshida, 住友由佳, Shusuke Yagi, Takashi Iwase, Toshio Matsumoto and Masataka Sata : Glucocorticoid Excess Causes Vascular Endothelial Cell Dysfunction through Activation of Mineral Corticoid Receptor, 第73回日本循環器学会総会・学術集会, Mar. 2009.
1502.	Masataka Sata : 急性冠症候群の発症因子と臨床的意義, 第93回日本循環器学会四国地方会, Dec. 2008.
1503.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 仁木敏之, 冨田紀子, 山口浩司, 小柴邦彦, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, 河野智彦 and Masataka Sata : 右心不全を契機に診断された肺動脈狭窄症の一例, 第93回日本循環器学会四国地方会, Dec. 2008.
1504.	Shusuke Yagi, Takashi Iwase, Kenya Kusunose, 仁木敏之, 山口浩司, 小柴邦彦, 冨田紀子, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 強皮症に伴う難治性末梢循環不全に対するエンドセリン受容体拮抗薬の有用性, 第93回日本循環器学会四国地方会, Dec. 2008.
1505.	小柴邦彦, Takeshi Soeki, 仁木敏之, Kenya Kusunose, 山口浩司, 冨田紀子, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 両側肺血栓症と多発性体循環系塞栓症を合併した1例, 第93回日本循環器学会四国地方会, Dec. 2008.
1506.	山口浩司, Tetsuzo Wakatsuki, 仁木敏之, Kenya Kusunose, 小柴邦彦, 冨田紀子, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : 冠動脈ステント3種(CYPHER, TAXUS, DRIVER)の慢性期病理組織所見の比較と局所凝固反応の関連性, 第93回日本循環器学会四国地方会, Dec. 2008.
1507.	Masataka Sata : Vascular Regeneration Utilizing Circulating Progenitors and Novel Biomaterials., The 24th Kumamoto Medical Bioscience Symposium, Nov. 2008.
1508.	Ken-ichi Aihara, Sumiko Yoshida, Takayuki Ise, 住友由佳, 倉橋清衛, Itsuro Endo, Yuichi Fujinaka, Toshio Matsumoto, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Masataka Sata : 左室拡張能に対する脂質代謝異常の意義, 第31回日本高血圧学会総会, Oct. 2008.
1509.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, 住友由佳, Toshio Matsumoto, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Masataka Sata : 副腎アンドロゲンDHEASは頚動脈血流の制御因子である, 第31回日本高血圧学会学術集会, Oct. 2008.
1510.	住友由佳, Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Toshio Matsumoto, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Masashi Akaike and Masataka Sata : ヘパリンコファクターⅡは抗酸化ストレス作用を介してアンジオテンシンIIによる心房および心室のリモデリングを抑制する, 第31回日本高血圧学会総会, Oct. 2008.
1511.	Masashi Akaike, Shusuke Yagi, Ken-ichi Aihara, 石川カズ江, Yasumasa Ikeda, Sumiko Yoshida, 住友由佳, Takashi Iwase, 阿部純一, Toshio Matsumoto and Masataka Sata : ピタバスタチンはERK5-KLF2経路の活性化を介して血管内皮細胞での一酸化窒素合成酵素の発現を亢進する, 第31回日本高血圧学会総会, Oct. 2008.
1512.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, 住友由佳, Toshio Matsumoto, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Masataka Sata : 副腎アンドロゲンDHEASの血管への作用(頚動脈エコーを用いた臨床的検討), 第13回武田高血圧シンポジウム, Oct. 2008.
1513.	西尾進, Hirotsugu Yamada, Kenya Kusunose, 佐藤光代, 高松直子, Takeshi Soeki, Masashi Akaike and Masataka Sata : 頸動脈狭窄性病変におけるB-Flowの有用性, 第18回日本超音波医学会四国地方会学術集会, Oct. 2008.
1514.	山中森晶, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 佐藤光代, Takeshi Soeki, Masashi Akaike and Masataka Sata : 壁運動正常例におけるpost systolic shortening (PSS) についての検討, 第18回日本超音波医学会四国地方会学術集会, Oct. 2008.
1515.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 佐藤光代, Takeshi Soeki, Masashi Akaike, 阿部美保, 河野和弘, 角谷昭佳 and Masataka Sata : リアルタイム3次元経食道心エコー図で診断しえた肺動脈狭窄症の一例, 第18回日本超音波医学会四国地方会学術集会, Oct. 2008.
1516.	西尾進, Hirotsugu Yamada, Kenya Kusunose, 仁木敏之, 山口浩司, Shusuke Yagi, 小柴邦彦, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Yasunori Nagamine and Masataka Sata : Automated Function Imaging法による左室局所壁運動異常評価:心エコー初心者による肉眼的評価との比較, 第56回日本心臓病学会学術集会, Sep. 2008.
1517.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 仁木敏之, 山口浩司, Shusuke Yagi, 小柴邦彦, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 高血圧性心疾患における左房ポンプ機能の評価:Left Atrial Ejection Forceを用いた検討, 第56回日本心臓病学会学術集会, Sep. 2008.
1518.	Tetsuzo Wakatsuki, 山口浩司, 仁木敏之, Kenya Kusunose, 小柴邦彦, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Masashi Akaike and Masataka Sata : 薬剤溶出ステント植え込み後の冠動脈内皮機能障害と局所炎症遷延の関連性, 第56回日本心臓病学会学術集会, Sep. 2008.
1519.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 仁木敏之, 山口浩司, Shusuke Yagi, 小柴邦彦, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 心房細動におけるTEI indexの有用性:Dual Doppler法を用いた検討, 第56回日本心臓病学会学術集会, Sep. 2008.
1520.	仁木敏之, Takeshi Soeki, 小柴邦彦, Kenya Kusunose, 山口浩司, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masashi Akaike, 福田大和, 篠原尚典, 福田信夫, 田村禎通 and Masataka Sata : 虚血性心疾患におけるHMGBI (high mobility group box 1) の診断的意義, 第56回日本心臓病学会学術集会, Sep. 2008.
1521.	Masataka Sata : 細胞からみたDESの弱点と薬物療法, 第17回日本心血管インターベンション学会学術集会"Very late stent thrombosisの発症機序と対策"(シンポジウム), Jul. 2008.
1522.	Masataka Sata : 脳血管スパズムとスタチンの多面的作用―前駆細胞による血管メンテナンス―, 第24回スパズムシンポジウム特別講演, Mar. 2008.
1523.	M Sahara, Masataka Sata, T Morita, Y Hirata and R Nagai : Genetic Deletion of Angiotensin-converting Enzyme 2 Accelerates Hyperlipidemia-induced Atherosclerosis in Apolipoprotein E-deficient Mice, 第72回日本循環器学会"Plenary Session 3 「炎症・免疫と動脈硬化」", Mar. 2008.
1524.	Masataka Sata : Vulnerable Plaques: Pathogenesis and Noninvasive Approaches to Detection, 第72回日本循環器学会(AHA-JCSジョイントシンポジウム), Mar. 2008.
1525.	Masataka Sata : 動脈硬化と血管新生におけるシグナル制御 Regulation of cell signal in atherosclerosis and angiogenesis, 第85回日本生理学会大会"心臓血管系のシグナル調節 Regulation of cell signal in the cardiovascular system"(シンポジウム32), Mar. 2008.
1526.	Masataka Sata : DES の陰から光を探る―血管生物医学の立場から―, 第15回日本血管生物医学会学術大会"―薬物溶出ステント(DES)の陰から光を探る―再浮上したDESの問題点(血栓症)から次のゴールを探る"(プレナリーセッション), Nov. 2007.
1527.	Masataka Sata and 永井良三 : 血管細胞生物学からみた動脈硬化, 第48回日本脈管学会総会"動脈硬化症のトピックに関するシンポジウム"(シンポジウム6), Oct. 2007.
1528.	Masataka Sata and R Nagai : Roles of Renin-Angiotensin System in the Pathogenesis of Heart Failure, 第11回日本心不全学会学術集会"心不全における薬剤の基礎的評価"(シンポジウム15), Sep. 2007.
1529.	岩田洋, Masataka Sata, 中村和人, 墨誠, 二宮幹夫, 酒井芳紀, 高本眞一 and 永井良三 : 合成 PGI2 アゴニスト ; ONO1301 の慢性虚血性心疾患に対する有効性, 第28回日本炎症再生医学会"心血管再生医療の最前線"(ワークショップ13), Aug. 2007.
1530.	墨誠, Masataka Sata, 榎本操一郎, 大木隆生, 朝倉哲郎 and 永井良三 : Silk 素材由来 fibroin による小口径人工血管の開発と応用, 第28回日本炎症再生医学会"心血管再生医療の最前線"(ワークショップ13), Aug. 2007.
1531.	M Sahara, Masataka Sata, T Morita, Y Hirata and R Nagai : Nicorand1 Attenuates Monocrotaline-induced Pulmonary Arterial Hypertension in Rats: The Promising Therapeutic Potential of a Novel Combination Therapy, 第71回日本循環器学会総会 Symposium4 Diagnosis and treatment of pulmonary hypertension, Mar. 2007.
1532.	M Sumi, Masataka Sata and R Nagai : Long-term Patency of a Small Diameter Vascular Prosthesis Made of Fibroin, a Silk-based Biodegradable Material, 第71回日本循環器学会総会 Plenary Session 6 Regeneration Therapy Using Tissue Engineering, Mar. 2007.
1533.	Masataka Sata, D Fukuda, K Tanaka and R Nagai : Bone Marrow-Derived Cells Play a Critical Role in Progression and Destabilization of Atherosclerotic Plaques, 第71回日本循環器学会総会 Plenary Session 2 A New Era in Atherosclerosis Research, Mar. 2007.
1534.	Masataka Sata and 永井良三 : 動脈硬化における骨髄細胞と血管新生, 第29回日本血栓止血学会学術集会"日本血栓止血学会・日本血管生物医学会ジョイントシンポジウム 1.血栓症:Virchow Code", Nov. 2006.
1535.	Masataka Sata, 墨誠, 三浦伸一郎, 朔啓二郎 and 永井良三 : 合成 HDL は内皮前駆細胞の分化を促進して血管新生を増強する, 第54回日本心臓病学会学術集会 "メタボリックシンドローム:最新の診断と治療"(パネルディスカッション7), Sep. 2006.
1536.	Masataka Sata and 永井良三 : 動脈硬化の進展と破綻における血中前駆細胞の役割, 第38回日本動脈硬化学会総会・学術総会 "動脈硬化と幹細胞"(シンポジウム8), Jul. 2006.
1537.	Masataka Sata : Potential contribution of circulating progenitors to vascular healing and remodeling, The 14th CDB Meeting "EPC Biology Conference", 2006.
1538.	Masataka Sata : Therapeutic angiogenesis for heart failure, The 22nd annual meeting of the Japanese Section of International Society for Heart Research. Problem-solving Panel Discussion 3 "What is the most appropriate method to perform regeneration therapy in cardiovascular medicine", Dec. 2005.
1539.	岩田洋, Masataka Sata, 中村和人, 墨誠, 酒井芳紀 and 永井良三 : 徐放性低分子化合物局所投与によるサイトカイン発現誘導と血管新生, 第46回日本脈管学会総会 "血管新生"(シンポジウム), Dec. 2005.
1540.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Hirotsugu Kurobe, Masataka Sata, Yasumasa Ikeda, 藤村光則, 橋詰俊二, Takashi Iwase, Shusuke Yagi, 大水章正, 塚田稔, Tetsuya Kitagawa, 加藤茂明 and Toshio Matsumoto : 新規血管リモデリング抑制因子ヘパリンコファクターIIの臨床および分子生物学的解析, 第13回日本血管生物医学会, Oct. 2005.
1541.	Masataka Sata : DES and circulating vascular progenitors, Complex Catheter Therapeutics 2005 Cpmcirremt Session, Sep. 2005.
1542.	Masataka Sata : Cardiovascular regeneration using small molecules, Complex Catheter Therapeutics 2005 Cpmcirremt Session, Sep. 2005.
1543.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Masataka Sata, Fujimura MItsunori, Hashizume Shunji, Yasumasa Ikeda, Shusuke Yagi, Kawano Hirotaka, Yamada Takashi, Fukuda Tohru, Sekine Keisuke, Sato Takashi, Nakamichi Yuko, Yamamoto Yoko, Yoshimura Kimihiro, Watanabe Tomoyuki, Nakamura Takashi, Ohmizu Akira, Tsukada Minoru, Shigeaki Kato and Toshio Matsumoto : Heparin cofactor II is required for fetal development and attenuates cuff-injured vascular remodeling in mice, The 37th Japan Atherosclerosis Society Annual Meeting, Jul. 2005.
1544.	Masataka Sata, 福田大受, 岩田洋, 中村和人 and 永井良三 : 組織幹細胞と血管新生，再生, 第42回日本臨床分子医学会学術集会:Translational Research Forum Ⅰ「再生医療」, Jul. 2005.
1545.	Masataka Sata, 酒井芳紀 and 永井良三 : 徐放性低分子化合物局所投与によるサイトカイン発現誘導と血管新生, 第37回日本動脈硬化学会総会:シンポジウム2「遺伝子治療から再生医療へ」, Jul. 2005.
1546.	Masataka Sata : Origin and proliferation of smooth muscle cells, 第78回日本薬理学会:シンポジウム7「Smooth muscle research update:Differentiation,cell proliferation,cell function,programmed cell death」, Mar. 2005.
1547.	Masataka Sata : Molecular Mechanism of In-stent restenosis, Complex Catheter Therapeutics 2004 Special Lecture, Oct. 2004.
1548.	Masataka Sata : 血中前駆細胞による血管の新生，再生，病態形成, 第51回日本臨床検査医学会総会:シンポジウム「幹細胞と再生医学」, Sep. 2004.
1549.	Masataka Sata and 永井良三 : 平滑筋細胞アポトーシスとプラークの不安定化, 第36回日本動脈硬化学会総会:コントロバーシー1「アポトーシス/プラーク破綻」, Jul. 2004.
1550.	Masataka Sata and 永井良三 : 骨髄由来血管壁細胞と炎症, 第36回日本動脈硬化学会総会シンポジウム「炎症・免疫機構と動脈硬化―現状と将来」, Jul. 2004.
1551.	Masataka Sata and 永井良三 : 動脈硬化形成への骨髄細胞の関与, 第26回日本血栓止血学会:座長指定演題シンポジウム, Nov. 2003.
1552.	Masataka Sata and 永井良三 : プラーク破綻の機序, 第44回日本脈管学会総会シンポジウム:コンセンサス/コントロバーシー3「冠動脈疾患‐病態，診断，治療をめぐって」, Nov. 2003.
1553.	Masataka Sata : Statin の pleiotropic action, 第51回日本心臓病学会学術集会「モーニングセミナー」, Sep. 2003.
1554.	Masataka Sata and 永井良三 : 骨髄由来細胞による再生およ病態形成, 第100回日本内科学会講演会パネルディスカッション「再生医療の展望」, Apr. 2003.
1555.	Masataka Sata : Molecular Strategies to Treat Vascular Diseases, 第67回日本循環器学会学術集会日本心臓財団佐藤賞受賞記念講演, Mar. 2003.
1556.	Masataka Sata, K Tanaka and R Nagai : Hematopoietic Stem Cells Differentiate into Vascular Cells that Participate in the Pathogenesis of Atherosclerosis, 日本循環器学会学術集会Plenary Session 5 "Frontier of Atherosclerosis Research", Mar. 2003.
1557.	Masataka Sata, 平田恭信 and 永井良三 : 骨髄由来血管前駆細胞による血管修復と再生, 第76回日本薬理学会年会シンポジウム「血管新生制御機構と治療戦略」, Mar. 2003.
1558.	Masataka Sata : 動脈硬化，再狭窄の病態に関する最近の話題―特に骨髄幹細胞の関与について, 第186回日本循環器学会関東甲信越地方会学術集会教育セミナー, Dec. 2002.
1559.	Masataka Sata, 田中君枝, 平田恭信 and 永井良三 : 骨髄由来血管前駆細胞による血管修復と再生, 第24回心筋生検研究会ワークショップ「心筋の細胞死と再生」, Nov. 2002.
1560.	Masataka Sata : 動脈硬化プラーク構成細胞の由来とその臨床的意義, 第43回日本脈管学会総会シンポジウム, Nov. 2002.
1561.	Masataka Sata, K Tanaka, Y Hirata, K Walsh and R Nagai : Hematopoietic stem cells differentiate into smooth muscle cells that contribute to vascular diseases, The 19th annual meeting of the Japanese Section of International Society for Heart Research. Symposium6 "Molecular biology for the mechanism of unstable plaque formation", Nov. 2002.
1562.	Masataka Sata : Vascular Remodeling and Function, International Symposium on Cardio Vascular Remodeling and Function, Oct. 2002.
1563.	Masataka Sata : 遺伝子治療, 第50回日本心臓病学会学術集会JCC教育プログラム―循環器疾患の病態評価と治療選択, Sep. 2002.
1564.	Masataka Sata, 平田恭信 and 永井良三 : スタチンによる血管新生促進作用, 第34回日本動脈硬化学会総会パネルディスカッション2「スタチンのpleiotropic effectを考える」, Jul. 2002.
1565.	Masataka Sata : 遺伝子治療のトピックス, 第6回心臓リハビリテーション公開シンポジウム「QOLの改善につながる心臓病治療」, Jul. 2002.
1566.	Masataka Sata and 永井良三 : 骨髄幹細胞と血管リモデリング, 第7回Vascular Medicine学会指定演題Ⅱ, Jul. 2002.
1567.	Masataka Sata and 永井良三 : 骨髄由来血管前駆細胞と血管リモデリング, 第23回日本炎症・再生医学会ワークショップ, Jul. 2002.
1568.	Masataka Sata and 永井良三 : 薬物による血管新生療法, 第120回日本医学会シンポジウム「血管新生の基礎と臨床」, Dec. 2001.
1569.	Masataka Sata and 永井良三 : 骨髄幹細胞由来新生内膜平滑筋と再狭窄, 第9回日本血管細胞生物学会シンポジウムⅡ「血管リモデリングの分子機構:PTCA後再狭窄を中心に」, Nov. 2001.
1570.	Masataka Sata : 動脈硬化病巣の平滑筋細胞の起源をさぐる, 第16回「大学と科学」公開シンポジウム「動脈効果のしくみをさぐる」, Oct. 2001.
1571.	Masataka Sata, 鈴木亨, 西田昌道, 二見覚, 平井久丸, 前川和彦 and 永井良三 : 骨髄由来血管前駆細胞の血管修復過程への関与, 第22回日本炎症再生医学会シンポジウム「炎症/再生医学に関わる重要な細胞」, Jul. 2001.
1572.	Masataka Sata, 吹野恵子, 斎浦明夫, 幕内雅敏, 平田恭信 and 永井良三 : 骨髄由来平滑筋前駆細胞の同定とその分化制御に関する検討, 第33回日本動脈硬化学会総会モーニングセミナー「血管創生の可能性」, Jun. 2001.
1573.	Masataka Sata, Y Hirata, K Walsh and R Nagai : Genetic therapy for vascular proliferative diseases utilizing Fas ligand, The 17th annual meeting of the Japanese Section of International Society for Heart Research. Symposium3 "Cell Survival and Apopotosis in the Cardiovascular System", Dec. 2000.
1574.	Masataka Sata, 杉浦清了, 平田恭信 and 永井良三 : 血管内皮におけるFasリガンド発現の生理的意義及びその遺伝子治療への応用に関する検討, 第32回日本動脈硬化学会総会シンポジウム「血管壁細胞機能の制御と動脈硬化」, Jun. 2000.
1575.	Masataka Sata and 他 : 血管内皮細胞によるFas ligand 発現の生理的意義ならびにその遺伝子治療への応用, 日本循環器学会学術集会シンポジウム, Mar. 1999.

Products:

1.	Shusuke Yagi, Daiju Fukuda, Yukina Hirata, Ganbaatar Byambasuren, Arief Rahadian, Takayuki Ise, Kenya Kusunose, Hirotsugu Yamada, Koji Yamaguchi, Tomomi Matsuura, Takeshi Tobiume, Tomohiro Soga, Takeshi Soeki, Tetsuzo Wakatsuki, Shinji Kawahito and Masataka Sata : 【糖尿病専門医に必要な心不全の知識update】SGLT2阻害薬と心不全(解説/特集), 糖尿病・内分泌代謝科, Vol.52, No.3, 257-264, Nov. 2021.
2.	Sae Morita, Susumu Nishio, Yukina Hirata, YAMAGUCHI Natsumi, Asami Yuasa, 松本力三, 山尾雅美, Miharu Arase, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : ハイエンド汎用超音波診断装置(LOGIQ E10)と循環器専用超音波診断装置(Vvid E95)におけるglobal longitudinal strainの装置間差に関する検討, Japanese Journal of Medical Ultrasound Technology, Vol.46, No.5, 463-470, Nov. 2021.

Et cetera, Workshop:

1.	伊藤直司, Yoshihito Saijyo, 手束一貴, Tomoko TAKAHASHI, Akihiro TANI, Ryo BANDO, ロバートゼング, TOMONORI Takahashi, Muneyuki Kadota, Yutaka Kawabata, Rie Ueno, Tomoya Hara, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Ryota Matsumoto, Hiroki Hata and Masataka Sata : ポスタ-セッション健康診断を契機に発見された巨大冠動脈瘤の一例, 第269回徳島医学会学術集会, Jul. 2024.
2.	Yuho Higashimura, Yoshiko Suzuki, Kotono Ohishi, 石井亜由美, 西川幸治, Sonoko Yasui-Yamada, Takayuki Ise, Shusuke Yagi, Akiko Matsumura, Masataka Sata and Yasuhiro Hamada : 心臓リハビリテーションと連携し，継続した栄養介入を行うことで減量が認められた一例, 日本心臓リハビリテーション学会第3回四国支部地方会, Apr. 2019.
3.	中川舞, 毛山剛, Kazuhide Mineda, Keisuke Kashiwagi, Soushi Ishida, Yoshiro Abe, Ichiro Hashimoto, 川端豊, Masataka Sata, Hiroki Arase, Eiki Fujimoto and Tetsuya Kitagawa : 集学的治療により下肢大切断を免れた重症下肢虚血肢の一例, 第254回徳島医学会学術集会, Feb. 2017.
4.	村上貴寛, Shusuke Yagi, 原知也, Takayuki Ise, Kenya Kusunose, Tomomi Matsuura, Takeshi Tobiume, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Masashi Akaike, 春藤譲治 and Masataka Sata : 原発性アルドステロン症の診断に有用な臨床所見の検討, 第253回徳島医学会学術集会(平成28年度夏期), Jul. 2016.
5.	山上圭, 西條良仁, Kenya Kusunose, Hirotsugu Yamada, 瀬野弘光, 原知也, 上野理絵, 門田宗之, 齋藤友子, 山﨑宙, 坂東左知子, 伊藤浩敬, 轟貴史, Tomomi Matsuura, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 生体腎移植後における腎静脈-外腸骨静脈間の血流動態変化が一因と考えられた深部静脈血栓症の一例, 第253回徳島医学会学術集会(平成28年度夏期), Jul. 2016.
6.	瀬野弘光, Kenya Kusunose, 西條良仁, 平田有紀奈, 鳥居裕太, 西尾進, 林修司, Hirotsugu Yamada and Masataka Sata : 右室ストレインはベンダー間で異なるか:3D-RVEFとの比較, 第1回関西リサーチクラブ, Dec. 2015.
7.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 平田有紀奈, Mika Bando, 西條良仁, 林修司, 鳥居裕太, 天野里江, 山尾雅美, Jun Kishi and Masataka Sata : 膠原病に伴う肺高血圧症の進展予測:6分間歩行負荷心エコー図検査を用いた検討, 第13回先進心血管エコー研究会, Aug. 2015.
8.	山下雄也, Mika Bando, Takayuki Ise, Kenya Kusunose, Hirotsugu Yamada, 原知也, 高島啓, 山﨑宙, 斎藤友子, 坂東左知子, 飛梅威, Koji Yamaguchi, Shusuke Yagi, Takeshi Soeki, Tetsuzo Wakatsuki, 木下肇, 藤本鋭貴, 北川哲也, 井上洋行 and Masataka Sata : 収縮期雑音を契機に発見された成人単純型大動脈狭窄症の1例, 第251回徳島医学会学術集会, Aug. 2015.
9.	瀬野弘光, 山﨑宙, Shusuke Yagi, 黒部裕嗣, 高森信行, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 急激な弁破壊を認めたメチシリン感受性表皮ブドウ球菌による感染性心内膜炎の一例, 第251回徳島医学会学術集会, Aug. 2015.
10.	Miho Sakata, Yasunobu Hayabuchi, Shoji Kagami, Kazuhiro Mori, 井上美紀, Takeshi Soeki, Takeshi Tobiume, 松浦朋美, 坂東佐知子, Masataka Sata, Takashi Kitaichi, Eiki Fujimoto, Tamotsu Kanbara, Hirotsugu Kurobe, Tetsuya Kitagawa, Mutsuo Onodera, Hideaki Imanaka and Masaji Nishimura : 経皮的心肺補助(PCPS)装着下にカテーテルアブレーションを施行し，救命し得た異所性接合部頻拍の1男児例, 第141回日本小児科学会徳島地方会, Dec. 2013.
11.	坂東左知子, Takeshi Soeki, 松浦朋美, Takeshi Tobiume and Masataka Sata : Aorta-mitral continuityが起源の心房頻拍の1例, 第25回カテーテルアブレーション委員会公開研究会, Nov. 2013.
12.	松浦朋美, Takeshi Tobiume, Takeshi Soeki, 坂東左知子, Koji Yamaguchi, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki and Masataka Sata : 室房ブロックを伴っても持続する2種類の房室結節リエントリー性頻拍を認め，上位共通路の存在が示唆された1例, 第25回カテーテルアブレーション委員会公開研究会, Nov. 2013.
13.	Takeshi Soeki, T Matsuura, S Bando, E Uematsu, Takayuki Ise, Takeshi Tobiume, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Takashi Iwase, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro, I Kishimoto, Kenji Kangawa and Masataka Sata : Ghrelin protects the heart against ischemia-induced arrhythmia by preserving connexin 43 protein., 第36回心筋代謝研究会, Jul. 2013.
14.	Takeshi Soeki, Hirotsugu Yamada, 松浦朋美, 坂東左知子, Mika Bando and Masataka Sata : カテーテルアブレーションハンズオンセミナー, 第4回四国研修会, Jul. 2012.
15.	Mika Bando, Hirotsugu Yamada, 西尾進, 冨田紀子, 發知淳子, 林修司, 中川摩耶, 玉井利奈, 平田有紀奈, 弘田大智, 小笠原梢, 髙島啓, 山崎宙, 坂東左知子, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 質低下療法による頸動脈プラーク安定化の評価, 第5回T0kushima Young Investigators Conference, Mar. 2012.
16.	Mika Bando, Hirotsugu Yamada, 冨田紀子, 發知淳子, 西尾進, 中川摩耶, 玉井利奈, 平田有紀奈, 弘田大智, 坂東左知子, Takayuki Ise, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : Fabry病の2家系, 第16回中四国心筋症・心不全研究会, Sep. 2011.
17.	Takashi Iwase, Takayuki Ise, 小笠原梢, 山崎宙, 高島啓, 坂東左知子, Toshiyuki Niki, Kenya Kusunose, 發知淳子, 冨田紀子, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, Shoichiro Takao, Hayato Nose, Masafumi Harada, Masashi Akaike and 足立克仁 : Duchenne型筋ジストロフィー女性キャリアの心病変検出における心臓MRI検査の有用性, 第16回中四国心筋症・心不全研究会, Sep. 2011.
18.	原知也, Takashi Iwase, 高島啓, 山崎宙, 小笠原梢, 坂東左知子, Takayuki Ise, Toshiyuki Niki, Kenya Kusunose, Yuka Ueda, 冨田紀子, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Masataka Sata, Masashi Akaike, Hayato Nose, Shoichiro Takao, Hideki Otsuka, Masafumi Harada and Yasuhiko Nishioka : 心サルコイドーシス診断の手引きにおける各種診断モダリティーの検討, 第16回中四国心筋症・心不全研究会, Sep. 2011.
19.	林修司, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 發知淳子, 冨田紀子, Toshiyuki Niki, Koji Yamaguchi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki and Masataka Sata : 高齢者の左室弛緩能に心拍数が与える影響について:僧帽弁口血流速パターンをどう解釈するか, 第1回四国symphony, Jul. 2011.
20.	清水拓, Kenya Kusunose, Hirotsugu Yamada, 西尾進, 玉井利奈, 遠藤桂輔, 佐藤光代, 河野裕美, Masashi Akaike and Masataka Sata : 運動負荷心エコー法を用いた膠原病例における潜在性肺動脈性高血圧症の検出, 第2回徳島肺高血圧研究会, Apr. 2011.
21.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : エイコサペンタエン酸の心血管リモデリング抑制効果の検討, 第3回Tokushima Young Investigators Conference, Mar. 2011.
22.	林修司, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 多田津陽子, 西尾進, 玉井利奈, Takashi Iwase, Takeshi Soeki and Masataka Sata : 体位変換により右室内圧較差が変化をきたす右室二腔症の一例, UCG談話会, Jan. 2011.
23.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : EPAによる心血管リモデリング抑制効果の検討, 第30回心血管セミナー, Jan. 2011.
24.	遠藤桂輔, Hirotsugu Yamada, Kenya Kusunose, 西尾進, 冨田紀子, 三木淳子, 林修司, 玉井利奈, 河野裕美, 平岡葉月, 佐藤光代, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Ken Saito and Masataka Sata : 陳旧性心筋梗塞症における心電図左房負荷所見の意義:心エコー・ドプラ法を用いた検討, 心・血管クラスターミニリトリート, Jan. 2011.
25.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 林修司, 三木淳子, Toshiyuki Niki, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 左室内同期不全に対する前負荷の影響拡張型心筋症における下肢陽圧負荷3次元心エコー法を用いた検討, 先進血管エコー研究会, Aug. 2010.
26.	Hirotsugu Yamada, 西尾進, 玉井利奈, 遠藤桂輔, 冨田紀子, Kenya Kusunose, 林修司, Yoshio Taketani and Masataka Sata : 頸動脈エコーによるプラークの超音波正常カラーイメージングの試み, 第6回西日本血管・機能研究会, Aug. 2010.
27.	遠藤桂輔, Hirotsugu Yamada, 西尾進, 冨田紀子, Kenya Kusunose, 林修司, 佐藤光代, 平岡葉月, 河野裕美, 三木淳子, 玉井利奈, Koji Yamaguchi, Yoshio Taketani, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masataka Sata and Ken Saito : 心電図異常を指摘され，心エコー検査で発見された左室緻密化障害の1例, 第3回蔵本エコーカンファレンス, Jul. 2010.
28.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : 虚血および血管新生におけるアンドロゲン作用の検討, 興和学術講演会, May 2010.
29.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : 下肢虚血モデルを用いたアンドロゲン受容体による虚血臓器保護効果の検討, 第15回徳島内分泌研究会, Nov. 2009.
30.	Kenya Kusunose, Hirotsugu Yamada, 西尾進, 冨田紀子, 遠藤桂輔, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Yoshio Taketani, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike and Masataka Sata : 心房細動におけるE/e'の計測法:dual Doppler法を用いた検討, 第8回先進血管エコー研究会, Aug. 2009.
31.	倉橋清衛, Shingen Nakamura, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Yuichi Fujinaka, Toshio Matsumoto, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Masataka Sata : 一酸化炭素中毒を契機に発見された急性心筋梗塞の一例, 第9回徳島総合診療研究会, Jul. 2009.
32.	山中森晶, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masataka Sata and 西尾進 : 脳卒中患者における心エコー検査の現状:徳島大学病院SCU搬送例における検討, 第11回徳島脳卒中研究会, Feb. 2009.
33.	山中森晶, Hirotsugu Yamada, Kenya Kusunose, 冨田紀子, 仁木敏之, Koji Yamaguchi, Kunihiko Koshiba, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Tetsuzo Wakatsuki, Masashi Akaike, Masataka Sata and 西尾進 : 脳卒中患者における心エコー検査の現状:徳島大学病院SCU搬送例における検討, 脳卒中研究会, Feb. 2009.

Report:

1.	西尾進, 笹田倫子, 平田有紀奈, 鳥居裕太, 山尾雅美, Hirotsugu Yamada, Toshio Doi and Masataka Sata : 推算糸球体濾過量 (eGFR) と関連する腎エコー検査指標について, 超音波検査技術, Vol.41, No.0, S201, Jun. 2016.
2.	平田有紀奈, Hirotsugu Yamada, Kenya Kusunose, 鈴川理乃, 衣川尚知, 鳥居裕太, 天野里江, 山尾雅美, 西尾進, 瀬野弘光, 西條良仁 and Masataka Sata : 心外膜下脂肪厚は虚血性心疾患の壁運動回復の有無を反映する, 超音波検査技術, Vol.41, No.0, S158, Jun. 2016.
3.	長瀬襟加, 鳥居裕太, 西尾進, 平田有紀奈, 山尾雅美, Seiji Iwamoto, Hirotsugu Yamada, Naoki Muguruma and Masataka Sata : 好酸球性胆管炎の1例, 超音波検査技術, Vol.41, No.1, 128, Feb. 2016.
4.	長瀬襟加, 鳥居裕太, 西尾進, 松本力三, 平田有紀奈, 山尾雅美, 中野万有里, Seiji Iwamoto, Shoichiro Takao, Hirotsugu Yamada and Masataka Sata : 重複下大静脈に血栓を認めた1例, 超音波検査技術, Vol.41, No.5, 584, 2016.
5.	鳥居裕太, 西尾進, 鈴川理乃, 平田有紀奈, 天野里江, 山尾雅美, Mika Bando, Hajime Kinoshita, Shoichiro Takao, Kenya Kusunose, Hirotsugu Yamada and Masataka Sata : 感染性心内膜炎が契機となった右脛骨腓骨動脈感染性動脈瘤の1例, 超音波検査技術, Vol.40, No.suppl, S158, May 2015.
6.	平田有紀奈, Hirotsugu Yamada, 西尾進, 堀家由貴, 玉井佑里恵, 鳥居裕太, 天野里江, 山尾雅美, Mika Bando, 林修司, Kenya Kusunose and Masataka Sata : 肺高血圧を伴う右肺動脈上行大動脈起始の1例, 超音波検査技術, Vol.40, No.1, 85, Mar. 2015.
7.	石井亜由美, Takayuki Ise, 西川幸治, 後藤強, Shusuke Yagi, Shinsuke Katoh and Masataka Sata : 徳島大学病院での心臓リハビリテーションの現状, 心臓リハビリテーション, Vol.19, No.1, 161-162, Feb. 2014.

Patent:

1.	Masataka Sata and Hirotsugu Yamada : 超音波エコーによる頚動脈プラークの性状判定方法, 2010-73153.
2.	Masataka Sata, 墨誠, 立石法史 and 小野佳子 : 虚血後血管新生促進剤および血流改善剤, 2007-111975.
3.	通元夫, 赤木正明, Yutaka Nakaya, Masataka Sata, Nagakatsu Harada, 小川和男, 野河信太郎, 甲斐伸二, 金子祐輔, 稲本潔 and 冨田雅巳 : 4-置換安息香酸誘導体の個体分散体，その製造方法およびそれを含む医薬組成物, (Jun. 2014), 2014-186501 (Jun. 2014).
4.	Masataka Sata, Hirotsugu Yamada, Kenya Kusunose and Junko Hotsuchi : 起立性調節障害の治療用加圧装置, (Feb. 2014), (Aug. 2014), PCT/JP2014/054779.
5.	Masataka Sata, Hirotsugu Yamada and Junko Hotsuchi : 体位性頻脈症候群の治療用加圧装置, (Jan. 2014), 2014-009175 (Jan. 2014).
6.	Masataka Sata and Hirotsugu Yamada : 頸動脈プラークのエコー画像生成方法及び評価, (Jan. 2011), 2012-506873 (Jun. 2015).
7.	Masataka Sata and Hirotsugu Yamada : 頸動脈プラークのエコー画像生成方法及び評価装置, (Jan. 2011), (Sep. 2011), 5765823 (Jun. 2015).
8.	Masataka Sata and 畑江和夫 : フィブロイン糸を使用した小動脈用人工血管, (Apr. 2008), (Jul. 2010), 4541336 (Sep. 2010).
9.	島村宗尚, 森下竜一, 若山幸示 and Masataka Sata : 頭蓋内血管障害非ヒト動物モデルおよびその作製方法, (Nov. 2006), (Jun. 2008), 5034045 (Jun. 2008).
10.	Masataka Sata : 臓器移植後拒絶反応としての移植後動脈硬化症の予防及び/又は治療剤, (Nov. 2002), PCT/JP02/11441 (Nov. 2002).
11.	Masataka Sata and 中村正一 : カテーテルを兼用する医療用ガイドワイヤー, (Jun. 2001), (Jun. 2004), 2002-510149 (Jun. 2001).

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

Studies on mechanism and therapeutic approach of atherosclerosis using genetically-modified mice and fresh cadavers (Project/Area Number: 23K24330 )
Research on iPS cell culture using silk nanofiber 3D structures fabricated by AI-controlled technology (Project/Area Number: 20K05629 )
Development of therapeutic approach to diabetes-related vascular dysfunction targeting DNA sensors (Project/Area Number: 19K08584 )
Novel mechanism of chronic inflammation in progression and destabilization of atherosclerotic plaque (Project/Area Number: 19H03654 )
Elucidation of the mechanism of cardiac remodeling and arrhythmogenesis via toll-like receptor (TLR) 9 (Project/Area Number: 18K08077 )
The role of TLR9, a DNA sensor, in the development of vascular inflammation and atherogenesis (Project/Area Number: 16K09517 )
A study to elucidate the mechanism by which sterile chronic inflammation occurs in arterial wall and perivascular adipose tissue (Project/Area Number: 16H05299 )
Development of novel analytical NMR system for regenerative medical materials and its application for silk artificial vascular grafts (Project/Area Number: 26248050 )
Development of therapies for severe ischemic cardiomyopathy to substute heart transplantation (Project/Area Number: 25670390 )
microRNA released from adipose cells regulate vascular remodeling (Project/Area Number: 25461131 )
The role of TLR9 in the development of insulin resistance (Project/Area Number: 25460369 )
Visualization of chronic inflammation in arterial wall and perivascular adipose tissue (Project/Area Number: 25293184 )
Development of a novel revascularization method to treat diffuse coronary artery diseases with transplantation of artery and adipose tissues (Project/Area Number: 24659392 )
A new treatment for refractory non-ischemic heart disease with ghrelin via multifaceted effects (Project/Area Number: 24591056 )
Development of a novel treatment for coronary artery diseases by replacement of the epicardial adipose tissue (Project/Area Number: 23659420 )
Development of new treatments for cardiac remodeling after myocardial infarction using heparin cofactor II (Project/Area Number: 23591046 )
周囲脂肪組織を標的とした新規血管保護療法の開発 (Project/Area Number: 22659155 )
The regulation of endothelial migration and angiogenesis by transcriptiona l coact I vator PGC-1aIpha (Project/Area Number: 22590825 )
Elucidation of molecular mechanism of plaque destabilization and identification of predictable factors for acute coronary syndrome (Project/Area Number: 22390159 )
Functional role of pathogen sensors and their endogenous ligands in the metabolic syndrome (Project/Area Number: 21117007 )
Bidirectional effects of statins on the formation and growth of cerebral aneurysms (Project/Area Number: 21591844 )
A new treatment for arrhythmia with ghrelin via the modulation of autonomic nerve activity (Project/Area Number: 21590899 )
molecular mechanisms in the formation and rupture of cerebral aneurysm and impact of drug treatment (Project/Area Number: 21390412 )
Identification of novel regulator of atherosclerosis and development of molecular imaging technique (Project/Area Number: 19390207 )
血管の恒常性維持とリモデリングにおける外膜周囲脂肪組織の役割 (Project/Area Number: 18052003 )
AMP活性化タンパクキナーゼの抗動脈硬化作用と血管新生作用の検討 (Project/Area Number: 17659229 )
ナノ粒子を用いた心筋組織幹細胞活性化療法の開発 (Project/Area Number: 17659228 )
Investigation on the functional significance of myosin subfragment-2 (Project/Area Number: 17590710 )
Molecular Mechanism of Plaque Destabilization and Development of Therapeutic Strategy (Project/Area Number: 17390227 )
血管細胞の起源と運命を可視化する分子イメージング技術の開発 (Project/Area Number: 16659194 )
Studies on visualization of arteriosclerotic lesion using vascular cell-derived vasoactive substances (Project/Area Number: 16390217 )
脂肪前駆細胞の同定ならびにその機能解析 (Project/Area Number: 16046204 )
成体幹細胞を用いたバイオ人工血管の開発 (Project/Area Number: 15659180 )
細胞外基質による血管前駆細胞の分化誘導-血管内膜増殖阻害の試み- (Project/Area Number: 15591344 )
ROLE OF ABERRANT IRON HOMEOSTASIS AND INCREASED PRODUCTION OF REACTIVE OXYGEN SPECIES IN THE DEVELOPMENT OF CARDIOVASCULAR DAMAGE INDUCED BY ANGIOTENSIN II (Project/Area Number: 15590722 )
Investigation on the functional significance of myosin light chain kinase and myosin light chain phosphorylation (Project/Area Number: 15590721 )
Idermfiration and Charactetizaiion of Bone Marrow-derived Vascular Progenitor Cells (Project/Area Number: 15390241 )
病的血管リモデリングに関与する成体幹細胞の同定と分化様式の解明 (Project/Area Number: 15039213 )
動脈硬化における増殖内膜を構成する血管平滑筋細胞の起源およびその除去に関する研究 (Project/Area Number: 14657162 )
Development of a Gene Transfer and Functional Evaluation System for an Isolated Single Cardiac Myocyte as a model for the Gene Therapy (Project/Area Number: 13670692 )
Development of novel therapeutic options for treating heart failure targeting the myosin light chain (Project/Area Number: 13670689 )
Identification and regulation of differentiation In bone marrow -derived vascular progenitor cells (Project/Area Number: 13557061 )
Role of apoptosis of vascular endothelial cells In atherosclerosis (Project/Area Number: 13470141 )
Research on mechanisms for vascular action of adrenomedullin (Project/Area Number: 10218202 )
Search by Researcher Number (80345214)

Professor : Sata, Masataka

Research

Personal Web Page

Field of Study

Subject of Study

Book / Paper

Book:

Academic Paper (Judged Full Paper):

Academic Paper (Unrefereed Paper):

Academic Letter:

Review, Commentary:

Proceeding of International Conference:

Proceeding of Domestic Conference:

Products:

Et cetera, Workshop:

Report:

Patent:

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)