Tokushima University / Educator and Researcher Directory --- Ikeda, Yasumasa

Personal Web Page

https://yasuike2.wixsite.com/website

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

https://orcid.org/0000-0003-4318-7349 (ORCID)

Field of Study

○	Pharmacology, Cardiovascular Medicine, Cardiovascular Endocrinology and Metabolism
○	Internal Medicine
○	Nephrology

Subject of Study

○	心血管・内分泌代謝疾患における鉄作用, 鉄を標的とした新規治療法の開発, 心血管疾患における性ホルモン，特に男性ホルモンの意義 (ferrum, androgen)
○
○

Book / Paper

Book:

1.	Toshiaki Tamaki and Yasumasa Ikeda : 疾病の成り立ちと回復の促進薬理学(第4版)(分担執筆各論4・5・6), Oct. 2023.
2.	Yasumasa Ikeda and Yuya Horinouchi : 8章血液・造血器・リンパ系( 新しい薬理学), 西村書店, May 2018.
3.	Yasumasa Ikeda and Toshiaki Tamaki : Annual Review2015腎臓---腎疾患と鉄代謝異常---, 株式会社中外医学社, Jan. 2015.
4.	Licht Miyamoto, 山根萌, 冨田洋輔, Keisuke Ishizawa, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : ヒト腎糸球体内皮細胞における亜硝酸塩によるAMPK-eNOS活性化経路の検討, TOKYO IGAKUSHA, Oct. 2014.
5.	Yasumasa Ikeda, 田島壮一郎, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 腎とフリーラジカル第11集, TOKYO IGAKUSHA, Tokyo, Jan. 2013.
6.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Shoko Fujii, Jumpei Taniguchi, Yuki Izawa-Ishizawa, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : 腎とフリーラジカル第11集, TOKYO IGAKUSHA, Tokyo, Jan. 2013.
7.	Koichiro Tsuchiya, Keisuke Ishizawa, Licht Miyamoto, Yuya Horinouchi, Yasumasa Ikeda, Yoshitaka Kihira, Shuhei Tomita and Toshiaki Tamaki : 腎とフリーラジカル第11集, TOKYO IGAKUSHA, Tokyo, Jan. 2013.
8.	田島壮一郎, Koichiro Tsuchiya, 濱本磨以, 久住祥子, Yuya Horinouchi, 八木祐子, 櫻田巧, Keisuke Ishizawa, Yasumasa Ikeda, Yoshitaka Kihira, Shuhei Tomita and Toshiaki Tamaki : 腎とフリーラジカル第10集, TOKYO IGAKUSHA, Tokyo, Jun. 2010.

Academic Paper (Judged Full Paper):

1.	Steeve Akumwami, Asadur Rahman, Masafumi Funamoto, Akram Hossain, Asahiro Morishita, Yasumasa Ikeda, Hiroaki Kitamura, Kento Kitada, Takahisa Noma, Yuichi Ogino and Akira Nishiyama : Effects of D-Allose on experimental cardiac hypertrophy., Journal of Pharmacological Sciences, Vol.156, No.2, 142-148, 2024. (Summary) The hallmark of pathological cardiac hypertrophy is the decline in myocardial contractility caused by an energy deficit resulting from metabolic abnormalities, particularly those related to glucose metabolism. Here, we aim to explore whether D-Allose, a rare sugar that utilizes the same transporters as glucose, may restore metabolic equilibrium and reverse cardiac hypertrophy. Isolated neonatal rat cardiomyocytes were stimulated with phenylephrine and treated with D-Allose simultaneously for 48 h. D-Allose treatment resulted in a pronounced reduction in cardiomyocyte size and cardiac remodelling markers accompanied with a dramatic reduction in the level of intracellular glucose in phenylephrine-stimulated cells. The metabolic flux analysis provided further insights revealing that D-Allose exerted a remarkable inhibition of glycolysis as well as glycolytic capacity. Furthermore, in mice subjected to a 14-day continuous infusion of isoproterenol (ISO) to induce cardiac hypertrophy, D-Allose treatment via drinking water notably reduced ISO-induced cardiac hypertrophy and remodelling markers, with minimal effects on ventricular wall thickness observed in echocardiographic analyses. These findings indicate that D-Allose has the ability to attenuate the progression of cardiomyocyte hypertrophy by decreasing intracellular glucose flux and inhibiting glycolysis. (Keyword) Animals / Cardiomegaly / Myocytes, Cardiac / Glycolysis / Isoproterenol / Glucose / Phenylephrine / male / Cells, Cultured / Mice, Inbred C57BL / Rats / knockout mice / Disease Models, Animal / Rats, Sprague-Dawley (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphs.2024.08.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39179333 ● Search Scopus @ Elsevier (PMID): 39179333 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jphs.2024.08.002 (DOI: 10.1016/j.jphs.2024.08.002, PubMed: 39179333)
2.	Xi Chen, Asadur Rahman, Steeve Akumwami, Asahiro Morishita, Kento Kitada, Yasumasa Ikeda, Masafumi Funamoto and Akira Nishiyama : Effects of D-allose on ATP production and cell viability in neonatal rat cardiomyocytes., Journal of Pharmacological Sciences, Vol.154, No.4, 274-278, 2024. (Summary) 2-Deoxy-d-glucose (2DG) induces anticancer effects through glycolytic inhibition but it may raise the risk of arrhythmia. The rare monosaccharide d-allose also has anticancer properties, but its cardiac effects are unknown. We examined the effects of d-allose on adenosine triphosphate (ATP) production in neonatal rat cardiomyocytes. We showed that 25 mM d-allose selectively reduced glycolytic ATP, but had minimal impact on mitochondrial ATP, while 1 mM 2DG strongly inhibited both. Furthermore, d-allose had less impact on cell viability and was less cytotoxic than 2DG; neither compound caused apoptosis. Thus, d-allose selectively diminished glycolytic ATP production with no apparent effects on cardiomyocytes. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphs.2024.02.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38485345 ● Search Scopus @ Elsevier (PMID): 38485345 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jphs.2024.02.009 (DOI: 10.1016/j.jphs.2024.02.009, PubMed: 38485345)
3.	Honoka Tsunematsu, Masaki Imanishi, Yuka Uemura, Yoshiya Higaki, Miyu Morisaki, Akari Katsura, Licht Miyamoto, Masafumi Funamoto, Mayuko Ichimura-Shimizu, Yuya Horinouchi, Yasumasa Ikeda, Koichi Tsuneyama and Koichiro Tsuchiya : Indigo Leaves-Induced Pulmonary Arterial Remodeling without Right Ventricular Hypertrophy in Rats., Biological & Pharmaceutical Bulletin, Vol.47, No.7, 1350-1359, 2024. (Summary) Indigo naturalis (IN), derived from the leaves of the indigo plant, is a traditional Chinese medicine that has historically been used for its anti-inflammatory properties in the treatment of various diseases, including ulcerative colitis (UC). However, long-term use of IN in UC patients is incontrovertibly associated with the onset of pulmonary arterial hypertension (PAH). To investigate the mechanisms by which IN induces PAH, we focused on the raw material of IN, indigo leaves (IL). Only the condition of long-term chronic (6 months) and high-dose (containing 5% IL in the control diet) administration of IL induced medial thickening in the pulmonary arteries without right ventricular hypertrophy in our rat model. IL administration for a month did not induce pulmonary arterial remodeling but increased endothelin-1 (ET-1) expression levels within endothelial cell (EC) layers in the lungs. Gene Expression Omnibus analysis showed that ET-1 is a key regulator of PAH and that the IL component indican and its metabolite IS induced ET-1 mRNA expression via reactive oxygen species-dependent mechanism. We identified the roles of indican and IS in ET-1 expression in ECs, which were linked to pulmonary arterial remodeling in an animal model. (Keyword) Animals / Plant Leaves / Pulmonary Artery / Male / Endothelin-1 / Vascular Remodeling / Hypertrophy, Right Ventricular / Rats, Sprague-Dawley / Hypertension, Pulmonary / Rats / Endothelial Cells / Lung (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b24-00289 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39085074 ● CiNii @ National Institute of Informatics (CRID): 1390863937794660096 ● Summary page in Scopus @ Elsevier: 2-s2.0-85199865455 (DOI: 10.1248/bpb.b24-00289, PubMed: 39085074, CiNii: 1390863937794660096, Elsevier: Scopus)
4.	Masaki Imanishi, Takahisa Inoue, Keijo Fukushima, Ryosuke Yamashita, Ryo Nakayama, Masataka Nojima, Kosuke Kondo, Yoshiki Gomi, Honoka Tsunematsu, Kohei Goto, Licht Miyamoto, Masafumi Funamoto, Masaya Denda, Keisuke Ishizawa, Akira Otaka, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya : CA9 and PRELID2; hypoxia-responsive potential therapeutic targets for pancreatic ductal adenocarcinoma as per bioinformatics analyses., Journal of Pharmacological Sciences, Vol.153, No.4, 232-242, 2023. (Summary) A strong hypoxic environment has been observed in pancreatic ductal adenocarcinoma (PDAC) cells, which contributes to drug resistance, tumor progression, and metastasis. Therefore, we performed bioinformatics analyses to investigate potential targets for the treatment of PDAC. To identify potential genes as effective PDAC treatment targets, we selected all genes whose expression level was related to worse overall survival (OS) in The Cancer Genome Atlas (TCGA) database and selected only the genes that matched with the genes upregulated due to hypoxia in pancreatic cancer cells in the dataset obtained from the Gene Expression Omnibus (GEO) database. Although the extracted 107 hypoxia-responsive genes included the genes that were slightly enriched in angiogenic factors, TCGA data analysis revealed that the expression level of endothelial cell (EC) markers did not affect OS. Finally, we selected CA9 and PRELID2 as potential targets for PDAC treatment and elucidated that a CA9 inhibitor, U-104, suppressed pancreatic cancer cell growth more effectively than 5-fluorouracil (5-FU) and PRELID2 siRNA treatment suppressed the cell growth stronger than CA9 siRNA treatment. Thus, we elucidated that specific inhibition of PRELID2 as well as CA9, extracted via exhaustive bioinformatic analyses of clinical datasets, could be a more effective strategy for PDAC treatment. (Keyword) Humans / Carbonic Anhydrase IX / Antigens, Neoplasm / Carcinoma, Pancreatic Ductal / Pancreatic Neoplasms / Hypoxia / RNA, Small Interfering / Computational Biology / Pancreatic Neoplasms (Tokushima University Institutional Repository) ● Metadata: 119176 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphs.2023.10.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37973221 ● CiNii @ National Institute of Informatics (CRID): 1050018428980929664 ● Search Scopus @ Elsevier (PMID): 37973221 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jphs.2023.10.003 (Tokushima University Institutional Repository: 119176, DOI: 10.1016/j.jphs.2023.10.003, PubMed: 37973221, CiNii: 1050018428980929664)
5.	Aoi Suenaga, Yasuyuki Seto, Masafumi Funamoto, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : TJ-17 (Goreisan) mitigates renal fibrosis in a mouse model of folic acid-induced chronic kidney disease., Journal of Pharmacological Sciences, Vol.153, No.1, 31-37, 2023. (Summary) TJ-17 may have a novel preventive effect against inflammation, oxidative stress, and fibrosis, contributing to innovation in the treatment of CKD. (Tokushima University Institutional Repository) ● Metadata: 118452 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphs.2023.07.001 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37524452 ● Search Scopus @ Elsevier (PMID): 37524452 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jphs.2023.07.001 (Tokushima University Institutional Repository: 118452, DOI: 10.1016/j.jphs.2023.07.001, PubMed: 37524452)
6.	Yuya Horinouchi, Yuka Murashima, Yuto Yamada, Shun Yoshioka, Keijo Fukushima, Takumi Kure, Naofumi Sasaki, Masaki Imanishi, Hiromichi Fujino, Koichiro Tsuchiya, Kazuaki Shinomiya and Yasumasa Ikeda : Pemafibrate inhibited renal dysfunction and fibrosis in a mouse model of adenine-induced chronic kidney disease., Life Sciences, Vol.321, 121590, 2023. (Summary) These results demonstrated the renoprotective effects of pemafibrate in CKD mice, confirming its potential as a therapeutic agent for renal disorders. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.lfs.2023.121590 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36940907 ● CiNii @ National Institute of Informatics (CRID): 1360017282221457024 ● Summary page in Scopus @ Elsevier: 2-s2.0-85151399970 (DOI: 10.1016/j.lfs.2023.121590, PubMed: 36940907, CiNii: 1360017282221457024, Elsevier: Scopus)
7.	Tomoyo Hara, Ryoko Uemoto, Akiko Sekine, Yukari Mitsui, Shiho Masuda, Hiroki Yamagami, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Yasumasa Ikeda, Itsuro Endo, Soichi Honda, Katsuhiko Yoshimoto, Akira Kondo, Toshiaki Tamaki, Toshio Matsumoto, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Plasma Heparin Cofactor II Activity Is Inversely Associated with Hepatic Fibrosis of Non-Alcoholic Fatty Liver Disease in Patients with Type 2 Diabetes Mellitus., Journal of Atherosclerosis and Thrombosis, 2022. (Summary) Plasma HCII activity was inversely associated with clinical hepatic fibrosis indices including FIB-4 index, NFS and APRI and with the prevalence of advanced hepatic fibrosis in patients with T2DM. The results suggest that HCII can serve as a novel biomarker for assessment of hepatic fibrosis of NAFLD in patients with T2DM. (Tokushima University Institutional Repository) ● Metadata: 118258 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.63752 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36244745 ● Search Scopus @ Elsevier (PMID): 36244745 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.63752 (Tokushima University Institutional Repository: 118258, DOI: 10.5551/jat.63752, PubMed: 36244745)
8.	Masafumi Funamoto, Yoichi Sunagawa, Yasufumi Katanasaka, Toru Kato, Junichi Funada, Yoichi Ajiro, Maki Komiyama, Masaharu Akao, Akihiro Yasoda, Hajime Yamakage, Noriko Satoh-Asahara, Hiromichi Wada, Yasumasa Ikeda, Tatsuya Morimoto and Koji Hasegawa : Effects of high-absorption curcumin for the prevention of hypertensive heart disease: a double-blind, placebo-controlled, randomized clinical study., European Heart Journal Open, Vol.107, 154457, 2022. (Summary) ' ratio, rather it significantly inhibited the increase in plasma BNP levels in patients with initial signs of hypertensive heart disease. (Tokushima University Institutional Repository) ● Metadata: 118447 (Link to Publication Site) ● Publication site (DOI): 10.1093/ehjopen/oeac057 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36172003 ● Search Scopus @ Elsevier (PMID): 36172003 ● Search Scopus @ Elsevier (DOI): 10.1093/ehjopen/oeac057 (Tokushima University Institutional Repository: 118447, DOI: 10.1093/ehjopen/oeac057, PubMed: 36172003)
9.	Yasumasa Ikeda, Masafumi Funamoto, Seiji Kishi, Masaki Imanishi, Ken-ichi Aihara, Yoshiki Kashiwada and Koichiro Tsuchiya : The novel preventive effect of a Japanese ethical Kampo extract formulation TJ-90 (Seihaito) against cisplatin-induced nephrotoxicity, Phytomedicine, Vol.103, No.8, 154213, 2022. (Tokushima University Institutional Repository) ● Metadata: 117134 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.phymed.2022.154213 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.phymed.2022.154213 (Tokushima University Institutional Repository: 117134, DOI: 10.1016/j.phymed.2022.154213)
10.	Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Licht Miyamoto, Hitayama Tasuku, Hideko Nagasawa, Toshiaki Tamaki and Koichiro Tsuchiya : Role of ferroptosis in cisplatin-induced acute nephrotoxicity in mice, Journal of Trace Elements in Medicine and Biology, Vol.67, 126798, 2021. (Tokushima University Institutional Repository) ● Metadata: 116131 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jtemb.2021.126798 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.jtemb.2021.126798 (Tokushima University Institutional Repository: 116131, DOI: 10.1016/j.jtemb.2021.126798)
11.	Tomoyo Hara, Ryoko Uemoto, Akiko Sekine, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Yasumasa Ikeda, Itsuro Endo, Soichi Honda, Katsuhiko Yoshimoto, Akira Kondo, Toshiaki Tamaki, Toshio Matsumoto, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Plasma Heparin Cofactor II Activity Is Inversely Associated with Albuminuria and Its Annual Deterioration in Patients with Diabetes., Journal of Diabetes Investigation, 2021. (Summary) The plasma HCII activity was inversely and specifically associated with glomerular injury in patients with diabetes. The results suggest that HCII can serve as a novel predictive factor for early-stage DKD development, as represented by albuminuria. (Tokushima University Institutional Repository) ● Metadata: 116545 (Link to Publication Site) ● Publication site (DOI): 10.1111/jdi.13602 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34043882 ● Search Scopus @ Elsevier (PMID): 34043882 ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.13602 (Tokushima University Institutional Repository: 116545, DOI: 10.1111/jdi.13602, PubMed: 34043882)
12.	Yuki Izawa-Ishizawa, Mitsuhiro Goda, Fuka Aizawa, Yoshito Zamami, Hirofumi Hamano, Kenta Yagi, Yasumasa Ikeda, Keisuke Ishizawa and Toshiaki Tamaki : 薬剤誘発性大動脈解離易発症モデルマウスを用いた薬効評価, Shikoku Acta Medica, Vol.77, No.1,2, 57-62, 2021. (Summary) Aortic dissection (or dissecting aortic aneurysm) is a condition in which the aortic wall is separated into two layers at the medial level to form a pseudocavity. The intima crack, called the ``entry'', allows blood to tear through the medial layer and flow in. The location of the ``entry'' and the extent of the dissection can cause a variety of serious complications, including rupture, cardiac tamponade, and obstruction of branched vessels. According to the Guideline on Diagnosis and Treatment of Aortic Aneurysm and Aortic Dissection 2020, it is estimated that 61.4% of the onset of dissection die before arrival at the hospital, and 93% will die within 24 hours after the onset. It has been suggested that the morbidity rate has been increasing in recent years. Since many of them have a fatal prognosis, it is an important issue to prevent the onset itself. However, no effective therapeutic agent or preventive strategy has been established so far. The first reason is that it is extremely difficult to design clinical studies because aortic dissection traced the rapid onset and progression. The second is that the pathophysiology and preventive drug search are not sufficiently conducted even at the basic research level. Epidemiologically, the results of the International Registry of Aortic Dissection (IRAD) revealed that aging, hypertension, atherosclerosis, and hereditary connective tissue diseases are risk factors. The aortic aneurysm also shows similar pathological conditions caused by these risk factors. However, one of the major differences between aneurysm and dissection is the presence of aortic intima rupture. Therefore, we attempted to establish a mouse model developing dissection at a high rate by adding the endothelial dysfunction to a pharmacologically induced aortic aneurysm model mouse. Furthermore, we evaluated the efficacy of pitavastatin and several nutrients using our novel model mice and verified its usefulness as a model animal. (Keyword) aortic dissection / endothelial dysfunction / statin / polyphenol / large medical databases (Tokushima University Institutional Repository) ● Metadata: 116038 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050851320431028352 (Tokushima University Institutional Repository: 116038, CiNii: 1050851320431028352)
13.	Shimon Takahashi, Kenshi Takechi, Natsumi Jozukuri, Takahiro Niimura, Masayuki Chuma, Mitsuhiro Goda, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya, Hiroaki Yanagawa and Keisuke Ishizawa : Examination of the antiepileptic effects of valacyclovir using kindling mice- search for novel antiepileptic agents by drug repositioning using a large medical information database., European Journal of Pharmacology, Vol.902, 2021. (Summary) Despite the availability of more than 20 clinical antiepileptic drugs, approximately 30% of patients with epilepsy do not respond to antiepileptic drug treatment. Therefore, it is important to develop antiepileptic products that function via novel mechanisms. In the present study, we evaluated data from one of the largest global databases to identify drugs with antiepileptic effects, and subsequently attempted to understand the effect of the combination of antiepileptic drugs and valacyclovir in epileptic seizures using a kindling model. To induce kindling in mice, pentylenetetrazol at a dose of 40 mg/kg was administered once every 48 h. Valacyclovir was orally administered 30 min before antiepileptic drug injection in kindled mice, and behavioral seizures were monitored for 20 min following pentylenetetrazol administration. Additionally, c-Fos expression in the hippocampal dentate gyrus was measured in kindled mice. Valacyclovir showed inhibitory effects on pentylenetetrazol-induced kindled seizures. In addition, simultaneous use of levetiracetam and valacyclovir caused more potent inhibition of seizure activity, and neither valproic acid nor diazepam augmented the anti-seizure effect in kindled mice. Furthermore, kindled mice showed increased c-Fos levels in the dentate gyrus. The increase in c-Fos expression was significantly inhibited by the simultaneous use of levetiracetam and valacyclovir. The findings of the present study indicate that a combination of levetiracetam and valacyclovir had possible anticonvulsive effects on pentylenetetrazol-induced kindled epileptic seizures. These results suggest that valacyclovir may have an antiseizure effect in patients with epilepsy. (Tokushima University Institutional Repository) ● Metadata: 116301 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2021.174099 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33910036 ● Search Scopus @ Elsevier (PMID): 33910036 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2021.174099 (Tokushima University Institutional Repository: 116301, DOI: 10.1016/j.ejphar.2021.174099, PubMed: 33910036)
14.	Kenji Nishimura, Kensei Taguchi, Seiji Kishi, R Craig Brooks, Arisa Ochi, Hiroyuki Kadoya, Yasumasa Ikeda, Masashi Miyoshi, Masanori Tamaki, Hideharu Abe, Ken-Ichi Aihara, Naoki Kashihara and Kojiro Nagai : Dual disruption of eNOS and ApoE gene accelerates kidney fibrosis and senescence after injury., Biochemical and Biophysical Research Communications, Vol.556, 142-148, 2021. (Summary) mice (DKO) were obtained by breeding. Unilateral ureteral obstruction (UUO) was performed on 8-10 week old male mice and the degree of renal tubular injury, fibrosis and kidney senescence were evaluated. DKO manifested elevated blood pressure, higher total cholesterol and lower HDL than WT. DKO showed sustained kidney injury molecule-1 protein expression. Kidney fibrosis was significantly higher in ApoEKO and DKO. mRNA expression of genes related to kidney fibrosis was the highest in DKO. The mRNA expression of Zinc-α2-Glycoprotein and heme oxygenase-1 were significantly decreased in DKO. Furthermore, mRNA expression of p53, p21 and p16 were increased both in ApoEKO and DKO, with DKO being the highest. Senescence associated β-gal positive tubule area was significantly increased in DKO. Increased DNA damage and target of rapamycin-autophagy spatial coupling compartments (TASCCs) formation was found in DKO. Mice with endothelial dysfunction and dyslipidemia developed kidney fibrosis and accelerated senescence even in young mice after injury. These data highlight the fact managing lifestyle-related diseases from a young age is important for CKD prevention. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2021.03.111 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33845306 ● Search Scopus @ Elsevier (PMID): 33845306 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2021.03.111 (DOI: 10.1016/j.bbrc.2021.03.111, PubMed: 33845306)
15.	Hirofumi Hamano, Yasumasa Ikeda, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, Masayuki Chuma, Michiko Yamashita, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Izawa-Ishizawa Yuki, Licht Miyamoto, Ishizawa Keisuke, Hiromichi Fujino, Toshiaki Tamaki, Ken-ichi Aihara and Koichiro Tsuchiya : Diphenhydramine may be a preventive medicine against cisplatin-induced kidney toxicity, Kidney International, Vol.99, No.4, 885-889, 2021. (Summary) Cisplatin is widely used as an anti-tumor drug for the treatment of solid tumors. Unfortunately, it causes kidney toxicity as a critical side effect, limiting its use, given that no preventive drug against cisplatin-induced kidney toxicity is currently available. Here, based on a repositioning analysis of the Food and Drug Administration Adverse Events Reporting System, we found that a previously developed drug, diphenhydramine, may provide a novel treatment for cisplatin-induced kidney toxicity. To confirm this, the actual efficacy of diphenhydramine was evaluated in in vitro and in vivo experiments. Diphenhydramine inhibited cisplatin-induced cell death in kidney proximal tubular cells. Mice administered cisplatin developed kidney injury with significant dysfunction (mean plasma creatinine: 0.43 vs 0.15 mg/dl) and showed augmented oxidative stress, increased apoptosis, elevated inflammatory cytokines, and MAPKs activation. However, most of these symptoms were suppressed by treatment with diphenhydramine. Furthermore, the concentration of cisplatin in the kidney was significantly attenuated in diphenhydramine-treated mice (mean platinum content: 70.0 vs 53.4 μg/g dry kidney weight). Importantly, diphenhydramine did not influence or interfere with the anti-tumor effect of cisplatin in any of the in vitro or in vivo experiments. In a selected cohort of 98 1:1 matched patients from a retrospective database of 1467 patients showed that patients with malignant cancer who had used diphenhydramine before cisplatin treatment exhibited significantly less acute kidney injury compared to ones who did not (6.1 % vs 22.4 %, respectively). Thus, diphenhydramine demonstrated efficacy as a novel preventive medicine against cisplatin-induced kidney toxicity. (Tokushima University Institutional Repository) ● Metadata: 115399 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.kint.2020.10.041 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33307103 ● Search Scopus @ Elsevier (PMID): 33307103 ● Search Scopus @ Elsevier (DOI): 10.1016/j.kint.2020.10.041 (Tokushima University Institutional Repository: 115399, DOI: 10.1016/j.kint.2020.10.041, PubMed: 33307103)
16.	Hirofumi Hamano, Chisato Mitsuhashi, Yoshiko Suzuki, Yoshito Zamami, Kaito Tsujinaka, Naoto Okada, Takahiro Niimura, Tatsuya Hayama, Toru Imai, Shunsuke Ishida, Kumiko Sakamoto, Mitsuhiro Goda, Kenshi Takechi, Kenta Yagi, Masayuki Chuma, Yuya Horinouchi, Kazuaki Shinomiya, Yasumasa Ikeda, Yasushi Kirino, Toshimi Nakamura, Hiroaki Yanagawa, Yasuhiro Hamada and Keisuke Ishizawa : Effects of Palonosetron on Nausea and Vomiting Induced by Multiple-Day Chemotherapy: A Retrospective Study., Biological & Pharmaceutical Bulletin, Vol.44, No.4, 478-484, 2021. (Summary) RAs in controlling multiple-day chemotherapy-induced nausea and vomiting. (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b20-00609 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33790099 ● Search Scopus @ Elsevier (PMID): 33790099 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.b20-00609 (DOI: 10.1248/bpb.b20-00609, PubMed: 33790099)
17.	Kenta Yagi, Marin Mitstui, Yoshito Zamami, Takahiro Niimura, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Masayuki Chuma, Kimiko Fukunaga, Takahiro Shibata, Shunsuke Ishida, Takumi Sakurada, Naoto Okada, Hirofumi Hamano, Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Yanagawa and Keisuke Ishizawa : Investigation of drugs affecting hypertension in bevacizumab-treated patients and examination of the impact on the therapeutic effect., Cancer Medicine, 2020. (Summary) PPIs prevent hypertension in bevacizumab-treated patients but may reduce bevacizumab's anti-tumoral effects by inducing VEGF expression. (Tokushima University Institutional Repository) ● Metadata: 116288 (Link to Publication Site) ● Publication site (DOI): 10.1002/cam4.3587 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33231381 ● Search Scopus @ Elsevier (PMID): 33231381 ● Search Scopus @ Elsevier (DOI): 10.1002/cam4.3587 (Tokushima University Institutional Repository: 116288, DOI: 10.1002/cam4.3587, PubMed: 33231381)
18.	Yasumasa Ikeda, Hiroaki Watanabe, Tetsuya Shiuchi, Hirofumi Hamano, Yuya Horinouchi, Masaki Imanishi, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Yuki Izawa-Ishizawa, Licht Miyamoto, Keisuke Ishizawa, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Deletion of H-ferritin in macrophages alleviates obesity and diabetes induced by high-fat diet in mice, Diabetologia, Vol.63, No.8, 1588-1602, 2020. (Summary) Iron accumulation affects obesity and diabetes, both of which are ameliorated by iron reduction. Ferritin, an iron-storage protein, plays a crucial role in iron metabolism. H-ferritin exerts its cytoprotective action by reducing toxicity via its ferroxidase activity. We investigated the role of macrophage H-ferritin in obesity and diabetes. Conditional macrophage-specific H-ferritin (Fth, also known as Fth1) knockout (LysM-Cre Fth KO) mice were used and divided into four groups: wild-type (WT) and LysM-Cre Fth KO mice with normal diet (ND), and WT and LysM-Cre Fth KO mice with high-fat diet (HFD). These mice were analysed for characteristics of obesity and diabetes, tissue iron content, inflammation, oxidative stress, insulin sensitivity and metabolic measurements. RAW264.7 macrophage cells were used for in vitro experiments. Iron concentration reduced, and mRNA expression of ferroportin increased, in macrophages from LysM-Cre Fth KO mice. HFD-induced obesity was lower in LysM-Cre Fth KO mice than in WT mice at 12 weeks (body weight: KO 34.6 ± 5.6 g vs WT 40.1 ± 5.2 g). mRNA expression of inflammatory cytokines and infiltrated macrophages and oxidative stress increased in the adipose tissue of HFD-fed WT mice, but was not elevated in HFD-fed LysM-Cre Fth KO mice. However, WT mice fed an HFD had elevated iron concentration in adipose tissue and spleen, which was not observed in LysM-Cre Fth KO mice fed an HFD (adipose tissue [μmol Fe/g protein]: KO 1496 ± 479 vs WT 2316 ± 866; spleen [μmol Fe/g protein]: KO 218 ± 54 vs WT 334 ± 83). Moreover, HFD administration impaired both glucose tolerance and insulin sensitivity in WT mice, which was ameliorated in LysM-Cre Fth KO mice. In addition, energy expenditure, mRNA expression of thermogenic genes, and body temperature were higher in KO mice with HFD than WT mice with HFD. In vitro experiments showed that iron content was reduced, and lipopolysaccharide-induced Tnf-α (also known as Tnf) mRNA upregulation was inhibited in a macrophage cell line transfected with Fth siRNA. Deletion of macrophage H-ferritin suppresses the inflammatory response by reducing intracellular iron levels, resulting in the prevention of HFD-induced obesity and diabetes. The findings from this study highlight macrophage iron levels as a potential therapeutic target for obesity and diabetes. (Tokushima University Institutional Repository) ● Metadata: 114409 (Link to Publication Site) ● Publication site (DOI): 10.1007/s00125-020-05153-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32430665 ● Summary page in Scopus @ Elsevier: 2-s2.0-85085484596 (Tokushima University Institutional Repository: 114409, DOI: 10.1007/s00125-020-05153-0, PubMed: 32430665, Elsevier: Scopus)
19.	Masaki Imanishi, Yusuke Yamakawa, Keijo Fukushima, Raiki Ikuto, Akiko Maegawa, Yuki Izawa-Ishizawa, Yuya Horinouchi, Masateru Kondo, Masatoshi Kishuku, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda, Koichiro Tsuchiya, Hiromichi Fujino, Koichi Tsuneyama and Keisuke Ishizawa : Fibroblast-specific ERK5 deficiency changes tumor vasculature and exacerbates tumor progression in a mouse model., Naunyn-Schmiedeberg's Archives of Pharmacology, Vol.393, No.7, 1239-1250, 2020. (Summary) The roles of cancer-associated fibroblasts (CAFs) have been studied in the tumor progression, and CAFs are expected to become the new targets for cancer pharmacotherapies. CAFs contribute to tumor cell survival and proliferation, tumor angiogenesis, immune suppression, tumor inflammation, tumor cell invasion and metastasis, and extracellular matrix remodeling. However, detailed mechanisms of how CAFs function in the living system remain unclear. CAFs include α-smooth muscle actin, expressing activated fibroblasts similar to myofibroblasts, and are highly capable of producing collagen. Several reports have demonstrated the contributions of extracellular-signal-regulated kinase 5 (ERK5) in fibroblasts to the fibrotic processes; however, the roles of CAF-derived ERK5 remain unclear. To investigate the roles of CAF-derived ERK5 in the tumor progression, we created mice lacking the ERK5 gene specifically in fibroblasts. Colon-26 mouse colon cancer cells were implanted into the mice subcutaneously, and the histological analyses of the tumor tissue were performed after 2 weeks. Immunofluorescence analyses showed that recipient-derived fibroblasts existed within the tumor tissue. The present study demonstrated that fibroblast-specific ERK5 deficiency exacerbated tumor progression and it was accompanied with thicker tumor vessel formation and the increase in the number of activated fibroblasts. We combined the results of The Cancer Genome Atlas (TCGA) database analysis with our animal studies, and indicated that regulating ERK5 activity in CAFs or CAF invasion into the tumor tissue can be important strategies for the development of new targets in cancer pharmacotherapies. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00210-020-01859-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32307577 ● Search Scopus @ Elsevier (PMID): 32307577 ● Search Scopus @ Elsevier (DOI): 10.1007/s00210-020-01859-5 (DOI: 10.1007/s00210-020-01859-5, PubMed: 32307577)
20.	Yuki Tsuchihashi, Shinji Abe, Licht Miyamoto, Honoka Tsunematsu, Toshihiro Izumi, Aya Hatano, Hiroko Okuno, Megumi Yamane, Takashi Yasuoka, Yasumasa Ikeda and Koichiro Tsuchiya : Novel Hydrophilic Camptothecin Derivatives Conjugated to Branched Glycerol Trimer Suppress Tumor Growth without Causing Diarrhea in Murine Xenograft Models of Human Lung Cancer., Molecular Pharmaceutics, Vol.17, No.4, 1049-1058, 2020. (Summary) Camptothecin possesses broad antitumor spectra on various cancers. In spite of its marked tumor-suppressing potency, camptothecin is too hydrophobic to be solved in water and therefore not currently in clinical use. CPT-11 (irinotecan) is one of the hydrophilic analogues of camptothecin and widely prescribed. However, its water solubility is still low and furthermore evokes severe diarrhea. Therefore, we designed and synthesized novel highly hydrophilic camptothecin derivatives by conjugating SN38 with branched glycerol trimer (SN38-BGL), which we have been developing as a unique strategy to endow hydrophobic molecule with much hydrophilicity, to maximize the benefit of CPT-11 and minimize the adverse effects. The SN38-BGLs exhibited equivalent or slightly stronger tumor-suppressing effects in murine xenograft human lung cancer models compared to CPT-11. However, neither early- nor late-onset diarrhea was observed when SN38-BGL was administered. Heights of villi in jejunum and ileum were bigger than those from CPT-11-treated mice, indicating that SN38-BGL is less harmful than CPT-11. Ex vivo digestion by liver microsome did not yield SN38 but a couple of other molecules against our expectations, which suggests the involvement of other active metabolites than SN38 and may explain the differences. Hence, SN38-BGLs can be a novel hydrophilic camptothecin derivative without causing severe diarrhea. (Keyword) A549 Cells / Animals / Antineoplastic Agents, Phytogenic / Camptothecin / Cell Line, Tumor / Diarrhea / Disease Models, Animal / Glycerol / Heterografts / Humans / Hydrophobic and Hydrophilic Interactions / Irinotecan / Lung Neoplasms / Male / Mice / Mice, Inbred BALB C / Mice, Nude / Microsomes, Liver / Rats, Sprague-Dawley / Xenograft Model Antitumor Assays (Link to Publication Site) ● Publication site (DOI): 10.1021/acs.molpharmaceut.9b00249 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32068412 ● Search Scopus @ Elsevier (PMID): 32068412 ● Search Scopus @ Elsevier (DOI): 10.1021/acs.molpharmaceut.9b00249 (DOI: 10.1021/acs.molpharmaceut.9b00249, PubMed: 32068412)
21.	Tatsuya Tsuda, Masaki Imanishi, Mizuho Oogoshi, Mitsuhiro Goda, Yoshitaka Kihira, Yuya Horinouchi, Yoshito Zamami, Keisuke Ishizawa, Yasumasa Ikeda, Ichiro Hashimoto, Toshiaki Tamaki and Yuki Izawa-Ishizawa : Rho-associated protein kinase and cyclophilin a are involved in inorganic phosphate-induced calcification signaling in vascular smooth muscle cells., Journal of Pharmacological Sciences, Vol.142, No.3, 109-115, 2020. (Summary) Arterial calcification, a risk factor of cardiovascular events, develops with differentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells. Cyclophilin A (CypA) is a peptidyl-prolyl isomerase involved in cardiovascular diseases such as atherosclerosis and aortic aneurysms, and rho-associated protein kinase (ROCK) is involved in the pathogenesis of vascular calcification. CypA is secreted in a ROCK activity-dependent manner and works as a mitogen via autocrine or paracrine mechanisms in VSMCs. We examined the involvement of the ROCK-CypA axis in VSMC calcification induced by inorganic phosphate (Pi), a potent cell mineralization initiator. We found that Pi stimulated ROCK activity, CypA secretion, extracellular signal-regulated protein kinase (ERK) 1/2 phosphorylation, and runt-related transcription factor 2 expression, resulting in calcium accumulation in rat aortic smooth muscle cells (RASMCs). The ROCK inhibitor Y-27632 significantly suppressed Pi-induced CypA secretion, ERK1/2 phosphorylation, and calcium accumulation. Recombinant CypA was found to be associated with increased calcium accumulation in RASMCs. Based on these results, we suggest that autocrine CypA is mediated by ROCK activity and is involved in Pi-induced ERK1/2 phosphorylation following calcification signaling in RASMCs. (Tokushima University Institutional Repository) ● Metadata: 115530 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphs.2019.12.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31882204 ● Search Scopus @ Elsevier (PMID): 31882204 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jphs.2019.12.005 (Tokushima University Institutional Repository: 115530, DOI: 10.1016/j.jphs.2019.12.005, PubMed: 31882204)
22.	Hirofumi Hamano, Takahiro Niimura, Yuya Horinouchi, Yoshito Zamami, Kenshi Takechi, Mitsuhiro Goda, Masaki Imanishi, Masayuki Chuma, Yuki Izawa-Ishizawa, Licht Miyamoto, Keijo Fukushima, Hiromichi Fujino, Koichiro Tsuchiya, Keisuke Ishizawa, Toshiaki Tamaki and Yasumasa Ikeda : Proton pump inhibitors block iron absorption through direct regulation of hepcidin via the aryl hydrocarbon receptor-mediated pathway, Toxicology Letters, Vol.318, 86-91, 2020. (Summary) Proton pump inhibitors (PPIs) have been used worldwide to treat gastrointestinal disorders. A recent study showed that long-term use of PPIs caused iron deficiency; however, it is unclear whether PPIs affect iron metabolism directly. We investigated the effect of PPIs on the peptide hepcidin, an important iron regulatory hormone. First, we used the FDA Adverse Event Reporting System database and analyzed the influence of PPIs. We found that PPIs, as well as H2 blockers, increased the odds ratio of iron-deficient anemia. Next, HepG2 cells were used to examine the action of PPIs and H2 blockers on hepcidin. PPIs augmented hepcidin expression, while H2 blockers did not. In fact, the PPI omeprazole increased hepcidin secretion, and omeprazole-induced hepcidin upregulation was inhibited by gene silencing or the pharmacological inhibition of the aryl hydrocarbon receptor. In mouse experiments, omeprazole also increased hepatic hepcidin mRNA expression and blood hepcidin levels. In mice treated with omeprazole, protein levels of duodenal and splenic ferroportin decreased. Taken together, PPIs directly affect iron metabolism by suppressing iron absorption through the inhibition of duodenal ferroportin via hepcidin upregulation. These findings provide a new insight into the molecular mechanism of PPI-induced iron deficiency. (Tokushima University Institutional Repository) ● Metadata: 113812 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.toxlet.2019.10.016 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31669099 ● Search Scopus @ Elsevier (PMID): 31669099 ● Search Scopus @ Elsevier (DOI): 10.1016/j.toxlet.2019.10.016 (Tokushima University Institutional Repository: 113812, DOI: 10.1016/j.toxlet.2019.10.016, PubMed: 31669099)
23.	Yasumasa Ikeda, Akiho Satoh, Yuya Horinouchi, Hirofumi Hamano, Hiroaki Watanabe, Mizuki Imao, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Yuki Izawa-Ishizawa, Licht Miyamoto, Hirayama Tasuku, Hideko Nagasawa, Keisuke Ishizawa, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Iron accumulation causes impaired myogenesis correlated with MAPK signaling pathway inhibition by oxidative stress, The FASEB journal, Vol.33, No.8, 9551-9564, 2019. (Summary) Skeletal muscle atrophy is caused by disruption in the homeostatic balance of muscle degeneration and regeneration under various pathophysiological conditions. We have previously reported that iron accumulation induces skeletal muscle atrophy a ubiquitin ligase-dependent pathway. However, the potential effect of iron accumulation on muscle regeneration remains unclear. To examine the effect of iron accumulation on myogenesis, we used a mouse model with cardiotoxin (CTX)-induced muscle regeneration and C2C12 mouse myoblast cells . In mice with iron overload, the skeletal muscles exhibited increased oxidative stress and decreased expression of satellite cell markers. Following CTX-induced muscle injury, these mice also displayed delayed muscle regeneration with a decrease in the size of regenerating myofibers, reduced expression of myoblast differentiation markers, and decreased phosphorylation of MAPK signaling pathways. , iron overload also suppressed the differentiation of C2C12 myoblast cells but the suppression could be reversed by superoxide scavenging using tempol. Excess iron inhibits myogenesis oxidative stress, leading to an imbalance in skeletal muscle homeostasis.-Ikeda, Y., Satoh, A., Horinouchi, Y., Hamano, H., Watanabe, H., Imao, M., Imanishi, M., Zamami, Y., Takechi, K., Izawa-Ishizawa, Y., Miyamoto, L., Hirayama, T., Nagasawa, H., Ishizawa, K., Aihara, K.-I., Tsuchiya, K., Tamaki, T. Iron accumulation causes impaired myogenesis correlated with MAPK signaling pathway inhibition by oxidative stress. (Tokushima University Institutional Repository) ● Metadata: 113746 (Link to Publication Site) ● Publication site (DOI): 10.1096/fj.201802724RR (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31145863 ● Search Scopus @ Elsevier (PMID): 31145863 ● Search Scopus @ Elsevier (DOI): 10.1096/fj.201802724RR (Tokushima University Institutional Repository: 113746, DOI: 10.1096/fj.201802724RR, PubMed: 31145863)
24.	Hirofumi Hamano, Marin Mitsui, Yoshito Zamami, Kenshi Takechi, Takahiro Nimura, Naoto Okada, Keijo Fukushima, Masaki Imanishi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasushi Kirino, Toshimi Nakamura, Kazuhiko Teraoka, Yasumasa Ikeda, Hiromichi Fujino, Hiroaki Yanagawa, Toshiaki Tamaki and Keisuke Ishizawa : Irinotecan-induced neutropenia is reduced by oral alkalization drugs: analysis using retrospective chart reviews and the spontaneous reporting database., Supportive Care in Cancer, Vol.27, No.3, 849-856, 2019. (Summary) These data indicate that oral alkalization drugs may reduce the frequency of neutropenia caused by irinotecan administration, making it possible to increase the dose safely. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00520-018-4367-y (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30062585 ● Search Scopus @ Elsevier (PMID): 30062585 ● Search Scopus @ Elsevier (DOI): 10.1007/s00520-018-4367-y (DOI: 10.1007/s00520-018-4367-y, PubMed: 30062585)
25.	Masateru Kondo, Masaki Imanishi, Keijo Fukushima, Raiki Ikuto, Yoichi Murai, Yuya Horinouchi, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : Xanthine Oxidase Inhibition by Febuxostat in Macrophages Suppresses Angiotensin II-induced Aortic Fibrosis., American Journal of Hypertension, Vol.32, No.3, 249-256, 2019. (Summary) Our results suggested that FEB ameliorates Ang II-induced aortic fibrosis via suppressing macrophage-derived TGF-1 expression. (Link to Publication Site) ● Publication site (DOI): 10.1093/ajh/hpy157 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30351343 ● Search Scopus @ Elsevier (PMID): 30351343 ● Search Scopus @ Elsevier (DOI): 10.1093/ajh/hpy157 (DOI: 10.1093/ajh/hpy157, PubMed: 30351343)
26.	Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Toya Hiroki, Nagao Tomoko, Marin Morishita, Koichi Tsuneyama, Yuya Horinouchi, Yoshitaka Kihira, Kenshi Takechi, Yasumasa Ikeda, Koichiro Tsuchiya, Masanori Yoshizumi, Toshiaki Tamaki and Keisuke Ishizawa : Development of a novel aortic dissection mouse model and evaluation of drug efficacy using in-vivo assays and database analyses., Journal of Hypertension, Vol.37, No.1, 73-83, 2019. (Summary) Aortic dissection is a life-threatening disease. At present, the only therapeutic strategies available are surgery and antihypertensive drugs. Moreover, the molecular mechanisms underlying the onset of aortic dissection are still unclear. We established a novel aortic dissection model in mice using pharmacologically induced endothelial dysfunction. We then used the Japanese Adverse Drug Event Report database to investigate the role of pitavastatin in preventing the onset of aortic dissection. To induce endothelial dysfunction, Nω-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, was administered to C57BL/6 mice. Three weeks later, angiotensin II (Ang II) and β-aminopropionitrile (BAPN), a lysyl oxidase inhibitor, were administered with osmotic mini-pumps. False lumen formation was used as the pathological determinant of aortic dissection. The incidences of aortic dissection and death from aneurysmal rupture were significantly higher in the Nω-nitro-L-arginine methyl ester, Ang II, and BAPN (LAB) group than they were in the Ang II and BAPN (AB) group.Pitavastatin was administered orally to LAB mice. It significantly lowered the incidences of dissection and rupture. It also decreased inflammation and medial degradation, both of which were exacerbated in the LAB group. The Japanese Adverse Drug Event Report database analysis indicated that there were 113 cases of aortic dissection out of 95 090 patients (0.12%) not receiving statins but only six cases out of 16 668 patients receiving statins (0.04%) (odds ratio: 0.30; P = 0.0043). Our results suggest that endothelial dysfunction is associated with the onset of aortic dissection and pitavastatin can help prevent this condition. (Tokushima University Institutional Repository) ● Metadata: 113264 (Link to Publication Site) ● Publication site (DOI): 10.1097/HJH.0000000000001898 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30303488 ● Search Scopus @ Elsevier (PMID): 30303488 ● Search Scopus @ Elsevier (DOI): 10.1097/HJH.0000000000001898 (Tokushima University Institutional Repository: 113264, DOI: 10.1097/HJH.0000000000001898, PubMed: 30303488)
27.	Masaki Imanishi, Yuki Izawa-Ishizawa, T Sakurada, Y Kohara, Yuya Horinouchi, E Sairyo, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yasumasa Ikeda, Hiromichi Fujino, M Yoshizumi, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : Nitrosonifedipine, a Photodegradation Product of Nifedipine, Suppresses Pharmacologically Induced Aortic Aneurysm Formation., Pharmacology, Vol.102, No.5-6, 281-286, 2018. (Summary) We have reported that nitrosonifedipine (NO-NIF), a photodegradation product of nifedipine, has strong antioxidant and endothelial protective effects, and can suppress several cardiovascular diseases in animal models. The objective of the present study was to investigate the effects of NO-NIF on aortic aneurysm formation. The mice were infused with β-aminopropionitrile for 2 weeks and angiotensin II for 6 weeks to induce aortic aneurysm formation. The oxidative stress was measured by dihydroethidium staining and nitrotyrosine staining. The expressions of inflammation-related genes were assessed by quantitative real-time PCR and immunohistochemical staining. To clarify the mechanisms of how NO-NIF suppresses vascular cell adhesion molecule (VCAM)-1, endothelial cells were used in in vitro system. NO-NIF suppressed pharmacologically induced the aortic aneurysm formation and aortic expansion without blood pressure changes. NO-NIF suppressed elastin degradation and matrix metalloproteinase-2 mRNA expression. NO-NIF suppressed the reactive oxygen species-cyclophilin A positive feedback loop. Upregulated mRNA expressions of inflammation-related genes and endothelial VCAM-1 were suppressed by NO-NIF co-treatment in aortae. NO-NIF has the potential to be a new, nifedipine-derived therapeutic drug for suppressing aortic aneurysm formation by directly improving aortic structure with its strong ability to reduce oxidative stress and inflammation. (Keyword) Aminopropionitrile / Angiotensin II / Animals / Antigens, Differentiation / Antioxidants / Aortic Aneurysm / Chemokine CCL2 / Cyclophilins / Disease Models, Animal / Elastin / Endothelial Cells / Human Umbilical Vein Endothelial Cells / Humans / Male / Matrix Metalloproteinase 2 / Mice / Nifedipine / Nitroso Compounds / Oxidative Stress / Photolysis / Reactive Oxygen Species / Vascular Cell Adhesion Molecule-1 (Link to Publication Site) ● Publication site (DOI): 10.1159/000492577 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30253416 ● Summary page in Scopus @ Elsevier: 2-s2.0-85054191604 (DOI: 10.1159/000492577, PubMed: 30253416, Elsevier: Scopus)
28.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Hirofumi Hamano, Yuki Izawa-Ishizawa, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Renoprotective effects of a factor Xa inhibitor: fusion of basic research and a database analysis., Scientific Reports, Vol.8, No.1, 2018. (Summary) Renal tubulointerstitial injury, an inflammation-associated condition, is a major cause of chronic kidney disease (CKD). Levels of activated factor X (FXa), a blood coagulation factor, are increased in various inflammatory diseases. Therefore, we investigated the protective effects of an FXa inhibitor against renal tubulointerstitial injury using unilateral ureteral obstruction (UUO) mice (a renal tubulointerstitial fibrosis model) and the Food and Drug Administration Adverse Events Reporting System (FAERS) database. The renal expression levels of FX and the FXa receptors protease-activated receptor (PAR)-1 and PAR-2 were significantly higher in UUO mice than in sham-operated mice. UUO-induced tubulointerstitial fibrosis and extracellular matrix expression were suppressed in UUO mice treated with the FXa inhibitor edoxaban. Additionally, edoxaban attenuated UUO-induced macrophage infiltration and inflammatory molecule upregulation. In an analysis of the FAERS database, there were significantly fewer reports of tubulointerstitial nephritis for patients treated with FXa inhibitors than for patients not treated with inhibitors. These results suggest that FXa inhibitors exert protective effects against CKD by inhibiting tubulointerstitial fibrosis. (Tokushima University Institutional Repository) ● Metadata: 112445 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-018-29008-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30022146 ● Search Scopus @ Elsevier (PMID): 30022146 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-018-29008-2 (Tokushima University Institutional Repository: 112445, DOI: 10.1038/s41598-018-29008-2, PubMed: 30022146)
29.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The uremic toxin indoxyl sulfate interferes with iron metabolism by regulating hepcidin in chronic kidney disease, Nephrology, Dialysis, Transplantation, Vol.33, No.4, 586-597, 2018. (Tokushima University Institutional Repository) ● Metadata: 110922 (Link to Publication Site) ● Publication site (DOI): 10.1093/ndt/gfx252 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28992067 ● Search Scopus @ Elsevier (PMID): 28992067 ● Search Scopus @ Elsevier (DOI): 10.1093/ndt/gfx252 (Tokushima University Institutional Repository: 110922, DOI: 10.1093/ndt/gfx252, PubMed: 28992067)
30.	Wenting Xu, Licht Miyamoto, Haruna Aihara, Tomomi Yamaoka, Naonobu Tanaka, Yuki Tsuchihashi, Yasumasa Ikeda, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : Methanol extraction fraction from Citrus Sudachi peel exerts lipid reducing effects in cultured cells., The Journal of Medical Investigation : JMI, Vol.65, No.3.4, 225-230, 2018. (Summary) Ectopic fat accumulation is associated with insulin resistance and type 2 diabetes mellitus. Citrus sudachi is an evergreen tree that is found mainly in Tokushima Prefecture in Japan. Previously, it was demonstrated that Citrus sudachi could inhibit the rising trend of blood glucose and fatty acid in human subjects. In the current study, we illustrated the function of methanol extracts from sudachi peel and investigated the mechanism of this effect. We got the five kinds of methanol extracts by using diaion HP-20, and those were named by hydrophobicity from M-F1 to M-F5. Among the 5 kinds of sudachi methanol extracts, only M-F4 significantly decreased the intracellular triglyceride of C2C12 cells. It augmented the AMPK activity and increased the transcription of PPARα and its downstream targets CPT-1b and UCP2. In conclusion, M-F4 improved the lipid metabolism possibly through AMPK, PPARα and their downstream targets like CPT-1b and UCP2. Furthermore, this extract may be useful for preventing obesity and diabetes related diseases. J. Med. Invest. 65:225-230, August, 2018. (Keyword) AMP-Activated Protein Kinases / Animals / Cell Line / Citrus / Humans / Hypolipidemic Agents / Lipid Metabolism / methanol / knockout mice / Models, Biological / PPAR alpha / Phytotherapy / Plant Extracts / signal transduction / Sirtuin 1 / Triglycerides (Tokushima University Institutional Repository) ● Metadata: 112243 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.65.225 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30282865 ● Search Scopus @ Elsevier (PMID): 30282865 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.65.225 (Tokushima University Institutional Repository: 112243, DOI: 10.2152/jmi.65.225, PubMed: 30282865)
31.	Katsunori Tsuda, Licht Miyamoto, Shuichi Hamano, Yuri Morimoto, Yumi Kangawa, Chika Fukue, Yoko Kagawa, Yuya Horinouchi, Wenting Xu, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : Mechanisms of the pH- and Oxygen-Dependent Oxidation Activities of Artesunate., Biological & Pharmaceutical Bulletin, Vol.41, No.4, 555-563, 2018. (Summary) Artemisinin was discovered in 1971 as a constituent of the wormwood genus plant (Artemisia annua). This plant has been used as an herbal medicine to treat malaria since ancient times. The compound artemisinin has a sesquiterpene lactone bearing a peroxide group that offers its biological activity. In addition to anti-malarial activity, artemisinin derivatives have been reported to exert antitumor activity in cancer cells, and have attracted attention as potential anti-cancer drugs. Mechanisms that might explain the antitumor activities of artemisinin derivatives reportedly induction of apoptosis, angiogenesis inhibitory effects, inhibition of hypoxia-inducible factor-1 (HIF-1) activation, and direct DNA injury. Reactive oxygen species (ROS) generation is involved in many cases. However, little is known about the mechanism of ROS formation from artemisinin derivatives and what types of ROS are produced. Therefore, we investigated the iron-induced ROS formation mechanism by using artesunate, a water-soluble artemisinin derivative, which is thought to be the underlying mechanism involved in artesunate-mediated cell death. The ROS generated by the coexistence of iron(II), artesunate, and molecular oxygen was a hydroxyl radical or hydroxyl radical-like ROS. Artesunate can reduce iron(III) to iron(II), which enables generation of ROS irrespective of the iron valence. We found that reduction from iron(III) to iron(II) was activated in the acidic rather than the neutral region and was proportional to the hydrogen ion concentration. (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b17-00855 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29607928 ● Search Scopus @ Elsevier (PMID): 29607928 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.b17-00855 (DOI: 10.1248/bpb.b17-00855, PubMed: 29607928)
32.	Takahiro Niimura, Yoshito Zamami, Toshihiro Koyama, Yuki Izawa-Ishizawa, Masashi Miyake, Tadashi Koga, Keisaku Harada, Ayako Ohshima, Toru Imai, Yutaka Kondo, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki, Shiro Hinotsu, R Mitsunobu Kano and Keisuke Ishizawa : Hydrocortisone administration was associated with improved survival in Japanese patients with cardiac arrest., Scientific Reports, Vol.7, No.1, 2017. (Summary) There are few reports on hydrocortisone administration after cardiac arrest, and those that have been published included few subjects. This study aimed to evaluate the effect of hydrocortisone administration on the outcomes of patients who experienced cardiac arrest. We investigated the survival discharge rates and the length of hospital stay from cardiac arrest to discharge, stratified by use of hydrocortisone, using a Japanese health-insurance claims dataset that covers approximately 2% of the Japanese population. The study included the data of 2233 subjects who experienced either in-hospital or out-of-hospital cardiac arrest between January 2005 and May 2014. These patients were divided into two groups, based on the administration of hydrocortisone. We adjusted the baseline characteristics, medical treatment, and drug administration data of the two groups using propensity scores obtained via the inverse probability of treatment weighted method. The hydrocortisone group had a significantly higher survival discharge rate (13/61 [21.1%] vs. 240/2172 [11.0%], adjusted odds ratio: 4.2, 95% CI: 1.60-10.98, p = 0.004). In addition, the administration of hydrocortisone was independent predictor of survival to discharge (hazard ratio: 4.6, p < 0.001). The results demonstrate a correlation between hydrocortisone administration and the high rates of survival to discharge. (Tokushima University Institutional Repository) ● Metadata: 112397 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-017-17686-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29263333 ● Search Scopus @ Elsevier (PMID): 29263333 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-017-17686-3 (Tokushima University Institutional Repository: 112397, DOI: 10.1038/s41598-017-17686-3, PubMed: 29263333)
33.	Yasumasa Ikeda, Yuya Horinouchi, Hamano Hirofumi, Hirayama Tasuku, Seiji Kishi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Ken-ichi Aihara, Hideko Nagasawa, Koichiro Tsuchiya and Toshiaki Tamaki : Dietary iron restriction alleviates renal tubulointerstitial injury induced by protein overload in mice, Scientific Reports, Vol.7, No.1, 10621, 2017. (Summary) Increased proteinuria causes tubulointerstitial injury due to inflammation in chronic kidney disease (CKD). Iron restriction exhibits protective effects against renal dysfunction; however, its effects against protein overload-induced tubulointerstitial damage remain unclear. Here, we investigated dietary iron restriction effect on tubulointerstitial damage in mice with protein-overload tubulointerstitial injury. Renal tubulointerstitial injury in animal model was induced by intraperitoneal injection of an overdose of bovine serum albumin (BSA). We divided mice into three groups: normal saline + normal diet (ND), BSA + ND, and BSA + iron-restricted diet (IRD). BSA overload induced renal tubulointerstitial injury in the ND mice, which was ameliorated in the IRD mice. Inflammatory cytokines and extracellular matrix mRNA expression was upregulated in BSA + ND mice kidneys and was inhibited by IRD. BSA-induced increase in renal superoxide production, NADPH oxidase activity, and p22(phox) expression was diminished in the IRD mice. IRD suppression increased BSA-induced renal macrophage infiltration. Moreover, BSA mice exhibited nucleotide-binding oligomerisation domain-like receptor pyrin domain-containing protein (NLRP) inflammasome activation, which was inhibited by IRD. Ferrous iron increased in kidneys with BSA overload and was inhibited by IRD. Thus, iron restriction inhibited oxidative stress and inflammatory changes, contributing to the protective effect against BSA overload-induced tubulointerstitial injury. (Tokushima University Institutional Repository) ● Metadata: 112368 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-017-11089-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28878231 ● Search Scopus @ Elsevier (PMID): 28878231 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-017-11089-0 (Tokushima University Institutional Repository: 112368, DOI: 10.1038/s41598-017-11089-0, PubMed: 28878231)
34.	Takeshi Mitsuhashi, Ryoko Uemoto, Kazue Ishikawa, Sumiko Yoshida, Yasumasa Ikeda, Shusuke Yagi, Toshio Matsumoto, Masashi Akaike and Ken-ichi Aihara : Endothelial Nitric Oxide Synthase-Independent Pleiotropic Effects of Pitavastatin Against Atherogenesis and Limb Ischemia in Mice., Journal of Atherosclerosis and Thrombosis, 2017. (Summary) Pitavastatin exerts eNOS-independent protective effects against atherogenesis and hind-limb ischemia in mice, which may occur via modifications on key molecules such as AMPK and diverse molecules. (Tokushima University Institutional Repository) ● Metadata: 115483 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.37747 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28592707 ● Search Scopus @ Elsevier (PMID): 28592707 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.37747 (Tokushima University Institutional Repository: 115483, DOI: 10.5551/jat.37747, PubMed: 28592707)
35.	Kiyoe Kurahashi, Seika Inoue, Sumiko Yoshida, Yasumasa Ikeda, Kana Morimoto, Ryoko Uemoto, Kazue Ishikawa, Takeshi Kondo, Tomoyuki Yuasa, Itsuro Endo, Masato Miyake, Seiichi Oyadomari, Toshio Matsumoto, Masahiro Abe, Hiroshi Sakaue and Ken-ichi Aihara : The Role of Heparin Cofactor in the Regulation of Insulin Sensitivity and Maintenance of Glucose Homeostasis in Humans and Mice., Journal of Atherosclerosis and Thrombosis, 2017. (Summary) The present studies provide evidence to support the idea that HC plays an important role in the maintenance of glucose homeostasis by regulating insulin sensitivity in both humans and mice. Stimulators of HC production may serve as novel therapeutic tools for the treatment of type 2 diabetes. (Tokushima University Institutional Repository) ● Metadata: 110925 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.37739 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28502917 ● Search Scopus @ Elsevier (PMID): 28502917 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.37739 (Tokushima University Institutional Repository: 110925, DOI: 10.5551/jat.37739, PubMed: 28502917)
36.	Keisuke Oshima, Yasumasa Ikeda, Yuya Horinouchi, Hiroaki Watanabe, Hirofumi Hamano, Yoshitaka Kihira, Seiji Kishi, Yuki Izawa-Ishizawa, Licht Miyamoto, Tasuku Hirayama, Hideko Nagasawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Iron suppresses erythropoietin expression via oxidative stress-dependent hypoxia-inducible factor-2 alpha inactivation, Laboratory Investigation; a Journal of Technical Methods and Pathology, Vol.97, No.5, 555-566, 2017. (Summary) Renal anemia is a major complication in chronic kidney disease (CKD). Iron supplementation, as well as erythropoiesis-stimulating agents, are widely used for treatment of renal anemia. However, excess iron causes oxidative stress via the Fenton reaction, and iron supplementation might damage remnant renal function including erythropoietin (EPO) production in CKD. EPO gene expression was suppressed in mice following direct iron treatment. Hypoxia-inducible factor-2 alpha (HIF-2α), a positive regulator of the EPO gene, was also diminished in the kidney of mice following iron treatment. Anemia-induced increase in renal EPO and HIF-2α expression was inhibited by iron treatment. In in vitro experiments using EPO-producing HepG2 cells, iron stimulation reduced the expression of the EPO gene, as well as HIF-2α. Moreover, iron treatment augmented oxidative stress, and iron-induced reduction of EPO and HIF-2α expression was restored by tempol, an antioxidant compound. HIF-2α interaction with the Epo promoter was inhibited by iron treatment, and was restored by tempol. These findings suggested that iron supplementation reduced EPO gene expression via an oxidative stress-HIF-2α-dependent signaling pathway. (Tokushima University Institutional Repository) ● Metadata: 113749 (Link to Publication Site) ● Publication site (DOI): 10.1038/labinvest.2017.11 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28263291 ● Search Scopus @ Elsevier (PMID): 28263291 ● Search Scopus @ Elsevier (DOI): 10.1038/labinvest.2017.11 (Tokushima University Institutional Repository: 113749, DOI: 10.1038/labinvest.2017.11, PubMed: 28263291)
37.	Yutaka Fukunaga, Yuki Izawa-Ishizawa, Yuya Horinouchi, Eriko Sairyo, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Yoshiro Abe, Ichiro Hashimoto and Toshiaki Tamaki : Topical Application of Nitrosonifedipine, a Novel Radical Scavenger, Ameliorates Ischemic Skin Flap Necrosis in a Mouse Model., Wound Repair and Regeneration, Vol.25, No.2, 217-223, 2017. (Summary) Ischemic skin flap necrosis can occur in random pattern flaps. An excess amount of reactive oxygen species is generated and causes necrosis in the ischemic tissue. Nitrosonifedipine (NO-NIF) has been demonstrated to possess potent radical scavenging ability. However, there has been no study on the effects of NO-NIF on ischemic skin flap necrosis. Therefore, they evaluated the potential of NO-NIF in ameliorating ischemic skin flap necrosis in a mouse model. A random pattern skin flap (1.0 × 3.0 cm) was elevated on the dorsum of C57BL/6 mice. NO-NIF was administered by topical injection immediately after surgery and every 24 hours thereafter. Flap survival was evaluated on postoperative day 7. Tissue samples from the skin flaps were harvested on postoperative days 1 and 3 to analyze oxidative stress, apoptosis and endothelial dysfunction. The viable area of the flap in the NO-NIF group was significantly increased (78.30 ± 7.041%) compared with that of the control group (47.77 ± 6.549%, p < 0.01). NO-NIF reduced oxidative stress, apoptosis and endothelial dysfunction, which were evidenced by the decrease of malondialdehyde, p22phox protein expression, number of apoptotic cells, phosphorylated p38 MAPK protein expression, and vascular cell adhesion molecule-1 protein expression while endothelial nitric oxide synthase protein expression was increased. In conclusion, they demonstrated that NO-NIF ameliorated ischemic skin flap necrosis by reducing oxidative stress, apoptosis, and endothelial dysfunction. NO-NIF is considered to be a candidate for the treatment of ischemic flap necrosis. (Tokushima University Institutional Repository) ● Metadata: 110118 (Link to Publication Site) ● Publication site (DOI): 10.1111/wrr.12510 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28090711 ● Search Scopus @ Elsevier (PMID): 28090711 ● Search Scopus @ Elsevier (DOI): 10.1111/wrr.12510 (Tokushima University Institutional Repository: 110118, DOI: 10.1111/wrr.12510, PubMed: 28090711)
38.	Yasumasa Ikeda, Mizuki Imao, Akiho Satoh, Hiroaki Watanabe, Hirofumi Hamano, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Iron-induced skeletal muscle atrophy involves an Akt-forkhead box O3-E3 ubiquitin ligase-dependent pathway, Journal of Trace Elements in Medicine and Biology, Vol.35, No.5, 66-76, 2016. (Summary) Skeletal muscle wasting or sarcopenia is a critical health problem. Skeletal muscle atrophy is induced by an excess of iron, which is an essential trace metal for all living organisms. Excessive amounts of iron catalyze the formation of highly toxic hydroxyl radicals via the Fenton reaction. However, the molecular mechanism of iron-induced skeletal muscle atrophy has remained unclear. In this study, 8-weeks-old C57BL6/J mice were divided into 2 groups: vehicle-treated group and the iron-injected group (10 mg iron·day-1·mouse-1) during 2 weeks. Mice in the iron-injected group showed an increase in the iron content of the skeletal muscle and serum and ferritin levels in the muscle, along with reduced skeletal muscle mass. The skeletal muscle showed elevated mRNA expression of the muscle atrophy-related E3 ubiquitin ligases, atrogin-1 and muscle ring finger-1(MuRF1), on days 7 and 14 of iron treatment. Moreover, iron-treated mice showed reduced phosphorylation of Akt and forkhead box O3 (FOXO3a) in skeletal muscles. Inhibition of FOXO3a using siRNA in vitro in C2C12 myotube cells inhibited iron-induced upregulation of atrogin-1 and MuRF1 and reversed the reduction in myotube diameters. Iron-load caused oxidative stress, and an oxidative stress inhibitor abrogated iron-induced muscle atrophy by reactivating the Akt-FOXO3 pathway. Iron-induced skeletal muscle atrophy is suggested to involve the E3 ubiquitin ligase mediated by the reduction of Akt-FOXO3a signaling by oxidative stress. (Tokushima University Institutional Repository) ● Metadata: 113750 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jtemb.2016.01.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27049128 ● Search Scopus @ Elsevier (PMID): 27049128 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jtemb.2016.01.011 (Tokushima University Institutional Repository: 113750, DOI: 10.1016/j.jtemb.2016.01.011, PubMed: 27049128)
39.	Yasumasa Ikeda, Hirofumi Hamano, Akiho Satoh, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Bilirubin exerts pro-angiogenic effects through an Akt-eNOS-dependent pathway, Hypertension Research, Vol.38, No.11, 733-740, 2015. (Summary) Low serum bilirubin levels are associated with the risk of cardiovascular diseases including peripheral artery disease. Bilirubin is known to exert its property such as antioxidant effect or the enhancement of flow-mediated vasodilation, however, bilirubin action on angiogenesis remains unclear. To investigate the molecular mechanism of bilirubin on angiogenic effect, we first employed C57BL/6J mice with unilateral hindlimb ischemia surgery and divided the mice into two groups (vehicle-treated group and bilirubin-treated group). The analysis of laser speckle blood flow demonstrated the enhancement of blood flow recovery in response to ischemia of mice with bilirubin treatment. The density of capillaries was significantly higher in ischemic-adductor muscles of bilirubin-treated mice. The phosphorylated levels of endothelial nitric oxide synthase (eNOS) and Akt were increased in ischemic skeletal muscles of mice with bilirubin treatment compared with vehicle treatment. In in vitro experiments by using human aortic endothelial cells, bilirubin augmented eNOS and Akt phosphorylation, cell proliferation, cell migration and tube formation. These bilirubin actions on endothelial cell activation were inhibited by LY294002, a phosphatidylinositol 3-kinase inhibitor. In conclusion, bilirubin promotes angiogenesis through endothelial cells activation via Akt-eNOS-dependent manner. (Tokushima University Institutional Repository) ● Metadata: 113751 (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2015.74 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26134126 ● Summary page in Scopus @ Elsevier: 2-s2.0-84946558014 (Tokushima University Institutional Repository: 113751, DOI: 10.1038/hr.2015.74, PubMed: 26134126, Elsevier: Scopus)
40.	Soichiro Tajima, Yasumasa Ikeda, Hideaki Enomoto, Mizuki Imao, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II alters the expression of duodenal iron transporters, hepatic hepcidin, and body iron distribution in mice, European Journal of Nutrition, Vol.54, No.5, 709-719, 2015. (Summary) Angiotensin II (ANG II) has been shown to affect iron metabolism through alteration of iron transporters, leading to increased cellular and tissue iron contents. Serum ferritin, a marker of body iron storage, is elevated in various cardiovascular diseases, including hypertension. However, the associated changes in iron absorption and the mechanism underlying increased iron content in a hypertensive state remain unclear. The C57BL6/J mice were treated with ANG II to generate a model of hypertension. Mice were divided into three groups: (1) control, (2) ANG II-treated, and (3) ANG II-treated and ANG II receptor blocker (ARB)-administered (ANG II-ARB) groups. Mice treated with ANG II showed increased serum ferritin levels compared to vehicle-treated control mice. In ANG II-treated mice, duodenal divalent metal transporter-1 and ferroportin (FPN) expression levels were increased and hepatic hepcidin mRNA expression and serum hepcidin concentration were reduced. The mRNA expression of bone morphogenetic protein 6 and CCAAT/enhancer-binding protein alpha, which are regulators of hepcidin, was also down-regulated in the livers of ANG II-treated mice. In terms of tissue iron content, macrophage iron content and renal iron content were increased by ANG II treatment, and these increases were associated with reduced expression of transferrin receptor 1 and FPN and increased expression of ferritin. These changes induced by ANG II treatment were ameliorated by the administration of an ARB. Angiotensin II (ANG II) altered the expression of duodenal iron transporters and reduced hepcidin levels, contributing to the alteration of body iron distribution. (Tokushima University Institutional Repository) ● Metadata: 113753 (Link to Publication Site) ● Publication site (DOI): 10.1007/s00394-014-0749-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25096756 ● Summary page in Scopus @ Elsevier: 2-s2.0-84937513465 (Tokushima University Institutional Repository: 113753, DOI: 10.1007/s00394-014-0749-1, PubMed: 25096756, Elsevier: Scopus)
41.	Yoshitaka Kihira, Ariunzaya Burentogtokh, Mari Itoh, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia decreases glucagon-like peptide-1 secretion from GLUTag cell line, Biological & Pharmaceutical Bulletin, Vol.38, No.4, 514-521, 2015. (Summary) Glucagon-like peptide-1 (GLP-1), an incretin hormone, is secreted from L cells located in the intestinal epithelium. It is known that intestinal oxygen tension is decreased postprandially. In addition, we found that the expression of hypoxia-inducible factor-1α (HIF-1α), which accumulates in cells under hypoxic conditions, was significantly increased in the colons of mice with food intake, indicating that the oxygen concentration is likely reduced in the colon after eating. Therefore, we hypothesized that GLP-1 secretion is affected by oxygen tension. We found that forskolin-stimulated GLP-1 secretion from GLUTag cells, a model of intestinal L cells, is suppressed in hypoxia (1% O2). Forskolin-stimulated elevations of preproglucagon (ppGCG) and proprotein convertase 1/3 (PC1/3) mRNA expression were decreased under hypoxic conditions. The finding that H89, a protein kinase A (PKA) inhibitor, inhibited the forskolin-stimulated increase of ppGCG and PC1/3 indicated that the cAMP-PKA pathway is involved in the hypoxia-induced suppression of the genes. Hypoxia decreased hexokinase 2 mRNA and protein expression and increased lactate dehydrogenase A mRNA and protein expression. Concomitantly, lactate production was increased and ATP production was decreased. Together, the results indicate that hypoxia decreases glucose utilization for ATP production, which probably causes a decrease in cAMP production and in subsequent GLP-1 production. Our findings suggest that the postprandial decrease in oxygen tension in the intestine attenuates GLP-1 secretion. (Tokushima University Institutional Repository) ● Metadata: 109948 (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b14-00612 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25832631 ● CiNii @ National Institute of Informatics (CRID): 1390001204631777920 ● Summary page in Scopus @ Elsevier: 2-s2.0-84928951796 (Tokushima University Institutional Repository: 109948, DOI: 10.1248/bpb.b14-00612, PubMed: 25832631, CiNii: 1390001204631777920, Elsevier: Scopus)
42.	Noriko Yamano, Yasumasa Ikeda, Minoru Sakama, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Licht Miyamoto, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : A Long-Term High-Fat Diet Changes Iron Distribution in Body, Increasing Iron Accumulation Specifically in the Mouse Spleen, Journal of Nutritional Science and Vitaminology, Vol.61, No.1, 20-27, 2015. (Summary) Although iron is an essential trace metal, its presence in excess causes oxidative stress in the human body. Recent studies have indicated that iron storage is a risk factor for type 2 diabetes mellitus. Dietary iron restriction or iron chelation ameliorates symptoms of type 2 diabetes in mouse models. However, whether iron content in the body changes with the development of diabetes is unknown. Here, we investigated the dynamics of iron accumulation and changes in iron absorption-related genes in mice that developed obesity and diabetes by consuming a high-fat diet (HFD-fed mice). HFD-fed mice (18-20 wk) were compared with control mice for hematologic features, serum ferritin levels, and iron contents in the gastrocnemius muscle, heart, epididymal fat, testis, liver, duodenum, and spleen. In addition, the spleen was examined histologically. Iron absorption-related gene expression in the liver and duodenum was also examined. Hemoglobin and serum ferritin levels were increased in HFD-fed mice. The HFD-fed mice showed iron accumulation in the spleen, but not in the heart or liver. Increased percentages of the splenic red pulp and macrophages were observed in HFD-fed mice and iron accumulation in the spleen was found mainly in the splenic red pulp. The HFD-fed mice also showed decreased iron content in the duodenum. The mRNA expression of divalent metal transporter-1 (DMT-1), an iron absorption-related gene, was elevated in the duodenum of HFD-fed mice. These results indicate that iron accumulation (specifically accumulation in the spleen) is enhanced by the development of type 2 diabetes induced by HFD. (Keyword) iron/spleen/diet / high fat/diabetes mellitus / type 2/DMT1 protein (iron transporter) (Link to Publication Site) ● Publication site (DOI): 10.3177/jnsv.61.20 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25994136 ● CiNii @ National Institute of Informatics (CRID): 1390282681302013696 ● Summary page in Scopus @ Elsevier: 2-s2.0-84929747372 (DOI: 10.3177/jnsv.61.20, PubMed: 25994136, CiNii: 1390282681302013696, Elsevier: Scopus)
43.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Masaki Ueno, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Noriko Yamano, Koichiro Tsuchiya and Toshiaki Tamaki : Smooth muscle cell specific Hif-1 deficiency suppresses angiotensin II-induced vascular remodeling in mice, Cardiovascular Research, Vol.102, No.3, 460-468, 2014. (Summary) Vascular remodelling is mediated by vascular smooth muscle cell (VSMC) proliferation and hypertrophy, both processes of which are linked to medial thickening and fibrosis. Here, we show that hypoxia-inducible factor-1α (Hif-1α) expressed in smooth muscle cells (SMCs) is involved in angiotensin II (Ang II)-induced vascular remodelling in an in vivo model. To clarify the role of Hif-1α in vascular remodelling, we created mice lacking the Hif-1α gene in SMCs (SMKO mice). Ang II infusion induced medial thickening and vascular fibrosis, accompanied by Hif-1α up-regulation, in the aortae of control mice, but not in those of SMKO mice. In accordance with those results, our in vitro studies showed that the deletion of SMC-derived Hif-1α suppressed the Ang II-induced hypertrophy of VSMCs, and our in vivo studies showed that the Ang II-induced expression of fibrosis-related genes in aortae was suppressed by SMC-specific Hif-1α deficiency. In addition, the SMC-specific Hif-1α deficiency suppressed Ang II-induced macrophage infiltration and Ang II-induced expression of inflammation-related genes in aortae. The superoxide production observed in the aortae of control mice with Ang II was suppressed in those of SMKO mice with Ang II, and this finding was consistent with the results of little Ang II-induced c-Src phosphorylation in SMKO mouse aortae. Loss- and gain-of-function analysis in in vitro experiments confirmed that VSMC-derived Hif-1α functions as an intrinsic modulator of vascular remodelling-related gene expression. Our results revealed that SMC-derived Hif-1α is a crucial mediator of Ang II-induced vascular remodelling. (Keyword) Angiotensin II / Animals / Fibrosis / Gene Expression Regulation / Hemodynamics / Hypoxia-Inducible Factor 1, alpha Subunit / Mice / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / phosphorylation / Superoxides / Vascular Remodeling (Tokushima University Institutional Repository) ● Metadata: 106145 (Link to Publication Site) ● Publication site (DOI): 10.1093/cvr/cvu061 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24623277 ● Summary page in Scopus @ Elsevier: 2-s2.0-84901457818 (Tokushima University Institutional Repository: 106145, DOI: 10.1093/cvr/cvu061, PubMed: 24623277, Elsevier: Scopus)
44.	Yuko Imamura, Shuhei Tomita, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : HIF-2α/ARNT complex regulates hair development via induction of p21Waf1/Cip1 and p27Kip1, The FASEB journal, Vol.28, No.6, 2517-2524, 2014. (Summary) The hypoxia-inducible factors HIF-1α or HIF-2α form heterodimeric complexes with the aryl hydrocarbon receptor nuclear translocator (ARNT). HIF-1α/ARNT and HIF-2α/ARNT complexes activate hypoxia-inducible genes that play critical roles in angiogenesis, anaerobic metabolism, and other processes in response to O2 deprivation. HIF-2α is known to regulate the function and/or differentiation of stem cells by activating the POU domain transcription factor Oct4; however, the precise underlying mechanism is unknown. This study examined the role of HIF-2α/ARNT in hair development using conditional-knockout mice, in which Arnt was specifically deleted in keratinocytes. In wild-type mice, HIF-2α and ARNT were highly expressed in the precortex above the hair matrix, an area containing differentiating stem cells. An analysis of hair size and type in these mice showed that loss of ARNT decreased the production of zigzag hairs, corresponding to reduced expression of HIF-2α and induction of the mammalian cyclin-dependent kinase inhibitors p21(Waf1/Cip1) and p27 (Kip1). The results suggest that the HIF-2α/ARNT complex regulates hair follicle differentiation via induction of p21(Waf1/Cip1) and possibly p27(Kip1), as p27(Kip1) expression was not altered in ARNT knockout mice. The findings provide insight into a possible mechanism underlying hair growth disorders and can be useful for future studies on hair follicle response to insults, such as chemotherapy and ionizing radiation.-Imamura, Y., Tomita, S., Imanishi, M., Kihira, Y., Ikeda, Y., Ishizawa, K., Tsuchiya, K., Tamaki, T. HIF-2α/ARNT complex regulates hair development via induction of p21(Waf1/Cip1) and p27(Kip1). (Keyword) Animals / Aryl Hydrocarbon Receptor Nuclear Translocator / Basic Helix-Loop-Helix Transcription Factors / cell differentiation / Cells, Cultured / Cyclin-Dependent Kinase Inhibitor p21 / Cyclin-Dependent Kinase Inhibitor p27 / Hair / Hair Follicle / Hypoxia-Inducible Factor 1, alpha Subunit / Keratinocytes / Mice / knockout mice (Link to Publication Site) ● Publication site (DOI): 10.1096/fj.13-244079 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24599965 ● Summary page in Scopus @ Elsevier: 2-s2.0-84901845393 (DOI: 10.1096/fj.13-244079, PubMed: 24599965, Elsevier: Scopus)
45.	Atsushi Morimoto, Shuhei Tomita, Masaki Imanishi, Go Shioi, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Mitsuru Takaku, Ichiro Hashimoto, Yasumasa Ikeda, Hideki Nakanishi and Toshiaki Tamaki : Overexpressed HIF-2α in Endothelial Cells Promotes Vascularization and Improves Random Pattern Skin Flap Survival., Plastic and Reconstructive Surgery. Global Open, Vol.2, No.4, e132, 2014. (Summary) Specific overexpression of HIF-2 in ECs promoted vascularization and enhanced skin flap survival in vivo in a mouse model. (Tokushima University Institutional Repository) ● Metadata: 106138 (Link to Publication Site) ● Publication site (DOI): 10.1097/GOX.0000000000000083 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25289325 ● Summary page in Scopus @ Elsevier: 2-s2.0-84897362750 (Tokushima University Institutional Repository: 106138, DOI: 10.1097/GOX.0000000000000083, PubMed: 25289325, Elsevier: Scopus)
46.	Yoshitaka Kihira, Mariko Miyake, Manami Hirata, Yoji Hoshina, Kana Kato, Hitoshi Shirakawa, Hiroshi Sakaue, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Deletion of hypoxia-inducible factor-1α in adipocytes enhances glucagon-like peptide-1 secretion and reduces adipose tissue inflammation., PLoS ONE, Vol.9, No.4, e93856, 2014. (Summary) It is known that obese adipose tissues are hypoxic and express hypoxia-inducible factor (HIF)-1α. Although some studies have shown that the expression of HIF-1α in adipocytes induces glucose intolerance, the mechanisms are still not clear. In this study, we examined its effects on the development of type 2 diabetes by using adipocyte-specific HIF-1α knockout (ahKO) mice. ahKO mice showed improved glucose tolerance compared with wild type (WT) mice. Macrophage infiltration and mRNA levels of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor α (TNFα) were decreased in the epididymal adipose tissues of high fat diet induced obese ahKO mice. The results indicated that the obesity-induced adipose tissue inflammation was suppressed in ahKO mice. In addition, in the ahKO mice, serum insulin levels were increased under the free-feeding but not the fasting condition, indicating that postprandial insulin secretion was enhanced. Serum glucagon-like peptide-1 (GLP-1) levels were also increased in the ahKO mice. Interestingly, adiponectin, whose serum levels were increased in the obese ahKO mice compared with the obese WT mice, stimulated GLP-1 secretion from cultured intestinal L cells. Therefore, insulin secretion may have been enhanced through the adiponectin-GLP-1 pathway in the ahKO mice. Our results suggest that the deletion of HIF-1α in adipocytes improves glucose tolerance by enhancing insulin secretion through the GLP-1 pathway and by reducing macrophage infiltration and inflammation in adipose tissue. (Keyword) Adipocytes / Animals / Blotting, Western / Chemokine CCL2 / DNA Primers / Diabetes Mellitus, Type 2 / Gene Deletion / Glucagon-Like Peptide 1 / Glucose Tolerance Test / Hypoxia-Inducible Factor 1, alpha Subunit / Immunohistochemistry / Insulin / Mice / Mice, Knockout / Real-Time Polymerase Chain Reaction / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0093856 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24705496 ● Summary page in Scopus @ Elsevier: 2-s2.0-84899440448 (DOI: 10.1371/journal.pone.0093856, PubMed: 24705496, Elsevier: Scopus)
47.	Yasumasa Ikeda, Iori Ozono, Soichro Tajima, Mizuki Imao, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Iron chelation by deferoxamine prevents renal interstitial fibrosis in mice with unilateral ureteral obstruction, PLoS ONE, Vol.9, No.2, e89355, 2014. (Summary) Renal fibrosis plays an important role in the onset and progression of chronic kidney diseases (CKD). Although several mechanisms underlying renal fibrosis and candidate drugs for its treatment have been identified, the effect of iron chelator on renal fibrosis remains unclear. In the present study, we examined the effect of an iron chelator, deferoxamine (DFO), on renal fibrosis in mice with surgically induced unilateral ureter obstruction (UUO). Mice were divided into 4 groups: UUO with vehicle, UUO with DFO, sham with vehicle, and sham with DFO. One week after surgery, augmented renal tubulointerstitial fibrosis and the expression of collagen I, III, and IV increased in mice with UUO; these changes were suppressed by DFO treatment. Similarly, UUO-induced macrophage infiltration of renal interstitial tubules was reduced in UUO mice treated with DFO. UUO-induced expression of inflammatory cytokines and extracellular matrix proteins was abrogated by DFO treatment. DFO inhibited the activation of the transforming growth factor-β1 (TGF-β1)-Smad3 pathway in UUO mice. UUO-induced NADPH oxidase activity and p22(phox) expression were attenuated by DFO. In the kidneys of UUO mice, divalent metal transporter 1, ferroportin, and ferritin expression was higher and transferrin receptor expression was lower than in sham-operated mice. Increased renal iron content was observed in UUO mice, which was reduced by DFO treatment. These results suggest that iron reduction by DFO prevents renal tubulointerstitial fibrosis by regulating TGF-β-Smad signaling, oxidative stress, and inflammatory responses. (Tokushima University Institutional Repository) ● Metadata: 113752 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0089355 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24586712 ● Summary page in Scopus @ Elsevier: 2-s2.0-84897786390 (Tokushima University Institutional Repository: 113752, DOI: 10.1371/journal.pone.0089355, PubMed: 24586712, Elsevier: Scopus)
48.	Keisuke Ishizawa, Yuki Izawa-Ishizawa, Noriko Yamano, Maki Urushihara, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Asami Nuno, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Shoji Kagami, Hiroyuki Kobori, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine ameliorates the progression of type 2 diabetic nephropathy by exerting antioxidative effects, PLoS ONE, Vol.9, No.1, e86335, 2014. (Summary) Diabetic nephropathy (DN) is the major cause of end-stage renal failure. Oxidative stress is implicated in the pathogenesis of DN. Nitrosonifedipine (NO-NIF) is a weak calcium channel blocker that is converted from nifedipine under light exposure. Recently, we reported that NO-NIF has potential as a novel antioxidant with radical scavenging abilities and has the capacity to treat vascular dysfunction by exerting an endothelial protective effect. In the present study, we extended these findings by evaluating the efficacy of NO-NIF against DN and by clarifying the mechanisms of its antioxidative effect. In a model of type 2 DN (established in KKAy mice), NO-NIF administration reduced albuminuria and proteinuria as well as glomerular expansion without affecting glucose metabolism or systolic blood pressure. NO-NIF also suppressed renal and systemic oxidative stress and decreased the expression of intercellular adhesion molecule (ICAM)-1, a marker of endothelial cell injury, in the glomeruli of the KKAy mice. Similarly, NO-NIF reduced albuminuria, oxidative stress, and ICAM-1 expression in endothelial nitric oxide synthase (eNOS) knockout mice. Moreover, NO-NIF suppressed urinary angiotensinogen (AGT) excretion and intrarenal AGT protein expression in proximal tubular cells in the KKAy mice. On the other hand, hyperglycemia-induced mitochondrial superoxide production was not attenuated by NO-NIF in cultured endothelial cells. These findings suggest that NO-NIF prevents the progression of type 2 DN associated with endothelial dysfunction through selective antioxidative effects. (Keyword) Animals / Antioxidants / Cell Line / Diabetic Nephropathies / Humans / Male / Mice / Mice, Inbred C57BL / knockout mice / Nifedipine / Nitric Oxide Synthase Type III / Nitroso Compounds / oxidative stress (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0086335 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24489716 ● Summary page in Scopus @ Elsevier: 2-s2.0-84900332178 (DOI: 10.1371/journal.pone.0086335, PubMed: 24489716, Elsevier: Scopus)
49.	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)
50.	Yasumasa Ikeda, Hideaki Enomoto, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Dietary iron restriction inhibits progression of diabetic nephropathy in db/db mice., American Journal of Physiology, Renal Physiology, Vol.304, No.7, F1028-F1036, 2013. (Summary) Excess iron causes oxidative stress through hydroxyl-radical production via Fenton/Haber-Weiss reactions. Recently, body iron reduction has been found to ameliorate diabetes. In the present study, we examined the protective effect of dietary iron restriction against diabetic nephropathy in the db/db mouse model of diabetic nephropathy using db/m mice as controls. The db/db mice were divided into 2 groups and fed a normal diet (ND) or a low iron diet (LID). Increasing urinary albumin excretion was observed in the ND db/db mice, but this was suppressed in db/db mice with LID. Histologically, the db/db mice in the ND group had increased glomerular volume and mesangial area compared to the LID group. Augmented deposition of extracellular matrices was decreased in db/db mice with LID. In terms of oxidative stress, increased superoxide production observed in the kidneys of the ND db/db mice was diminished in the LID group. NADPH oxidase activity and renal expression of NADPH oxidase components p22(phox) and NOX4 were augmented in the ND group, and this was abolished by LID. There were no differences in expression of renal iron importers, transferrin receptor, or divalent metal transporter-1 between db/m mice and db/db mice. The level of ferroportin, an iron exporter, increased in the kidneys of the db/db mice. Urinary iron excretion was significantly higher in ND db/db mice and was reduced in the LID group. These findings suggest that dietary iron restriction exerts a preventive effect on the progression of diabetic nephropathy partly due to the reduction of oxidative stress. (Link to Publication Site) ● Publication site (DOI): 10.1152/ajprenal.00473.2012 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23389454 ● Search Scopus @ Elsevier (PMID): 23389454 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00473.2012 (DOI: 10.1152/ajprenal.00473.2012, PubMed: 23389454)
51.	Yasumasa Ikeda, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Sumiko Yoshida, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Bovine milk-derived lactoferrin exerts proangiogenic effects in an Src-Akt-eNOS-dependent manner in response to ischemia, Journal of Cardiovascular Pharmacology, Vol.61, No.5, 423-429, 2013. (Summary) Lactoferrin (LF) exerts a variety of biological effects, including the promotion of angiogenesis by increasing the expression of angiogenesis-related genes and reducing blood pressure via a nitric oxide-dependent mechanism. In this study, we investigated the effects of LF on angiogenesis using C57BL/6J mice that received daily unilateral treatment with or without bovine milk-derived LF (bLF) after unilateral hindlimb surgery. The analysis of laser speckle blood flow showed that bLF treatment promoted blood flow recovery in response to ischemic hindlimb. The capillary density of ischemic adductor muscles and the phosphorylation of Src, Akt, and endothelial nitric oxide synthase (eNOS) were also significantly higher in bLF-treated mice than in vehicle-treated mice. Furthermore, bLF increased the phosphorylation levels of Src, Akt, and eNOS in in vitro experiments using human aortic endothelial cells. The action of bLF on eNOS phosphorylation was abolished by both LY294002, a phosphatidylinositol 3-kinase inhibitor, and 4-amino-5-(4-chlorophenyl)-7-(dimethylethyl)pyrazolo [3,4-d]pyrimidine (PP2), an Src inhibitor. Similarly, bLF-induced acceleration of tube formation, cell proliferation, and cell migration in human aortic endothelial cells were inhibited by LY294002 or PP2. Thus, bLF promotes vascular endothelial cell function via an Src Akt eNOS-dependent pathway, thereby contributing to revascularization in response to ischemia. (Keyword) Animals / Aorta / Cell Movement / Cell Proliferation / Cells, Cultured / Endothelial Cells / Endothelium, Vascular / Enzyme Activation / Hindlimb / Humans / Ischemia / Lactoferrin / Laser-Doppler Flowmetry / Mice / Mice, Inbred C57BL / Milk / Neovascularization, Physiologic / Nitric Oxide Synthase Type III / Phosphorylation / Proto-Oncogene Proteins c-akt / Reperfusion Injury / Signal Transduction / src-Family Kinases (Tokushima University Institutional Repository) ● Metadata: 113754 (Link to Publication Site) ● Publication site (DOI): 10.1097/FJC.0b013e318287d526 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23364610 ● Search Scopus @ Elsevier (PMID): 23364610 ● Search Scopus @ Elsevier (DOI): 10.1097/FJC.0b013e318287d526 (Tokushima University Institutional Repository: 113754, DOI: 10.1097/FJC.0b013e318287d526, PubMed: 23364610)
52.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Yuki Izawa-Ishizawa, Shoko Fujii, Erika Tominaga, Teppei Tsuneishi, Yuya Horinouchi, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Ken-ichi Aihara, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine ameliorates angiotensin II-induced vascular remodeling via antioxidative effects, Naunyn-Schmiedeberg's Archives of Pharmacology, Vol.386, No.1, 29-39, 2013. (Summary) Nifedipine is unstable under light and decomposes to a stable nitroso analog, nitrosonifedipine (NO-NIF). The ability of NO-NIF to block calcium channels is quite weak compared with that of nifedipine. Recently, we have demonstrated that NO-NIF reacts with unsaturated fatty acid leading to generate NO-NIF radical, which acquires radical scavenging activity. However, the effects of NO-NIF on the pathogenesis related with oxidative stress, such as atherosclerosis and hypertension, are unclear. In this study, we investigated the effects of NO-NIF on angiotensin II (Ang II)-induced vascular remodeling. Ang II-induced thickening and fibrosis of aorta were inhibited by NO-NIF in mice. NO-NIF decreased reactive oxygen species (ROS) in the aorta and urinary 8-hydroxy-20-deoxyguanosine. Ang II-stimulated mRNA expressions of p22(phox), CD68, F4/80, monocyte chemoattractant protein-1, and collagen I in the aorta were inhibited by NO-NIF. Moreover, NO-NIF inhibited Ang II-induced cell migration and proliferation of vascular smooth muscle cells (VSMCs). NO-NIF reduced Ang II-induced ROS to the control level detected by dihydroethidium staining and lucigenin chemiluminescence assay in VSMCs. NO-NIF suppressed phosphorylations of Akt and epidermal growth factor receptor induced by Ang II. However, NO-NIF had no effects on intracellular Ca(2+) increase and protein kinase C-δ phosphorylation induced by Ang II in VSMCs. The electron paramagnetic resonance spectra indicated the continuous generation of NO-NIF radical of reaction with cultured VSMCs. These findings suggest that NO-NIF improves Ang II-induced vascular remodeling via the attenuation of oxidative stress. (Keyword) Angiotensin II / Animals / Antioxidants / Aorta, Thoracic / calcium / Cell Movement / Cell Proliferation / Fibrosis / Male / Mice / Mice, Inbred C57BL / Muscle, Smooth, Vascular / Nifedipine / Nitroso Compounds / oxidative stress / Rats / reactive oxygen species (Link to Publication Site) ● Publication site (DOI): 10.1007/s00210-012-0810-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23149861 ● Summary page in Scopus @ Elsevier: 2-s2.0-84872316103 (DOI: 10.1007/s00210-012-0810-7, PubMed: 23149861, Elsevier: Scopus)
53.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Licht Miyamoto, Shoko Fujii, Hironori Taira, Yoshitaka Kihira, Yasumasa Ikeda, Shuichi Hamano, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II receptor blocker improves tumor necrosis factor-α-induced cytotoxicity via antioxidative effect in human glomerular endothelial cells, Pharmacology, Vol.90, No.5-6, 324-331, 2012. (Summary) Tumor necrosis factor-α (TNF-α) is known to involve the progression of renal dysfunction through its cytotoxicity and proinflammatory effects such as the induction of intercellular adhesion molecule (ICAM)-1 expression in vascular endothelial cells (ECs). Olmesartan, one of the angiotensin II type 1 receptor blockers (ARBs), has been reported to show protective effects on injured ECs by some causal factors of renal disorder other than angiotensin II. However, the effects of olmesartan on TNF-α-induced glomerular EC damage have not been investigated. In the present study, we investigated the effects of RNH-6270, an active metabolite of olmesartan, on TNF-α-induced human glomerular EC (HGEC) damage to clarify the renoprotective mechanisms of ARBs. Cultured HGECs were stimulated by TNF-α, and then cell viability and cytotoxicity were measured by MTT assay and lactate dehydrogenase release assay, respectively. TNF-α-induced oxidative stress was estimated by dihydroethidium assay and lucigenin chemiluminescence assay. ICAM-1 expression and the phosphorylations of mitogen-activated protein kinases were measured using Western blotting assay. RNH-6270 suppressed cell death and the increase in ICAM-1 expression induced by TNF-α via the inhibition of reactive oxygen species in HGECs. Our findings suggested that olmesartan might have protective effects against TNF-α-induced glomerular EC dysfunction. (Keyword) Angiotensin II Type 1 Receptor Blockers / apoptosis / Cell Survival / Cells, Cultured / Endothelial Cells / Humans / Imidazoles / Intercellular Adhesion Molecule-1 / Kidney Glomerulus / reactive oxygen species / Tetrazoles / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1159/000343244 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23052181 ● Summary page in Scopus @ Elsevier: 2-s2.0-84867214872 (DOI: 10.1159/000343244, PubMed: 23052181, Elsevier: Scopus)
54.	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)
55.	Mitsuru Takaku, Shuhei Tomita, Hirotsugu Kurobe, Yoshitaka Kihira, Atsushi Morimoto, Mayuko Higashida, Yasumasa Ikeda, Akira Ushiyama, Ichiro Hashimoto, Hideki Nakanishi and Toshiaki Tamaki : Systemic Preconditioning by a Prolyl Hydroxylase Inhibitor Promotes Prevention of Skin Flap Necrosis via HIF-1-Induced Bone Marrow-Derived Cells., PLoS ONE, Vol.7, No.8, 2012. (Summary) We demonstrated that transient activation of the HIF signaling pathway by a single systemic DMOG treatment upregulates not only anti-apoptotic pathways but also enhances neovascularization with concomitant increase in the numbers of bone marrow-derived progenitor cells. (Tokushima University Institutional Repository) ● Metadata: 105965 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0042964 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22880134 ● Search Scopus @ Elsevier (PMID): 22880134 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0042964 (Tokushima University Institutional Repository: 105965, DOI: 10.1371/journal.pone.0042964, PubMed: 22880134)
56.	Yasumasa Ikeda, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Estrogen regulates hepcidin expression via GPR30-BMP6-dependent signaling in hepatocytes, PLoS ONE, Vol.7, No.7, e40465, 2012. (Summary) Hepcidin, a liver-derived iron regulatory protein, plays a crucial role in iron metabolism. It is known that gender differences exist with respect to iron storage in the body; however, the effects of sex steroid hormones on iron metabolism are not completely understood. We focused on the effects of the female sex hormone estrogen on hepcidin expression. First, ovariectomized (OVX) and sham-operated mice were employed to investigate the effects of estrogen on hepcidin expression in an in vivo study. Hepcidin expression was decreased in the livers of OVX mice compared to the sham-operated mice. In OVX mice, bone morphologic protein-6 (BMP6), a regulator of hepcidin, was also found to be downregulated in the liver, whereas ferroportin (FPN), an iron export protein, was upregulated in the duodenum. Both serum and liver iron concentrations were elevated in OVX mice relative to their concentrations in sham-operated mice. In in vitro studies, 17β-estradiol (E(2)) increased the mRNA expression of hepcidin in HepG2 cells in a concentration-dependent manner. E(2)-induced hepatic hepcidin upregulation was not inhibited by ICI 182720, an inhibitor of the estrogen receptor; instead, hepcidin expression was increased by ICI 182720. E(2) and ICI 182720 exhibit agonist actions with G-protein coupled receptor 30 (GPR30), the 7-transmembrane estrogen receptor. G1, a GPR30 agonist, upregulated hepcidin expression, and GPR30 siRNA treatment abolished E(2)-induced hepcidin expression. BMP6 expression induced by E(2) was abolished by GPR30 silencing. Finally, both E(2) and G1 supplementation restored reduced hepatic hepcidin and BMP6 expression and reversed the augmentation of duodenal FPN expression in the OVX mice. In contrast, serum hepcidin was elevated in OVX mice, which was reversed in these mice with E(2) and G1. Thus, estrogen is involved in hepcidin expression via a GPR30-BMP6-dependent mechanism, providing new insight into the role of estrogen in iron metabolism. (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0040465 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22792339 ● Summary page in Scopus @ Elsevier: 2-s2.0-84863827034 (DOI: 10.1371/journal.pone.0040465, PubMed: 22792339, Elsevier: Scopus)
57.	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.
58.	Soichiro Tajima, Yasumasa Ikeda, Kaori Sawada, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Yuki Izawa-Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Iron reduction by deferoxamine leads to amelioration of adiposity via the regulation of oxidative stress and inflammation in obese and type 2 diabetes KKAy mice., American Journal of Physiology, Endocrinology and Metabolism, Vol.302, No.1, E77-86, 2012. (Summary) Iron is an essential trace metal for most organisms. However, excess iron causes oxidative stress through production of highly toxic hydroxyl radicals via the Fenton/Haber-Weiss reaction. Iron storage in the body is reported to be associated with fat accumulation and type 2 diabetes mellitus. We investigated the role of iron in adiposity by using KKAy mice and obese and diabetic model mice. Eight-week-old KKAy mice were divided into two groups and treated with deferoxamine (DFO), an iron chelator agent, or a vehicle for 2 wk. DFO treatment diminished fat iron concentration and serum ferritin levels in KKAy mice. Fat weight and adipocyte size were reduced significantly in DFO-treated mice compared with vehicle-treated mice. Macrophage infiltration into fat was also decreased in DFO-treated mice compared with vehicle-treated mice. Superoxide production and NADPH oxidase activity in fat, as well as urinary 8-hydroxy-2'-deoxyguanosine excretion, were decreased in KKAy mice after DFO treatment while p22(phox) expression in adipose tissue was diminished in such mice. Ferritin expression in the fat of DFO-treated KKAy mice was decreased. In addition, F4/80-positive cells also presented through both p22(phox) and ferritin expression. The mRNA expression levels of inflammatory cytokines were also reduced in fat tissue of DFO-treated mice. These findings suggest that reduction of iron levels ameliorates adipocyte hypertrophy via suppression of oxidative stress, inflammatory cytokines, and macrophage infiltration, thereby breaking a vicious cycle in obesity. (Keyword) ferrum / oxidative stress / obesity (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpendo.00033.2011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21917632 ● Search Scopus @ Elsevier (PMID): 21917632 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.00033.2011 (DOI: 10.1152/ajpendo.00033.2011, PubMed: 21917632)
59.	Yoshitaka Kihira, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Basic fibroblast growth factor regulates glucose metabolism through glucose transporter 1 induced by hypoxia-inducible factor-1α in adipocytes, The International Journal of Biochemistry & Cell Biology, Vol.43, No.11, 1602-1611, 2011. (Summary) Hypoxia-inducible factor-1 (HIF-1), which is a transcription factor that enhances glycolysis in cells in response to hypoxia, is induced in hypertrophied adipocytes in obesity. Recent studies have shown that growth factors are able to induce HIF-1 by mechanisms independent of hypoxia. Since basic fibroblast growth factor (bFGF), an angiogenic factor, is concentrated in expanding adipose tissue, the possible effects of bFGF on regulation of HIF-1 in adipocytes were investigated. Treatment of differentiated 3T3-L1 adipocytes with bFGF induced HIF-1. Concomitantly, glucose transporter 1 (GLUT1), which is a target gene of HIF-1, was induced at both mRNA and protein levels and was translocated to the plasma membrane. A chromatin immunoprecipitation assay and an RNA interference study indicated that bFGF-induced HIF-1 directly upregulates GLUT1. In addition, it was observed that bFGF increases lactate production of adipocytes. This result indicates that bFGF reprograms the metabolism toward glycolysis. Intraperitoneal injection of bFGF into mice upregulated HIF-1 and GLUT1 in adipose tissues, suggesting that bFGF regulates the metabolism of adipocytes via HIF-1-GLUT1 regulation in vivo. We also found that bFGF inhibits insulin-induced phosphorylation of insulin receptor substrate-1 and Akt, suggesting that bFGF attenuates the insulin signal in adipocytes. Taken together, the findings suggest that bFGF has a harmful effect on the development of type 2 diabetes through metabolism reprogramming and attenuation of the insulin signal. (Keyword) 3T3-L1 Cells / Adipocytes / Animals / Anoxia / Diabetes Mellitus, Type 2 / Fibroblast Growth Factor 2 / Glucose / Glucose Transporter Type 1 / Glycolysis / Hypoxia-Inducible Factor 1, alpha Subunit / Injections, Intraperitoneal / Insulin / Insulin Receptor Substrate Proteins / Male / Mice / Obesity / Phosphorylation / Proto-Oncogene Proteins c-akt / Signal Transduction / Transcriptional Activation / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biocel.2011.07.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21810481 ● Search Scopus @ Elsevier (PMID): 21810481 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biocel.2011.07.009 (DOI: 10.1016/j.biocel.2011.07.009, PubMed: 21810481)
60.	Shuhei Tomita, Yoshitaka Kihira, Masaki Imanishi, Yayoi Fukuhara, Yuko Imamura, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Pathophysiological Response to Hypoxia From the Molecular Mechanisms of Malady to Drug Discovery: Inflammatory Responses of Hypoxia-Inducible Factor 1 (HIF-1) in T Cells Observed in Development of Vascular Remodeling, Journal of Pharmacological Sciences, Vol.115, No.4, 433-439, 2011. (Summary) Recent studies have shown that the cellular immune response to the hypoxic microenvironment constructed by vascular remodeling development modulates the resulting pathologic alterations. A major mechanism mediating adaptive responses to reduced oxygen availability is the regulation of transcription by hypoxia-inducible factor 1 (HIF-1). Impairment of HIF-1-dependent inflammatory responses in T cells causes an augmented vascular remodeling induced by arterial injury, which is shown as prominent neointimal hyperplasia and increase in infiltration of inflammatory cells at the adventitia in mice lacking Hif-1α specifically in T cells. Studies to clarify the mechanism of augmented vascular remodeling in the mutant mice have shown enhanced production of cytokines in activated T cells and augmented antibody production in response to a T-dependent antigen in the mutant mice. This minireview shows that HIF-1α in T cells plays a crucial role in vascular inflammation and remodeling in response to cuff injury as a negative regulator of the T cell-mediated immune response and suggests potential new therapeutic strategies that target HIF-1α. (Keyword) Animals / Anoxia / Drug Discovery / Humans / Hypoxia-Inducible Factor 1, alpha Subunit / Immunity, Cellular / Reperfusion Injury / T lymphocytes / Vasculitis (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.10R22FM (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21422726 ● Summary page in Scopus @ Elsevier: 2-s2.0-79955046642 (DOI: 10.1254/jphs.10R22FM, PubMed: 21422726, Elsevier: Scopus)
61.	Keisuke Ishizawa, Masanori Yoshizumi, Yoshichika Kawai, Junji Terao, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Pharmacology in health food: Metabolism of quercetin in vivo and its protective effect against arteriosclerosis, Journal of Pharmacological Sciences, Vol.115, No.4, 466-470, 2011. (Summary) Quercetin, a member of the bioflavonoids family, has been proposed to have anti-atherogenic, anti-inflammatory, and anti-hypertensive properties leading to the beneficial effects against cardiovascular diseases. It was recently demonstrated that quercetin 3-O-β-D-glucuronide (Q3GA) is one of the major quercetin conjugates in human plasma, in which the aglycone could not be detected. Although most of the in vitro pharmacological studies have been carried out using only the quercetin aglycone form, experiments using Q3GA would be important to discover the preventive mechanisms of cardiovascular diseases by quercetin in vivo. Therefore we examined the effects of the chemically synthesized Q3GA, as an in vivo form, on vascular smooth muscle cell (VSMC) disorders related to the progression of arteriosclerosis. Platelet-derived growth factor-induced cell migration and proliferation were inhibited by Q3GA in VSMCs. Q3GA attenuated angiotensin II-induced VSMC hypertrophy via its inhibitory effect on JNK and the AP-1 signaling pathway. Q3GA scavenged 1,1-diphenyl-2-picrylhydrazyl radical measured by the electron paramagnetic resonance method. In addition, immunohistochemical studies with monoclonal antibody 14A2 targeting the Q3GA demonstrated that the positive staining specifically accumulates in human atherosclerotic lesions, but not in the normal aorta. These findings suggest Q3GA would be an active metabolite of quercetin in plasma and may have preventative effects on arteriosclerosis relevant to VSMC disorders. (Keyword) Animals / Antioxidants / Arteriosclerosis / Cell Movement / Cell Proliferation / Drug Evaluation, Preclinical / Free Radicals / Health Food / Humans / Hypertrophy / Muscle, Smooth, Vascular / Quercetin / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.10R38FM (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21436601 ● Search Scopus @ Elsevier (PMID): 21436601 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.10R38FM (DOI: 10.1254/jphs.10R38FM, PubMed: 21436601)
62.	Yuya Horinouchi, Koichiro Tsuchiya, Chiaki Taoka, Soichiro Tajima, Yoshitaka Kihira, Yuko Matsuda, Kozo Shishido, Masahiro Yoshida, Shuichi Hamano, Kazuyoshi Kawazoe, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita and Toshiaki Tamaki : Antioxidant effects of photodegradation product of nifedipine, Chemical & Pharmaceutical Bulletin, Vol.59, No.2, 208-214, 2011. (Summary) Recently, increasing evidence suggests that the antihypertensive drug nifedipine acts as a protective agent for endothelial cells, and that the activity is unrelated to its calcium channel blocking. Nifedipine is unstable under light and reportedly decomposes to a stable nitrosonifedipine (NO-NIF). NO-NIF has no antihypertensive effect, and it has been recognized as a contaminant of nifedipine. The present study for the first time demonstrated that NO-NIF changed to a NO-NIF radical in a time-dependent manner when it interacted with human umbilical vein endothelial cells (HUVECs). The electron paramagnetic resonance (EPR) signal of NO-NIF radicals in HUVECs showed an asymmetric pattern suggesting that the radicals were located in the membrane. The NO-NIF radicals had radical scavenging activity for 1,1-diphenyl-2-picrylhydrazyl, whereas neither NO-NIF nor nifedipine did. In addition, the NO-NIF radical more effectively quenched lipid peroxides than NO-NIF or nifedipine. Furthermore, NO-NIF attenuated the superoxide-derived free radicals in HUVECs stimulated with LY83583, and suppressed iron-nitrilotriacetic acid (Fe-NTA)-induced cytotoxicity in rat pheochromocytoma (PC12) cells. Our findings suggest that NO-NIF is a candidate for a new class of antioxidative drugs that protect cells against oxidative stress. (Keyword) Animals / Antioxidants / Cells, Cultured / Endothelial Cells / Humans / Nifedipine / PC12 Cells / Photolysis / Rats (Link to Publication Site) ● Publication site (DOI): 10.1248/cpb.59.208 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21297301 ● Summary page in Scopus @ Elsevier: 2-s2.0-79551489998 (DOI: 10.1248/cpb.59.208, PubMed: 21297301, Elsevier: Scopus)
63.	Yayoi Fukuhara, Koichiro Tsuchiya, Yuya Horinouchi, Soichiro Tajima, Yoshitaka Kihira, Shuichi Hamano, Kazuyoshi Kawazoe, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita and Toshiaki Tamaki : Protective effect of photodegradation product of nifedipine against tumor necrosis factor alpha-induced oxidative stress in human glomerular endothelial cells, The Journal of Medical Investigation : JMI, Vol.58, No.1, 2, 118-126, 2011. (Summary) Recently, increasing evidence suggests that the antihypertensive drug nifedipine acts as a protective agent for endothelial cells, and that the activity is unrelated to its calcium channel blocking. Nitrosonifedipine (NO-NIF) is metabolically and photochemically produced from nifedipine, and NO-NIF has been recognized as a contaminant of nifedipine because it has no antihypertensive effect. Treatment of tumor necrosis factor-α (TNF-α) suppressed the cell viability and facilitated the expression of Inter-Cellular Adhesion Molecule 1(ICAM-1) in human glomerular endothelial cells (HGECs) though, pretreatment of NO-NIF significantly recovered the TNF-α-induced cell damage to the same extent as Trolox-C did, and suppressed the ICAM-1 expression in a concentration dependent manner. In addition, NO-NIF inhibited the cell toxicity induced by cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, as effective as Trolox-c. These data suggest that NO-NIF is a candidate for a new class of antioxidative drug that protect cells against oxidative stress in glomerular endothelial cells. (Keyword) Antioxidants / Benzene Derivatives / Cell Survival / Cells, Cultured / Endothelial Cells / Humans / Intercellular Adhesion Molecule-1 / Kidney Glomerulus / Nifedipine / Nitroso Compounds / oxidative stress / Tumor Necrosis Factor-alpha (Tokushima University Institutional Repository) ● Metadata: 72667 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.58.118 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21372496 ● CiNii @ National Institute of Informatics (CRID): 1390001204242892288 ● Search Scopus @ Elsevier (PMID): 21372496 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.58.118 (Tokushima University Institutional Repository: 72667, DOI: 10.2152/jmi.58.118, PubMed: 21372496, CiNii: 1390001204242892288)
64.	Yasumasa Ikeda, Soichiro Tajima, Sumiko Yoshida, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Ken-ichi Aihara, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Deferoxamine promotes angiogenesis via the activation of vascular endothelial cell function., Atherosclerosis, Vol.215, No.2, 339-347, 2011. (Summary) BACKGROUND: Deferoxamine (DFO), an iron chelator for disorders of excess iron, upregulates the expression of angiogenic factors, such as vascular endothelial growth factor (VEGF) and cyclooxygenase-2 (COX-2), indicating that it affects angiogenesis. Herein, we clarify the effect and mechanism of action of DFO on angiogenesis. METHODS AND RESULTS: In an in vitro study, DFO increased endothelial nitric oxide synthesis (eNOS) phosphorylation in human aortic endothelial cells (HAECs), which were inhibited by the phosphatidylinositol 3-kinase inhibitor LY294002. Tube formation, cell proliferation, and cell migration in HAECs were promoted by DFO, which were significantly reduced by LY294002. In an in vivo study, DFO promoted blood flow recovery in response to the hindlimb ischemia in mice with unilateral hindlimb surgery. The density of capillaries and arterioles in ischemic muscle was higher in DFO-treated mice compared to vehicle-treated mice. Endothelial cell proliferation increased and oxidative stress and apoptosis decreased in ischemic muscles of DFO-treated mice. The phosphorylation of Akt and eNOS on the ischemic side was elevated and urinary nitric oxide/nitric dioxide (NOx) excretion was higher in DFO-treated mice compared to vehicle-treated mice. The effect of DFO on angiogenesis was abolished in eNOS-deficient mice with hindlimb ischemia. CONCLUSION: These findings indicate that DFO promotes revascularization via the activation of vascular endothelial cell function by an Akt-eNOS-dependent mechanism. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2011.01.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21315355 ● Search Scopus @ Elsevier (PMID): 21315355 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2011.01.009 (DOI: 10.1016/j.atherosclerosis.2011.01.009, PubMed: 21315355)
65.	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)
66.	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)
67.	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)
68.	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)
69.	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)
70.	Yasumasa Ikeda, Ken-ichi Aihara, Masashi Akaike, Takashi Sato, Kazue Ishikawa, Takayuki Ise, Shusuke Yagi, Takashi Iwase, Yuka Ueda, Sumiko Yoshida, Hiroyuki Azuma, Kenneth Walsh, Toshiaki Tamaki, Shigeaki Kato and Toshio Matsumoto : Androgen receptor counteracts Doxorubicin-induced cardiotoxicity in male mice., Molecular Endocrinology, Vol.24, No.7, 1338-1348, 2010. (Summary) Doxorubicin (Dox) has been used as a potent anticancer agent, but serious cardiotoxicity precludes its use in a wide range of patients. We have reported that the androgen-androgen receptor (AR) system plays important roles in cardiac growth and protection from angiotensin II-induced cardiac remodeling. The present study was undertaken to clarify whether the androgen-AR system exerts a cardioprotective effect against Dox-induced cardiotoxicity. Male AR knockout (ARKO) and age-matched littermate male wild-type (WT) mice at 25 wk of age were given ip injections of Dox (20 mg/kg) or a vehicle. The survival rate and left ventricular function in Dox-treated male ARKO mice were reduced compared with those in Dox-treated male WT mice. Electron microscopic study showed prominent vacuole formation of myocardial mitochondria in Dox-treated male ARKO mice. Cardiac oxidative stress and apoptosis of cardiomyocytes were increased more prominently by Dox treatment in male ARKO mice than in male WT mice. In addition, Dox-induced reduction in the expression of cardiac mitochondria transcription factor A (Tfam) and phosphorylation of serine-threonine kinase (Akt) was more pronounced in male ARKO mice than in male WT mice. In cardiac myoblast cells, testosterone up-regulated Akt phosphorylation and Tfam expression and exerted an antiapoptotic effect against Dox-induced cardiotoxicity. Collectively, the results demonstrate that Dox-induced cardiotoxicity is aggravated in male ARKO mice via exacerbation of mitochondrial damage and superoxide generation, leading to enhanced apoptosis of cardiomyocytes. Thus, the androgen-AR system is thought to counteract Dox-induced cardiotoxicity partly through activation of the Akt pathway and up-regulation of Tfam to protect cardiomyocytes from mitochondrial damage and apoptosis. (Keyword) Androgens / Animals / Antineoplastic Agents / Apoptosis / Blotting, Western / Cell Line / Cell Survival / DNA-Binding Proteins / Doxorubicin / Echocardiography / High Mobility Group Proteins / Immunoprecipitation / In Situ Nick-End Labeling / Male / Mice / Mice, Knockout / Microscopy, Electron / Myocardium / Myocytes, Cardiac / Oxidative Stress / Phosphorylation / Protein-Serine-Threonine Kinases / Rats / Receptors, Androgen / Superoxides / Testosterone / Thiobarbituric Acid Reactive Substances / Ventricular Function, Left (Link to Publication Site) ● Publication site (DOI): 10.1210/me.2009-0402 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20501642 ● Search Scopus @ Elsevier (PMID): 20501642 ● Search Scopus @ Elsevier (DOI): 10.1210/me.2009-0402 (DOI: 10.1210/me.2009-0402, PubMed: 20501642)
71.	Soichiro Tajima, Koichiro Tsuchiya, Yuya Horinouchi, Keisuke Ishizawa, Yasumasa Ikeda, Yoshitaka Kihira, Masayuki Shono, Kazuyoshi Kawazoe, Shuhei Tomita and Toshiaki Tamaki : Effect of angiotensin II on iron-transporting protein expression and subsequent intracellular labile iron concentration in human glomerular endothelial cells, Hypertension Research, Vol.33, No.7, 713-721, 2010. (Summary) Angiotensin II (Ang II)-induced endothelial injury, which is associated with atherosclerosis, is believed to be mediated by intracellular reactive oxygen species (ROS) through stimulation of nicotinamide adenine dinucleotide phosphate oxidase (NOX). Iron is essential for the amplification of oxidative stress. In this study, we investigated whether Ang II altered iron metabolism and whether the Ang II-induced endothelial injury is attributable to changes in iron metabolism of human glomerular endothelial cells (HGECs). When 90% iron-saturated human transferrin (90% Tf) was applied to HGECs without Ang II, the labile ferrous iron level was same as the effect of control in spite of a significant increase in the total cellular iron concentration. Treatment with Ang II and 30% Tf or 90% Tf significantly (P<0.01) increased the intracellular iron concentration, as well as labile ferrous iron and protein oxidation levels, compared with the effect of separate administration of each compound. Ang II treatment facilitated the protein expression of the Tf receptor, divalent metal transporter 1, and ferroportin 1 in a dose- and time-dependent manner. It was also found that simultaneous exposure of HGECs to Ang II and 90% Tf accelerated hydroxyl radical production, as shown by using an electron paramagnetic resonance spectrometer. These results suggest that Ang II not only induces production of ROS by NOX activation but also iron incorporation followed by an increase in labile iron in HGECs. Both of these events may participate in the progression of oxidative stress because of endothelial cell dysfunction through ferrous iron-mediated ROS generation. (Keyword) Angiotensin II / Cation Transport Proteins / Endothelial Cells / Humans / Hydroxyl Radical / Iron / Kidney Glomerulus / oxidation and reduction / Receptors, Transferrin / Transferrin (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2010.63 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20431588 ● Summary page in Scopus @ Elsevier: 2-s2.0-77954369377 (DOI: 10.1038/hr.2010.63, PubMed: 20431588, Elsevier: Scopus)
72.	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)
73.	Keisuke Ishizawa, Yuki Izawa-Ishizawa, Narantungalag Dorjsuren, Erika Miki, Yoshitaka Kihira, Yasumasa Ikeda, Shuichi Hamano, Kazuyoshi Kawazoe, Kazuo Minakuchi, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II receptor blocker attenuates PDGF-induced mesangial cell migration in a receptor-independent manner, Nephrology, Dialysis, Transplantation, Vol.25, No.2, 364-372, 2010. (Summary) Clinical studies have shown that angiotensin II (Ang II) type 1 (AT1) receptor blockers (ARBs) are able to provide renoprotection independent of their blood pressure lowering effects. ARBs also are reported to suppress oxidative stress, inflammation and certain other cellular responses in a receptor-independent manner. We investigated the effects of an ARB, olmesartan, on the cell migration induced by platelet-derived growth factor (PDGF), a major mitogen involved in the pathogenesis of glomerulonephritis in rat mesangial cells (RMCs). Cell migration was determined by a modified Boyden chamber assay. The intracellular signalling pathway was examined by western blotting. AT1 receptor expression was knocked down by small interfering RNAs. The intracellular reactive oxygen species (ROS) was measured by using a fluorescent probe. The O(2)(.-) scavenging activities were studied by the electron paramagnetic resonance-spin trapping method. PDGF-induced cell migration was inhibited by olmesartan in AT1 receptor knockdown RMCs. Olmesartan attenuated big mitogen-activated protein (MAP) kinase 1 (BMK1) and Src activation by PDGF in AT1 receptor knockdown RMCs. PDGF-induced BMK1 activation was suppressed by the Src family tyrosine kinase inhibitors, indicating that Src exists upstream of BMK1. The NADPH oxidase inhibitors inhibited not only PDGF-induced BMK1 and Src activation but also RMC migration. The elevation in ROS generation induced by PDGF was decreased by olmesartan. Olmesartan displayed neither directly ROS scavenging activity nor the inhibition of ROS-mediated intracellular signalling in RMCs. Olmesartan attenuates ROS generation by PDGF, leading to the subsequent inhibition of Src/ BMK1/migration in an AT1 receptor-independent manner in RMCs. (Keyword) Angiotensin II Type 1 Receptor Blockers / Animals / Cell Movement / Cells, Cultured / Imidazoles / Male / Mesangial Cells / Platelet-Derived Growth Factor / Rats / Rats, Sprague-Dawley / Signal Transduction / Tetrazoles (Link to Publication Site) ● Publication site (DOI): 10.1093/ndt/gfp520 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19812233 ● Search Scopus @ Elsevier (PMID): 19812233 ● Search Scopus @ Elsevier (DOI): 10.1093/ndt/gfp520 (DOI: 10.1093/ndt/gfp520, PubMed: 19812233)
74.	Koichiro Tsuchiya, Shuhei Tomita, Keisuke Ishizawa, Shinji Abe, Yasumasa Ikeda, Yoshitaka Kihira and Toshiaki Tamaki : Dietary nitrite ameliorates renal injury in l-NAME-induced hypertensive rats, Nitric Oxide: Biology and Chemistry, Vol.22, No.2, 98-103, 2010. (Summary) Nitric oxide (NO) has numerous important functions in the kidney, and long-term blockage of nitric oxide synthases in rats by L-NAME results in severe hypertension and progressive kidney damage. On the other hand, NO production seems to be low in patients with chronic kidney disease (CKD), and NO deficiency may play a role in CKD progression. In this review, we summarized the mechanisms of amelioration of renal injury induced by L-NAME treated rats by treatment of nitrite. First, we demonstrate whether orally-administrated nitrite-derived NO can shift to the circulation. When 3mg/kg body weight Na(15)NO(2) was orally administered to rats, an apparent EPR signal derived from Hb(15)NO (A(z)=23.4 gauss) appeared in the blood, indicating that orally ingested nitrite can be a source of NO in vivo. Next, in order to clarify the capacity of nitrite to prevent renal disease, we administered low-dose nitrite (LDN: 0.1mg of sodium nitrite in 1L of drinking water), medium-dose nitrite (MDN: 1mg sodium nitrite/L, which corresponds to the amount of nitrite ingested by vegetarians), or high-dose nitrite (HDN: 10mg sodium nitrite/L) to rats simultaneously with L-NAME (1 g l-NAME/L) for 8 weeks, then examined the blood NO level as a hemoglobin-NO adduct (iron-nitrosyl-hemoglobin) using electron paramagnetic resonance spectroscopy, urinary protein excretion, and renal histological changes at the end of the experiment. It was found that oral administration of MDN and HDN but not LDN increased the blood iron-nitrosyl-hemoglobin concentration to the normal level, ameliorated the L-NAME-induced proteinuria, and reduced renal histological damage. The findings demonstrate that chronic administration of a mid-level dietary dose of nitrite restores the circulating iron-nitrosyl-hemoglobin levels reduced by L-NAME and that maintenance of the circulating iron-nitrosyl-hemoglobin level in a controlled range protects against L-NAME-induced renal injury. Taking these findings together, we propose that dietary supplementation of nitrite is a potentially useful nonpharmacological strategy for maintaining circulating NO level in order to prevent or slow the progression of renal disease. It had been believed that nitrite could result in intragastric formation of nitrosamines, which had been linked to esophageal and other gastrointestinal cancers. However, there is no positive association between the intake of nitrate or nitrite and gastric and pancreatic cancer by recent researches. Furthermore, nitrate-derived NO formation pathway is a possible mechanism for the hypotensive effect of vegetable- and fruit-rich diets, which may explain, at least in part, the mechanism of the Dietary Approach to Stop Hypertension (DASH) diet-induced hypotensive and organ-protective effects. Further research is needed to investigate the interaction between nitrite-nitrate intakes and human health. (Keyword) Animals / Diet / Hypertension / Kidney Diseases / NG-Nitroarginine Methyl Ester / Rats / Sodium Nitrite (Link to Publication Site) ● Publication site (DOI): 10.1016/j.niox.2009.12.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20005970 ● Search Scopus @ Elsevier (PMID): 20005970 ● Search Scopus @ Elsevier (DOI): 10.1016/j.niox.2009.12.002 (DOI: 10.1016/j.niox.2009.12.002, PubMed: 20005970)
75.	Masatomo Mihara, Ken-ichi Aihara, Yasumasa Ikeda, Sumiko Yoshida, Mizuho Kinouchi, Kiyoe Kurahashi, Yuichi Fujinaka, Masashi Akaike and Toshio Matsumoto : Inhibition of thrombin action ameliorates insulin resistance in type 2 diabetic db/db mice., Endocrinology, Vol.151, No.2, 513-519, 2009. (Summary) The binding of thrombin to its receptor stimulates inflammatory cytokines including IL-6 and monocyte chemoattractant protein-1 (MCP-1); both are associated with the development of insulin resistance. Because increased adiposity enhanced the expression of coagulation factor VII that stimulates the coagulation pathway in adipose tissue, we tested whether the inhibition of thrombin action ameliorates insulin resistance in obese diabetic (Lpr(-/-):db/db) mice. The 4-wk administration of argatroban, a selective thrombin inhibitor, reduced fasting plasma glucose and ameliorated insulin resistance in these mice. It also reduced adipocyte size and macrophage infiltration into adipose tissue. The aberrant gene expression of MCP-1, IL-6, adiponectin, and factor VII and suppressed insulin receptor substrate-1-Akt signaling in adipose tissue of db/db mice were reversed by argatroban treatment. These results demonstrate that increased adiposity enhances the production of thrombin in adipose tissue by stimulating factor VII expression and suggest that increased thrombin activity in adipose tissue plays an important role in the development of insulin resistance via enhancing MCP-1 production, leading to macrophage infiltration and insulin receptor substrate-1-Akt pathway inactivation. (Link to Publication Site) ● Publication site (DOI): 10.1210/en.2009-0661 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19966184 ● Search Scopus @ Elsevier (PMID): 19966184 ● Search Scopus @ Elsevier (DOI): 10.1210/en.2009-0661 (DOI: 10.1210/en.2009-0661, PubMed: 19966184)
76.	Yasumasa Ikeda, Kaori Sato, R David Pimentel, Flora Sam, J Reuben Shaw, B Jason R Dyck and Kenneth Walsh : Cardiac-specific deletion of LKB1 leads to hypertrophy and dysfunction., The Journal of Biological Chemistry, Vol.284, No.51, 35839-35849, 2009. (Summary) LKB1 encodes a serine/threonine kinase, which functions upstream of the AMP-activated protein kinase (AMPK) superfamily. To clarify the role of LKB1 in heart, we generated and characterized cardiac myocyte-specific LKB1 knock-out (KO) mice using alpha-myosin heavy chain-Cre deletor strain. LKB1-KO mice displayed biatrial enlargement with atrial fibrillation and cardiac dysfunction at 4 weeks of age. Left ventricular hypertrophy was observed in LKB1-KO mice at 12 weeks but not 4 weeks of age. Collagen I and III mRNA expression was elevated in atria at 4 weeks, and atrial fibrosis was seen at 12 weeks. LKB1-KO mice displayed cardiac dysfunction and atrial fibrillation and died within 6 months of age. Indicative of a prohypertrophic environment, the phosphorylation of AMPK and eEF2 was reduced, whereas mammalian target of rapamycin (mTOR) phosphorylation and p70S6 kinase phosphorylation were increased in both the atria and ventricles of LKB1-deficient mice. Consistent with vascular endothelial growth factor mRNA and protein levels being significantly reduced in LKB1-KO mice, these mice also exhibited a reduction in capillary density of both atria and ventricles. In cultured cardiac myocytes, LKB1 silencing induced hypertrophy, which was ameliorated by the expression of a constitutively active form AMPK or by treatment with the inhibitor of mTOR, rapamycin. These findings indicate that LKB1 signaling in cardiac myocytes is essential for normal development of the atria and ventricles. Cardiac hypertrophy and dysfunction in LKB1-deficient hearts are associated with alterations in AMPK and mTOR/p70S6 kinase/eEF2 signaling and with a reduction in vascular endothelial growth factor expression and vessel rarefaction. (Keyword) Animals / Antibiotics, Antineoplastic / Atrial Fibrillation / Carrier Proteins / Collagen Type I / Collagen Type II / Fibrosis / Gene Expression Regulation / Heart Atria / Hypertrophy, Left Ventricular / Mice / Mice, Knockout / Myocardium / Organ Specificity / Peptide Elongation Factor 2 / Phosphorylation / Phosphotransferases (Alcohol Group Acceptor) / Protein Kinases / Protein-Serine-Threonine Kinases / RNA, Messenger / Ribosomal Protein S6 Kinases, 70-kDa / Signal Transduction / Sirolimus (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M109.057273 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19828446 ● Search Scopus @ Elsevier (PMID): 19828446 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M109.057273 (DOI: 10.1074/jbc.M109.057273, PubMed: 19828446)
77.	Mitsunori Fujimura, Masashi Akaike, Takashi Iwase, Sumiko Yoshida, Yuka Sumitomo, Shusuke Yagi, Yasumasa Ikeda, Shunji Hashizume, Ken-ichi Aihara, Takeshi Nishiuchi, Yoshio Yasumura and Toshio Matsumoto : Decrease in plasma brain natriuretic peptide level in the early phase after the start of carvedilol therapy is a novel predictor of long-term outcome in patients with chronic heart failure., Acta Cardiologica, Vol.64, No.5, 589-595, 2009. (Summary) OBJECTIVE: The purpose of the present study was to determine whether change in plasma brain natriuretic peptide (BNP) level at an early phase of carvedilol therapy is a predictor of improvement in cardiac function and long-term prognosis in patients with systolic chronic heart failure (CHF). METHODS AND RESULTS: Neurohumoral factors and haemodynamics were examined in 64 patients with systolic CHF (left ventricular ejection fraction (LVEF) below 45%) before and one month (early phase) and 3 to 6 months (late phase) after the start of carvedilol therapy. These patients were followed up for a mean period of 57 months. Plasma BNP levels were already decreased in the early phase before improvement of LVEF in response to carvedilol therapy. Univariate and multivariate linear regression analyses showed that Delta log brain natriuretic peptide (BNP)E (= log BNP at baseline--log BNP at early phase) (P < 0.0001) was a significant independent predictor of improvement in LVEF in the late phase. Cardiac events occurred in I I patients during the follow-up period. In addition, multivariate Cox proportional hazards regression analysis showed that Delta log BNPE (P = 0.0045) and systolic blood pressure at baseline (P = -0.048) were significant independent predictors of the development of cardiac events. CONCLUSIONS: Decrease in plasma BNP level in the early phase of carvedilol therapy is a novel predictor of not only improvement of LVEF in the late phase but also prognosis in patients with systolic CHF. (Link to Publication Site) ● Publication site (DOI): 10.2143/AC.64.5.2042687 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20058503 ● Search Scopus @ Elsevier (PMID): 20058503 ● Search Scopus @ Elsevier (DOI): 10.2143/AC.64.5.2042687 (DOI: 10.2143/AC.64.5.2042687, PubMed: 20058503)
78.	Keisuke Ishizawa, Narantungalag Dorjsuren, Yuki Izawa-Ishizawa, Rika Sugimoto, Yasumasa Ikeda, Yoshitaka Kihira, Kazuyoshi Kawazoe, Shuhei Tomita, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : Inhibitory effects of adiponectin on platelet-derived growth factor-induced mesangial cell migration, The Journal of Endocrinology, Vol.202, No.2, 309-316, 2009. (Summary) Adiponectin, an adipocyte-derived hormone, has been involved in metabolic syndrome, a known risk factor for the development of chronic kidney disease (CKD). Recent studies have demonstrated that plasma adiponectin levels are elevated when kidney function declines in patients with CKD. Excessive mesangial cell (MC) turnover is one of the important features of CKD. The aim of the present study is to elucidate the effects of adiponectin on platelet-derived growth factor (PDGF)-induced cell migration and intracellular signaling pathways, in cultured rat MCs (RMCs). PDGF-induced RMC migration was significantly inhibited by the pretreatment of adiponectin. Adiponectin alone had no effect on RMC migration. Big mitogen-activated protein (MAP) kinase 1 (BMK1), p38 MAP kinase, and Akt were activated by PDGF stimulation in a time- and concentration-dependent manner in RMC. Adiponectin alone did not affect BMK1, p38 MAP kinase, and Akt phosphorylations in RMC. PDGF-induced BMK1 and p38 MAP kinase phosphorylations were significantly attenuated by the pretreatment of adiponectin in RMCs. On the other hand, the phosphorylation of Akt by PDGF was not diminished by the pretreatment of adiponectin. Adiponectin had no effects on PDGF-receptor autophosphorylation by PDGF. We also confirmed that PDGF-induced RMC migration was significantly suppressed by siBMK1 transfection or SB203580, a p38 MAP kinase inhibitor. From these findings, it is implied that the elevated plasma adiponectin levels in patients with CKD might play a compensatory role aimed at counteracting renal dysfunction related to MC disorders. (Keyword) Adiponectin / Animals / Cell Movement / Cells, Cultured / Dose-Response Relationship, Drug / Enzyme Inhibitors / Glomerular Mesangium / Imidazoles / Male / Mitogen-Activated Protein Kinase 7 / Phosphorylation / Platelet-Derived Growth Factor / Pyridines / RNA, Small Interfering / Rats / Rats, Sprague-Dawley / Recombinant Proteins / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1677/JOE-08-0469 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19460854 ● Search Scopus @ Elsevier (PMID): 19460854 ● Search Scopus @ Elsevier (DOI): 10.1677/JOE-08-0469 (DOI: 10.1677/JOE-08-0469, PubMed: 19460854)
79.	Ross Summer, A Christopher Fiack, Yasumasa Ikeda, Kaori Sato, Daniel Dwyer, Noriyuki Ouchi, Alan Fine, W Harrison Farber and Kenneth Walsh : Adiponectin deficiency: a model of pulmonary hypertension associated with pulmonary vascular disease., American Journal of Physiology. Lung Cellular and Molecular Physiology, Vol.297, No.3, L432-8, 2009. (Summary) Adiponectin (APN) is an adipocyte-derived factor that exists at high concentrations in serum and has anti-inflammatory and systemic vascular-protective properties. In this study, we investigated the role of APN in pulmonary vascular homeostasis. We found that APN localizes to the luminal side of blood vessels in lung and acts in vitro to block TNF-alpha-induced E-selectin upregulation in pulmonary artery endothelial cells. Targeted deletion of the APN gene in mice leads to a vascular phenotype in lung characterized by E-selectin upregulation and age-dependent increases in perivascular inflammatory cell infiltration and pulmonary arterial pressures. Taken together, these findings demonstrate an important role for APN in lung vascular homeostasis and suggest that APN-deficient states may contribute to the pathogenesis of inflammatory pulmonary vascular disease and to the development of pulmonary hypertension. (Keyword) Adiponectin / Aging / Animals / Cell Line / Disease Models, Animal / E-Selectin / Endothelium, Vascular / Heart Catheterization / Humans / Hypertension, Pulmonary / Inflammation / Lung / Mice / Phenotype / Pressure / Protein Transport / Pulmonary Artery / Tumor Necrosis Factor-alpha / Up-Regulation / Vascular Diseases (Link to Publication Site) ● Publication site (DOI): 10.1152/ajplung.90599.2008 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19561137 ● Search Scopus @ Elsevier (PMID): 19561137 ● Search Scopus @ Elsevier (DOI): 10.1152/ajplung.90599.2008 (DOI: 10.1152/ajplung.90599.2008, PubMed: 19561137)
80.	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)
81.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Takashi Sato, Shusuke Yagi, Takashi Iwase, Yuka Sumitomo, Takayuki Ise, Kazue Ishikawa, Hiroyuki Azuma, Masashi Akaike, Shigeaki Kato and Toshio Matsumoto : Androgen-androgen receptor system protects against angiotensin II-induced vascular remodeling., Endocrinology, Vol.150, No.6, 2857-2864, 2009. (Summary) Age-related andropause promotes cardiovascular disease in males. Although we had previously reported that the androgen-androgen receptor (AR) system plays important roles in cardiac growth and remodeling, the system's involvement in vascular remodeling remains unclear. To clarify this role, 25-wk-old male AR knockout (ARKO) mice and littermate male wild-type (WT) mice were divided into two groups with and without angiotensin II (Ang II) administration (2.0 mg/kg . d) for 14 d, respectively. No morphological differences in the coronary artery and thoracic aorta were observed between the groups without Ang II. Ang II stimulation markedly increased medial thickness and perivascular fibrosis in ARKO mice, with enhanced TGF-beta1, collagen type I, and collagen type III gene expression in the aorta. Ang II stimulation also prominently increased superoxide production, lipid peroxidation, and gene expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase components in ARKO mice compared with WT mice. In addition, phosphorylation of c-Jun N-terminal kinase (JNK) and phosphorylated (Smad2/3) was remarkably enhanced in Ang II-treated ARKO mice compared with Ang II-treated WT mice. Notably, daily urinary nitric oxide (NO) metabolites excretion as a marker of NO bioavailability, aortic endothelial NO synthase expression and phosphorylation, and Akt phosphorylation were significantly reduced in ARKO mice compared with WT mice, regardless of Ang II stimulation. In conclusion, the androgen-AR system is required for the preservation of NO bioavailability through Akt-endothelial NO synthase system activation and exerts protective effects against Ang II-induced vascular remodeling by regulating oxidative stress, c-Jun N-terminal kinase (JNK) signaling, and the TGF-beta-phosphorylated Smad pathway. (Keyword) Androgens / Angiotensin II / Animals / Aorta, Thoracic / Atherosclerosis / Coronary Vessels / Disease Models, Animal / Lipid Peroxidation / MAP Kinase Kinase 4 / Male / Mice / Mice, Inbred C57BL / Mice, Knockout / Nitric Oxide / Proto-Oncogene Proteins c-akt / Receptor, Angiotensin, Type 1 / Receptor, Angiotensin, Type 2 / Receptors, Androgen / Superoxides / Thiobarbituric Acid Reactive Substances / Transforming Growth Factor beta1 / Vasoconstrictor Agents (Link to Publication Site) ● Publication site (DOI): 10.1210/en.2008-1254 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19196803 ● Search Scopus @ Elsevier (PMID): 19196803 ● Search Scopus @ Elsevier (DOI): 10.1210/en.2008-1254 (DOI: 10.1210/en.2008-1254, PubMed: 19196803)
82.	Ken-ichi Aihara, Masashi Akaike, Yasumasa Ikeda, Yuka Ueda, Sumiko Yoshida, Takayuki Ise, Shusuke Yagi, Takashi Iwase, 近藤彰, 田村克也 and Toshio Matsumoto : アンジオテンシンII受容体拮抗薬バルサルタンのNO bioavailability改善効果に関する臨床的検討, Progress in Medicine, Vol.29, No.7, 1777-1782, 2009. (Summary) バルサルタンの降圧作用，動脈硬化抑制作用および糖代謝改善作用に一酸化窒素(NO)のバイオアベイラビリティの改善効果が関与しているか検討した．高血圧治療目的で通院加療中の42例を対象とした．バルサルタン投与にて，BMIやリポプロテイン(a)を含む脂質プロファイルに有意な変化は認めなかったが，収縮期血圧，脈圧，baPWVおよびHbA1cは有意に低下した．投与3ヵ月後には投与前と比較して，NOのバイオアベイラビリティのマーカーである血清硝酸/亜硝酸イオン(NOx)は約1.5倍に増加した．血清NOxの増加が，他の測定因子にどのように影響を与えているか，単変量および多変量解析を用いて解析し，血清NOxの増加量は収縮期血圧の低下と脈圧の減少との間においてそれぞれ有意な相関がみられた．また，HbA1cはバルサルタン投与3ヵ月後に有意に低下していたが，その変化はNOxの増加量と有意な相関がみられた． (Keyword) Nitrogen Oxides(血液) Glycosylated Hemoglobin A 降圧剤(治療的利用,薬理学) 高血圧(薬物療法) 生物学的利用率動脈硬化症-アテローム性(予防,診断) 経口投与一酸化窒素 Valsartan(治療的利用,薬理学) Angiotensin II Type 1 Receptor Blockers(治療的利用,薬理学) 脈波伝播速度ヒト中年(45~64) 高齢者(65~79) 男女
83.	Shusuke Yagi, Masahi Akaike, Mitsunori Fujimura, Takayuki Ise, Sumiko Yoshida, Yuka Sumitomo, Yasumasa Ikeda, Takashi Iwase, Ken-ichi Aihara, Hiroyuki Azuma, Atsushi Kurushima, Youichi Ichikawa, Tetsuya Kitagawa, Takehiko Kimura, Takeshi Nishiuchi and Toshio Matsumoto : Infective endocarditis caused by lactobacillus., Internal Medicine, Vol.47, No.12, 1113-1116, 2008. (Summary) Lactobacillus (LB) is a gram-positive rod-shaped bacterium that inhabits the oral cavity, gastrointestinal tract, vagina and nasal cavity. Although LB plays a role in the prevention of infections caused by pathogenic bacteria, it causes some critical infectious diseases such as infective endocarditis (IE). IE due to LB is rare; however, early diagnosis and early treatment are important because of its high mortality rate. We report the onset of IE after otologic treatment in a heavy drinker of alcohol, the second case of IE due to LB in Japan. (Keyword) Adult / Alcoholism / Endocarditis, Bacterial / Gram-Positive Bacterial Infections / Heart Valve Prosthesis Implantation / Humans / Immunocompromised Host / Lactobacillus / Male / Mitral Valve Insufficiency (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.47.0744 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18552468 ● Search Scopus @ Elsevier (PMID): 18552468 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.47.0744 (DOI: 10.2169/internalmedicine.47.0744, PubMed: 18552468)
84.	Yasumasa Ikeda, Koji Ohashi, Rei Shibata, R David Pimentel, Shinji Kihara, Noriyuki Ouchi and Kenneth Walsh : Cyclooxygenase-2 induction by adiponectin is regulated by a sphingosine kinase-1 dependent mechanism in cardiac myocytes., FEBS Letters, Vol.582, No.7, 1147-1150, 2008. (Summary) The adipose-derived plasma protein, adiponectin (APN), has various protective effects on cardiovascular diseases. In this study, we show that endogenous APN is required for full cyclooxygenase-2 (COX-2) induction by ischemia-reperfusion injury in the heart in vivo. In rat neonatal cardiac myocytes, APN-induced COX-2 expression was reduced by treatment with a sphingosine kinase-1 (SphK-1) inhibitor or siRNA targeting SphK-1. Treatment with a sphingosine-1-phosphate (S1P) receptor antagonist also diminished COX-2 expression in response to APN stimulation. These findings suggest that APN is a physiological regulator of COX-2 signaling in the heart and that this regulation occurs in part via a SphK-1-S1P receptor dependent mechanism in cardiac myocytes. (Keyword) Adiponectin / Animals / Cyclooxygenase 2 / Mice / Mice, Knockout / Myocardial Reperfusion Injury / Myocytes, Cardiac / Phosphotransferases (Alcohol Group Acceptor) / Receptors, Lysosphingolipid / Signal Transduction / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.febslet.2008.03.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18339320 ● Search Scopus @ Elsevier (PMID): 18339320 ● Search Scopus @ Elsevier (DOI): 10.1016/j.febslet.2008.03.002 (DOI: 10.1016/j.febslet.2008.03.002, PubMed: 18339320)
85.	Masashi Akaike, 小原卓爾, 日浅光春, 藤村光則, 加藤みどり, 横井健治, 小島章裕, 岡崎誠司, 井内貴彦, 井上利彦, 住友由佳, Shusuke Yagi, Yasumasa Ikeda, Takashi Iwase, Ken-ichi Aihara and Hiroyuki Azuma : 高コレステロール血症患者に対するピタバスタチンの有効性総合的脂質プロファイルに関する検討, Progress in Medicine, Vol.28, No.11, 2745-2751, 2008. (Summary) 高コレステロール血症患者を対象にピタバスタチンを投与し，総合的脂質プロファイルへの影響について検討した．高コレステロール血症と診断され，ピタバスタチンを投与した87例を対象とした．ピタバスタチン投与によりTC，LDL-Cは有意に低下した．HDL-Cは有意な上昇，TGは有意な低下を認めた．ピタバスタチンを新規に投与した症例で，TC，LDL-Cは有意かつ良好な低下作用を認めた．また，HDL-Cは有意な上昇，TGは有意な低下作用を示した．Non HDL-Cは有意に低下し，LDL-C/HDL-C比は有意に減少した．動脈硬化指数は，いずれも有意に改善した．投与前後でLp(a)を測定した76例で，有意な変化は認めなかった．投与前後におけるALT，ASTの平均変化量に，有意な変化は認めなかった．CKも有意な変化は認めなかった．治療上，問題となる副作用は認めなかった． (Keyword) Cholesterol(血液) HDL Cholesterol(血液) LDL Cholesterol(血液) Triglycerides(血液) 高コレステロール血症(薬物療法) Lipoprotein(a)(血液) 治療成績 Pitavastatin(治療的利用) ヒト中年(45~64) 高齢者(65~79) 男女
86.	Shusuke Yagi, Ken-ichi Aihara, Yasumasa Ikeda, Yuka Sumitomo, Sumiko Yoshida, Takayuki Ise, Takashi Iwase, Kazue Ishikawa, Hiroyuki Azuma, Masashi Akaike and Toshio Matsumoto : Pitavastatin, an HMG-CoA reductase inhibitor, exerts eNOS-independent protective actions against angiotensin II induced cardiovascular remodeling and renal insufficiency., Circulation Research, Vol.102, No.1, 68-76, 2007. (Summary) Angiotensin II (Ang II) plays a pivotal role in cardiovascular remodeling leading to hypertension, myocardial infarction, and stroke. Pitavastatin, an HMG-CoA reductase inihibitor, is known to have pleiotropic actions against the development of cardiovascular remodeling. The objectives of this study were to clarify the beneficial effects as well as the mechanism of action of pitavastatin against Ang II-induced organ damage. C57BL6/J mice at 10 weeks of age were infused with Ang II for 2 weeks and were simultaneously administered pitavastatin or a vehicle. Pitavastatin treatment improved Ang II-induced left ventricular hypertrophy and diastolic dysfunction and attenuated enhancement of cardiac fibrosis, cardiomyocyte hypertrophy, coronary perivascular fibrosis, and medial thickening. Ang II-induced oxidative stress, cardiac TGFbeta-1 expression, and Smad 2/3 phosphorylation were all attenuated by pitavastatin treatment. Pitavastatin also reduced Ang II-induced cardiac remodeling and diastolic dysfunction in eNOS-/- mice as in wild-type mice. In eNOS-/- mice, the Ang II-induced cardiac oxidative stress and TGF-beta-Smad 2/3 signaling pathway were enhanced, and pitavastatin treatment attenuated the enhanced oxidative stress and the signaling pathway. Moreover, pitavastatin treatment reduced the high mortality rate and improved renal insufficiency in Ang II-treated eNOS-/- mice, with suppression of glomerular oxidative stress and TGF-beta-Smad 2/3 signaling pathway. In conclusion, pitavastatin exerts eNOS-independent protective actions against Ang II-induced cardiovascular remodeling and renal insufficiency through inhibition of the TGF-beta-Smad 2/3 signaling pathway by suppression of oxidative stress. (Keyword) Angiotensin II / Animals / Cardiotonic Agents / Hydroxymethylglutaryl-CoA Reductase Inhibitors / Hypertrophy, Left Ventricular / Mice / Mice, Inbred C57BL / Mice, Knockout / Nitric Oxide Synthase Type III / Oxidative Stress / Quinolines / Renal Insufficiency / Signal Transduction / Smad2 Protein / Smad3 Protein / Transforming Growth Factor beta / Ventricular Remodeling (Link to Publication Site) ● Publication site (DOI): 10.1161/CIRCRESAHA.107.163493 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17967781 ● Search Scopus @ Elsevier (PMID): 17967781 ● Search Scopus @ Elsevier (DOI): 10.1161/CIRCRESAHA.107.163493 (DOI: 10.1161/CIRCRESAHA.107.163493, PubMed: 17967781)
87.	Shusuke Yagi, Masashi Akaike, Shuji Ozaki, Chikako Moriya, Kyoko Takeuchi, Tomoko Hara, Mitsunori Fujimura, Yuka Sumitomo, Takashi Iwase, Yasumasa Ikeda, Ken-ichi Aihara, Takehiko Kimura, Takeshi Nishiuchi, Masahiro Abe and Toshio Matsumoto : Improvement of cardiac diastolic function and prognosis after autologous peripheral blood stem cell transplantation in AL cardiac amyloidosis., Internal Medicine, Vol.46, No.20, 1705-1710, 2007. (Summary) AL amyloidosis is a disease in which immunoglobulin L chain is deposited in multiple organs, and the prognosis of cardiac amyloidosis is extremely poor. Although several treatments based on that for multiple myeloma, have been performed, there is no clear evidence that cardiac function is improved. We report a case of AL cardiac amyloidosis with moderate cardiac dysfunction for which we performed autologous peripheral blood stem cell transplantation (auto-PBSCT) in combination with high-dose melphalan therapy. This treatment resulted in significant improvement in cardiac function and good prognosis for about 3.5 years after the diagnosis. Therefore, auto-PBSCT is a possible option as up-front therapy for AL cardiac amyloidosis. (Keyword) Amyloidosis / Cardiomyopathies / Combined Modality Therapy / Female / Heart / Humans / Melphalan / Middle Aged / Peripheral Blood Stem Cell Transplantation / Prognosis (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.46.0142 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17938525 ● Search Scopus @ Elsevier (PMID): 17938525 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.46.0142 (DOI: 10.2169/internalmedicine.46.0142, PubMed: 17938525)
88.	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)
89.	Yasumasa Ikeda, Shusuke Yagi, Hiroshi Yamaguchi, Mitsunori Fujimura, Shunji Hashizume, Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : Intra-vascular ultrasound findings of diffuse coronary atherosclerotic change in systemic lupus erythematosus with secondary antiphospholipid syndrome, Circulation Journal, Vol.70, No.8, 1082-1085, 2006. (Summary) Systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) are autoimmune inflammatory diseases associated with juvenile atherosclerosis and thrombosis, respectively. A 44-year-old woman who had SLE with secondary APS had been treated with corticosteroid therapy, however, her inflammatory marker had never been within a normal range in her clinical course, and finally acute myocardial infarction was developed. Intra-vascular ultrasound also revealed diffuse coronary atherosclerosis progression for her age, which might result from SLE and APS, including vascular inflammation. (Keyword) Adrenal Cortex Hormones / Adult / Antiphospholipid Syndrome / Coronary Artery Disease / Coronary Vessels / Female / Humans / Lupus Erythematosus, Systemic / Myocardial Infarction / Ultrasonography, Interventional (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.70.1082 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16864946 ● Search Scopus @ Elsevier (PMID): 16864946 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.70.1082 (DOI: 10.1253/circj.70.1082, PubMed: 16864946)
90.	Tomonori Watanabe, Hiroyuki Fujinaga, Yasumasa Ikeda, Teruo HIgashi, Masaru Murakami, Keiji Kawahara, Ikuo Hayashi, Toshiharu Niki, Toshio Shigekiyo and Tetsuzo Wakatsuki : Acute myocardial infarction in a patient with essential thrombocythemia who underwent successful stenting. A case report, Angiology, Vol.56, No.6, 771-774, 2005. (Summary) Essential thrombocythemia (ET) can cause systemic vascular thrombosis, but involvement of coronary arteries in the setting of ET is rare. This report describes a case of acute myocardial infarction (MI) in a patient with ET. A 67-year-old man with ET complained of severe acute chest pain. Emergent coronary angiography revealed subtotal thrombotic occlusion of the left main trunk (LMT) coronary artery. Coronary angioplasty and stenting were performed successfully. Coronary angiography 4 weeks later revealed no significant restenosis. The patient has done well after primary coronary stenting with the use of only an antiplatelet agent to treat the thrombocythemia. (Keyword) Aged / Angioplasty, Balloon, Coronary / Humans / Male / Myocardial Infarction / Platelet Aggregation Inhibitors / Stents / Thrombocythemia, Essential (Link to Publication Site) ● Publication site (DOI): 10.1177/000331970505600616 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16327955 ● Search Scopus @ Elsevier (PMID): 16327955 ● Search Scopus @ Elsevier (DOI): 10.1177/000331970505600616 (DOI: 10.1177/000331970505600616, PubMed: 16327955)
91.	Yasumasa Ikeda, Ken-ichi Aihara, Takashi Sato, Masashi Akaike, Masanori Yoshizumi, Yuki Suzaki, Yuki Izawa-Ishizawa, Mitsunori Fujimura, Shunji Hashizume, Midori Kato, Shusuke Yagi, Toshiaki Tamaki, Hirotaka Kawano, Takahiro Matsumoto, Hiroyuki Azuma, Shigeaki Kato and Toshio Matsumoto : Androgen receptor gene knockout male mice exhibit impaired cardiac growth and exacerbation of angiotensin II-induced cardiac fibrosis., The Journal of Biological Chemistry, Vol.280, No.33, 29661-29666, 2005. (Summary) Androgen has anabolic effects on cardiac myocytes and has been shown to enhance left ventricular enlargement and function. However, the physiological and patho-physiological roles of androgen in cardiac growth and cardiac stress-induced remodeling remains unclear. We aimed to clarify whether the androgen-nuclear androgen receptor (AR) system contributes to the cardiac growth and angiotensin II (Ang II)-stimulated cardiac remodeling by using systemic AR-null male mice. AR knock-out (ARKO) male mice, at 25 weeks of age, and age-matched wild-type (WT) male mice were treated with or without Ang II stimulation (2.0 mg/kg/day) for 2 weeks. ARKO mice with or without Ang II stimulation showed a significant reduction in the heart-to-body weight ratio compared with those of WT mice. In addition, echocardiographic analysis demonstrated impairments of both the concentric hypertrophic response and left ventricular function in Ang II-stimulated ARKO mice. Western blot analysis of the myocardium revealed that activation of extracellular signal-regulated kinases (ERK) 1/2 and ERK5 by Ang II stimulation were lower in ARKO mice than those of WT mice. Ang II stimulation caused more prominent cardiac fibrosis in ARKO mice than in WT mice with enhanced expression of types I and III collagen and transforming growth factor-beta1 genes and with increased Smad2 activation. These results suggest that, in male mice, the androgen-AR system participates in normal cardiac growth and modulates cardiac adaptive hypertrophy and fibrosis during the process of cardiac remodeling under hypertrophic stress. (Keyword) Angiotensin II / Animals / blood pressure / Cardiomegaly / DNA-Binding Proteins / pulmonary fibrosis / Heart Rate / Male / Mice / Mice, Inbred C57BL / Mice, Inbred CBA / knockout mice / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinase 7 / myocardium / RNA, Messenger / Receptors, Androgen / Smad2 Protein / Trans-Activators / Transforming Growth Factor beta / Transforming Growth Factor beta1 / Ventricular Remodeling (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M411694200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15961403 ● Search Scopus @ Elsevier (PMID): 15961403 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M411694200 (DOI: 10.1074/jbc.M411694200, PubMed: 15961403)
92.	Midori Kato, Hiroyuki Azuma, Masashi Akaike, Takahiko Iuchi, Ken-ichi Aihara, Yasumasa Ikeda, Mitsunori Fujimura, Tomonori Yoshida, Hiroshi Yamaguchi, Shunji Hashizume and Toshio Matsumoto : Aspirin inhibits thrombin action on endothelial cells via up-regulation of aminopeptidase N/CD13 expression., Atherosclerosis, Vol.183, No.1, 49-55, 2005. (Summary) OBJECTIVE: We hypothesized that aspirin may exhibit its anti-atherosclerotic effects via mechanisms other than cyclooxygenase inhibition in platelets. METHODS AND RESULTS: Using enhanced subtraction hybridization analysis, we found in human umbilical vein endothelial cells (HUVECs) that aspirin up-regulates the expression of aminopeptidase N (APN/CD13) mRNA and its surface protein levels in a dose-dependent manner. Enzymatic activity of APN/CD13 on HUVECs was increased approximately 1.5-fold by 1 mmol L(-1) of aspirin, and treatment with bestatin, an inhibitor for APN/CD13 metalloprotease activity, attenuated the enhanced activities of APN/CD13. Since activated thrombin receptor is reported to be inactivated by APN/CD13 in vitro, protective actions of aspirin on HUVECs by thrombin stimulation were examined, resulting in the suppression of endothelin-1 and reactive oxygen species productions in HUVECs. These inhibitory actions of aspirin were partially abrogated by bestatin. CONCLUSIONS: Aspirin may exert its anti-atherothrombotic effects in part via the inhibition of thrombin action by up-regulating APN/CD13 on endothelial cells. (Keyword) Antigens, CD13 / Aspirin / Cells, Cultured / Endothelial Cells / Endothelin-1 / Endothelium, Vascular / Enzyme Induction / Fibrinolytic Agents / Genes, Reporter / Humans / Leucine / Protease Inhibitors / RNA, Messenger / reactive oxygen species / Subtraction Technique / Thrombin / Transcription, Genetic / Transfection / Umbilical Veins (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2005.03.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16216591 ● Search Scopus @ Elsevier (PMID): 16216591 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2005.03.003 (DOI: 10.1016/j.atherosclerosis.2005.03.003, PubMed: 16216591)
93.	Yasumasa Ikeda, Hiroyuki Fujinaga and Toshiharu Niki : Successful percutaneous coronary intervention for acute myocardial infarction caused by simultaneous occlusion of two major coronary arteries in patients with diabetes mellitus. A report of two cases., Acta Cardiologica, Vol.60, No.2, 225-228, 2005. (Summary) Percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) is a common therapeutic method. Although two or more culprit lesions are rarely observed simultaneously in AMI patients, we present two cases of AMI caused by simultaneous occlusion of two major coronary arteries, the left anterior descending and right coronary arteries. In both cases, emergency PCI for the two major vessels was successful. Both patients had type 2 diabetes mellitus, which might have contributed to simultaneous occlusion of the two coronary arteries. (Keyword) Aged / Angioplasty, Transluminal, Percutaneous Coronary / Coronary Disease / Diabetic Angiopathies / Electrocardiography / Female / Humans / Intra-Aortic Balloon Pumping / Myocardial Infarction (Link to Publication Site) ● Publication site (DOI): 10.2143/AC.60.2.2005037 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15887482 ● Search Scopus @ Elsevier (PMID): 15887482 ● Search Scopus @ Elsevier (DOI): 10.2143/AC.60.2.2005037 (DOI: 10.2143/AC.60.2.2005037, PubMed: 15887482)
94.	山口普史, Yasumasa Ikeda, 藤村光則, 森岡将臣, 橋詰俊二, 加藤みどり, Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma, Toshio Matsumoto, 稲山真美 and Masaki Hanibuchi : アミオダロン肺合併症との鑑別を要したマイコプラズマ肺炎合併拡張型心筋症の1例, Progress in Medicine, Vol.25, No.Suppl.1, 1552-1556, 2005. (Summary) 52歳男.47歳時に拡張型心筋症と診断され,持続性心室頻拍でアミオダロン150mg/日を開始した.その後,心室頻拍が頻回となり,心臓電気生理学的検査で心室細動が誘発されたため除細動器植込み術を受け,アミオダロンは増量して継続していた.今回,乾性咳が出現し,胸部X線で左右下肺野にスリガラス状陰影を指摘された.検査所見では高度の炎症所見を認めたが,KL-6は正常範囲で,C型肝炎ウイルスとヒトT細胞性白血病ウイルスI型のキャリアであった.胸部CTでは両側下肺野を中心として壁の肥厚を伴う気管支拡張や小葉中心性の粒状・樹枝状の陰影が多発しており,周囲の肺野に淡い濃度上昇を認めた.アミオダロンの副作用か感染症かは判断できなかったが,アミオダロンは中止し,アンピシリンナトリウム・スルバクタムナトリウム合剤を開始すると共にサイトメガロウイルス高力価免疫グロブリン投与を行った.入院10日目にマイコプラズマ抗体異常高値が判明し,マイコプラズマ肺炎と診断しミノサイクリン100mg/日を開始した.その結果,炎症所見,画像所見は徐々に軽快し,アミオダロンも再開して退院となった (Keyword) Amiodarone(治療的利用,毒性・副作用) Minocycline(治療的利用) 胸部X線診断心筋症-拡張型(合併症) 鑑別診断 X線CT 肺炎-マイコプラズマ性(合併症,X線診断) 頻拍-心室性(薬物療法) 肺炎-細菌性(合併症,X線診断,薬物療法) 肺炎-間質性(化学的誘発,X線診断) 胸部CT ヒト中年(45~64) 男
95.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Yasumasa Ikeda, Michiko Yamashita, Toshiki Sudo, Hideki Hayashi, Yoshihisa Yamada, Fuminari Endoh, Mitsunori Fujimura, Tomonori Yoshida, Hiroshi Yamaguchi, Shunji Hashizume, Midori Kato, Kimihiro Yoshimura, Yoko Yamamoto, Shigeaki Kato and Toshio Matsumoto : Disruption of nuclear vitamin D receptor gene causes enhanced thrombogenicity in mice, The Journal of Biological Chemistry, Vol.279, No.34, 35798-35802, 2004. (Summary) Vitamin D metabolites influence the expression of various genes involved in calcium homeostasis, cell differentiation, and regulation of the immune system. Expression of these genes is mediated by the activation of the nuclear vitamin D receptor (VDR). Previous studies have shown that a hormonally active form of vitamin D, 1alpha,25-dihydroxyvitamin D3, exerts anticoagulant effects in cultured monocytic cells. To clarify whether activation of VDR plays any antithrombotic actions in vivo, hemostatic/thrombogenic systems were examined in normocalcemic VDR knock-out (KO) mice on a high calcium diet and compared with wild type and hypocalcemic VDRKO mice that were fed a regular diet. Platelet aggregation was enhanced significantly in normocalcemic VDRKO mice compared with wild type and hypocalcemic VDRKO mice. Aortic endothelial nitric-oxide (NO) synthase expression and urinary NOx excretions were reduced in hypocalcemic VDRKO mice, but not in normocalcemic VDRKO mice. Northern blot and RT-PCR analyses revealed that the gene expression of antithrombin in the liver as well as that of thrombomodulin in the aorta, liver and kidney was down-regulated in hypo- and normocalcemic VDRKO mice. Whereas tissue factor mRNA expression in the liver and kidney was up-regulated in VDRKO mice regardless of plasma calcium level. Furthermore, VDRKO mice manifested an exacerbated multi-organ thrombus formation after exogenous lipopolysaccharide injection regardless of the calcemic conditions. These results demonstrate that activation of nuclear VDR elicits antithrombotic effects in vivo, and suggest that the VDR system may play a physiological role in the maintenance of antithrombotic homeostasis. (Keyword) FILTRATION PRESSURE METHOD / TISSUE-FACTOR / 1,25-DIHYDROXYVITAMIN D-3 / ANTITHROMBIN DEFICIENCY / WHOLE-BLOOD / EXPRESSION / cells / AGGREGATION / inhibition / ALOPECIA (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M404865200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15205460 ● CiNii @ National Institute of Informatics (CRID): 1362262945661168512 ● Summary page in Scopus @ Elsevier: 2-s2.0-4143096123 (DOI: 10.1074/jbc.M404865200, PubMed: 15205460, CiNii: 1362262945661168512, Elsevier: Scopus)
96.	Ken-ichi Aihara, Hiroyuki Azuma, Nobuyuki Takamori, Yasuhiko Kanagawa, Masashi Akaike, Mitsunori Fujimura, Tomonori Yoshida, Shunji Hashizume, Midori Kato, Hiroshi Yamaguchi, Shuji Kato, Yasumasa Ikeda, Tomoko Arase, Akira Kondo and Toshio Matsumoto : Heparin cofactor II is a novel protective factor against carotid atherosclerosis in elderly individuals., Circulation, Vol.109, No.22, 2761-2765, 2004. (Summary) Thrombin plays a crucial role in atherothrombotic changes. Because heparin cofactor II (HCII) inhibits thrombin actions after binding to dermatan sulfate at injured arterial walls, HCII may negatively regulate thrombin actions in vascular walls. We hypothesized that plasma HCII activity is a preventive factor against atherosclerotic changes, especially in elderly individuals who already have atherosclerotic vascular injuries. Maximum plaque thickness (MPT) in the carotid artery was measured by ultrasonography in 306 Japanese elderly individuals (154 men and 152 women; age, 40 to 91 years; 68.9+/-11.1 years, mean+/-SD). The relevance of cardiovascular risk factors including plasma HCII activity to the severity of MPT was statistically evaluated. Plasma HCII activity decreased with age. Simple linear regression analysis after adjustments for age and sex showed that lipoprotein(a), glycosylated hemoglobin A1c, and presence of diabetes mellitus significantly contributed to an increase in MPT values (r=0.119, P<0.05; r=0.196, P<0.001; and r=0.227, P<0.0001, respectively). In contrast, high-density lipoprotein (HDL) cholesterol and HCII activity were negatively correlated with MPT values (r=-0.117, P<0.05, and r=-0.202, P<0.0005, respectively). Multiple regression analysis revealed that plasma HCII activity and HDL cholesterol independently contributed to the suppression of MPT values and that the antiatherogenic contribution of HCII activity was stronger than that of HDL cholesterol (P<0.001 and P<0.05, respectively). These results suggest that HCII can be a novel and independent antiatherogenic factor. Moreover, HCII is a stronger predictive factor than HDL cholesterol against carotid atherosclerosis in elderly individuals. (Keyword) Adult / Aged / Aged, 80 and over / aging / Antithrombins / Cardiovascular Diseases / Carotid Artery Diseases / Female / Heparin Cofactor II / Humans / Male / Middle Aged / Regression Analysis / Risk Factors / Severity of Illness Index (Link to Publication Site) ● Publication site (DOI): 10.1161/01.CIR.0000129968.46095.F3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15148272 ● Search Scopus @ Elsevier (PMID): 15148272 ● Search Scopus @ Elsevier (DOI): 10.1161/01.CIR.0000129968.46095.F3 (DOI: 10.1161/01.CIR.0000129968.46095.F3, PubMed: 15148272)
97.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, 藤村光則, 吉田智則, 橋詰俊二, 加藤みどり, 山口普史, Yasumasa Ikeda, 加藤茂明 and Toshio Matsumoto : ビタミンD-ビタミンD受容体システムは生体における血液凝固調節因子である, 第25回日本血栓止血学会学術集会, Vol.14, No.5, 420, 2003. (Keyword) *Vitamin D(薬理学) 遺伝子発現血液凝固 Calcitriol Receptors Thrombomodulin マウス動物
98.	Ken-ichi Aihara, Hiroyuki Azuma, Yasumasa Ikeda, Masashi Akaike, Masahiro Abe, Takashi Sugihara and Toshio Matsumoto : Successful combination therapy--flunarizine,pentoxifylline, and cholestyramine--for spur cell anemia, International Journal of Hematology, Vol.73, No.3, 351-355, 2001. (Summary) Spur cell anemia, a hemolytic anemia observed in patients with alcoholic cirrhosis, is characterized by unusual erythrocyte morphology and an increased ratio of free cholesterol to phospholipid in the erythrocyte membrane. The prognosis of spur cell anemia is usually extremely poor, however, we describe here a patient with spur cell anemia who was successfully treated with combination therapy consisting of flunarizine, pentoxifylline, and cholestyramine. Initial therapy with flunarizine alone for 6 weeks did not significantly decrease the number of spur cells on peripheral blood smears. So pentoxifylline was added to the regimen. The patient recovered from the anemia, showed remarkable improvement with regard to the hyperbilirubinemia, and the changes were accompanied by a significant decrease in the number of spur cells in peripheral blood smears. To correct the hypercholesterolemia, cholestyramine was added to the regimen, which resulted in a reduction in the serum level of free cholesterol and an increase in the molar ratio of free cholesterol to phospholipid in erythrocyte membrane. However, 6 months later a skin eruption developed that was considered an adverse reaction to the drugs, so the flunarizine and pentoxifylline were discontinued. With cholestyramine therapy alone, the remission of spur cell anemia was maintained for more than 11 months. These observations suggest that non-invasive combination therapy with flunarizine, pentoxifylline, and cholestyramine is effective and valuable in the treatment of patients with spur cell anemia. (Keyword) Spur cell anemia / Free cholesterol / Hepatosplenomegaly / Pentoxifylline / Cholestyramine (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11345202 ● Search Scopus @ Elsevier (PMID): 11345202 (PubMed: 11345202)

Academic Letter:

1.	Hirofumi Hamano, Masayuki Chuma, Kenshi Takechi and Yasumasa Ikeda : The authors reply. Response to In Response to Diphenhydramine may be a Preventive Medicine Against Cisplatin- Induced Kidney Toxicity, Kidney International, Vol.99, No.4, 1026, 2021. (Keyword) Cisplatin / Diphenhydramine / Drug-Related Side Effects and Adverse Reactions / Humans / kidney disease / Renal Insufficiency (Tokushima University Institutional Repository) ● Metadata: 116786 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.kint.2021.01.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33745535 ● Search Scopus @ Elsevier (PMID): 33745535 ● Search Scopus @ Elsevier (DOI): 10.1016/j.kint.2021.01.009 (Tokushima University Institutional Repository: 116786, DOI: 10.1016/j.kint.2021.01.009, PubMed: 33745535)

Review, Commentary:

1.	Yasumasa Ikeda, Masafumi Funamoto and 山本みずほ : 腎性貧血の新規治療標的ヘプシジンとエリスロフェロン(今この研究が面白い!2024年9月増大号), 臨床雑誌内科, Vol.134, No.3, 788-791, Sep. 2024.
2.	Yasumasa Ikeda and Masafumi Funamoto : [A new attempt of integrated practice of basic medicine in Tokushima University]., Folia Pharmacologica Japonica, Vol.158, No.6, 440-443, Nov. 2023. (Summary) The Japan Accreditation Council for Medical Education has strengthened the promotion of horizontal and vertical integration of medical education, assuring the quality of medical education in Japan from an international perspective. Pharmacology plays an important role as a central hub that connects basic medical education with clinical medical education. As part of promoting horizontal integration of medical education, Tokushima University has started a joint practice with three basic medical subjects such as Biochemistry, Physiology, and Pharmacology for 2nd grade medical students in 2019. Each subject is in charge of two or four items of practice, and a total 8 of items are performed for 10 days in integrated practice every year. This joint practice has become an official subject in 2022. We introduce our experiences of unique practices based on their advantages and limitations. (Keyword) Humans / Universities / Education, Medical / Japan (Link to Publication Site) ● Publication site (DOI): 10.1254/fpj.23017 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37914318 ● Search Scopus @ Elsevier (PMID): 37914318 ● Search Scopus @ Elsevier (DOI): 10.1254/fpj.23017 (DOI: 10.1254/fpj.23017, PubMed: 37914318)
3.	Yasumasa Ikeda : Novel role of the biometal element iron in the development of therapeutic strategies, Shikoku Acta Medica, Vol.79, No.5,6, 229-236, Nov. 2023. (Keyword) iron / macrophage / inflammation / oxidative stress (Tokushima University Institutional Repository) ● Metadata: 119145 (Link to Publication Site) ● Publication site (DOI): 10.57444/shikokuactamedica.79.5.6_229 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390018141480002944 ● Search Scopus @ Elsevier (DOI): 10.57444/shikokuactamedica.79.5.6_229 (Tokushima University Institutional Repository: 119145, DOI: 10.57444/shikokuactamedica.79.5.6_229, CiNii: 1390018141480002944)
4.	Masafumi Funamoto and Yasumasa Ikeda : The association between COVID-19 and cardiovascular diseases, Shikoku Acta Medica, Vol.79, No.1,2, 37-42, Jun. 2023. (Keyword) COVID-19 / cardiovascular disease / cytokine storm / herbal medicines (Tokushima University Institutional Repository) ● Metadata: 118415 (Link to Publication Site) ● Publication site (DOI): 10.57444/shikokuactamedica.79.1.2_37 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390015191534393344 ● Search Scopus @ Elsevier (DOI): 10.57444/shikokuactamedica.79.1.2_37 (Tokushima University Institutional Repository: 118415, DOI: 10.57444/shikokuactamedica.79.1.2_37, CiNii: 1390015191534393344)
5.	Masafumi Funamoto, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : Roles of histone acetylation sites in cardiac hypertrophy and heart failure., Frontiers in Cardiovascular Medicine, Vol.10, Mar. 2023. (Summary) Heart failure results from various physiological and pathological stimuli that lead to cardiac hypertrophy. This pathological process is common in several cardiovascular diseases and ultimately leads to heart failure. The development of cardiac hypertrophy and heart failure involves reprogramming of gene expression, a process that is highly dependent on epigenetic regulation. Histone acetylation is dynamically regulated by cardiac stress. Histone acetyltransferases play an important role in epigenetic remodeling in cardiac hypertrophy and heart failure. The regulation of histone acetyltransferases serves as a bridge between signal transduction and downstream gene reprogramming. Investigating the changes in histone acetyltransferases and histone modification sites in cardiac hypertrophy and heart failure will provide new therapeutic strategies to treat these diseases. This review summarizes the association of histone acetylation sites and histone acetylases with cardiac hypertrophy and heart failure, with emphasis on histone acetylation sites. (Link to Publication Site) ● Publication site (DOI): 10.3389/fcvm.2023.1133611 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37008337 ● Search Scopus @ Elsevier (PMID): 37008337 ● Search Scopus @ Elsevier (DOI): 10.3389/fcvm.2023.1133611 (DOI: 10.3389/fcvm.2023.1133611, PubMed: 37008337)
6.	Yasumasa Ikeda, Masafumi Funamoto and Koichiro Tsuchiya : The role of iron in obesity and diabetes., The Journal of Medical Investigation : JMI, Vol.69, No.1.2, 1-7, Apr. 2022. (Summary) Iron is an essential trace metal for all life, but excess iron causes oxidative stress through catalyzing the toxic hydroxy-radical production via the Fenton reaction. The number of patients with obesity and diabetes has been increasing worldwide, and their onset and development are affected by diet. In both clinical and experimental studies, a high body iron content was associated with obesity and diabetes, and the reduction of body iron content to an appropriate level can ameliorate the status and development of obesity and diabetes. Macrophages play an essential role in the pathophysiology of obesity and diabetes, and in the metabolism and homeostasis of iron in the body. Recent studies demonstrated that macrophage polarization is related to adipocyte hypertrophy and insulin resistance through their capabilities of iron handling. Control of iron in macrophages is a potential therapeutic strategy for obesity and diabetes. J. Med. Invest. 69 : 1-7, February, 2022. (Keyword) Adipose Tissue / Diabetes Mellitus / Humans / Insulin Resistance / Iron / Macrophages / obesity (Tokushima University Institutional Repository) ● Metadata: 116403 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.69.1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35466128 ● Search Scopus @ Elsevier (PMID): 35466128 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.69.1 (Tokushima University Institutional Repository: 116403, DOI: 10.2152/jmi.69.1, PubMed: 35466128)
7.	Yasumasa Ikeda : Novel roles of HIF-PHIs in CKD: the link between iron metabolism, kidney function, and FGF23, Kidney International, Vol.100, No.1, 14-16, Jul. 2021. (Summary) Hanudel et al. investigated the effects of hypoxia-inducible factor-prolyl hydroxylase domain inhibitors (HIF-PHIs) on iron metabolism in a chronic kidney disease (CKD) mouse model and showed that vadadustat, an HIF-PHI, exerted beneficial effects on anemia and iron disorders independently of erythroferrone. Vadadustat also inhibited the progression of CKD and the CKD-associated increase of plasma fibroblast growth factor 23 in CKD mice. This study provides new insights into the action of HIF-PIHs in CKD. (Keyword) Anemia / Animals / Fibroblast Growth Factors / Glycine / Hypoxia-Inducible Factor-Proline Dioxygenases / Iron / Kidney / Mice / Picolinic Acids / Renal Insufficiency, Chronic (Tokushima University Institutional Repository) ● Metadata: 116787 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.kint.2021.04.030 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34154707 ● Search Scopus @ Elsevier (PMID): 34154707 ● Search Scopus @ Elsevier (DOI): 10.1016/j.kint.2021.04.030 (Tokushima University Institutional Repository: 116787, DOI: 10.1016/j.kint.2021.04.030, PubMed: 34154707)
8.	Yasumasa Ikeda : Abnormal iron metabolism in kidney disease, Nephrology, Vol.11, No.2, 146-152, Feb. 2020. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520291856216639360 (CiNii: 1520291856216639360)
9.	Yasumasa Ikeda and 深田俊幸 : 序文(特集:必須微量金属研究のパラダイムシフト), Folia Pharmacologica Japonica, Vol.2019, No.6, 309, Dec. 2019.
10.	Yuya Horinouchi, Yasumasa Ikeda and Toshiaki Tamaki : Body iron accumulation in obesity, diabetes and complications, and thepossibility of therapeutic application by iron regulation, Folia Pharmacologica Japonica, Vol.154, No.6, 316-321, Dec. 2019. (Summary) <p>Iron is an essential trace metal element for maintaining vital functions, and it is involved in hemoglobin synthesis, redox reaction, enzyme activity, cell proliferation and apoptosis in various cells. Iron deficient-related diseases represented anemia are well-known, on the other hand, iron overload disease has attracted little attention. Excessive iron produces hydroxyl radicals via Fenton/Haber-Weiss reaction, causing organ damage in hereditary iron overload diseases. Additionally, it has been clarified that iron accumulation is involved in the pathological conditions even in metabolic diseases thought to be unrelated to iron so far. Therefore, the role of iron in the living body has been raised attention again. Recent studies have reported that body iron content is associated with both obesity and diabetes, and iron might be an aggravating factor of obesity and diabetes. We have revealed that iron chelating agent reduced oxidative stress and inflammation, suppressing the development of adipose hypertrophy in KKAy mice. Dietary iron restriction also diminishes oxidative stress, leading to the inhibition of increased albuminuria excretion and glomerular lesions in <i>db/db</i> mice. In this review, we give an outline of the role of iron on obese and diabetes, and diabetic kidney disease, and present the possibility of application to treatment with iron regulation in those disorders.</p> (Keyword) 鉄 / 酸化ストレス / 肥満 / 糖尿病 (Link to Publication Site) ● Publication site (DOI): 10.1254/fpj.154.316 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001277399772544 ● Search Scopus @ Elsevier (DOI): 10.1254/fpj.154.316 (DOI: 10.1254/fpj.154.316, CiNii: 1390001277399772544)
11.	Yasumasa Ikeda : The role of iron, a trace nutrient, on diabetes, Shikoku Acta Medica, Vol.74, No.1,2, 13-20, Apr. 2018. (Summary) The nutrient balance is an important factor to keep healthy state in the body. In various nutrients, iron is a most abundant trace metal element. Iron-deficient anemia is often seen in the iron-related disorders, therefore, lots of functional food, drink, and nutritional supplement are widely provided and used to prevent iron deficiency. On the other hand, over iron intake induces excess iron status, causing increased oxidative stress production via catalyzing Fenton reaction. Recent evidences suggest that iron involves the pathological conditions of non-iron accumulating diseases, and the role of iron is noticed again.Diabetes is associated with poor prognosis to develop a variety of complications such as cardiovascular disease and diabetic kidney disease(DKD)in addition to diabetic retinopathy and neuropathy. Moreover, patients with diabetes often present reduced skeletal muscle mass, and it causes more impaired insulin resistance by diminishing glucose uptake. Recent studies have shown that iron content is associated with diabetic and obese condition, and high iron intake increases diabetes risk. We have clarified the favorable effect of iron reduction on obesity and DKD through diminishing oxidative stress. In addition, excess iron caused skeletal muscle atrophy and it was ameliorated by an anti-oxidant drug.Thus, iron plays an important role in diabetes and its complication through oxidative stress production. Further studies are clarifying an important role of trace nutrient including iron and so on, contributing to the development of new therapeutic strategy. (Keyword) Iron / Diabetes / Oxidative stress (Tokushima University Institutional Repository) ● Metadata: 111571 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050564288435540608 (Tokushima University Institutional Repository: 111571, CiNii: 1050564288435540608)
12.	Sumiko Yoshida, Yasumasa Ikeda and Ken-ichi Aihara : Roles of the Androgen - Androgen Receptor System in Vascular Angiogenesis., Journal of Atherosclerosis and Thrombosis, Vol.23, No.3, 257-265, Mar. 2016. (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.31047 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26522430 ● Summary page in Scopus @ Elsevier: 2-s2.0-84959258899 (DOI: 10.5551/jat.31047, PubMed: 26522430, Elsevier: Scopus)
13.	Masaki Imanishi, Keisuke Ishizawa, TAKUMI SAKURADA, Yuki Izawa-Ishizawa, Noriko Yamano, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Drug development for cardiorenal disease based on oxidative stress control, Journal of the Pharmaceutical Society of Japan, Vol.134, No.6, 715-719, Jun. 2014. (Summary) Oxidative stress is a key factor involved in the pathogenesis and progression of cardiovascular disease (CVD) and chronic kidney disease (CKD). Reactive oxygen species (ROS), produced as a result of redox reactions in various cells, have been recognized as key chemical mediators causing cellular damage and organ dysfunction in CVD and CKD. Nifedipine, a well-known calcium channel blocker, is extremely sensitive to light which gets converted to its nitroso analog, nitrosonifedipine (NO-NIF) in the presence of ultraviolet and visible light. The so formed NO-NIF blocks calcium channel quite weakly compared to that of nifedipine. However, we elucidated for the first time that NO-NIF is converted to NO-NIF radical which acquires extremely strong antioxidant property via reaction with unsaturated fatty acid or endothelial cells. We have already reported that NO-NIF reduces the cytotoxicity of cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, in endothelial cells. Additionally, we demonstrated that NO-NIF restored acetylcholine-responsive vascular relaxation and suppressed intercellular adhesion molecule-1 expression in the aorta of N(ω)-nitro-L-arginine methyl ester-treated rats, a model of vascular endothelial dysfunction. Recently, we reported that NO-NIF ameliorates angiotensin II-induced vascular remodeling via antioxidative effects in vivo and in vitro. These observations point towards the plausible, unique role of NO-NIF as a novel antioxidant which improves vascular dysfunction for overcoming CVD and CKD and the same has been highlighted in this review. (Keyword) oxidative stress / chronic kidney disease / cardiovascular disease / nitrosonifedipine (Link to Publication Site) ● Publication site (DOI): 10.1248/yakushi.13-00255-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24882646 ● Search Scopus @ Elsevier (PMID): 24882646 ● Search Scopus @ Elsevier (DOI): 10.1248/yakushi.13-00255-4 (DOI: 10.1248/yakushi.13-00255-4, PubMed: 24882646)
14.	Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 抗酸化薬, 腎・高血圧の最新治療, Vol.3, No.2, 93-99, Apr. 2014.
15.	Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Role of Dietary Essential Trace Metals in the Pathogenesis of Diabetes Mellitus, Journal of the The Japan Diabetes Society, Vol.56, No.12, 919-921, Dec. 2013. (Keyword) 金属元素 / 糖尿病 / 酸化ストレス (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520290882774966784 ● Summary page in Scopus @ Elsevier: 2-s2.0-84892762387 (CiNii: 1520290882774966784, Elsevier: Scopus)
16.	櫻田巧, Keisuke Ishizawa, Masaki Imanishi, 藤井聖子, 谷口順平, Yuki Izawa-Ishizawa, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipineはangiotensin IIによるマウス血管リモデリングを抑制する, 腎とフリーラジカル, Vol.11, 78-81, Jan. 2013.
17.	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)
18.	Yasumasa Ikeda, Soichiro Tajima, Koichiro Tsuchiya and Toshiaki Tamaki : Iron metabolism in the progression of adipocyte hypertrophy, The Cell, Vol.44, No.6, 282-286, Jun. 2012.
19.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Masashi Akaike and Toshio Matsumoto : Effects of androgens on cardiovascular remodeling., The Journal of Endocrinology, Apr. 2012. (Summary) Androgens, the male sex hormones, exert various biological effects on many target organs through the transcriptional effects of the nuclear androgen receptor (AR). ARs are expressed not only in classical target organs, such as the brain, genital organs, bone, and skeletal muscles, but also in the cardiovascular system. Because the female sex hormones estrogens are well known to protect against cardiovascular disease, sex has been considered to have a significant clinical impact on cardiovascular mortality. However, the influence of androgens on the cardiovascular system has not been fully elucidated. To clarify this issue, we analyzed the effects of administration of angiotensin II and doxorubicin, an anticancer agent, in a loading model in male wild-type and AR-deficient mice. In this review, we focus on the actions of androgens as potential targets for the prevention of cardiovascular diseases in males. (Link to Publication Site) ● Publication site (DOI): 10.1530/JOE-12-0126 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22493003 ● Search Scopus @ Elsevier (PMID): 22493003 ● Search Scopus @ Elsevier (DOI): 10.1530/JOE-12-0126 (DOI: 10.1530/JOE-12-0126, PubMed: 22493003)
20.	Yasumasa Ikeda, 田島壮一郎, Noriko Yamano, Koichiro Tsuchiya and Toshiaki Tamaki : The role of iron on cardiovascular disease and diabetes mellitus, Japanese Journal of Circulation Research, Vol.34, No.2, 75-85, Jul. 2011. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1572543024868677632 (CiNii: 1572543024868677632)
21.	Shuhei Tomita, Masaki Imanishi, Takumi Sakurada, Noriko Yamano, Yoshitaka Kihira, Yasumasa Ikeda and Toshiaki Tamaki : Role of Hypoxia-Inducible Factor1a (HIF-1a) in T cells in development of vascular remodeling, Shikoku Acta Medica, Vol.67, No.1, 2, 3-6, Apr. 2011. (Summary) Recent studies have shown that the cellular immune response to the hypoxic microenvironment constructed by vascular remodeling development modulates the resulting pathologic alterations. A major mechanism mediating adaptive responses to reduced oxygen availability is the regulation of transcription by hypoxia-inducible factor1(HIF‐1). Impairment of HIF‐1‐ dependent inflammatory responses in T cells causes an augmented vascular remodeling induced by arterial injury, which is shown as prominent neointimal hyperplasia and increase in infiltration of inflammatory cells at the adventitia in mice lacking Hif‐1α specifically in T cells. Studies to clarify the mechanism of augmented vascular remodeling in the mutant mice have shown enhanced production of cytokines in activated T cells and augmented antibody production in response to a T-dependent antigen in the mutant mice. This minireview shows that HIF‐1α in T cells plays a crucial role in vascular inflammation and remodeling in response to cuff injury as a negative regulator of the T cell-mediated immune response and suggests potential new therapeutic strategies that target HIF‐1α. (Keyword) vascular remodeling / hypoxia / hypoxia-inducible factor (Tokushima University Institutional Repository) ● Metadata: 110344 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050564287418524160 (Tokushima University Institutional Repository: 110344, CiNii: 1050564287418524160)
22.	Ken-ichi Aihara, Yasumasa Ikeda, Shusuke Yagi, Masashi Akaike and Toshio Matsumoto : Transforming Growth Factor-1 as a Common Target Molecule for Development of Cardiovascular Diseases, Renal Insufficiency and Metabolic Syndrome., Cardiology Research and Practice, Vol.2011, 175381, Dec. 2010. (Summary) Transforming growth factor-1 (TGF-1) is a polypeptide member of the transforming growth factor superfamily of cytokines. It is a secreted protein that performs many cellular functions including control of cell growth, cell proliferation, cell differentiation and apoptosis. In the cardiovascular system, TGF-1 plays pivotal roles in the pathogenesis of hypertension, restenosis after percutaneous coronary intervention, atherosclerosis, cardiac hypertrophy and heart failure. In addition, TGF-1 has been shown to be increased in adipose tissue of obese subjects with insulin resistance. Furthermore, TGF-1 is a potent initiator of proliferation of renal mesangial cells leading to chronic kidney disease. Some currently available agents can manipulate TGF-1 expression leading to amelioration of cardiovascular diseases. Thus, an understanding of interactions between chronic kidney disease and metabolic syndrome and the development of cardiovascular diseases is an important issue, and attention should be given to TGF-1 as a crucial factor for regulation and modulation of those pathological conditions. (Link to Publication Site) ● Publication site (DOI): 10.4061/2011/175381 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21234356 ● Search Scopus @ Elsevier (PMID): 21234356 ● Search Scopus @ Elsevier (DOI): 10.4061/2011/175381 (DOI: 10.4061/2011/175381, PubMed: 21234356)
23.	Ken-ichi Aihara, Yasumasa Ikeda and Toshio Matsumoto : 【慢性心不全の分子機構新しい治療戦略を求めて】性ステロイドと心保護作用, Cardioangiology, Vol.59, No.6, 579-584, 2006. (Keyword) Androgens / *Estrogens(薬理学) / Androgen Receptors / Estrogen Receptors / 心不全 / ノックアウトマウス / 心室リモデリング / マウス / 動物

Proceeding of International Conference:

1.	Amiho Muramatsu, Masafumi Funamoto, Miyako Ueno, Masaki Imanishi, Yasumasa Ikeda and Koichiro Tsuchiya : Kampo medicine, orengedokuto, suppresses Doxorubicin-induced cardiotoxicity, 28th International Society of Cardiovascular Pharmacotherapy Annual Scientific Meeting, Nov. 2023.
2.	Masafumi Funamoto, Yoichi Sunagawa, Yasufumi Katanasaka, Toru Kato, Yoichi Ajiro, Maki Komiyama, Masaharu Akao, Hajime Yamakage, Noriko Satoh-Asahara, Hiromichi Wada, Yasumasa Ikeda, Tatsuya Morimoto and Koji Hasegawa : Effects of high-absorption curcumin for the prevention of hypertensive heart disease, 28th International Society of Cardiovascular Pharmacotherapy Annual Scientific Meeting, Nov. 2023.
3.	Masafumi Funamoto, Yoichi Sunagawa, Yasufumi Katanasaka, Maki Komiyama, Masaharu Akao, Akihiro Yasoda, Hajime Yamakage, Noriko Satoh-Asahara, Hiromichi Wada, Yasumasa Ikeda, Tatsuya Morimoto and Koji Hasegawa : Clinical trial for high-absorption curcumin, targeting p300-histonetransferase activity, in patients with hypertensive heart disease, 27TH ASIAN PACIFIC SOCIETY OF CARDIOLOGY CONGRESS, Jul. 2023.
4.	Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Mitsuhiro Goda, Naoto Okada, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : Development of therapeutic agents using drug discovery tools and large-scale medical information, FIP2019, Abu Dhabi, Sep. 2019.
5.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Utilizing Real-World Big Data in the Search for New Renoprotective Drugs, Joint Hypertension 2018 Scientific Sessions, Sep. 2018.
6.	Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Masayuki Chuma, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : Drug repositioning for post cardiopulmonary resuscitation syndrome using large-scale medical claims, FIP2018, グラスゴー, Sep. 2018.
7.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Renoprotective effects of edoxaban, a factor Xa inhibitor, 18th World Congress of Basic and Clinical Pharmacology, Jul. 2018.
8.	Yuki Izawa-Ishizawa, Masaki Imanishi, kotoko suzuki, Yuya Horinouchi, Kenshi Takechi, Yoshito Zamami, Koichiro Tsuchiya, Toshiaki Tamaki, Keisuke Ishizawa and Yasumasa Ikeda : The effect of quercetin on aortic aneurysms in mice, WCP2018, Jul. 2018.
9.	濱野裕章, Yasumasa Ikeda, Yuya Horinouchi, Yoshito Zamami, Masaki Imanishi, Yuki Izawa-Ishizawa, Licht Miyamoto, Koichiro Tsuchiya, Keisuke Ishizawa and Toshiaki Tamaki : Proton Pump Inhibitor Involves Abnormality of Iron Metabolism through Hepcidin Regulation, 18th World Congress of Basic and Clinical Pharmacology, Jul. 2018.
10.	Yoshito Zamami, Yuki Izawa-Ishizawa, Kenshi Takechi, Masaki Imanishi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Toshiaki Tamaki and Keisuke Ishizawa : Search for drugs that attenuate the anti tumor effect of bevacizumab using adverse event database, 18th World Congress of Basic and Clinical Pharmacology, Jul. 2018.
11.	Yuya Horinouchi, Yasumasa Ikeda, Hirofumi Hamano, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Kenshi Takechi, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The effect of iron on skeletal muscle atrophy in chronic kidney disease., Free Radical Biology and Medicine, Vol.112, No.1, 204-205, Dec. 2017. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.freeradbiomed.2017.10.323 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.freeradbiomed.2017.10.323 (DOI: 10.1016/j.freeradbiomed.2017.10.323)
12.	hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Indoxyl Sulfate Disturbs Normal Iron Metabolism via Hepcidin Upregulation in Chronic Kidney Disease, ASN Kidney Week 2017 Annual Meeting, Nov. 2017.
13.	Yuya Horinouchi, Yasumasa Ikeda, Masaki Imanishi, Yoshito Zamami, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Direct activated factor X inhibitor attenuates renal fibrosis on unilateral ureteral obstruction-induced nephrotoxicity., 53rd Congress of the European Societies of Toxicology (eurotox2017), Sep. 2017.
14.	Yuya Horinouchi, Yasumasa Ikeda, Masaki Imanishi, Yoshito Zamami, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : FACTOR XA INHIBITOR ATTENUATES RENAL INTERSTITIAL FIBROSIS IN MICE WITH UNILATERAL URETERAL OBSTRUCTION, THE 13TH CONGRESS OF THE EUROPEAN ASSOCIATION FOR CLINICAL PHARMACOLOGY AND THERAPEUTICS(EACPT2017), Jun. 2017.
15.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 田淵正樹, Masaki Imanishi, Mai Takata, Eriko Sairyo, Yoshito Zamami, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : NITROSONIFEDIPINE, A NOVEL ANTIOXIDANT, AMELIORATES NEUROLOGICALSYMPTOMS AND PROLONGS THE SURVIVAL IN A MALIGNANT STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RATS, 27th European Meeting on Hypertension and Cardiovascular Protection, Jun. 2017.
16.	Masaki Imanishi, Kyohei Tanaka, Raiki Ikutoh, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : THE EFFECTS OF FEBUXOSTAT ON ANGIOTENSIN II-INDUCED VASCULAR REMODELING, 27th European Meeting on Hypertension and Cardiovascular Protection, Jun. 2017.
17.	Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa and Toshiaki Tamaki : IRON RESTRICTION PREVENTS RENAL TUBULOINTERSTITIAL INJURY INDUCED BY ALBUMIN OVERLOAD IN MICE, 54th ERA-EDTA Congress, Madrid, Jun. 2017.
18.	Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa and Toshiaki Tamaki : DIRECT FACTOR XA INHIBITOR PREVENTS RENAL INTERSTITIAL FIBROSIS IN MICE WITH UNILATERAL URETERAL OBSTRUCTION, 54th ERA-EDTA Congress, Madrid, Jun. 2017.
19.	Licht Miyamoto, Fukuta Keisuke, Takahashi Rie, Umemoto Kana, Okuno Hiroko, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : Fragrance of aromatic oil from peels of Citrus sudachi causes adipose browning and ameliorates glucose and lipid metabolism, EMBO workshop, Sitges, Spain, May 2017.
20.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Indoxyl Sulfate Involves Abnormality of Iron Metabolism through Hepcidin Regulation, Experimental Bioogy 2017, Chicago, Apr. 2017.
21.	Koichiro Tsuchiya, Aihara Haruna, Xu Wenting, Jin Meina, Tomida Yosuke, Yamaoka Tomomi, Naonobu Tanaka, Yasumasa Ikeda, Akira Shigenaga, Akira Otaka, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : A limonene-derivative from Sudachi peel activates sirt1 and improves lipid and glucose metabolism in high fat diet-fed mice., 欧州糖尿病学会, Dec. 2016.
22.	Ota Kazuma, Yoshitaka Kihira, Kishibuchi Reina, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda and Toshiaki Tamaki : Disruption of hypoxia-inducible factor-1a deteriorates renal ischemia-reperfusion injury through dysregulation of Kv2.2-induced apoptosis in tubules., ASN KIDNEY WEEK 2016, Chicago, Nov. 2016.
23.	Maki Urushihara, T Nagai, Shuji Kondo, Toshiaki Tamaki, Yasumasa Ikeda and Shoji Kagami : (Pro)renin receptor-mediated ERK1/2 and Wnt signaling pathway in crescent glomerulonephritis., Kidney Week 2016, Nov. 2016.
24.	Yoshito Zamami, Mitsui Marin, Moriguchi Hiroshi, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Kawasaki Hiromu, Toshiaki Tamaki and Keisuke Ishizawa : Search for a preventative therapy for Bevacizumab-induced hypertension using the drug repositioning approach, 7th Scientific Meeting of Asian Society for Vascular Biology, Oct. 2016.
25.	Yutaka Fukunaga, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Ichiro Hashimoto : Topical Application of Nitrosonifedipine, a Novel Free Radical Scavenger, Ameliorate the Ischemic Skin Flap Necrosis, Plastic Surgery THE MEETING 2016, Los Angeles, Sep. 2016.
26.	Ken-ichi Aihara, Masashi Akaike, Sumiko Yoshida, Yasumasa Ikeda, Shusuke Yagi and Masahiro Abe : Pleiotropic Effects of Pitavastatin against Vascular Stress in eNOS-deficient Mice, The 10th Congress of the Asian-Pacific Society of Atherosclerosis and Vascular Diseases, Tokyo, Jul. 2016.
27.	Yuki Izawa-Ishizawa, Masaki Imanishi, Yuya Horinouchi, Kenshi Takechi, Yoshito Zamami, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : The effects of pitavastatin, a lipid-lowering agent, against aortic dissection model mice induced by L-NAME, a nitric oxide synthase inhibitor., The 9th International Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide/16th Annual Scientific Meeting of the Nitric Oxide Society of Japan., May 2016.
28.	Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa and Toshiaki Tamaki : The new insight of iron on tissue damage in metabolic disorders., The 9th International Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide/16th Annual Scientific Meeting of the Nitric Oxide Society of Japan., May 2016.
29.	Koichiro Tsuchiya, Licht Miyamoto, Tomida Yosuke, Yamane Megumi, Tsuda Katsunori, Yasumasa Ikeda and Toshiaki Tamaki : Dietary nitrite ameliorates glucose tolerance and hyperlipidemia in diet-induced obesity rats., The 16th Annual Scientific Meeting of the Nitric Oxide Society of Japan / The 9th Internatinal Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide. (Seindai, Japan) 2016.5, May 2016.
30.	Yasumasa Ikeda, Keisuke Oshima, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The Involvement of Iron Supplementation on Erythropoietin Expression, Experimental Biology 2016, Apr. 2016.
31.	Licht Miyamoto, 粟飯原遥奈, 許文てい, ジン美娜, 冨田洋介, 山岡朋美, Naonobu Tanaka, Yasumasa Ikeda, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : スダチ果皮からの抗メタボリックシンドローム活性を有する物質の同定, Journal of the The Japan Diabetes Society, No.59, Kyoto, 2016.
32.	FUKUTA Keisuke, Licht Miyamoto, TAKAHASHI Rie, Toshiaki Tamaki, Yasumasa Ikeda and Koichiro Tsuchiya : 11th IDF-WPR Congress 2016 & 8th AASD Scientific MeetingPosterEessentialoil fromsudachipealimprovesglucoseandlipidmetabolism, 2016.
33.	Licht Miyamoto, Yuki Tsuchihashi, Yosuke Tomida, Megumi Yamane, Kazuya Takenokuma, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : Dietary nitrite ameliorates glucose tolerance and hyperlipidemia in diet-induced obese rats, The 6th International Conference on Food Factors, Seoul, Nov. 2015.
34.	Yasumasa Ikeda, Hamano Hirofumi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Bilirubin Enhances Ischimia-induced Angiogenesis Through Akt-eNOS-Dependent Signaling Pathway, American Heart Association Scientific Sessions 2015, Orlando, Nov. 2015.
35.	Licht Miyamoto, 粟飯原遥奈, Wenting Xu, Meina Jin, 冨田洋介, 山岡朋美, Naonobu Tanaka, Yasumasa Ikeda, Akira Shigenaga, Akira Otaka, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : リモネン誘導体によるsirt1活性化を介した脂質低下作用, 日本肥満学会，アジアオセアニア糖尿病学会, Nagoya, Oct. 2015.
36.	Licht Miyamoto, Haruna Aihara, Wenting Xu, Meina Jin, Yosuke Tomida, Tomomi Yamaoka, Naonobu Tanaka, Yasumasa Ikeda, Akira Shigenaga, Akira Otaka, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : Limonene-derivative Ameliorates Lipid Profiles by Upregulation of Sirt1 Activity and Expression in Cultured Cells and High Fat Diet-Fed Mice, American diabetes association, Boston, Jun. 2015.
37.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Toya Hiroki, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Novel aortic dissection model by pharmacologically-induced endothelial dysfunction, 17th International Congress on Atherosclerosis 2015, Amsterdam, May 2015.
38.	Yasumasa Ikeda, Yusuke Kanai, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The Effects of Bilirubin on Angiogenesis in Mice with Hindlimb Ischemia, Experimental Biology 2015, Boston, Mar. 2015.
39.	Keisuke Ishizawa, Kohara Yusuke, Sakurada Takumi, Toya Hiroki, Iki Yutaka, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine ameliorates the progression of aortic aneurysms by exerting antioxidative effects, ESC Congress 2014, Barcelona, Sep. 2014.
40.	Yasumasa Ikeda, Soichiro Tajima, Mizuki Imao, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Ferritin induces IL-1 production through inflammasome activation via NF-B-dependent manner in macrophages, Experimental Biology 2014, San Diego, Apr. 2014.
41.	Keisuke Ishizawa, Noriko Yamano, Hiroyuki Kobori, Maki Urushihara, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine prevents the progression of diabetic nephropathy via attenuating the expression of intrarenal angiotensinogen and oxidative stress, High Blood Pressure Research 2013 Scientific Sessions, Sep. 2013.
42.	Sumiko Yoshida, Ken-ichi Aihara, Yasumasa Ikeda and Toshio Matsumoto : Androgen receptor promotes angiogenesis in response to ischemia via activation of VEGF receptor signaling pathway regardless of sex, ENDO 2013;The Endocrine Society's 95th Annual Meeting & Expo, San Francisco, Jun. 2013.
43.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Sakiko Doi, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Rho-kinase is involved in inorganic phosphate-induced ERK1/2 activation in vascular smooth muscle cells, World Biotechnology Congress 2013, Jun. 2013.
44.	Yasumasa Ikeda, Hideaki Enomoto, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : The effect of dietary iron restriction against diabetic nephropathy in db/db mice, Experimental Biology 2013, Apr. 2013.
45.	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.
46.	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.
47.	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.
48.	Yasumasa Ikeda, Hideaki Enomoto, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Iron Restriction Prevents the Progression of Diabetic Nephropathy in db/db Mice, American Heart Association Scientific Sessions 2012, Nov. 2012.
49.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia-inducible Factor-1a in Vascular Smooth Muscle Cells Regulates Angiotensin -induced Vascular Remodeling and AT1 Receptor Expression in Mouse Aortic Media, American Heart Association Scientific Sessions 2012, Nov. 2012.
50.	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.
51.	Hideaki Enomoto, Yasumasa Ikeda, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Protective Effects of Iron-Restricted Food against Diabetic Nephropathy in db/db Mice, American Heart Association High Blood Pressure Research 2012, Sep. 2012.
52.	Shoko Fujii, Keisuke Ishizawa, Takumi Sakurada, Noriko Yamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine, a Photodegradation Product of Nifedipine, Prevents the Progression of Diabetic Nephropathy in Type II Diabetic Mice, American Heart Association High Blood Pressure Research 2012, Sep. 2012.
53.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible factor-1a deficiency in smooth muscle cell attenuates angiotensin -induced vascular remodeling in mice, ISOTT (International Society on Oxygen Transport to Tissue) 2012, Aug. 2012.
54.	Takumi Sakurada, Keisuke Ishizawa, Shoko Fujii, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Effects of nitrosonifedipine, a photodegradation product of nifedipine, on diabetic nephropathy in type II diabetic mice, Experimental Biology 2012, Apr. 2012.
55.	Ken-ichi Aihara, Sumiko Yoshida, Yasumasa Ikeda, Masashi Akaike and Toshio Matsumoto : Heparin cofactor II, a serine protease inhibitor, is a novel regulating factor for glucose metabolism and albuminuria, Keystone Symposia: Complications of Diabetes: Mechanisms of Injury and Failure of Repair, Mar. 2012.
56.	Yasumasa Ikeda, Hideaki Enomoto, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Iron restriction prevents progression of diabetic nephropathy, KEYSTONE SYMPOSIA 40th ANNIVERSARY 1972-2012 Complications of Diabetes: Mechanisms of Injury and Failure of Repair, Mar. 2012.
57.	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.
58.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia-inducible Factor-1 in Vascular Smooth Muscle Cells Regulates Angiotensin -induced Vascular Remodeling and AT1 Receptor Expression in Mouse Aortic Media, AHA SCIENTIFIC SESSIONS 2012, 2012.
59.	Fujii Shoko, Keisuke Ishizawa, Takumi Sakurada, Noriko Yamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine, a Photodegradation Product of Nifedipine, Prevents the Progression of Diabetic Nephropathy in Type II Diabetic Mice, HIGH BLOOD PRESSURE RESEARCH 2012 SCIENTIFIC SESSIONS, 2012.
60.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible factor-1 deficiency in smooth muscle cell attenuates angiotensin II-induced vascular remodeling in mice, The International Society on Oxygen Transport to Tissue 2012, 2012.
61.	Takumi Sakurada, Keisuke Ishizawa, Shoko Fujii, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Effects of nitrosonifedipine, a photodegradation product of nifedipine, on diabetic nephropathy in type II diabetic mice, Experimental Biology 2012, 2012.
62.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Smooth Muscle Cell-Specific Hypoxia-Inducible Factor-1a Deficiency Attenuates Angiotensin II-Induced Vascular Remodeling in Mice, AHA scientific sessions 2011, Orlando, Nov. 2011.
63.	Soichiro Tajima, Yasumasa Ikeda, Noriko Yamano, Koichiro Tsuchiya, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : Inhibition of Adipocyte Hypertrophy by Deferoxiamine Diabetic KKAy mice, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
64.	Kazuyuki Yamaguchi, Yoshitaka Kihira, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : Glucose Metabolism of Adipocytes is Regulated by Basic Fibroblast Growth Factor via Hypoxia-inducible Factor-1a, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
65.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible Factor-1a Deficiency in Smooth Muscle Cells Suppresses Angiotensin -induced Vascular Remodeling in Mice, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
66.	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.
67.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin -induced Vascular Remodeling is Improved by Nitrosonifedipine, a Possible New Class Drug Against Oxidative Stress, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
68.	Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitorosonifedipine is a new class drug to improves angiotensin II-induced vascular remodeling, European Society of Cardiology Congress 2011, Aug. 2011.
69.	Shuhei Tomita, Yoshitaka Kihira, Noriko Yamano, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Characterization on mice lacking HIF1a gene in renal ischemia-reperfusion injury, ISOTT (International Society on Oxygen Transport to Tissue) 2011, Washington, D.C., Jul. 2011.
70.	Yasumasa Ikeda, Soichiro Tajima, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Estrogen action on iron metabolism, ENDO 2011: The 93rd Annual Meeting & Expo, Boston, Jun. 2011.
71.	Masaki Imanishi, Soichiro Tajima, Yoshitaka Kihira, Keisuke Ishizawa, Shuji Kondo, Shoji Kagami, Shuhei Tomita, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Increment intracellular labile iron enhances Angiotensin-induced intracellular adhesion molecule-1 (ICAM-1) expression in human glomerular endothelial cells, World congress of Nephrology 2011, Vancouver, Apr. 2011.
72.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Smooth Muscle Cell-specific Hypoxia-inducible Factor-1a Deficiency Attenuates Angiotensin II-induced Vascular Remodeling In Mice, AHA SCIENTIFIC SESSIONS 2011, 2011.
73.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Sakurada Takumi, Masaki Imanishi, Fujii Shoko, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II-induced Vascular Remodeling Is Improved By Nitrosonifedipine, A Possible New Class Drug, HIGH BLOOD PRESSURE RESEARCH 2011 SCIENTIFIC SESSIONS, 2011.
74.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible Factor-1 Deficiency In Smooth Muscle Cells Suppresses Angiotensin II-induced Vascular Remodeling In Mice, HIGH BLOOD PRESSURE RESEARCH 2011 SCIENTIFIC SESSIONS, 2011.
75.	Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitorosonifedipine is a new class drug to improve angiotensin II-induced vascular remodeling, ESC Congress 2011, 2011.
76.	Masaki Imanishi, Soichiro Tajima, Yoshitaka Kihira, Keisuke Ishizawa, Shuji Kondo, Shoji Kagami, Shuhei Tomita, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : INCREMENT INTRACELLULAR LABILE IRON ENHANCES ANGIOTENSIN II-INDUCED INTRACELLULAR ADHESION MOLECULE-1 (ICAM-1) EXPRESSION IN HUMAN GLOMERULAR ENDOTHELIAL CELLS, World Congress of Nephrology 2011, 2011.
77.	Toshiaki Tamaki, Kunihisa Yamaguchi, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Shuji Kondo, Shoji Kagami and Shuhei Tomita : Global gene expression analyses in renal ischemia-reperfusion injury (IRI) from mice lucking Hif-1a gene, ASN RENAL WEEK 2010 EXHIBIT, Nov. 2010.
78.	Koichiro Tsuchiya, Yuya Horinouchi, Soichiro Tajima, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Yoshiyuki Yoshimura, Shuhei Tomita, Shuichi Hamano and Toshiaki Tamaki : Antioxidant effects of photodegradation product of nifedipine, 17th Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2010), Nov. 2010.
79.	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.
80.	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.
81.	Shuhei Tomita, Masahisa Urata, Yayoi Fukuhara, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Tetsuya Kitagawa and Toshiaki Tamaki : Endothelial-targeted hypoxia-inducible factor-1b (HIF-1b) loss-of function alleviates the monocrotaline-induced pulmonary hypertension in mice, American Heart Association Scientific Sessions 2010, Chicago, Nov. 2010.
82.	Keisuke Ishizawa, Masaki Imanishi, Yuya Horinouchi, Yayoi Fukuhara, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Yoshitaka Kihira, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitroso-nifedipine is a new class drug to protect endothelial function for overcoming organ damage, International Society of Hypertension 2010, Vancouver, Sep. 2010.
83.	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.
84.	Soichiro Tajima, Yasumasa Ikeda, Noriko Yamano, Koichiro Tsuchiya, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : IRON DERIVATION AMELIORATES GLUCOSE TOLERANCE THROUGH REDUCTION OF OXIDATIVE STRESS AND INFLAMMATION IN DIABETIC KKAY MICE, 2010 American Physiological Society Conference Inflammation, Immunity and Cardiovascular Disease, Aug. 2010.
85.	Yoshitaka Kihira, Shuhei Tomita, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Basic fibroblast growth factor upregulates hypoxia inducible factor 1 and glucose transporter 1 in adipose cells, The 16th World Congress of Basic and Clinical Pharmacology (WorldPharma 2010), Copenhagen, Jul. 2010.
86.	Soichiro Tajima, Yasumasa Ikeda, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi, Toshiaki Tamaki and Koichiro Tsuchiya : Deferoxamine, an iron chelator, promotes angiogenesis after ischemic hind limb through Akt-eNOS-dependent pathway, The 6th International Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide, Jun. 2010.
87.	Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Toshiaki Tamaki and Koichiro Tsuchiya : Metabolism of quercetin in vivo and its protective effect against cardiovascular diseases, 2nd International On-Board Symposium: Human Health, Energy and Environment, May 2010.
88.	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.
89.	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.
90.	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.
91.	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.
92.	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.
93.	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.
94.	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.
95.	Yasumasa Ikeda, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Deferoxamine, an iron chelator, promotes angiogenesis after ischemic hind limb through Akt-eNOS-dependent pathway, XX World Congress ISHR 2010 KYOTO, May 2010.
96.	Toshiaki Tamaki, Kunihisa Yamaguchi, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Shuhei Tomita : Amelioration of acute tubular necrosis in ischemic acute renal failure was impaired in mice lucking hypoxia inducible factor-1 gene, ISN (International Society of Nephrology) nexus sympojium 2010, Apr. 2010.
97.	Souichiro Tajima, Yasumasa Ikeda, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi, Toshiaki Tamaki and Koichiro Tsuchiya : Deferoxamine, an iron chelator, promotes angiogenesis after ischemic hind limb through Akt-eNOS-dependent pathway, The 6th International Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide, Kyoto, Apr. 2010.
98.	Koichiro Tsuchiya, Soichiro Tajima, Keisuke Ishizawa, Shuhei Tomita, Yoshitaka Kihira, Yasumasa Ikeda, Yoshiyuki Yoshimura, Shuichi Hamano and Toshiaki Tamaki : Effect of Angiotensin II on the intracellular labile iron concentration in HGECs, 16th Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2009), Nov. 2009.
99.	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.
100.	Yasumasa Ikeda, Kaori Sato, David Pimentel, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Flora Sam, Toshiaki Tamaki and Kenneth Walsh : LKB1 gene in myocytes plays a critical role to regulate the coordinated cardiac growth and capillary development, American Heart Association Scientific Sessions 2009, Orlando, Nov. 2009.
101.	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.
102.	Masashi Akaike, Ken-ichi Aihara, Shusuke Yagi, Yasumasa Ikeda, Ishikawa Kazue, Takayuki Ise, Sumiko Yoshida, Sumitomo Yuka, Takashi Iwase and Toshio Matsumoto : Pitavastatin, an HMG-CoA Reductase Inhibitor, Prevents Glucocorticoid-induced Hypertension through Increased Nitric Oxide Production as a Pleiotropic Effect on Vascular Endothelial Cells, Hypertension 2008 18th Scientific Meeting of the European Society of Hypertension 22nd Scientific Meeting of the International Society of Hypertension, Berlin, Jun. 2008.
103.	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.
104.	Ken-ichi Aihara, Masashi Akaike, Yasumasa Ikeda, Fujimura Mitsunori, Hashizume Shunji, Takashi Iwase, Shusuke Yagi, Kondo Akira, Hiroyuki Azuma and Toshio Matsumoto : Valsartan Enhances Nitric Oxide Bioavailability and Reduces Arterial Stiffness in Patients with Essential Hypertension, The 21st Scientific Meeting of the International Society of Hypertension, 2006, Fukuoka, Japan, Oct. 2006.
105.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Hirotsugu Kurobe, Fujimura Mitsunori, Shusuke Yagi, Hashizume Shunji, Yasumasa Ikeda, Takashi Iwase, Takamori Nobuyuki, Tetsuya Kitagawa and Toshio Matsumoto : Plasma Heparin Cofactor II Activity is a Predictor for Incidence of Peripheral Arterial Disease in Patients with Cardiovascular Risk Factors, XIV International Symposium on Atherosclerosis, 2006 Rome, Italy, Jun. 2006.
106.	Ken-ichi Aihara, Mihara Masatomo, Hiroyuki Azuma, Masashi Akaike, Takaya Matsushita, Yasumasa Ikeda, Shusuke Yagi, Takashi Iwase, Hashizume Shunji, Fujimura Mitsunori and Toshio Matsumoto : Argatroban, a synthetic thrombin antagonist, can reduce insulin resistance though thrombin inactivation in the db/db mouse model of type 2 diabetes mellitus, XIV International Symposium on Atherosclerosis, 2006 Rome, Italy, Jun. 2006.
107.	Ken-ichi Aihara, Takamori Nobuyuki, Yasuhiko Kanagawa, Masashi Akaike, Fujimura Mitsunori, Yoshida Tomonori, Hashizume Shunji, Kato Midori, Yasumasa Ikeda, Hiroyuki Azuma and Toshio Matsumoto : Heparin cofactor II is inversely related to the severity of carotid atherosclerosis, American Heart Association, Scientific Sessions 2003 Orland Florida USA, Nov. 2003.

Proceeding of Domestic Conference:

1.	Masafumi Funamoto, Amiho Muramatsu, YAMAMOTO Mizuho, Shunji Hirose, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : 黄連解毒湯によるドキソルビシン誘導性心毒性に対する効果検討, 第8回黒潮カンファレンス, Sep. 2024.
2.	YAMAMOTO Mizuho, Masafumi Funamoto, 上原渉, 眞鍋智弘, 砂川陽一, 刀坂泰史, 浜辺俊秀, 川瀬裕斗, 鳴田竜也, 小見山麻紀, 長谷川浩二, Yasumasa Ikeda and 森本達也 : p300/CBPのヒストンアセチル化酵素活性を阻害する低分子化合物であるA485は圧負荷による収縮機能低下を改善した, 第8回黒潮カンファレンス, Sep. 2024.
3.	Shunji Hirose, Masafumi Funamoto, YAMAMOTO Mizuho, Masaki Imanishi, Yasumasa Ikeda and Koichiro Tsuchiya : 糖尿病性心筋症に対する漢方薬五苓散の抑制効果, 第8回黒潮カンファレンス, Sep. 2024.
4.	Yasumasa Ikeda : 薬剤性腎障害の病態の解明と予防薬同定―シスプラチン腎障害について(教育講演1 AKIの病態機序解明に迫る! ), 第67回日本腎臓学会学術総会, Jun. 2024.
5.	中西俊輔, 高井秀通, 砂川陽一, Masafumi Funamoto, 川瀬裕斗, 鳴田竜也, 刀坂泰史, 浜辺俊秀, 今泉厚, Yasumasa Ikeda, 橋本正, 長谷川浩二 and 森本達也 : 新規クルクミン製剤であるcurcuRougeTMは心筋梗塞モデルラットにおいて心収縮能の低下を抑制した, 第9回日本心血管協会(JCVA)学術集会, 60, May 2024.
6.	眞鍋智弘, 上原渉, Masafumi Funamoto, 山本みずほ, 砂川陽一, 刀坂泰史, 浜辺俊秀, 川瀬裕斗, 鳴田竜也, Yasumasa Ikeda, 長谷川浩二 and 森本達也 : 圧負荷心不全モデルマウスにおいてBRG1阻害剤PFI-3は心収縮機能悪化を改善した, 第9回日本心血管協会(JCVA)学術集会, 61, May 2024.
7.	Mizuho Yamamoto, Masafumi Funamoto, 上原渉, 眞鍋智弘, 砂川陽一, 刀坂泰史, 浜辺俊秀, 川瀬裕斗, 鳴田竜也, 小見山麻紀, 長谷川浩二, Yasumasa Ikeda and 森本達也 : 低分子化合物A485はp300-HAT阻害作用により圧負荷心不全モデルマウスの心不全悪化を抑制した, 第9回日本心血管協会(JCVA)学術集会, 71, May 2024.
8.	Masafumi Funamoto, Amiho Muramatsu, Masaki Imanishi, Hidenori Yasuda, Koichiro Tsuchiya and Yasumasa Ikeda : アントラサイクリン系抗がん剤による心毒性に対する黄連解毒湯の検討, 第9回日本心血管協会(JCVA)学術集会, 72, May 2024.
9.	Shunji Hirose, Masafumi Funamoto, Hidenori Yasuda, Masaki Imanishi, Yasumasa Ikeda and Koichiro Tsuchiya : 糖尿病合併心不全に対する漢方薬五苓散の抑制効果, 第144回日本薬理学会近畿部会, Mar. 2024.
10.	Yasumasa Ikeda, Masafumi Funamoto, Hidenori Yasuda, Masaki Imanishi and Koichiro Tsuchiya : 低重力下における消化管と骨髄における鉄動態の検討, 第144回日本薬理学会近畿部会, Mar. 2024.
11.	Masafumi Funamoto, Amiho Muramatsu, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : ドキソルビシン誘導性心毒性を抑制する漢方薬と作用機序の解明, 第53回日本心脈管作動物質学会, Feb. 2024.
12.	Masaki Imanishi, Takahisa Inoue, Keijo Fukushima, GOMI Yoshiki, HIGAKI Yoshiya, Masataka Nojima, Kohsuke Kondoh, SAWAMURA Takaya, Ryosuke Yamashita, Ryo Nakayama, Honoka Tsunematsu, GOTOH Kohei, Licht Miyamoto, Masafumi Funamoto, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya : TCGAがんゲノムビッグデータによる膵がん悪性化因子の網羅的探索と腫瘍血管新生の寄与についての検討, 第53回日本心脈管作動物質学会年会, Feb. 2024.
13.	眞鍋智弘, 上原渉, Masafumi Funamoto, 山本みずほ, 砂川陽一, 刀坂泰史, 浜辺俊秀, 川瀬裕斗, 鳴田竜也, Yasumasa Ikeda, 長谷川浩二 and 森本達也 : 圧負荷心不全モデルマウスにおいて心収縮機能悪化をBRG1阻害剤 PFI-3は抑制した, 第33回循環薬理学会, Jan. 2024.
14.	Masafumi Funamoto, Amiho Muramatsu, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : ドキソルビシン心毒性を抑制する漢方薬と作用機序の解明, 第33回日本循環薬理学会, Jan. 2024.
15.	Licht Miyamoto, Yuki Tsuchihashi, Shinji Abe, Toshihiro Izumi, Aya Hatano, Masaki Imanishi, Yasumasa Ikeda and Koichiro Tsuchiya : 新規水溶性カンプトテシン誘導体，SN38-BGLによる，ヒト肺がん細胞移植モデルマウスにおける抗腫瘍効果と副作用の解析, 第97回日本薬理学会年会(神戸), Dec. 2023.
16.	Yasumasa Ikeda, SUENAGA Aoi, SETO Yasuyuki, Masafumi Funamoto, Masaki Imanishi and Koichiro Tsuchiya : 慢性腎臓病に対する漢方薬五苓散の効果の検討, 第97回日本薬理学会年会(神戸), Dec. 2023.
17.	Masafumi Funamoto, Amiho Muramatsu, Miyako Ueno, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : 漢方薬のドキソルビシン心毒性に対する効果の検討, 第97回日本薬理学会年会(神戸)2023年12月16日, Dec. 2023.
18.	Shunji Hirose, Masafumi Funamoto, Amiho Muramatsu, Miyako Ueno, Masaki Imanishi, Yasumasa Ikeda and Koichiro Tsuchiya : 糖尿病性心筋症におけるエピジェネティック制御機構, 第97回日本薬理学会年会(神戸), Dec. 2023.
19.	Honoka Tsunematsu, Masaki Imanishi, Yuka Uemura, HIGAKI Yoshiya, Keijo Fukushima, Miyu Morisaki, Akari Katsura, Licht Miyamoto, Masafumi Funamoto, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichi Tsuneyama and Koichiro Tsuchiya : 藍含有成分はendothelin-1発現を制御して肺動脈血管リモデリングを形成させる, 次世代を担う若手のための創薬・医療薬理シンポジウム2023, Aug. 2023.
20.	SAWAMURA Takaya, Masaki Imanishi, Keijo Fukushima, Ryosuke Yamashita, Kohsuke Kondoh, Ryo Nakayama, GOMI Yoshiki, Honoka Tsunematsu, Takahisa Inoue, GOTOH Kohei, Licht Miyamoto, Masafumi Funamoto, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya : PARP阻害剤は低酸素環境下において生じる5-FU治療効果の減弱を回復させる, 生体機能と創薬シンポジウム2023, Aug. 2023.
21.	Natsuki Toyota, Masaki Imanishi, Takahisa Inoue, Honoka Tsunematsu, GOTOH Kohei, Licht Miyamoto, Masafumi Funamoto, Yasumasa Ikeda and Koichiro Tsuchiya : 亜硝酸塩が有するヒドロキシルラジカル消去活性の検討, 生体機能と創薬シンポジウム2023, Aug. 2023.
22.	GOMI Yoshiki, Masaki Imanishi, Takahisa Inoue, Keijo Fukushima, Ryosuke Yamashita, Ryo Nakayama, Masataka Nojima, Kohsuke Kondoh, SAWAMURA Takaya, Honoka Tsunematsu, GOTOH Kohei, Licht Miyamoto, Masafumi Funamoto, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya : TCGAがんゲノムビッグデータとGEOトランスクリプトームデータとの統合解析による膵がん治療標的候補遺伝子の探索, 生体機能と創薬シンポジウム2023, Aug. 2023.
23.	Yasumasa Ikeda : 生命金属元素鉄の新たな役割と治療応用(教授就任記念講演), 第267回徳島医学会学術集会, Aug. 2023.
24.	Amiho Muramatsu, Masafumi Funamoto, Miyako Ueno, Masaki Imanishi, Yasumasa Ikeda and Koichiro Tsuchiya : ドキソルビシン心毒性に対する漢方薬効果の検討, 第7回黒潮カンファレンス(宮崎), Jul. 2023.
25.	Masafumi Funamoto, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : 病的心肥大と老化におけるマクロファージ鉄ストレスの役割の検討, ,第7回黒潮カンファレンス(宮崎), Jul. 2023.
26.	Amiho Muramatsu, Masafumi Funamoto, 上野実弥子, Masaki Imanishi, Yasumasa Ikeda and Koichiro Tsuchiya : 黄連解毒湯を用いたcGAS/STING/IRF3経路を介したドキソルビシン誘導性心毒性に対する検討, 第8回日本心血管協会(JCVA)学術集会(大分) 2023年6月10日, Jun. 2023.
27.	Masafumi Funamoto, Shunji Hirose, Amiho Muramatsu, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : 糖尿病性心筋症におけるエピジェネティックな老化制御機構の解明, 第8回日本心血管協会(JCVA)学術集会(大分), Jun. 2023.
28.	Kohsuke Kondoh, Masaki Imanishi, Ryosuke Yamashita, Keijo Fukushima, Ryo Nakayama, Honoka Tsunematsu, Takahisa Inoue, GOTOH Kohei, Licht Miyamoto, Masafumi Funamoto, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya : 5-FUの膵がん細胞増殖抑制効果に対する低酸素―PARP活性化シグナルの役割, 第262回徳島医学会学術集会(徳島), Feb. 2023.
29.	Shunji Hirose, Masafumi Funamoto, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : 2型糖尿病による心筋症モデルマウスの検討, 第262回徳島医学会学術集会, Feb. 2023.
30.	SETO Yasuyuki, Masafumi Funamoto and Yasumasa Ikeda : 黄連解毒湯を用いたドキソルビシン誘導性心毒性に対する検討, 第262回徳島医学会学術集会, Feb. 2023.
31.	Tatsuki Itoh, Masafumi Funamoto and Yasumasa Ikeda : 急性腎障害に対するマクロファージ鉄ストレスの役割の検討, 第262回徳島医学会学術集会, Feb. 2023.
32.	SUENAGA Aoi, Masafumi Funamoto and Yasumasa Ikeda : 慢性腎臓病に対する五苓散の効果, 第262回徳島医学会学術集会, Feb. 2023.
33.	Masaki Imanishi, 山下竜介, Keijo Fukushima, 近藤宏祐, 中山涼, 常松保乃加, 井上貴久, 後藤廣平, Masafumi Funamoto, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya : 5-FU膵がん細胞増殖抑制効果に対する低酸素-PARPシグナルの役割, 第52回心脈管作動物質学会, Feb. 2023.
34.	Yasumasa Ikeda, Masafumi Funamoto and Hiroyoshi Sei : New Attempt of Practice in Pharmacology Joint Practice with Basic Medical Departments in Tokushima University-, 第96回日本薬理学会年会教育企画シンボジウム, Nov. 2022.
35.	村嶋優香, Yuya Horinouchi, 山田佑人, 吉岡駿, Keijo Fukushima, 久禮匠, 佐々木尚史, Hiromichi Fujino, 四宮一昭 and Yasumasa Ikeda : フィブラート系薬剤の腎保護効果に関する検討, 第61回日本薬学会中四国支部学術大会, Nov. 2022.
36.	山下竜介, Masaki Imanishi, Keijo Fukushima, 近藤宏祐, 中山涼, 常松保乃加, 井上貴久, 後藤廣平, Masafumi Funamoto, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya : 低酸素がん微小環境におけるPARP活性化は5-FUによる膵がん細胞増殖抑制効果の減弱に寄与する, 第142回日本薬理学会近畿部会, Nov. 2022.
37.	Masafumi Funamoto, 砂川陽一, 刀坂泰史, 清水果奈, 清水聡志, 長谷川浩二, Yasumasa Ikeda and 森本達也 : 心不全発症時におけるBRG1を介したヒストンのアセチル修飾部位の検討, 第51回日本心脈管作動物質学会, Jul. 2022.
38.	Yasumasa Ikeda and Masafumi Funamoto : 漢方薬の腎保作用の検討, 第51回日本心脈管作動物質学会, Jul. 2022.
39.	Masafumi Funamoto, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : ドキソルビシン誘導性心毒性に対するオウゴン成分オウゴニンの効果検討, 第141回日本薬理学会近畿部会, Jul. 2022.
40.	山田佑人, Yuya Horinouchi, 吉岡駿, 村嶋優香, 久禮匠, 佐々木尚史, Masaki Imanishi, Koichiro Tsuchiya, 四宮一昭 and Yasumasa Ikeda : 慢性腎臓病に対するSPPARMαペマフィブラートの腎保護効果, 第141回日本薬理学会近畿部会, Jul. 2022.
41.	Tatsuki Itoh, Masafumi Funamoto, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : 急性腎障害におけるマクロファージ鉄ストレスの役割の検討, 第141回日本薬理学会近畿部会, Jul. 2022.
42.	Masafumi Funamoto, Yoichi Sunagawa, Yasufumi Katanasaka, Kana Shimizu, Satoshi Shimizu, Koji Hasegawa, Yasumasa Ikeda and Tatsuya Morimoto : The Interaction of the p300 with the BRG1 Increases the Acetylation levels of the H3K122 in Heart Failure, 第95回日本薬理学会年会, Mar. 2022.
43.	Yasumasa Ikeda, Masafumi Funamoto, Masaki Imanishi and Koichiro Tsuchiya : 漢方薬の新規腎保護作用の検討, 第95回日本薬理学会年会, Mar. 2022.
44.	Masafumi Funamoto, 砂川陽一, 刀坂泰史, 清水果奈, 清水聡志, 長谷川浩二, Yasumasa Ikeda and 森本達也 : 心不全期にp300/BRG1複合体がH3K122のアセチル化レベルを増加させた, 第95回日本薬理学会年会, Mar. 2022.
45.	Masafumi Funamoto and Yasumasa Ikeda : 生薬由来化合物のオウゴニンによるドキソルビシンの心毒性に対する効果検討, 第31回日本循環薬理学会, Dec. 2021.
46.	Masafumi Funamoto and Yasumasa Ikeda : ドキソルビシンの心毒性に対する生薬由来化合物オウゴニンの効果検討, 第140回日本薬理学会近畿部会, Nov. 2021.
47.	Masafumi Funamoto, 砂川陽一, 刀坂泰史, 清水果奈, 宮崎雄輔, 清水聡史, 長谷川浩二, Yasumasa Ikeda and 森本達也 : 心肥大期から心不全期におけるヒストンのアセチル化修飾部位の検討, 第5回黒潮カンファレンス, Sep. 2021.
48.	Masafumi Funamoto, 砂川陽一, 刀坂泰史, 清水果奈, 宮崎雄輔, 清水聡史, 長谷川浩二, Yasumasa Ikeda and 森本達也 : 心不全発症時におけるヒストンのアセチル化修飾部位の検討, 第263回徳島医学会学術集会, Aug. 2021.
49.	Masafumi Funamoto, 砂川陽一, 刀坂泰史, 清水果奈, 宮崎雄輔, 清水聡史, 長谷川浩二, Yasumasa Ikeda and 森本達也 : 心不全発症におけるヒストンのアセチル化修飾部位の変化を介した転写制御機構の解明, 第28回市大フォーラム, Aug. 2021.
50.	Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Licht Miyamoto, Toshiaki Tamaki and Koichiro Tsuchiya : シスプラチン誘発性腎毒性における鉄依存性細胞死の役割の検討, 第64回日本腎臓学会学術集会, Jun. 2021.
51.	Yasumasa Ikeda, Hirofumi Hamano, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, Masayuki Chuma, Yoshito Zamami, Licht Miyamoto, 石澤啓介, Hiromichi Fujino, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Identification of a candidate drug for the prevention of cisplatin-induced nephrotoxicity by a database analysis -basic research-clinical study, 第94回日本薬理学会年会, Mar. 2021.
52.	Yasumasa Ikeda, Hirofumi Hamano, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, 石澤啓介, Koichiro Tsuchiya and Toshiaki Tamaki : シスプラチン起因性腎障害を予防する既存薬の同定, 第63回日本腎臓学会学術総会, Aug. 2020.
53.	Masateru Kondoh, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Kotoko Suzuki, Rie Matsuoka, Yoshito Zamami, Masayuki Chuma, Yasumasa Ikeda and Keisuke Ishizawa : 薬剤誘発性急性大動脈疾患に対するケルセチンの抑制効果, 第137回日本薬理学会近畿部会, Jun. 2020.
54.	Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Mitsuhiro Goda, Yoshito Zamami, Licht Miyamoto, Keisuke Ishizawa and Koichiro Tsuchiya : The involvement of ferroptosis on cisplatin-induced nephrotoxicity, 第93回日本薬理学会年会, Mar. 2020.
55.	Licht Miyamoto, Yuko Yagi, Aya Hatano, Yasumasa Ikeda, Shinji Abe, Toshiaki Tamaki and Koichiro Tsuchiya : Chronic exposure to hypoxia facilitates chemotherapy sensitivity with downregulation of MDR1, 日本薬理学会, Mar. 2020.
56.	Tatsuya Tsuda, Mitsuhiro Goda, Yuya Horinouchi, Yoshito Zamami, Yasumasa Ikeda, Keisuke Ishizawa, Ichiro Hashimoto and Yuki Izawa-Ishizawa : 血管平滑筋細胞石灰化シグナルにおけるRhoキナーゼーサイクロフィリンA経路の関与, 第260回徳島医学会学術集会(令和元年度冬期), Feb. 2020.
57.	Hirofumi Hamano, Yasumasa Ikeda, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, Kenshi Takechi, Masayuki Chuma, Yoshito Zamami, Yuya Horinouchi, Licht Miyamoto, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : シスプラチン誘発性腎障害を予防する既存薬物の同定, 第260回徳島医学会学術集会(令和元年度冬期), Feb. 2020.
58.	Yasumasa Ikeda and Yuya Horinouchi : シスプラチン腎障害における鉄依存性細胞死の役割の検討, 第23回日本心血管内分泌代謝学会学術総会【CVMW2019 心血管代謝週間】, Dec. 2019.
59.	Mitsuhiro Goda, Masaya Kanda, 前川晃子, Takahiro Niimura, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Kenshi Takechi, Hirofumi Hamano, Naoto Okada, Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Yanagawa and Keisuke Ishizawa : 大規模医療情報データベースを活用したシスプラチン誘発腎障害に対する新規予防薬の探索とその有効性の検証, 第40回日本臨床薬理学会学術総会, Dec. 2019.
60.	Takahiro Niimura, Yoshito Zamami, Yutaroh Naitoh, 川尻雄大, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda and Keisuke Ishizawa : 抗がん剤誘発末梢神経障害の予防薬開発を目的とした医療ビッグデータ解析および基礎研究, 第40回日本臨床薬理学会学術総会, Dec. 2019.
61.	Yasumasa Ikeda, Yuya Horinouchi, Hirofumi Hamano, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : シスプラチン腎障害における鉄依存性細胞死の検討, 第29回日本循環薬理学会/第55回高血圧関連疾患モデル学会合同学会, Nov. 2019.
62.	Yuya Horinouchi, Yasumasa Ikeda, Hirofumi Hamano, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全関連サルコペニアにおける鉄代謝異常, 第6回日本サルコペニア・フレイル学会大会, Nov. 2019.
63.	近藤友宏, Licht Miyamoto, 福田恵介, 高橋梨恵, Yuya Horinouchi, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : スダチ果皮香気成分由来物質による糖脂質代謝の影響, 第58回中国四国支部学術大会, Nov. 2019.
64.	Hirofumi Hamano, Yasumasa Ikeda, Yuya Horinouchi, Mitsuhiro Goda, Yoshito Zamami, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : プロトンポンプ阻害剤はヘプシジンを介して鉄代謝異常に関与する, 第29回日本医療薬学会年会, Nov. 2019.
65.	Mitsuhiro Goda, 神田将哉, 前川晃子, Ami Yoshida, Takahiro Niimura, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Kenshi Takechi, Yasumasa Ikeda and Keisuke Ishizawa : ドラッグリポジショニング手法を用いたシスプラチン誘発腎障害に対する新規予防薬探索, 第29回日本循環薬理学会・第55回高血圧関連疾患モデル学会合同学術集会, Nov. 2019.
66.	Takahiro Niimura, Yoshito Zamami, Hiroumi Saito, 神田将哉, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : 大規模医療情報を活用した抗がん剤誘発心筋症予防薬の探索, 第29回日本循環薬理学会・第55回高血圧関連疾患モデル学会合同学術集会, Nov. 2019.
67.	鈴木琴子, Yuki Izawa-Ishizawa, Mitsuhiro Goda, 近藤正輝, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda and Keisuke Ishizawa : ケルセチンによる薬剤誘発性急性大動脈疾患発症抑制効果の検討, 第58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, Nov. 2019.
68.	Hiroumi Saito, Takahiro Niimura, Yoshito Zamami, Masaya Kanda, Mitsuhiro Goda, Yuki Izawa-Ishizawa, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : 大規模医療情報データベースを活用したドキソルビシン誘発心筋炎に対する予防薬の探索, 第58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, Nov. 2019.
69.	内藤優太朗, Yoshito Zamami, Takahiro Niimura, 川尻雄大, 相澤風花, Shiori Nishiuchi, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, 島添隆雄, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : 大規模医療情報データベースを活用したオキサリプラチン誘発末梢神経障害に対する予防薬探索, 第58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, Nov. 2019.
70.	JOHZUKURI Natsumi, Shimon Takahashi, Kenshi Takechi, Masayuki Chuma, Mitsuhiro Goda, Yoshito Zamami, Yuki Izawa-Ishizawa, Yuya Horinouchi, Hirofumi Hamano, Naoto Okada, Kenshi Takechi, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : ドラッグリポジショニングによる大規模医療情報データベースを用いた新規抗てんかん薬の探索研究, 第58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, Nov. 2019.
71.	村井陽一, Mitsuhiro Goda, 神田将哉, Takahiro Niimura, Ami Yoshida, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Hirofumi Hamano, Naoto Okada, Kenshi Takechi, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : シスプラチンと各種5-HT3受容体拮抗薬の併用による腎機能への影響, 第58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, Nov. 2019.
72.	Masaya Kanda, Mitsuhiro Goda, Takahiro Niimura, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Hirofumi Hamano, Naoto Okada, Kenshi Takechi, Yuya Horinouchi, Yasumasa Ikeda, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : シスプラチン誘発腎障害に対する各種 5-HT3 受容体拮抗薬の影響, 第29回日本医療薬学会年会, Nov. 2019.
73.	定作奈津美, Shimon Takahashi, Kenshi Takechi, Masayuki Chuma, Mitsuhiro Goda, Yoshito Zamami, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : ビッグデータを活用した新規抗てんかん薬の検討, 第29回日本医療薬学会年会, Nov. 2019.
74.	Masayuki Chuma, Mitsuhiro Goda, Takahiro Niimura, Yoshito Zamami, Kenshi Takechi, Yuki Izawa-Ishizawa, 濱野裕章, 石田俊介, Takahiro Niimura, Masateru Kondoh, Takashi Bandoh, Naoto Okada, Keijo Fukushima, Hiromichi Fujino, Koichiro Tsuchiya, Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Yanagawa and Keisuke Ishizawa : ドラッグリポジショニング手法を用いたバンコマイシン関連腎障害の予防薬探索とその有用性の検討, 第13回日本腎臓病薬物療法学会学術集会・総会, Nov. 2019.
75.	Sumiko Yoshida, Yasumasa Ikeda, Ken-ichi Aihara and Masahiro Abe : 心血管病におけるアンドロゲン受容体の意義, 第30回日本性機能学会学術総会, Sep. 2019.
76.	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.
77.	Takahiro Niimura, Yoshito Zamami, Takahiro Niimura, Yutaroh Naitoh, 川尻雄大, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda and Keisuke Ishizawa : 医療ビッグデータ解析と基礎研究を融合した抗がん剤誘発末梢神経障害の予防薬開発, 次世代を担う創薬・医療薬理シンポジウム2019, Aug. 2019.
78.	Takahiro Niimura, Yoshito Zamami, Takahiro Niimura, 内藤優太朗, 川尻雄大, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda and Keisuke Ishizawa : 医療ビッグデータ解析と基礎研究を融合した抗がん剤誘発末梢神経障害の予防薬開発, 生体機能と創薬シンポジウム2019, Aug. 2019.
79.	齊藤広海, Yoshito Zamami, Takahiro Niimura, Masaya Kanda, Mitsuhiro Goda, Yuki Izawa-Ishizawa, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : 大規模医療情報データベースを活用したドキソルビシン誘発心筋炎にたいする予防薬の探索, 第30回霧島神経薬理フォーラム, Aug. 2019.
80.	新村貴博, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : 大規模医療情報を用いたニコランジルの心肺停止後予後改善効果の検討, 医療薬学フォーラム2019/第27回クリニカルファーマシーシンポジウム, Jul. 2019.
81.	Yutaroh Naitoh, Takahiro Niimura, Yoshito Zamami, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda and Keisuke Ishizawa : オキサリプラチン誘発末梢神経障害の予防薬探索を目的としたドラッグリポジショニング研究, 医療薬学フォーラム2019/第27回クリニカルファーマシーシンポジウム, Jul. 2019.
82.	齊藤広海, 新村貴博, Yoshito Zamami, Masaya Kanda, Mitsuhiro Goda, Yuki Izawa-Ishizawa, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : 医療ビッグデータ解析を活用したドキソルビシン誘発心筋炎に対する予防薬探索研究, 医療薬学フォーラム2019/第27回クリニカルファーマシーシンポジウム, Jul. 2019.
83.	JOHZUKURI Natsumi, Shimon Takahashi, Kenshi Takechi, Masayuki Chuma, Mitsuhiro Goda, Yoshito Zamami, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : 大規模医療情報データベースを活用した新規抗てんかん薬の探索研究, 医療薬学フォーラム2019/第27回クリニカルファーマシーシンポジウム, Jul. 2019.
84.	Mitsuhiro Goda, 斉家和仁, Akiko Maegawa, Masaya Kanda, Ami Yoshida, Yoichi Murai, Takahiro Niimura, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Kenshi Takechi, Hirofumi Hamano, Naoto Okada, Keijo Fukushima, Hiromichi Fujino, Koichiro Tsuchiya, Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Yanagawa and Keisuke Ishizawa : 医療ビッグデータを活用したシスプラチン誘発腎障害に対する新規予防薬の探索とその有効性の検証, 第4回中四国臨床薬理学会, Jul. 2019.
85.	新村貴博, Yoshito Zamami, 川尻雄大, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda and Keisuke Ishizawa : ドラッグリポジショニング手法を用いたオキサリプラチン誘発末梢神経障害の予防薬探索, 第4回中四国臨床薬理学会, Jul. 2019.
86.	Kotoko Suzuki, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Masateru Kondoh, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda and Keisuke Ishizawa : 薬剤誘発性急性大動脈疾患に対するケルセチンの効果, 第135回日本薬理学会近畿部会, Jun. 2019.
87.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : 医療ビッグデータ解析と基礎研究を融合した薬剤性副作用の機序解明および治療薬の開発, 第29回日本医療薬学会年会シンポジウム13, Mar. 2019.
88.	Kenshi Takechi, Masayuki Chuma, 石田俊介, 坂東寛, Yoshito Zamami, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda, Keisuke Ishizawa and Hiroaki Yanagawa : 向精神薬の副作用対策を基盤とした臨床研究とその活用, 第139回日本薬学会年会一般シンポジウムS48, Mar. 2019.
89.	近藤正輝, Masaki Imanishi, Keijo Fukushima, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : キサンチンオキシダーゼ阻害剤による新規血管線維化抑制機構の検討, 日本薬学会第139年会大学院生シンポジウムGS03, Mar. 2019.
90.	Yuya Horinouchi, Yasumasa Ikeda, Hirofumi Hamano, Masaki Imanishi, Keijo Fukushima, Mitsuhiro Goda, Kenshi Takechi, Licht Miyamoto, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全関連骨格筋萎縮における鉄代謝異常, 第92回日本薬理学会年会, Mar. 2019.
91.	Yasumasa Ikeda, Akiho Satoh, Yuya Horinouchi, Yuki Izawa-Ishizawa, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Iron accumulation negatively regulates skeletal muscle myogenesis, 第92回日本薬理学会年会, Mar. 2019.
92.	Yuya Horinouchi, Yasumasa Ikeda and Toshiaki Tamaki : 疾患における鉄の意義と治療応用, 第92回日本薬理学会年会シンポジウム2:必須微量金属研究のパラダイムシフト, Mar. 2019.
93.	Licht Miyamoto, Nakayama Suguru, Hatano Aya, Hattori Mana, Inoue Haruka, Yasumasa Ikeda and Koichiro Tsuchiya : Significance of SGLT2 in glucagon secretion from α-TC cells, 日本薬理学会, Mar. 2019.
94.	Mitsuhiro Goda, Masaya Kanda, Takahiro Niimura, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, 濱野裕章, 生田賢治, Naoto Okada, Kenshi Takechi, Yuya Horinouchi, Yasumasa Ikeda, Yasushi Kirino, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : ビッグデータを用いたシスプラチン誘発腎障害に対する新規予防薬の探索とその有効性の検証, 日本薬学会第139年会, Mar. 2019.
95.	Mitsuhiro Goda, Masaya Kanda, Takahiro Niimura, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, 濱野裕章, 生田賢治, Naoto Okada, Kenshi Takechi, Yuya Horinouchi, Yasumasa Ikeda, Yasushi Kirino, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : シスプラチン誘発腎障害に対する新規予防薬の有効性の基礎的検証, 日本臨床腫瘍薬学会学術大会2019, Mar. 2019.
96.	Mitsuhiro Goda, 神田将哉, 新村貴博, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, 濱野裕章, 生田賢治, Naoto Okada, Kenshi Takechi, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : シスプラチン誘発腎障害に対する新規予防薬の有効性の検証, 第92回日本薬理学会年会, Mar. 2019.
97.	鈴木琴子, Yuki Izawa-Ishizawa, Masateru Kondoh, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Kenshi Takechi, Mitsuhiro Goda, Masayuki Chuma, Yasumasa Ikeda and Keisuke Ishizawa : 薬物誘発性大動脈瘤または大動脈解離モデルマウスに対するケルセチンの効果, 第92回日本薬理学会年会, Mar. 2019.
98.	新村貴博, Yoshito Zamami, 川尻雄大, Mitsuhiro Goda, Naoto Okada, 萱野純史, 小山敏広, Masaki Imanishi, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, 小林大介, 島添隆雄 and Keisuke Ishizawa : ドラッグリポジショニング手法を用いたオキサリプラチン誘発末梢神経障害の予防薬探索, 第92回日本薬理学会年会学生セッション, Mar. 2019.
99.	Yoshito Zamami, Takahiro Niimura, 川尻雄大, Mitsuhiro Goda, Naoto Okada, Hirofumi Hamano, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, 島添隆雄 and Keisuke Ishizawa : 大規模医療情報データベースを活用した抗がん剤誘発副作用に対する予防薬の探索, 第92回日本薬理学会年会年会企画シンポジウム, Mar. 2019.
100.	Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Watanabe, Hirofumi Hamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : マクロファージフェリチン欠損は肥満・糖尿病における脂肪炎症を抑制する, 第48回日本心脈管作動物質学会, Feb. 2019.
101.	Yuya Horinouchi, Yasumasa Ikeda and Toshiaki Tamaki : 肥満・糖尿病における鉄制御の意義, 第48回日本心脈管作動物質学会シンポジウム4:心疾患腎代謝疾患の制御因子としての微量金属栄養素「鉄」の新たな展開, Feb. 2019.
102.	藤本望, 村田梨菜, Keiji Murakami, Hideki Fujii, Licht Miyamoto, 井上貴久, Koichiro Tsuchiya, Yasumasa Ikeda, Yuki Izawa-Ishizawa and Shuichi Hamano : 唾液中の硝酸イオンが口腔細菌に与える影響について·, 第42回徳島県医学検査学会, Dec. 2018.
103.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Hiroumi Saito, Masaki Imanishi, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : 大規模医療情報データベースおよび遺伝子発現データベースを活用した薬剤性心筋炎に対する予防薬の探索, 第28回日本医療薬学会年会シンポジウム, Nov. 2018.
104.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Hirofumi Hamano, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Kenshi Takechi, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : リアルワールドビッグデータを活用した新規腎保護薬の探索, 第28回日本医療薬学会年会, Nov. 2018.
105.	Yoshito Zamami, Yuki Izawa-Ishizawa, 新村貴博, Masaki Imanishi, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yasumasa Ikeda, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 救急・集中治療領域において大規模医療情報データベースを活用したトランスレーショナルリサーチ, 第29回霧島神経薬理フォーラム, Nov. 2018.
106.	井上陽加, Licht Miyamoto, 服部真奈, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 亜硝酸塩による脂肪組織への抗肥満的な影響, 第134回日本薬理学会近畿部会, Nov. 2018.
107.	Yuya Horinouchi, Yasumasa Ikeda, Hirofumi Hamano, Masaki Imanishi, Keijo Fukushima, Mitsuhiro Goda, Kenshi Takechi, Licht Miyamoto, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全関連サルコペニアにおける鉄の関与, 第134回日本薬理学会近畿部会, Nov. 2018.
108.	斉家和仁, Mitsuhiro Goda, 伊勢諒, 新村貴博, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Naoto Okada, Kenshi Takechi, Masaki Imanishi, Yasumasa Ikeda, 演野裕章, Yuya Horinouchi, Koichiro Tsuchiya and Keisuke Ishizawa : シスプラチン誘発腎障害に対する脂質異常症治療薬の影響, 第57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, Nov. 2018.
109.	生藤来希, Masaki Imanishi, 山川祐介, Keijo Fukushima, 前川晃子, Yuya Horinouchi, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda, Hiromichi Fujino and Koichiro Tsuchiya : 大腸がん増大におけるがん関連線維芽細胞由来ERKSの役割, 第57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, Nov. 2018.
110.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Yuki Izawa-Ishizawa, Hiromichi Fujino and Toshiaki Tamaki : リアルワールドデータを活用した新規腎保護薬の探索, 第48回日本腎臓学会西部学術大会, Sep. 2018.
111.	Yasumasa Ikeda and Toshiaki Tamaki : シンポジウム1「腎疾患(CKD)の治療と研究の最前線」慢性腎臓病における鉄代謝の意義と治療応用, 第48回日本腎臓学会西部学術大会, Sep. 2018.
112.	Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Watanabe, Hirofumi Hamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Yoshito Zamami, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : マクロファージ鉄の肥満・糖尿病における役割第42回日本鉄バイオサイエンス学会学術集会 2018/9/2 石川県金沢医科大学病院北辰講堂, 第42回日本鉄バイオサイエンス学会学術集会, Sep. 2018.
113.	新村貴博, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : 大規模医療情報を活用した新規心肺蘇生後脳症治療薬の探索, 第29回霧島神経薬理フォーラム, Aug. 2018.
114.	Yuki Izawa-Ishizawa, Yu Kagimoto, Masaki Imanishi, Yusuke Iwata, Kotoko Suzuki, Yuya Horinouchi, Kenshi Takechi, Yoshito Zamami, Yasumasa Ikeda, Keisuke Ishizawa and Toshiaki Tamaki : 第40回徳島医学会賞受賞講演動脈硬化性疾患発症に対するケルセチンの効果, 第257回徳島医学会学術集会(平成30年度夏季), Aug. 2018.
115.	Yoshito Zamami, 新村貴博, Yuki Izawa-Ishizawa, Kenshi Takechi, Masaki Imanishi, Masayuki Chuma, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : 医療情報データベースを活用した抗がん剤誘発副作用に対する予防薬の探索研究, 第21回日本医薬品情報学会総会・学術大会, Jul. 2018.
116.	Masaki Imanishi, Masateru Kondoh, 山川裕介, 生藤来希, 村井陽一, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Keijo Fukushima, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : Angiotensin II誘発性心臓線維化は線維芽細胞特異的ERK5欠損マウスにおいて亢進される, 第133回日本薬理学会近畿部会, Jun. 2018.
117.	Koichiro Tsuchiya, Licht Miyamoto, Shuichi Hamano, Yuya Horinouchi, Yasumasa Ikeda, Toshiaki Tamaki and 津田勝範 : 抗マラリア薬artesunateからの鉄依存活性酸素生成メカニズムの検討, 第71回日本酸化ストレス学会，第18回日本NO学会合同学術集会, May 2018.
118.	Yasumasa Ikeda : シンポジウム2:「心血管系のNO/活性酸素と臨床応用展開」心腎血管代謝疾患における鉄の新たな知見, 第18回日本NO学会学術集会・第71回日本酸化ストレス学会学術集会合同大会, May 2018.
119.	Yoshito Zamami, Marin Mitsui, Yuki Izawa-Ishizawa, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Keijo Fukushima, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 有害事象自発報告データベースを活用したベバシズマブの抗腫瘍効果を減弱させる薬剤の探索研究, 日本薬学会第138年会, Mar. 2018.
120.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : ドラッグリポジショニング手法を用いた心肺蘇生後脳症治療薬の探索, 日本薬学会第138年会, Mar. 2018.
121.	Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa and Toshiaki Tamaki : Factor Xa Inhibitor Exerts a Protective Effect against Renal Injury, 第82回日本循環器学会学術集会, Mar. 2018.
122.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Hirofumi Hamano, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 大規模医療情報データベース解析と基礎研究の融合による新規腎保護薬の探索, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
123.	Yuki Izawa-Ishizawa, Yu Kagimoto, Masaki Imanishi, Yusuke Iwata, Yuya Horinouchi, Kenshi Takechi, Yoshito Zamami, Yasumasa Ikeda, Keisuke Ishizawa and Toshiaki Tamaki : マウス大動脈瘤形成に対するケルセチンの効果, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
124.	Masaki Imanishi, Masateru Kondoh, Kyohei Tanaka, Raiki Ikutoh, Yoichi Murai, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : Febuxostatの尿酸合成抑制作用とは独立した血管線維化抑制機構の解明, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
125.	Kenshi Takechi, Yoshito Zamami, Masaki Imanishi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Toshiaki Tamaki, Keisuke Ishizawa and Hiroaki Yanagawa : てんかん誘発性精神症状の行動学的解析および治療薬の探索と作用機序の解明, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
126.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 大規模医療情報を活用した心肺停止患者に対するニコランジルの有効性に関する検討, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
127.	Yasumasa Ikeda : 糖尿病における微量栄養素「鉄」の役割, 第256回徳島医学会市民公開シンポジウム「加齢で起こる病気の検査と治療薬」, Feb. 2018.
128.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 第Xa因子阻害剤の腎保護効果, 第47回日本心脈管作動物質学会, Feb. 2018.
129.	Licht Miyamoto, 梅本果奈, 上島沙弥香, 友成奈央実, 土橋有希, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 食後生じるAMPKの新たな翻訳後修飾を介した代謝制御機構, 心脈管作動物質学会, Feb. 2018.
130.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Yuki Izawa-Ishizawa, Hiromichi Fujino and Toshiaki Tamaki : 医療ビッグデータを活用した腎保護薬の探索, 2017年度肥満・糖尿病クラスター・ミニリトリート, Feb. 2018.
131.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 第Xa因子阻害薬の腎保護効果, 第10回心・血管クラスター・ミニリトリート, 2017.
132.	Masahiro Betsushiyo, 村上圭史, 藤猪英樹, Katsunori Tsuda, Licht Miyamoto, Koichiro Tsuchiya, Yasumasa Ikeda, Toshiaki Tamaki and Shuichi Hamano : Actinomyces spp. による硝酸イオンの還元と生理作用の検討, 第41回徳島県医学検査学会, Dec. 2017.
133.	Sakiko Hino, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Yuya Horinouchi, Yasumasa Ikeda, Toshiaki Tamaki and Keisuke Ishizawa : 大規模医療情報を活用した薬剤性腎障害に対する予防薬の探索, 西日本医学生学術フォーラム2017, Dec. 2017.
134.	Yusuke Iwata, Yuki Izawa-Ishizawa, Yu Kagimoto, Kotoko Suzuki, Yuya Horinouchi, Yasumasa Ikeda, Keisuke Ishizawa and Toshiaki Tamaki : マウス大動脈瘤形成に対するケルセチンの効果, 西日本医学生学術フォーラム2017, Dec. 2017.
135.	Yuki Izawa-Ishizawa, Yu Kagimoto, Masaki Imanishi, Yuya Horinouchi, Kotoko Suzuki, Yusuke Iwata, Yoshito Zamami, Kenshi Takechi, Yasumasa Ikeda, Toshiaki Tamaki and Keisuke Ishizawa : ケルセチンによる動脈硬化性疾患発症に対する予防効果の検討, 第27回日本循環薬理学会, Dec. 2017.
136.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 大規模医療情報を用いて新規心肺蘇生後症候群治療薬の開発を志向したドラッグリポジショニング研究, 第38回日本臨床薬理学会学術総会, Dec. 2017.
137.	Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 臨床薬理学集中講座修了後の研究活動∼大規模医療情報を活用したドラッグリポジショニング研究を中心に∼, 第38回日本臨床薬理学会学術総会臨床薬理学集中講座フォローアップ・セミナー, Dec. 2017.
138.	Hiroaki Watanabe, Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 肥満・糖尿病におけるマクロファージ鉄制御機構の検討, 第132回日本薬理学会近畿部会, Nov. 2017.
139.	Takahiro Niimura, Yoshito Zamami, 小山敏広, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : ドラッグリポジショニングを切り口とした心肺蘇生後症候群治療薬の探索研究, 第27回日本医療薬学会年会, Nov. 2017.
140.	Yoshito Zamami, 小山敏広, Yuki Izawa-Ishizawa, Takahiro Niimura, Masaki Imanishi, Kenshi Takechi, Yuya Horinouchi, 桐野靖, 中村敏己, 寺岡和彦, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 大規模医療情報を活用して心肺停止患者の生存率向上を志向したドラッグリポジショニング研究, 第27回日本医療薬学会年会, Nov. 2017.
141.	Marin Mitsui, Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 有害事象自発報告データベースを基にしたベバシズマブと相互作用を起こす薬剤の探索研究, 第56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, Oct. 2017.
142.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 心肺停止患者の予後に与えるニコランジルの影響-大規模レセプト情報を用いた検討, 第56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, Oct. 2017.
143.	Shiori Urushizaki, Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 大規模医療情報を活用して新規心肺蘇生後症候群治療薬の開発を志向したドラッグリポジショニング研究, 第56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, Oct. 2017.
144.	Yu Kagimoto, Yuki Izawa-Ishizawa, Mayuko Hosohka, Naoko Saito, Kotoko Suzuki, Masaki Imanishi, Yuya Horinouchi, Yoshito Zamami, Kenshi Takechi, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 急性大動脈解離易発症マウスにおけるquercetinの効果, 第56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, Oct. 2017.
145.	Kyohei Tanaka, Masaki Imanishi, Masateru Kondoh, Raiki Ikutoh, Yoichi Murai, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : フェブキソスタットの尿酸合成抑制剤作用とは独立した血管線維化抑制作用の検討, 第56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, Oct. 2017.
146.	Hiroaki Watanabe, Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 肥満・糖尿病におけるマクロファージ鉄の役割の検討, 第56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, Oct. 2017.
147.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎臓病における尿毒素蓄積によるヘプシジン制御と鉄代謝破綻のメカニズムの解明, 第41回日本鉄バイオサイエンス学会学術集会, Sep. 2017.
148.	Yasumasa Ikeda, Yuya Horinouchi, Hirofumi Hamano, 平山祐, Seiji Kishi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Ken-ichi Aihara, Hideko Nagasawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄摂取制限による尿細管間質障害の抑制効果の検討, 第41回日本鉄バイオサイエンス学会学術集会, Sep. 2017.
149.	Licht Miyamoto, Kana Umemoto, Sayaka Ueshima, Naomi Tomonari, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 食後のエネルギー代謝調節を担うAMPK活性制御機構, 次世代を担う創薬医療薬理シンポジウム2017, Aug. 2017.
150.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全における尿毒素蓄積はヘプシジンを介した鉄代謝恒常性破綻に関与する, 大阪市大フォーラム, Aug. 2017.
151.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 心肺蘇生後症候群治療薬の開発を目的としたドラッグリポジショニング研究-大規模医療情報を活用した検討-, 第255回徳島医学会学術集会, Aug. 2017.
152.	Yoshito Zamami, Yuki Izawa-Ishizawa, 桐野靖, Marin Mitsui, Shiori Urushizaki, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 有害事象自発報告データベースを切り口としたベバシズマブの抗腫瘍効果を減弱させる薬剤の探索研究, 医療薬学フォーラム2017 第25回クリニカルファーマシーシンポジウム, Jul. 2017.
153.	Yuya Horinouchi, Yasumasa Ikeda, Masaki Imanishi, Yoshito Zamami, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 経口FXa阻害剤の腎線維化抑制効果, 医療薬学フォーラム2017 第25回クリニカルファーマシーシンポジウム, Jul. 2017.
154.	Yuya Horinouchi, Yasumasa Ikeda, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 第Xa因子阻害剤は腎間質線維化を抑制する, 第131回日本薬理学会近畿部会, Jun. 2017.
155.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : インドキシル硫酸蓄積はヘプシジン制御を介して鉄代謝恒常性破綻に関与する, 第131回日本薬理学会近畿部会, Jun. 2017.
156.	Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa and Toshiaki Tamaki : Inhibitory effect of dietary iron restriction on albumin-induced renal tubulointerstitial injury, 第60回日本腎臓学会学術総会, May 2017.
157.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : インドキシル硫酸はヘプシジンを介した鉄代謝異常に関与する, 第60回日本腎臓学会学術総会, May 2017.
158.	Yuya Horinouchi, Yasumasa Ikeda, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : FXa阻害剤は腎間質線維化を抑制する, 第60回日本腎臓学会学術総会, May 2017.
159.	Licht Miyamoto, Aihara Haruna, Xu Wenting, Jin Meina, Tomida Yosuke, Yamaoka Tomomi, Tanaka Naonobu, Yasumasa Ikeda, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : A limonene-derivative purified from Sudachi peel upregulates sirt1 and improves lipid /glucose metabolism in HFD-fed mice., 第60回日本糖尿病学会, May 2017.
160.	Marin Mitsui, Yoshito Zamami, Yuki Izawa-Ishizawa, Shiori Urushizaki, 桐野靖, Kazuhito Saike, Hiroshi Moriguchi, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 有害事象自発報告データベースを基にしたベバシズマブの抗腫瘍効果を減弱させる薬剤の探索研究, 日本薬学会第137年会, Mar. 2017.
161.	Yuya Horinouchi, Yasumasa Ikeda, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : FXa 阻害剤の片側尿管結紮モデルマウスにおける腎間質線維化抑制作用, 日本薬学会第137年会, Mar. 2017.
162.	Raiki Ikutoh, Masaki Imanishi, Kyohei Tanaka, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : アンジオテンシンII 誘発性血管リモデリングに対するキサンチンオキシダーゼ阻害剤の影響, 日本薬学会第137年会, Mar. 2017.
163.	Yasumasa Ikeda and Toshiaki Tamaki : Excess iron on the risk of tissue injury, 第90回日本薬理学会年会, Mar. 2017.
164.	Yasumasa Ikeda and Toshiaki Tamaki : Excess iron action on risk of tissue injury, 第90回日本薬理学会年会年会企画ナノシンポジウム「機能性食品における薬理学」, Mar. 2017.
165.	Yuya Horinouchi, Yasumasa Ikeda, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Factor Xa inhibitor attenuates renal fibrosis in mice with unilateral ureteral obstruction, 第90回日本薬理学会年会, Mar. 2017.
166.	Masaki Imanishi, Kyohei Tanaka, Raiki Ikuto, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : Febuxostat suppresses angiotensin II-induced aortic fibrosis, 第90回日本薬理学会年会, Mar. 2017.
167.	Masaki Imanishi, 田中恭平, 生藤来希, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : フェブキソスタットはアンジオテンシンII誘発性大動脈繊維化を抑制する, 第90回日本薬理学会年会(長崎), Mar. 2017.
168.	Yuki Izawa-Ishizawa, Mayuko Hosooka, Naoko Saito, Masaki Imanishi, Yuya Horinouchi, Yoshito Zamami, Kenshi Takechi, Yasumasa Ikeda, Koichiro Tsuchiya, Keisuke Ishizawa and Toshiaki Tamaki : The effect of quercetin on the aortic dissection onset via its endothelial protective effect in mice, 第90回日本薬理学会年会, Mar. 2017.
169.	Licht Miyamoto, Goki Tomokawa, Yuki Matsuda, Moe Yamane, Mana Hattori, Reina Oonishi, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : Significance of central regulation in physical exercise-induced metabolic alterations in skeletal muscles, The 90th Annual Meeting of The Japanese Pharmacology Society, Mar. 2017.
170.	Koichiro Tsuchiya, Yasumasa Ikeda, Yuki Izawa-Ishizawa, Yuya Horinouchi, Licht Miyamoto and Toshiaki Tamaki : 鉄ストレスと代謝性疾患-鉄ストレスによる疾患と，鉄ストレスによる治療, 日本薬学会第137年会, Mar. 2017.
171.	Yoshito Zamami, Yuki Izawa-Ishizawa, 桐野靖, 三井茉綸, 漆崎汐里, 斉家和仁, 森口浩史, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 有害事象自発報告データベースを切り口としたベバシズマブと相互作用を起こす薬剤の探索研究, 第46回日本心脈管作動物質学会年会, Feb. 2017.
172.	Masaki Imanishi, 田中恭平, 生藤来希, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : Angiotensin II誘発性血管リモデリングに対するfebuxostatの効果, 第46回日本心脈管作動物質学会, Feb. 2017.
173.	Licht Miyamoto, 友川剛己, 松田裕樹, 山根萌, 服部真奈, 大西伶奈, Yasumasa Ikeda, Toshiaki Tamaki, Koichiro Tsuchiya and Koichiro Tsuchiya : 身体運動時に生じる骨格筋代謝状態の変化における，中枢を介した調節機構の意義, 第46回日本心脈管作動物質学会, Feb. 2017.
174.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Akiho Satoh, Keisuke Oshima, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全における尿毒素蓄積が生体内鉄代謝に与える影響の検討, 第46回日本心脈管作動物質学会, Feb. 2017.
175.	Yuki Izawa-Ishizawa, 細岡真由子, 斎藤尚子, 鍵本優有, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : ケルセチンによるマウス大動脈解離発症予防効果の検討, 第46回日本心脈管作動物質学会年会, Feb. 2017.
176.	友川剛己, Licht Miyamoto, 松田裕樹, 山根萌, 服部真奈, 大西怜奈, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 水泳運動負荷時に生じる骨格筋AMPK活性化の新たなメカニズム，第46回日本心脈管作動物質学会年会, Feb. 2017.
177.	Yumi Kangawa, Chiharu Fukue, Katsunori Tsuda, Licht Miyamoto, Koichiro Tsuchiya, Yasumasa Ikeda, Toshiaki Tamaki and Shuichi Hamano : Artesunateによる細胞傷害発現機序の解明1, 第40回徳島県医学検査学会, Dec. 2016.
178.	Chiharu Fukue, Yumi Kangawa, Katsunori Tsuda, Licht Miyamoto, Koichiro Tsuchiya, Yasumasa Ikeda, Toshiaki Tamaki and Shuichi Hamano : Artesunateによる細胞傷害発現機序の解明2, 第40回徳島県医学検査学会, Dec. 2016.
179.	Yuki Izawa-Ishizawa, Yutaka Fukunaga, 西良恵理子, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Yoshito Zamami, Kenshi Takechi, Keisuke Ishizawa, Koichiro Tsuchiya, Ichiro Hashimoto and Toshiaki Tamaki : ニトロソニフェジピンは虚血性皮弁モデルにおいて皮弁壊死を抑制する, 第26回日本循環薬理学会, Dec. 2016.
180.	高橋梨恵, Licht Miyamoto, 友川剛己, 宮武由実子, Hiroshi Sakaue, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 脳内グリコーゲンによる代謝調節効果の検討, 第130回日本薬理学会近畿部会, Nov. 2016.
181.	福田恵介, Licht Miyamoto, 高橋梨恵, Toshiaki Tamaki, Yasumasa Ikeda and Koichiro Tsuchiya : スダチ果皮芳香成分が糖脂質代謝に与える影響, 第130回日本薬理学会近畿部会, Nov. 2016.
182.	細岡真由子, Yuki Izawa-Ishizawa, 斎藤尚子, Masaki Imanishi, Yoshito Zamami, Licht Miyamoto, Yuya Horinouchi, Yasumasa Ikeda, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : Quercetin による血管内皮細胞保護効果の検討, 第130回日本薬理学会近畿部会, Nov. 2016.
183.	Akiho Satoh, Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Mizuki Imao, Hiroaki Watanabe, Yuki Izawa-Ishizawa, Licht Miyamoto, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : 鉄欠乏が骨格筋に与える作用の検討, 第55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, Nov. 2016.
184.	Yutaka Fukunaga, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Ichiro Hashimoto : 虚血性皮弁壊死モデルにおける抗酸化薬ニトロソニフェジピンの壊死抑制効果, 第25回日本形成外科学会基礎学術集会, Sep. 2016.
185.	三井茉綸, Yoshito Zamami, 漆崎汐里, 斉家和仁, 森口浩史, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Licht Miyamoto, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : ドラッグリポジショニングを切り口としたベバシズマブ誘発高血圧に対する予防薬の探索研究, 第27回霧島神経薬理フォーラム(福岡), Aug. 2016.
186.	Licht Miyamoto, 秦野彩, 竹之熊和也, 土橋有希, 矢野友章, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 速効型インスリン分泌促進薬とSGLT2阻害薬の併用による薬効の検討, 第129回日本薬理学会近畿部会, Jun. 2016.
187.	Yuki Izawa-Ishizawa, 細岡真由子, 斎藤尚子, Yuya Horinouchi, Masaki Imanishi, Yoshito Zamami, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : ケルセチン代謝産物Q3GAの血管内皮膚細胞に対する短期及び長期効果の検討, 第129回日薬理学会学会近畿部会( 広島), Jun. 2016.
188.	Yasumasa Ikeda, 佐藤明穂, Yuya Horinouchi, Yuki Izawa-Ishizawa, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 骨格筋分化における鉄の役割, 第129回日薬理学会学会近畿部会 (広島), Jun. 2016.
189.	Yasumasa Ikeda, Keisuke Oshima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄は低酸素誘導因子を抑制してエリスロポエチン発現を低下させる, 第59回日本腎臓学会学術総会, Jun. 2016.
190.	Licht Miyamoto, 粟飯原遥菜, 許文婷, 靳美娜, 冨田洋輔, 山岡朋美, Naonobu Tanaka, Yasumasa Ikeda, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : スダチ果皮における抗メタボリックシンドローム作用を有する物質の同定, 日本薬学会第136年会(横浜), Mar. 2016.
191.	細岡真由子, Yuki Izawa-Ishizawa, 斎藤尚子, Licht Miyamoto, Masaki Imanishi, Yoshito Zamami, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : ケルセチン生体内代謝産物 quercetin -3-O-β-Dglucuronideによる血管内皮細胞保護効果, 日本薬学会第136年会(横浜), Mar. 2016.
192.	鍵本優有, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 無機リン刺激による血管平滑筋細胞石灰化におけるrho-kinase 及び cyclophilinA の関与, 日本薬学会第136年会(横浜), Mar. 2016.
193.	Hiroaki Watanabe, Yasumasa Ikeda, Hirofumi Hamano, Akiho Satoh, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 慢性腎臓病におけるヘプシジン制御メカニズムの検討, 日本薬学会第136年会(横浜), Mar. 2016.
194.	佐藤明穂, Yasumasa Ikeda, Yuya Horinouchi, 濱野裕章, 今尾瑞季, 渡邉大晃, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Toshiaki Tamaki, Licht Miyamoto and Koichiro Tsuchiya : 鉄過剰による骨格筋分化抑制作用の解明, 日本薬学会第136年会(横浜), Mar. 2016.
195.	Yasumasa Ikeda, Keisuke Oshima, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Iron Supplementation Suppressed Erythropoietin Expression through HIF-dependent Pathway, The 80th Annual Scientific Meeting of the Japanese Circulation Society, Mar. 2016.
196.	太田和馬, Yoshitaka Kihira, 岸渕麗奈, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : 電位依存性カリウムチャネルKv2.2は腎虚血再灌流障害の軽減に関与する, 第89回日本薬理学会年会(神奈川), Mar. 2016.
197.	岸渕麗奈, Yoshitaka Kihira, Kunihisa Yamaguchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : HIF-1aはアポトーシス制御因子Bcl-2及びCHAC1の発現制御を介して腎虚血再灌流障害からの回復に関与する, 第89回日本薬理学会年会(神奈川), Mar. 2016.
198.	斎藤尚子, Yuki Izawa-Ishizawa, 細岡真由子, Yoshitaka Kihira, Masaki Imanishi, Yoshito Zamami, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : ケルセチン代謝物Q3GAによる血管内皮細胞保護効果の検討, 第89回日本薬理学会年会(神奈川), Mar. 2016.
199.	青木友里, Yuki Izawa-Ishizawa, 高田真衣, 田渕正樹, Masaki Imanishi, Yoshito Zamami, 福永豊, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya, Keisuke Ishizawa and Toshiaki Tamaki : 神経突起伸長および脳卒中後神経症状に対するニトロソニフェジピンの効果, 第89回日本薬理学会年会(神奈川), Mar. 2016.
200.	大島啓亮, Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄のエリスロポエチン発現への影響の検討, 第89回日本薬理学会年会(神奈川), Mar. 2016.
201.	佐藤明穂, Yasumasa Ikeda, Yuya Horinouchi, 濱野裕章, 今尾瑞季, 渡邉大晃, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄欠乏に伴う骨格筋萎縮メカニズム, 第89回日本薬理学会年会(神奈川), Mar. 2016.
202.	Licht Miyamoto, Haruna Aihara, Wenting Xu, Meina Jin, Yosuke Tomida, Tomomi Yamaoka, Naonobu Tanaka, Yasumasa Ikeda, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : Identification of an active compound on lipid metabolism from Sudachi peel, 薬理学会(パシフィコ), Mar. 2016.
203.	Licht Miyamoto, 粟飯原遥菜, Xu Wenting, Jin Meina, 冨田洋輔, 山岡朋美, Naonobu Tanaka, Yasumasa Ikeda, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : 脂質低下作用を有するスダチ果皮由来化合物の薬理作用, 第89回日本薬理学会年会(神奈川), Mar. 2016.
204.	濱野裕章, Yasumasa Ikeda, 渡邉大晃, 佐藤明穂, 大島啓亮, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 尿毒素は慢性腎不全におけるヘプシジン発現に関与する, 第89回日本薬理学会年会(神奈川), Mar. 2016.
205.	Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshitaka Kihira, Licht Miyamoto, Yoshito Zamami, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : Development of endothelial dysfunction-induced aortic dissection model and search for a preventive strategy, 第89回日本薬理学会年会(神奈川), Mar. 2016.
206.	Masaki Imanishi, Keisuke Ishizawa, 小原佑介, 櫻田巧, 戸谷紘基, 長尾朋子, 壱岐豊, 細岡真由子, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニフェジピン光分解産物による血管リモデリング抑制効果, 第252回徳島医学会学術集会(平成27年度冬期), Feb. 2016.
207.	Keisuke Oshima, Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄のエリスロポエチン発現への影響の検討, 第45回日本心脈管作動物質学会, Feb. 2016.
208.	Masaki Imanishi, Keisuke Ishizawa, 小原佑介, 櫻田巧, 戸谷紘基, 長尾朋子, 壱岐豊, 細岡真由子, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンによる抗大動脈瘤機序の検討, 第45回日本心脈管作動物質学会, Feb. 2016.
209.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 鍵本優有, 斎藤尚子, 高田真衣, Yoshitaka Kihira, Masaki Imanishi, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 高リン刺激は血管平滑筋細胞においてrho-kinase-cyclophilin A経路を活性化させる, 第45回日本心脈管作動物質学会, Feb. 2016.
210.	Yasumasa Ikeda and Toshiaki Tamaki : 臓器障害における生体内鉄代謝の意義と鉄除去による病態改善効果, 心血管代謝週間(CVMW)(第19回日本心血管内分泌代謝学会学術総会) シンポジウム, Dec. 2015.
211.	Yasumasa Ikeda, 濱野裕章, 渡邉大晃, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎臓病におけるヘプシジン制御メカニズムの検討, 第25回日本循環薬理学会, Dec. 2015.
212.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 高田真衣, 田渕正樹, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンは悪性脳卒中易発性高血圧自然発症ラットの生命予後を改善する, 第25回日本循環薬理学会, Dec. 2015.
213.	斎藤尚子, Yuki Izawa-Ishizawa, Keisuke Ishizawa, 戸谷紘基, Masaki Imanishi, 鍵本優有, 細岡真由子, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 大動脈解離発症における内皮障害の関与, 第25回日本循環薬理学会, Dec. 2015.
214.	Hirofumi Hamano, Yasumasa Ikeda, Yuya Horinouchi, Akiho Satoh, Hiroaki Watanabe, Keisuke Oshima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全における尿毒素によるヘプシジン制御機構, 第128回日本薬理学会近畿部会, Nov. 2015.
215.	今尾瑞季, Yasumasa Ikeda, 佐藤明穂, 濱野裕章, Yuya Horinouchi, Licht Miyamoto, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : 鉄蓄積によって引き起こされる骨格筋萎縮のメカニズム, 第54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, Nov. 2015.
216.	高田真衣, Keisuke Ishizawa, 田渕正樹, Yuki Izawa-Ishizawa, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 悪性脳卒中易発性高血圧自然発症ラットの神経症状に対するニトロソニフェジピンの効果, 第54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, Nov. 2015.
217.	戸谷紘基, Keisuke Ishizawa, Yuki Izawa-Ishizawa, 細岡真由子, 鍵本優有, 斎藤尚子, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 大動脈解離発症における内皮障害の関与の検討, 第54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, Nov. 2015.
218.	Yasumasa Ikeda, 佐藤明穂, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄欠乏は骨格筋量減少の原因となる, 第39回日本鉄バイオサイエンス学会学術集会, Aug. 2015.
219.	Ariunzaya Burentogtokh, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : YC1 increased adiponectin expression in 3T3-L1 adipocytes, 次世代を担う創薬・医療薬理シンポジウム2015, Aug. 2015.
220.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 大越瑞穂, 土肥紗希子, Yoshitaka Kihira, Yasumasa Ikeda and Toshiaki Tamaki : 血管石灰化シグナルにおけるRhoキナーゼおよびサイクロフィリンAの関与, 第47回日本動脈硬化学会総会・学術集会, Jul. 2015.
221.	Sumiko Yoshida, Yasumasa Ikeda, Ken-ichi Aihara and Toshio Matsumoto : 心血管病におけるアンドロゲン-AR系の役割, 第33回内分泌代謝学サマーセミナー, Jul. 2015.
222.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Masashi Akaike, Toshiaki Tamaki and Toshio Matsumoto : 心血管疾患における男性ホルモンの意義, 第15回日本抗加齢医学会総会シンポジウム「知って得するテストステロンアップデート」, May 2015.
223.	Yasumasa Ikeda, Kanai Yusuke, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Bilirubin Promotes Ischemic-Induced Revascularization through Akt-eNOS Pathway, 第79回日本循環器学会学術集会, Apr. 2015.
224.	Yoshitaka Kihira, 岸渕麗奈, Kunihisa Yamaguchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 腎虚血再灌流障害において低酸素誘導因子が制御する因子の探索, 日本薬学会第135年会(神戸), Mar. 2015.
225.	Mai Takata, Keisuke Ishizawa, 田渕正樹, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 悪性脳卒中易発性高血圧自然発症ラットに対するニトロソニフェジピンの効果, 日本薬学会第135年会(神戸), Mar. 2015.
226.	Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : ビリルビンは虚血後血管新生を促進する, 第88回日本薬理学会年会(愛知), Mar. 2015.
227.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 田渕正樹, Mai Takata, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンは悪性脳卒中易発性高血圧自然発症ラットの生存期間を延長させる, 第88回日本薬理学会年会(愛知), Mar. 2015.
228.	Hiroki Toya, Keisuke Ishizawa, Yuki Izawa-Ishizawa, Yusuke Kohara, Tomoko Nagao, 今西正樹, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 大動脈解離発症における血管内皮機能障害の関与, 第88回日本薬理学会年会(愛知), Mar. 2015.
229.	岸渕麗奈, Yoshitaka Kihira, Kunihisa Yamaguchi, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia-inducible factor-1 participates in induction of apoptosis in renal reperfusion injury, 第88回日本薬理学会年会(愛知), Mar. 2015.
230.	Mizuho Ogoshi, Yuki Izawa-Ishizawa, Sakiko Doi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 血管平滑筋細胞において無機リンによる石灰化シグナルにはRho-kinaseおよびcyclophilin Aが関与する, 第88回日本薬理学会年会(愛知), Mar. 2015.
231.	Burentogtokh Ariunzaya, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia decreases glucagon-like peptide-1 secretion from glutag cell lines, 第88回日本薬理学会年会(愛知), Mar. 2015.
232.	Yasumasa Ikeda, 金井佑亮, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : ビリルビンの血管新生促進作用の検討, 第44回日本心脈管作動物質学会, Feb. 2015.
233.	Yasumasa Ikeda, 金井佑亮, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : ビリルビンは血管内皮細胞を活性化させて，虚血後血管新生を促進する, 第24回循環薬理学会, Dec. 2014.
234.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 長尾朋子, 戸谷紘基, 小原佑介, 細岡真由子, 高田真衣, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 新規薬剤誘発性大動脈解離モデルを用いたスタチンの効果の検討, 第24回循環薬理学会, Dec. 2014.
235.	岸渕麗奈, Yoshitaka Kihira, Kunihisa Yamaguchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 低酸素誘導因子の機能不全は腎虚血再灌流障害からの回復を阻害する, 第36回生体膜と薬物の相互作用シンポジウム, Nov. 2014.
236.	Yoshitaka Kihira, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : 高脂肪食誘発肥満に対する脂肪特異的低酸素誘導因子欠損の影響, 第36回生体膜と薬物の相互作用シンポジウム, Nov. 2014.
237.	長尾朋子, Keisuke Ishizawa, 戸谷紘基, 小原佑介, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : HMG-CoA 還元酵素阻害薬の大動脈解離に対する効果, 第53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, Nov. 2014.
238.	長尾朋子, Keisuke Ishizawa, 戸谷紘基, 小原佑介, 今西正樹, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : HMG-CoA 還元酵素阻害薬の大動脈解離に対する効果, 第53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, Nov. 2014.
239.	小原佑介, Keisuke Ishizawa, 櫻田巧, 戸谷紘基, 長尾朋子, 壱岐豊, 細岡真由子, 今西正樹, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 大動脈瘤形成に対する新規抗酸化薬の効果, 第53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, Nov. 2014.
240.	岸渕麗奈, Yoshitaka Kihira, Kunihisa Yamaguchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 低酸素誘導因子の腎虚血再灌流障害に対する役割, 第126回日本薬理学会近畿部会, Oct. 2014.
241.	長尾朋子, Keisuke Ishizawa, 戸谷紘基, 小原佑介, 今西正樹, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 大動脈解離に対するピタバスタチンの効果, 第126回日本薬理学会近畿部会, Oct. 2014.
242.	Yasumasa Ikeda, 今尾瑞季, 佐藤明穂, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄による骨格筋萎縮メカニズムの検討, 日本鉄バイオサイエンス学会第38回学術集会, Sep. 2014.
243.	小原佑介, Keisuke Ishizawa, 櫻田巧, 戸谷紘基, 長尾朋子, 壱岐豊, 細岡真由子, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンは大動脈瘤の形成を抑制する, 次世代を担う創薬・医療薬理シンポジウム 2014, Aug. 2014.
244.	戸谷紘基, Keisuke Ishizawa, 小原佑介, 長尾朋子, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 血管内皮障害を介する新規大動脈解離モデルの作製, 次世代を担う創薬・医療薬理シンポジウム 2014, Aug. 2014.
245.	矢野友章, Licht Miyamoto, 竹之熊和也, 福田恵介, 津田勝範, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 食事による血中NOレベル変動の検討, 第249回徳島医学会, Jul. 2014.
246.	Ken-ichi Aihara, Sumiko Yoshida, Yasumasa Ikeda, 上元良子, 石川カズ江, Masashi Akaike and Toshio Matsumoto : 動脈硬化および虚血に対するeNOS非依存的なピタバスタチンの臓器保護効果の検討, 第46回日本動脈硬化学会総会・学術集会, Jul. 2014.
247.	小原佑介, Keisuke Ishizawa, 櫻田巧, 戸谷紘基, 長尾朋子, 壱岐豊, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 薬剤誘導性大動脈瘤モデルに対するニトロソニフェジピンの効果, 第125回日本薬理学会近畿部会, Jun. 2014.
248.	Yasumasa Ikeda, 田島壮一郎, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : アンジオテンシンIIは鉄吸収制御と生体内鉄分布変化に関与する, 第125回日本薬理学会近畿部会, Jun. 2014.
249.	今西正樹, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Noriko Yamano, Koichiro Tsuchiya and Toshiaki Tamaki : 血管リモデリングにおける低酸素誘導因子HIF-1αの役割, 日本薬学会第134年会, Mar. 2014.
250.	Yoshitaka Kihira, Ariunzaya BURENTOGTOKH, Mari Itoh, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 腸管L細胞のグルカゴン様ペプチド-1分泌に対する低酸素の影響, 日本薬学会第134年会, Mar. 2014.
251.	Keisuke Ishizawa, Yuki Izawa-Ishizawa, Noriko Yamano, 布あさ美, 今西正樹, 櫻田巧, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine ameliorates the progression of renal disease associated with endothelial dysfunction independently of eNOS, 第87回日本薬理学会年会, Mar. 2014.
252.	Mizuki Imao, Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The mechanism of sj=keletal muscle atroph induced by iron, 第87回日本薬理学会年会, Mar. 2014.
253.	Yasumasa Ikeda : The effects of iron reduction on obesity, diabetes and diabetic complications, 第87回日本薬理学会年会, Mar. 2014.
254.	Yasumasa Ikeda, 田島壮一郎, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : アンジオテンシンIIは十二指腸鉄輸送体発現とマクロファージ鉄量を増加させる, 第43回日本心脈管作動物質学会, Feb. 2014.
255.	Masaki Imanishi, Shuhei Tomita, Hirotsugu Kurobe, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 薬剤誘導性大動脈瘤モデルにおける平滑筋由来hypoxia-inducible factor-1αの役割, 第23回日本循環薬理学会, Dec. 2013.
256.	Atsushi Morimoto, Shuhei Tomita, Yoshitaka Kihira, Yasumasa Ikeda, Ichiro Hashimoto, 高久暢, Hideki Nakanishi and Toshiaki Tamaki : 血管内皮細胞特異的HIF-2α強制発現マウスを用いた虚血皮弁モデルの作製と検討, 第22回日本形成外科学会基礎学術集会, Nov. 2013.
257.	Yoshitaka Kihira, Shuhei Tomita, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 肥満に伴う脂肪組織炎症に対する低酸素誘導因子の役割, 第124回日本薬理学会近畿部会, Nov. 2013.
258.	布あさ美, Keisuke Ishizawa, Noriko Yamano, Yuki Izawa-Ishizawa, 櫻田巧, Masaki Imanishi, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : ニトロソニフェジピンは血管内皮機能を改善することで糖尿病性腎症の進展を抑制する, 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, Oct. 2013.
259.	Yuta Suzuki, Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 平滑筋由来HIF-1 αがアンジオテンシンII 誘発血管リモデリングに関与するメカニズム, 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, Oct. 2013.
260.	Masaki Murakami, Yusaku Maeda, Shuhei Tomita, Masaki Imanishi, Yoshitaka Kihira, Keisuke Ishizawa, Noriko Yamano, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 血管傷害モデルに伴う血管リモデリングにおける骨髄由来細胞のHIF1 αの役割, 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, Oct. 2013.
261.	Mariko Miyake, Yoshitaka Kihira, Shuhei Tomita, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 脂肪細胞の低酸素誘導因子欠損による耐糖能改善メカニズムの解析, 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, Oct. 2013.
262.	Yasumasa Ikeda, 田島壮一郎, Mizuki Imao, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : フェリチンの炎症惹起作用, 第37回日本鉄バイオサイエンス学会, Sep. 2013.
263.	Masaki Murakami, Shuhei Tomita, Yusaku Maeda, Masaki Imanishi, Noriko Yamano, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 血管傷害モデルに伴う血管リモデリング形成過程には，傷害部位に動員される骨髄由来細胞のHIFが関与する, 次世代を担う創薬・医療薬理シンポジウム2013, Aug. 2013.
264.	Noriko Yamano, Keisuke Ishizawa, 小堀浩幸, Maki Urushihara, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 糖尿病性腎症における腎内局所アンジオテンシノーゲンに対するニトロソニフェジピンの効果, 第123回日本薬理学会近畿部会, Jul. 2013.
265.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : 血管平滑筋細胞のhypoxia-inducible factor-1αがangiotensinⅡ誘発血管リモデリング形成に関与するメカニズムの解析, 第34回日本炎症・再生医学会, Jul. 2013.
266.	Keisuke Ishizawa, Noriko Yamano, Yuki Izawa-Ishizawa, 櫻田巧, Masaki Imanishi, Asami Nuno, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンは血管内皮保護作用を示して糖尿病性腎症進展を抑制する, 第56回日本腎臓学会学術総会, May 2013.
267.	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.
268.	Masaki Imanishi, Keisuke Ishizawa, Takumi Sakurada, Yuki Izawa-Ishizawa, Noriko Yamano, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 酸化ストレスに起因する心腎血管障害の克服を目指す新規治療薬開発, 日本薬学会第133年会, Mar. 2013.
269.	Koichiro Tsuchiya, Yasumasa Ikeda, 田島壮一郎, Yoshitaka Kihira, Keisuke Ishizawa, Yuki Izawa-Ishizawa, Licht Miyamoto, Noriko Yamano and Toshiaki Tamaki : 糖尿病に対する鉄の関与とキレート療法, 日本薬学会第133年会, Mar. 2013.
270.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia-inducible factor-1a; in vascular smooth muscle cells contributes to AT1 receptor expression in angiotensin II-induced vascular remodeling in mice, 第86回日本薬理学会年会, Mar. 2013.
271.	Mari Itoh, Yoshitaka Kihira, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : Secretion of glucagon-like peptide-1 from Intestinal L cell in hypoxia, 第86回日本薬理学会年会, Mar. 2013.
272.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, Takumi Sakurada, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Kazuyoshi Kawazoe, Kazuo Minakuchi and Toshiaki Tamaki : The influence of angiotensin II on duodenal iron absorption, 第86回日本薬理学会年会, Mar. 2013.
273.	Yasumasa Ikeda, 田島壮一郎, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Bovine lactoferrin stimulated angiogenesis in response to ischemic hindlimb, 第86回日本薬理学会年会, Mar. 2013.
274.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Sakiko Doi, Masaki Imanishi, Takumi Sakurada, Noriko Yamano, Yusuke Kohara, Tomoko Nagao, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Y-27632, a rho-kinase inhibitor, inhibits inorganic phosphate-induced ERK1/2 phosphorylation and ALP activity in vascular smooth muscle cells, 第86回日本薬理学会年会, Mar. 2013.
275.	Iori Ohzono, Yasumasa Ikeda, Souichirou Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The Effects of Iron chelatoion against Renal Fibrosis in Unilateral Ureteral Obstruction Mice Model, 第86回日本薬理学会年会, Mar. 2013.
276.	Yoji Hoshina, Yoshitaka Kihira, Shuhei Tomita, Mariko Miyake, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Adipocyte-specific hypoxia-inducible factor-1alpha knockout stimulated GLP-1 and insulin secretions in mice, 第86回日本薬理学会年会, Mar. 2013.
277.	Noriko Yamano, Keisuke Ishizawa, Shoko Fujii, Asami Nuno, Masaki Imanishi, Takumi Sakurada, Yuta Suzuki, Furi Endo, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Effects of nitrosonifedipine on the diabetic nephropathy with the endothelial dysfunction, 第86回日本薬理学会年会, Mar. 2013.
278.	Yasumasa Ikeda, Hideaki Enomoto, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Low Iron Diet Limits Development of Diabetic Nephropathy In db/db Mice, 第77回日本循環器学会学術集会, Mar. 2013.
279.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Noriko Yamano, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Asami Nuno, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンは血管内皮細胞障害を伴う糖尿病性腎症の進展を抑制する, 第42回日本心脈管作動物質学会, Feb. 2013.
280.	田島壮一郎, Yasumasa Ikeda, Hideaki Enomoto, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : 鉄制限食によってdb/dbマウスの糖尿病性腎症進展は抑制される, 第42回日本心脈管作動物質学会, Feb. 2013.
281.	Sakiko Doi, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Yusuke Kohara, Tomoko Nagao, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 無機リン刺激による血管平滑筋細胞石灰化におけるRho-kinaseの関与, 第42回日本心脈管作動物質学会, Feb. 2013.
282.	Yoshitaka Kihira, Shuhei Tomita, Mariko Miyake, Yoji Hoshina, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 脂肪細胞特異的低酸素誘導因子欠損マウスに観察される耐糖能の改善にはglucagon-like peptide-1が関与する, 第42回日本心脈管作動物質学会, Feb. 2013.
283.	Keisuke Ishizawa, Masaki Imanishi, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Angiotensin II慢性投与はhypoxia-inducible factor-1αを介して血管リモデリングを惹起する, 第33回日本臨床薬理学会学術総会, Dec. 2012.
284.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 血管平滑筋細胞のhypoxia-inducible factor-1αがangiotensinⅡ誘発血管リモデリング形成に寄与するメカニズムの解析, 第22回日本循環薬理学会, Nov. 2012.
285.	Yasumasa Ikeda, 田島壮一郎, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄吸収機構におけるAngiotensinⅡの効果の検討, 第122回日本薬理学会近畿部会, Nov. 2012.
286.	Shoko Fujii, Keisuke Ishizawa, Takumi Sakurada, Noriko Yamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : Nifedipine 光分解産物であるnitrosonifedipine は糖尿病性腎症進展を抑制する, 第51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, Nov. 2012.
287.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : 血管平滑筋細胞におけるHIF-1αのangiotensinⅡ誘発血管リモデリング形成およびAT1受容体発現への関与;平滑筋特異的HIF-1α遺伝子欠損マウスを用いた検討 The Role of HIF-1α in angiotensin Ⅱ-induced Vascular Remodeling and AT1 Receptor Expression in Vascular Smooth Muscle Cells, 第35回日本高血圧学会総会, Sep. 2012.
288.	Asami Nuno, Keisuke Ishizawa, Shoko Fujii, 櫻田巧, Noriko Yamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 糖尿病性腎症進展に対するニトロソニフェジピンの抑制作用, 次世代を担う創薬・医療薬理シンポジウム2012, Sep. 2012.
289.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : AngiotensinⅡ誘発血管リモデリングにおける血管平滑筋細胞内HIFシグナルの解析, 次世代を担う創薬・医療薬理シンポジウム2012, Sep. 2012.
290.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, 櫻田巧, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 十二指腸からの鉄吸収に対するAngiotensinⅡの影響, 第36回日本鉄バイオサイエンス学会学術集会, Sep. 2012.
291.	Yusaku Maeda, Shuhei Tomita, Masaki Murakami, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 血管傷害モデルに伴う血管リモデリング形成過程には，傷害部位に動員される骨髄由来細胞のHIFが関与する, 第121回日本薬理学会近畿部会, Jun. 2012.
292.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 平滑筋特異的hypoxia-inducible factor-1α欠損がangiotensin II誘発血管リモデリング形成に及ぼす影響, 第121回日本薬理学会近畿部会, Jun. 2012.
293.	Yasumasa Ikeda, 田島壮一郎, Koichiro Tsuchiya and Toshiaki Tamaki : 肥満進展における鉄と酸化ストレス, 第65回日本酸化ストレス学会学術集会シンポジウム「金属と酸化ストレスの関係を探る:基礎から臨床研究へ」, Jun. 2012.
294.	Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Yuki Izawa-Ishizawa, Licht Miyamoto, Noriko Yamano, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine はangiotensin II 誘発のマウス血管リモデリングを改善する, 第65回日本酸化ストレス学会学術集会, Jun. 2012.
295.	Shoko Fujii, Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 糖尿病モデルマウスにおいてニトロソニフェジピンは腎症の進展を抑制する, 第55回日本腎臓学会学術総会, Jun. 2012.
296.	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
297.	Mariko Miyake, Yoshitaka Kihira, Manami Hirata, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : 脂肪細胞における低酸素誘導因子1a欠損は高脂肪食負荷による耐糖能異常の発現を抑制する, 日本薬学会第132年会, Mar. 2012.
298.	Asami Nuno, Keisuke Ishizawa, 藤井聖子, Yuki Izawa-Ishizawa, Masaki Imanishi, Takumi Sakurada, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 2型糖尿病性腎症に対するニトロソニフェジピンの効果, 日本薬学会第132年会, Mar. 2012.
299.	Yasumasa Ikeda, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Bovine Lactoferin Promotes Angiogenesis Via Akt-eNOS Dependent Pathway in Vascular Endothelial Cells, 第76回日本循環器学会学術集会, Mar. 2012.
300.	Hideaki Enomoto, Yasumasa Ikeda, 田島壮一郎, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Protective effect of dietary iron restriction on diabetic nephropathy, 第85回日本薬理学会年会, Mar. 2012.
301.	Noriko Yamano, Yasumasa Ikeda, Minoru Sakama, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Accumulated iron storage in high fat diet-induced obese and diabetic mice, 第85回日本薬理学会年会, Mar. 2012.
302.	Shoko Fujii, Keisuke Ishizawa, Takumi Sakurada, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine prevents the progression of diabetic nephropathy in type 2 diabetic mice, 第85回日本薬理学会年会, Mar. 2012.
303.	Shuhei Tomita, Mitsuru Takaku, Noriko Yamano, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Preoperative stabilization of HIF-1 by systemic introduction of dimethyloxalylglycine (DMOG), improves skin flap survival, 第85回日本薬理学会年会, Mar. 2012.
304.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : The inhibitory effects of smooth muscle cell-specific hypoxia-inducible factor-1a deficiency on angiotensin 2-induced vascular remodeling in mice, 第85回日本薬理学会年会, Mar. 2012.
305.	Manami Hirata, Yoshitaka Kihira, Mariko Miyake, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : High fat diet-induced inflammation in adipose tissues is reduced in adipocyte-specific hypoxia-inducible factor-1a knockout mice, 第85回日本薬理学会年会, Mar. 2012.
306.	Keisuke Ishizawa, Shoko Fujii, Asami Nuno, Yuki Izawa-Ishizawa, Masaki Imanishi, Takumi Sakurada, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipineは2型糖尿病モデルマウスにおける腎症進展を抑制する, 第41回心脈管作動物質学会, Feb. 2012.
307.	Yoshitaka Kihira, Mariko Miyake, Manami Hirata, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : 肥満に伴う耐糖能異常の発現に対する脂肪細胞の低酸素誘導因子の役割, 第41回心脈管作動物質学会, Feb. 2012.
308.	Noriko Yamano, Yasumasa Ikeda, Minoru Sakama, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : The alternation of iron metabolism in high fat diet-induced obese and diabetic mice, 第34回日本分子生物学会年会, Dec. 2011.
309.	Yasumasa Ikeda, Hideaki Enomoto, 田島壮一郎, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 糖尿病腎症進展における鉄除去の効果, 腎と高血圧update, Dec. 2011.
310.	Mitsuru Takaku, Shuhei Tomita, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Hideki Nakanishi and Toshiaki Tamaki : PHD阻害剤の虚血皮弁生存拡大に対する効果, 第21回日本循環薬理学会, Dec. 2011.
311.	Jumpei Taniguchi, Keisuke Ishizawa, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Kazuo Minakuchi, Toshiaki Tamaki and Shuhei Tomita : 血管平滑筋細胞のhypoxia-inducible factor-1αはangiotensinⅡ誘発血管リモデリングの形成に関与する, 第50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, Nov. 2011.
312.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : AngiotensinⅡ誘発性血管リモデリングは平滑筋特異的HIF-1α遺伝子欠損により抑制される, 第34回日本高血圧学会総会, Oct. 2011.
313.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : AngiotensinⅡ誘発性血管リモデリングは平滑筋特異的HIF-1α遺伝子欠損により抑制される, 第34回日本高血圧学会総会, Oct. 2011.
314.	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.
315.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Takumi Sakurada, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 肥満の脂肪組織における鉄の役割, 第35回日本鉄バイオサイエンス学会学術集会, Sep. 2011.
316.	Sumiko Yoshida, Ken-ichi Aihara, Yasumasa Ikeda and Toshio Matsumoto : 心血管臓器におけるアンドロゲン作用の意義, 第11回日本内分泌学会四国支部学術集会高知, Sep. 2011.
317.	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.
318.	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.
319.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible factor-1a in vascular smooth muscle cells contributes to the development of angiotensin -induced vascular remodeling, 第43回日本動脈硬化学会総会・学術集会, Jul. 2011.
320.	Jumpei Taniguchi, Keisuke Ishizawa, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, 久次米敏秀, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Kazuo Minakuchi, Toshiaki Tamaki and Shuhei Tomita : 動脈硬化におけるhypoxia-inducible factor-1αの新規治療標的分子としての可能性, 医療薬学フォーラム2011/第19回クリニカルファーマシーシンポジウム, Jul. 2011.
321.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : AngiotensisⅡ誘発血管リモデリングは血管平滑筋細胞のhypoxia-inducible factor-1αを介して形成される, 第119回日本薬理学会近畿部会, Jul. 2011.
322.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : ヒト腎糸球体血管内皮細胞において細胞内遊離鉄はangiotensin ⅡによるICAM-1の発現を増強する, 第54回日本腎臓学会学術集会, Jun. 2011.
323.	Yasumasa Ikeda, 田島壮一郎, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄除去薬による糖尿病の病態改善効果の検討, 第84回日本内分泌学会学術集会, Apr. 2011.
324.	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.
325.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, 佐藤隆史, Masashi Akaike, Toshiaki Tamaki, 加藤茂明 and Toshio Matsumoto : 心血管リモデリングにおける男性ホルモンの作用, 第84回日本内分泌学会学術集会シンポジウム「心血管病を内分泌・代謝面から考察する」, Apr. 2011.
326.	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.
327.	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.
328.	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.
329.	Yasumasa Ikeda, Soichiro Tajima, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Iron elimination ameliorated glucose tolerance through suppression of oxidative stress and inflammation on fat in diabetic mice, 第75回日本循環器学会総会・学術集会, Mar. 2011.
330.	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.
331.	Noriko Yamano, Yasumasa Ikeda, Minoru Sakama, Soichiro Tajima, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : The alternation of iron transport-related genes in high fat diet-induced obese and diabetic mice, 第84回日本薬理学会年会, Mar. 2011.
332.	Yoshitaka Kihira, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : bFGF and insulin differentially regulate hypoxia-inducible factor-1 alpha in adipocytes, 第84回日本薬理学会年会, Mar. 2011.
333.	Yayoi Fukuhara, Shuhei Tomita, Masahisa Urata, Yoshitaka Kihira, Mitsuru Takaku, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Role of HIF-1b in endothelial cells in monocrotaline-induced pulmonary hypertension, 第84回日本薬理学会年会, Mar. 2011.
334.	Yasumasa Ikeda, Soichiro Tajima, Sumiko Yoshida, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Ken-ichi Aihara, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Deferoxamine, an iron chelator, promotes revascularization via endothelial cells activation, 第84回日本薬理学会年会, Mar. 2011.
335.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Erika Tominaga, Junpei Taniguchi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine, a photodegrative metabolite of nifedipine, improves angiotensin -induced vascular remodeling, 第84回日本薬理学会年会, Mar. 2011.
336.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Angiotensin -induced vascular remodeling is surpressed in smooth muscle cell-specific hypoxia-inducible factor-1a deficient mice, 第84回日本薬理学会年会, Mar. 2011.
337.	Masaki Imanishi, Keisuke Ishizawa, Takumi Sakurada, 富永えりか, Yuya Horinouchi, Jumpei Taniguchi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipineによる血管リモデリング抑制効果の検討, 日本薬学会第131回年会, Mar. 2011.
338.	Yuya Horinouchi, Koichiro Tsuchiya, 田島壮一郎, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita, Kazuyoshi Kawazoe, Toshiaki Tamaki and Kazuo Minakuchi : Nitrosonifedipine の細胞保護効果に関する検討, 日本薬学会第131年会, Mar. 2011.
339.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : AngiotensinⅡ誘発血管リモデリングにおけるhypoxia-inducible factor-1αの役割, 第40回日本心脈管作動物質学会, Feb. 2011.
340.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 鉄除去は脂肪肥大を抑制して糖尿病を改善する, 第40回日本心脈管作動物質学会, Feb. 2011.
341.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Yuya Horinouchi, 富永えりか, Jumpei Taniguchi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : AngiotensinⅡ誘発血管リモデリングに対するニトロソニフェジピンの抑制作用, 第40回日本心脈管作動物質学会, Feb. 2011.
342.	Yasumasa Ikeda, 田島壮一郎, Sumiko Yoshida, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Ken-ichi Aihara, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : マウス下肢虚血モデルにおいて鉄キレート剤Deferoxamineは酸化ストレスとアポトーシスを抑制する, 第40回日本心脈管作動物質学会, Feb. 2011.
343.	Noriko Yamano, Yasumasa Ikeda, 田島壮一郎, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 高脂肪食負荷肥満マウスにおける鉄吸収動態の検討, 第40回日本心脈管作動物質学会, Feb. 2011.
344.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 鉄除去は脂肪肥大を抑制して糖尿病を改善する, 第40回日本心脈管作動物質学会, Feb. 2011.
345.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Yuya Horinouchi, 富永えりか, Jumpei Taniguchi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : AngiotensinⅡ誘発血管リモデリングに対するニトロソニフェジピンの抑制作用, 第40回日本心脈管作動物質学会, Feb. 2011.
346.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : AngiotensinⅡ誘発血管リモデリングにおけるhypoxia-inducible factor-1αの役割, 第40回日本心脈管作動物質学会, Feb. 2011.
347.	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.
348.	Yasumasa Ikeda, 田島壮一郎, Sumiko Yoshida, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Ken-ichi Aihara, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Deferoxamine, an iron chelator, enhances angiogenesis through Akt-eNOS-dependent pathway in endothelial cells, 第18回日本血管生物医学会学術集会, Dec. 2010.
349.	Yuuko Imamura, Yoshitaka Kihira, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : HIF-2/ARNT control hair differentiation by up-regulating p21Waf1/Cip1, 第33回日本分子生物学会年会, Dec. 2010.
350.	Yoshitaka Kihira, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : 脂肪細胞における塩基性繊維芽細胞増殖因子による低酸素誘導因子誘導とそれを介した糖輸送担体発現誘導, 第118回日本薬理学会近畿部会, Nov. 2010. (Keyword) 第118回日本薬理学会近畿部会
351.	田島壮一郎, Yasumasa Ikeda, Yuya Horinouchi, Yoshitaka Kihira, Shuhei Tomita, Noriko Yamano, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄キレート剤 deferoxamine は内皮細胞活性化により血管新生を促進する, 第20回日本循環薬理学会, Nov. 2010.
352.	Koichiro Tsuchiya, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita and Toshiaki Tamaki : 亜硝酸塩由来血中NO動態に与える経口鉄の影響, 第22回腎とフリーラジカル研究会, Oct. 2010.
353.	Masaki Imanishi, Keisuke Ishizawa, 富永えりか, 櫻田巧, Yuya Horinouchi, 谷口順平, 藤井聖子, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II による血管平滑筋細胞の遊走および増殖に対するnifedipine代謝物の抑制作用とそのメカニズム, 第33回日本高血圧学会, Oct. 2010.
354.	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
355.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 2型糖尿病モデルマウスに対する鉄キレート剤による糖尿病改善効果の検討, 第34回日本鉄バイオサイエンス学会学術集会, Sep. 2010.
356.	藤井聖子, Keisuke Ishizawa, Masaki Imanishi, 富永えりか, 桜田巧, 谷口順平, Yuya Horinouchi, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Toshiaki Tamaki and Koichiro Tsuchiya : AngiotensinⅡ誘発血管リモデリングに対するnitrosonifedipineの抑制効果, 次世代を担う創薬・医療薬理シンポジウム2010, Sep. 2010.
357.	Shuhei Tomita, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 動脈硬化に伴う血管リモデリングに対してT細胞のHIF-1 は抑制的に機能する．, 第31回日本炎症再生医学会, Aug. 2010.
358.	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.
359.	Masaki Imanishi, Keisuke Ishizawa, 富永えりか, Yuya Horinouchi, 谷口順平, 藤井聖子, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nifedipine代謝物によるangiotensin II 誘発血管平滑筋細胞遊走及び増殖に対する抑制作用, 第117回日本薬理学会近畿部会, Jul. 2010.
360.	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.
361.	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.
362.	Keisuke Ishizawa, Masaki Imanishi, Erika Tminaga, Yuya Horinouchi, Takumi Sakurada, Zyunpei Taniguchi, Seiko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Toshiaki Tamaki and Koichiro Tsuchiya : Nifedipine代謝物はangiotensinⅡによる血管平滑筋細胞遊走および増殖を抑制する, 第63回日本酸化ストレス学会, Jun. 2010.
363.	Yasumasa Ikeda, Koichiro Tsuchiya, 田島壮一郎, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Yoshihisa Takaishi and Toshiaki Tamaki : The effect of SUDACHI peel, a specialty of Tokushima, as anti-metabolic syndrome, 第83回日本薬理学会年会シンポジウム「肥満の栄養ゲノミクスと薬理ゲノミクス」, Mar. 2010.
364.	Keisuke Ishizawa, Masanori Yoshizumi, Dortsuren Naruantungalag, 今村優子, Yasumasa Ikeda, Junji Terao, Koichiro Tsuchiya and Toshiaki Tamaki : ケルセチンの生体内代謝と動脈硬化予防効果, 第83回日本薬理学会年会シンポジウム「健康食品の薬理学」, Mar. 2010.
365.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, 櫻田巧, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : KK-Ay マウスにおける鉄キレート剤Deferoxamineによる糖尿病病態改善効果の検討, 第83回日本薬理学会, Mar. 2010.
366.	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.
367.	Yayoi Fukuhara, Shuhei Tomita, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Masanori Yoshizumi and Toshiaki Tamaki : T細胞のHIF-1aは，動脈硬化に伴う血管リモデリングを抑制的に制御する, 第39回日本心脈管作動物質学会, Feb. 2010.
368.	Yasumasa Ikeda, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita and Toshiaki Tamaki : 鉄キレート剤 Deferoxamine の血管新生左葉―マウス下肢虚血モデルにおける検討―, 第39回日本心脈管作動物質学会, Feb. 2010.
369.	富永えりか, Keisuke Ishizawa, 櫻田巧, 今西正樹, 谷口順平, Kazuyoshi Kawazoe, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : Angiotensin IIによる血管平滑筋細胞遊走に対するnifedipine代謝物の影響, 第30回日本臨床薬理学会年会, Dec. 2009.
370.	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
371.	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
372.	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.
373.	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.
374.	Shusuke Yagi, Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, 住友由佳, Yasumasa Ikeda, 岩瀬俊, Takeshi Soeki, Masashi Akaike and Toshio Matsumoto : ピタバスタチンはRac-1を介した酸化ストレス制御によりeNOS非依存的にアンジオテンシンIIによる心房リモデリングを抑制する, 第40回日本動脈硬化学会総会, 203, Jul. 2008. (Keyword) Angiotensin II 抗酸化剤(治療的利用) 心房動脈硬化症(薬物療法) 酸化ストレス rac GTP-Binding Proteins 心室リモデリング *Pitavastatin(治療的利用) マウス動物
375.	Masashi Akaike, Shusuke Yagi, Ken-ichi Aihara, Yasumasa Ikeda, 石川カズ江, Takayuki Ise, Sumiko Yoshida, 住友由佳, Takashi Iwase, Abe Jun-ichi and Toshio Matsumoto : HMG-CoA Reductase Inhibitor Pitavastatin Increases the Expression of Endothelial NOS through Activation of ERK5-KLF2 Pathway in Vascular Endothelial Cells, 第72回日本循環器学会学術集会, Mar. 2008.
376.	Shusuke Yagi, Ken-ichi Aihara, Yasumasa Ikeda, Takayuki Ise, 住友由佳, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : Pitavastatinはangiotensin IIによる心腎障害をeNOS非依存性にrac1抑制による酸化ストレス抑制を介して改善する, 第30回日本高血圧学会総会, 205, Oct. 2007. (Keyword) Angiotensin II 心臓疾患(実験的) 腎臓疾患(実験的) 酸化ストレスノックアウトマウス rac GTP-Binding Proteins Pitavastatin(薬理学) マウス動物
377.	Masashi Akaike, Ken-ichi Aihara, Shusuke Yagi, Yasumasa Ikeda, 石川カズ江, 住友由佳, Takashi Iwase and Toshio Matsumoto : グルココルチコイド誘発性高血圧に対するピタバスタチンの効果とその機序の検討, 第30回日本高血圧学会総会プログラム, 210, Oct. 2007. (Keyword) Glucocorticoids 高血圧(薬物療法,実験的) C57BLマウス Pitavastatin(治療的利用,薬理学) マウス動物オス
378.	Ken-ichi Aihara, Yasumasa Ikeda, Shusuke Yagi, Takayuki Ise, 住友由佳, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : 血管リモデリング制御因子としての活性化ビタミンD, 第30回日本高血圧学会総会, 260, Oct. 2007. (Keyword) Vitamin D(治療的利用) 動脈硬化症(薬物療法,診断) *血管リモデリングヒト男女
379.	Ken-ichi Aihara, Yasumasa Ikeda, Shusuke Yagi, 住友由佳, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : 活性化ビタミンDは臨床的動脈硬化抑制因子である, 第39回日本動脈硬化学会総会・学術集会, 250, Jul. 2007. (Keyword) Calcitriol(血液) 断面研究動脈硬化症(予防) ヒト中年(45~64) 高齢者(65~79) 男女
380.	Ken-ichi Aihara, Yasumasa Ikeda, Shusuke Yagi, 住友由佳, Takashi Iwase, Takeshi Kondo, 重清友理, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka, Masashi Akaike and Toshio Matsumoto : 活性化ビタミンDの抗動脈硬化作用に関する臨床的検討, 第80回日本内分泌学会学術総会, Vol.83, No.1, 159, Jun. 2007. (Keyword) Calcitriol(治療的利用,薬理学) 動脈硬化症(薬物療法,診断) Maxacalcitol(血液) ヒト中年(45~64) 高齢者(65~79) 男女
381.	Takashi Iwase, 住友由佳, Shusuke Yagi, Yasumasa Ikeda, Ken-ichi Aihara, Shuji Ozaki, Masashi Akaike, Masahiro Abe, Toshio Matsumoto and Tetsuya Kitagawa : エリスロポイエチンを用いた新たな血管新生療法の試み, 第104回日本内科学会総会・講演会, Vol.96, No.Suppl., 133, Apr. 2007. (Keyword) Erythropoietin(治療的利用) 血液成分除去法動脈閉塞性疾患(治療) *末梢血幹細胞移植ヒト
382.	Ken-ichi Aihara, Masashi Akaike, Yasumasa Ikeda, Shusuke Yagi, 住友由佳, Takashi Iwase, Hiroyuki Azuma and Toshio Matsumoto : 活性化ビタミンDによる血管リモデリング制御作用, 第104回日本内科学会総会・講演会, Vol.96, No.Suppl., 194, Apr. 2007. (Keyword) Vitamin D(治療的利用) 動脈閉塞性疾患(診断,薬物療法) 末梢血管疾患(診断,薬物療法) 血管リモデリングヒト中年(45~64) 高齢者(65~79) 男女
383.	Shusuke Yagi, Ken-ichi Aihara, Yasumasa Ikeda, 住友由佳, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : PitavastatinはAngiotensin IIによる心血管リモデリングと腎障害をeNOS非依存性に抑制する, 第36回日本心脈管作動物質学会, Vol.30, No.1, 24, Feb. 2007. (Keyword) Angiotensin II(毒性・副作用) 腎臓疾患(実験的,化学的誘発) 経口投与酸化ストレス心室リモデリング Pitavastatin(薬理学) 血管リモデリング *Nitric Oxide Synthase Type III マウス動物
384.	Yasumasa Ikeda, Ken-ichi Aihara, Masashi Akaike, 住友由佳, Shusuke Yagi, Takashi Iwase, Hiroyuki Azuma, 加藤茂明 and Toshio Matsumoto : アンドロゲン-アンドロゲン受容体システムによる血管リモデリング制御機構の解析, 第36回日本心脈管作動物質学会, Vol.30, No.1, 35, Feb. 2007. (Keyword) Androgens Angiotensin II Androgen Receptors 酸化ストレス一酸化窒素 *血管リモデリングマウス動物オス
385.	Masashi Akaike, Ken-ichi Aihara, Yasumasa Ikeda, 石川カズ江, Shusuke Yagi, 住友由佳, Takashi Iwase and Toshio Matsumoto : ピタバスタチンは血管内皮機能の改善を介してグルココルチコイド過剰による高血圧を予防する, 第36回日本心脈管作動物質学会, Vol.30, No.1, 39, Feb. 2007. (Keyword) Dexamethasone(毒性・副作用) Glucocorticoids(毒性・副作用) 血管内皮高血圧(予防,化学的誘発,実験的) Pitavastatin(治療的利用,薬理学) マウス動物オス
386.	Ken-ichi Aihara, Yasumasa Ikeda, Shusuke Yagi, 住友由佳, Takashi Iwase, Hiroyuki Azuma, 加藤茂明, Masashi Akaike and Toshio Matsumoto : ApoE欠損マウスにおける血漿ヘパリンコファクターII活性の低下は酸化ストレスを増大させ粥状動脈硬化を促進させる, 第36回日本心脈管作動物質学会, Vol.30, No.1, 41, Feb. 2007. (Keyword) Apolipoproteins E Heparin Cofactor II 動脈硬化症-アテローム性(実験的) 免疫組織化学酸化ストレスノックアウトマウスマウス動物
387.	Ken-ichi Aihara, Mihara Masatomo, Azuma Hiroyuki, Masashi Akaike, Takaya Matsushita, Yasumasa Ikeda, Shusuke Yagi, Takashi Iwase, Hashizume Shunji, Fujimura Mitsunori and Toshio Matsumoto : Thrombin inactivation by synthetic thrombin antagonist argatroban ameliorates insulin resistance in type 2 diabetic db/db mice, The 70th Anniversary Annual Scientific Meetings of the Japanese Circulation Society, Mar. 2006.
388.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Hirotsugu Kurobe, 藤村光則, Shusuke Yagi, 橋詰俊二, Yasumasa Ikeda, Takashi Iwase, Tetsuya Kitagawa and Toshio Matsumoto : ヘパリンコファクターIIは末梢動脈閉塞症に対する独立した防御因子である, 第28回日本血栓止血学会学術集会, Nov. 2005.
389.	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.
390.	Shusuke Yagi, Ken-ichi Aihara, Masashi Akaike, 藤村光則, Yasumasa Ikeda, 橋詰俊二, Hiroyuki Azuma and Toshio Matsumoto : Pitavastatinは,Angiotensin IIによるマウス冠動脈リモデリングを抑制する, 第37回日本動脈硬化学会総会, 232, Jul. 2005. (Keyword) Angiotensin II 心臓血管疾患(診断,外科的療法,実験的) *Pitavastatin(薬理学) 血管リモデリング頸動脈内膜中膜肥厚度マウス動物
391.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Yasumasa Ikeda, 藤村光則, 橋詰俊二, 大水正章, 塚田稔, 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の分子生物学的解析, 第37回日本動脈硬化学会総会, 233, Jul. 2005. (Keyword) *Heparin Cofactor II 遺伝子発現血管疾患(病理学,実験的) 分子生物学血管リモデリングマウス動物
392.	Ken-ichi Aihara, 三原正朋, Yasumasa Ikeda, Shusuke Yagi, 藤村光則, 橋詰俊二, Takaya Matsushita, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : トロンビン作用の阻害は2型糖尿病モデルdb/dbマウスのインスリン抵抗性を改善する, 第78回日本内分泌学会総会学術集会, Vol.81, No.1, 190, Jul. 2005. (Keyword) Thrombin(拮抗物質・阻害物質) *インスリン抵抗性糖尿病-2型(診断,実験的) Argatroban(薬理学) メタボリックシンドローム(病因) マウス動物
393.	Yasumasa Ikeda, Ken-ichi Aihara, Masashi Akaike, Shusuke Yagi, Takashi Iwase, 橋詰俊二, 藤村光則, Hiroyuki Azuma, 加藤茂明 and Toshio Matsumoto : アンドロゲン-アンドロゲン受容体システムはドキソルビシンによる心筋酸化ストレスに対して防御的に作用する, 第78回日本内分泌学会総会学術集会, Vol.81, No.2, 548, Jul. 2005. (Keyword) Androgens(薬理学) Doxorubicin(毒性・副作用) Androgen Receptors(薬理学) 心筋疾患(実験的,化学的誘発) 心臓ミトコンドリア酸化ストレスノックアウトマウスマウス動物オス
394.	Shusuke Yagi, Ken-ichi Aihara, Masashi Akaike, Yasumasa Ikeda, Takashi Iwase, 橋詰俊二, 藤村光則, Hiroyuki Azuma and Toshio Matsumoto : Pitavastatinは,Angiotensin IIによるマウス冠動脈および心筋リモデリングを抑制する, 第78回日本内分泌学会総会学術集会, Vol.81, No.2, 564, Jul. 2005. (Keyword) Angiotensin II 冠血管 C57BLマウス心室リモデリング *Pitavastatin(薬理学) 冠状動脈マウス動物
395.	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.
396.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Hirotsugu Kurobe, 藤村光則, Shusuke Yagi, 橋詰俊二, Yasumasa Ikeda, Tetsuya Kitagawa and Toshio Matsumoto : ヘパリンコファクターIIは末梢動脈閉塞性病変進展に対する新規抑制因子である, 第102回日本内科学会総会・講演会, Vol.94, No.Suppl., 228, Apr. 2005. (Keyword) Heparin Cofactor II 血圧測定動脈閉塞性疾患(診断) 足関節上腕血圧比ヒト中年(45~64) 高齢者(65~79)
397.	Ken-ichi Aihara, Masashi Akaike, Yasumasa Ikeda, Kato Midori, Fujimura Mitsunori, Hashizume Shunji, Shusuke Yagi, Hiroyuki Azuma and Toshio Matsumoto : Angiotensin II Antagonist Valsartan Ameliorates Nitric Oxide Bioavailability and Arterial Stiffness Accompanied with The Reduction of Blood Pressure and Pulse Pressure in Elderly Hypertensives, 第69回日本循環器学会総会・学術集会, Mar. 2005.
398.	Ken-ichi Aihara, Masashi Akaike, Yasumasa Ikeda, Shusuke Yagi and Toshio Matsumoto : Arterial Cuff Injury Causes Enhanced Neointimal Formation and Increased Adventitial Area in Heterozygous Heparin Cofactor II Deficient Mice, 第69回日本循環器学会総会・学術集会, Mar. 2005.
399.	Yasumasa Ikeda, Ken-ichi Aihara, Masashi Akaike, 藤村光則, Shusuke Yagi, 橋詰俊二, Hiroyuki Azuma, 加藤茂明 and Toshio Matsumoto : アンドロゲン-アンドロゲン受容体系は生体の心筋防御機構である, 第42回日本臨床分子医学会学術総会, 78, 2005. (Keyword) Androgens Angiotensin II Androgen Receptors 心筋心室リモデリングマウス動物オス
400.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Yasumasa Ikeda, 藤村光則, 橋詰俊二, Shusuke Yagi, 加藤茂明 and Toshio Matsumoto : ヘパリンコファクターII欠乏マウスにおける血管リモデリング異常の解析, 第27回日本血栓止血学会学術集会, Nov. 2004.
401.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, 藤村光則, 吉田智則, 橋詰俊二, 加藤みどり, Yasumasa Ikeda, 周藤俊樹, 加藤茂明 and Toshio Matsumoto : ビタミンD-ビタミンD受容体システムによる血液凝固調節作用の解析, 第77回日本内分泌学会学術総会, Vol.80, No.1, 138, Jun. 2004. (Keyword) Thromboplastin *Vitamin D(薬理学) 遺伝子発現血液凝固血小板凝集 Calcitriol Receptors マウス動物
402.	Yasumasa Ikeda, Ken-ichi Aihara, Masashi Akaike, 森岡将臣, 加藤みどり, 橋詰俊二, 山口普史, 藤村光則, 吉田智則, Hiroyuki Azuma, 加藤茂明 and Toshio Matsumoto : アンドロゲン-アンドロゲン受容体システムは生体における心筋肥大及び心筋線維化の調節因子である, 第77回日本内分泌学会学術総会, Vol.80, No.1, 96, Jun. 2004. (Keyword) Androgens Androgen Receptors 心筋疾患 *心筋症-肥大性(診断,病理学,実験的) 線維症ノックアウトマウス心筋線維症(診断,病理学,実験的) マウス動物
403.	山口普史, 七條加奈, Takaya Matsushita, Yasumasa Ikeda, 森岡将臣, 加藤みどり, 橋詰俊二, 藤村光則, 吉田智則, Ken-ichi Aihara, Daisuke Inoue, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : 拡張型心筋症様病態を呈したCushing病の一例, Circulation journal : official journal of the Japanese Circulation Society, Vol.68, No.0, 828, Apr. 2004. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1573387451866119936 (CiNii: 1573387451866119936)
404.	Yasumasa Ikeda, 山口普史, 七條加奈, 森岡将臣, 加藤みどり, 橋詰俊二, 吉田智則, 藤村光則, Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma, Toshio Matsumoto, 木村建彦 and 西内健 : Torsade de pointesを合併した汎下垂体機能低下症の一例, Circulation journal : official journal of the Japanese Circulation Society, Vol.68, No.0, 828, Apr. 2004. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1571135652052441728 (CiNii: 1571135652052441728)
405.	橋詰俊二, Yasumasa Ikeda, 加藤みどり, 山口普史, 吉田智則, 藤村光則, Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : 核内受容体PPARαの活性化は巨核球/血小板内PDGF-BBの産生を抑制する, 第36回日本動脈硬化学会総会, 196, 2004. (Keyword) 血小板由来増殖因子巨核球血小板培養腫瘍細胞白血病-急性赤芽球性細胞質受容体と核内受容体ペルオキシソーム増殖因子活性化受容体ヒト in vitro
406.	Ken-ichi Aihara, 高森信行, Yasuhiko Kanagawa, 藤村光則, 加藤みどり, 橋詰俊二, Yasumasa Ikeda, 田村克也, 近藤彰, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : ヘパリンコファクターIIの動脈硬化抑制作用に関する臨床的検討, 第41回日本臨床分子医学会学術総会, 55, 2004. (Keyword) Heparin Cofactor II Serine Proteinase Inhibitors(血液) ステント動脈硬化症血管平滑筋細胞増殖 Cofactor ヒト
407.	山口普史, Yasumasa Ikeda, 橋詰俊二, 加藤みどり, 吉田智則, 藤村光則, Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : 遺伝性出血性末梢血管拡張症9家系における臨床病型と遺伝子変異に関する解析, 第25回日本血栓止血学会学術集会, Vol.14, No.5, 456, Nov. 2003. (Keyword) 遺伝性疾患出血変異 *毛細血管拡張症-遺伝性出血性(診断,遺伝学) 遺伝学的検査骨形成因子受容体I型ヒト
408.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, 高森信行, Yasuhiko Kanagawa, 藤村光則, 吉田智則, 橋詰俊二, 加藤みどり, 山口普史, Yasumasa Ikeda, 加藤修司, 荒瀬友子, 近藤彰 and Toshio Matsumoto : ヘパリンコファクターIIは高齢者における新規動脈硬化抑制因子である, 第25回日本血栓止血学会学術集会, Vol.14, No.5, 439, Nov. 2003. (Keyword) Antithrombins *Heparin Cofactor II(薬理学) HDL Cholesterol 動脈硬化症(診断,予防) 高齢者 Lipoprotein(a) ヒト中年(45~64) 高齢者(65~79) 高齢者(80~) 男女
409.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Yasumasa Ikeda, Fujimura Mitsunori, Sudo Toshiki, Hayashi Hideki, Yamada Yoshihisa, Yoshida Tomonori, Yamaguchi Hiroshi, Hashizume Shunji, Kato Midori and Toshio Matsumoto : Vitamin D/Vitamin D Receptor System Regulates Antithrombogenicity in vivo, 第68回日本循環器学会総会学術集会, Mar. 2003.

Et cetera, Workshop:

1.	Yasumasa Ikeda : 生命金属元素鉄と代謝疾患, 2022年度肥満・糖尿病クラスター・ミニリトリート, Feb. 2023.
2.	Yasumasa Ikeda : 鉄代謝と糖尿病, 徳島大学糖尿病臨床・研究開発センター設立 10 周年記念シンポジウム, Feb. 2020.
3.	Yasumasa Ikeda : The role of iron in obesity and diabetes, Joint Symposium (Hannover Medical School- Institute of Advanced Medical Sciences in Tokushima University), May 2019.
4.	Yasumasa Ikeda : 健康と微量栄養素ー鉄の役割についてー, 市民公開講座「食と薬から健康長寿を考える」, Dec. 2018.
5.	池田裕美子, 斎藤尚子, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda, Keisuke Ishizawa and Toshiaki Tamaki : ケルセチンによる血管保護効果の検討, 西日本医学生学術フォーラム(第5回医学研究学生フォーラム), Dec. 2016.
6.	Yasumasa Ikeda : 慢性腎不全における鉄代謝変化と腎性貧血との関連, 第9回慢性腎臓病(CKD)病態研究会, Sep. 2016.
7.	Yoshito Zamami, Masaki Imanishi, Kenshi Takechi, Yuya Horinouchi, Licht Miyamoto, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Toshiaki Tamaki and Keisuke Ishizawa : ドラッグリポジショニング手法を用いた新規循環器治療薬の探索研究, 第23回大阪市大フォーラム, Aug. 2016.
8.	Ken-ichi Aihara, Sumiko Yoshida, Yasumasa Ikeda, 上元良子 and 石川カズ江 : -, 第6回テストステロン研究会, Sep. 2015.
9.	津田勝範, Licht Miyamoto, 森本悠里, Shuichi Hamano, Keisuke Ishizawa, 木平考高, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 鉄過剰ストレスに対するニトロソニフェジピン(NO-NIF)の抗酸化メカニズム検討, 徳島医学会, Aug. 2015.
10.	Ken-ichi Aihara, Sumiko Yoshida, Yasumasa Ikeda, 上元良子, 石川カズ江 and Toshio Matsumoto : 心血管ストレス制御におけるアンドロゲン受容体機能の性差, 第4回テストステロン研究会, Nov. 2013.
11.	Ken-ichi Aihara, Sumiko Yoshida, Yasumasa Ikeda, Masashi Akaike, 加藤茂明 and Toshio Matsumoto : 虚血耐性における性差非依存性のアンドロゲン受容体作用, 第5回核内受容体・ホルモン研究会, Mar. 2013.
12.	Sumiko Yoshida, Ken-ichi Aihara, Yasumasa Ikeda, Masashi Akaike, 加藤茂明 and Toshio Matsumoto : アンドロゲン受容体は，虚血ストレスに対する骨格筋アポトーシス防御および血管新生に必須である, 第4回核内受容体研究会, Apr. 2012.
13.	Sumiko Yoshida, Ken-ichi Aihara, Yasumasa Ikeda, Masashi Akaike, 加藤茂明 and Toshio Matsumoto : アンドロゲン受容体は，虚血ストレスに対する骨格筋アポトーシス防御および血管新生に必須である, 第3回核内受容体研究会帝人ファーマ株式会社, Mar. 2011.
14.	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.
15.	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.
16.	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.
17.	Ken-ichi Aihara, Sumiko Yoshida, Yasumasa Ikeda, Masashi Akaike, 加藤茂明 and Toshio Matsumoto : 心血管ストレスに対するandrogen-androgen 受容体系の役割, 第2回核内受容体研究会, Mar. 2010.
18.	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.
19.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Yasumasa Ikeda, Shusuke Yagi, 住友由佳, Sumiko Yoshida, Takayuki Ise, Takashi Iwase 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の分子生物学的解析, 第9回四国循環器研究会, Sep. 2007.

Patent:

1.	Toshiaki Tamaki, Yasumasa Ikeda and Koichiro Tsuchiya : マクロファージの浸潤抑制によるインスリン抵抗性改善剤, (2011), 2011-174001 (2011).

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

Investigation of the role of iron stress and identification of therapeutic targets in CKD and renal senescence (Project/Area Number: 24K11388 )
非アルコール性脂肪肝炎における新規病態制御因子の臨床的意義と分子機構の解明 (Project/Area Number: 22K08033 )
The role of macrophage Iron stress in NASH (Project/Area Number: 21K07914 )
The role of autophagy in mesangial cells in the development of chronic kidney disease (Project/Area Number: 19K08705 )
Pathophysiological Role of Heparin Cofactor II in Diabetic Kidney Diseases (Project/Area Number: 19K08680 )
Elucidation of the conversion mechanism from white adipocytes to beige cells by nitrite anion (Project/Area Number: 19K07100 )
The function and therapeutic application of macrophage-specific H-ferritin in chronic inflammation of obese adipose tissue (Project/Area Number: 18K08480 )
Effect of glucagon on antidiabetic effect induced by nitrite (Project/Area Number: 16K08550 )
Clarification of ERK5-mediated endothelial mesenchymal transition suppression mechanism and its application to the prevention of arteriosclerosis (Project/Area Number: 16K08549 )
The role of iron on sarcopenia, and the therapeutic significance of iron regulation for anti-sarcopenia (Project/Area Number: 15K01716 )
Physiological role of dietary nitrite (Project/Area Number: 15H02898 )
Role of androgen receptor in sex dependent and independent manner (Project/Area Number: 25461389 )
Activation mechanisms of AMPK by nitrite (Project/Area Number: 25460332 )
Clarification of the mechanism of iron metabolism in diabetic nephropathy and search of therapeutic factor for anti-diabetic nephropathy (Project/Area Number: 24591203 )
Elucidation of the mechanism of iron action against anti-diabetes and search for a new therapeutic target of diabetes研究代表池田康将(IKEDA YASUMASA) (Project/Area Number: 22790864 )
Search by Researcher Number (60432754)

Professor : Ikeda, Yasumasa

Research

Personal Web Page

Field of Study

Subject of Study

Book / Paper

Book:

Academic Paper (Judged Full Paper):

Academic Letter:

Review, Commentary:

Proceeding of International Conference:

Proceeding of Domestic Conference:

Et cetera, Workshop:

Patent:

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