徳島大学 / 教育研究者総覧 --- 粟飯原賢一

個人のホームページ

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

専門分野

○	医学 (Medicine)

研究テーマ

○	動脈硬化症，心血管内分泌・代謝

著書・論文

著書:

1.	吉田守美子, 原倫世, 山口佑樹, 近藤剛史, 遠藤ふうり, 筒井康継, 桝田志保, 倉橋清衛, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 中島公平, 安倍正博 : 急速に腫瘍が増大し悪性転化が疑われたCushing病の1例, 2019年6月.
2.	粟飯原賢一 : 歯科医師のための医学ハンドブック, 2014年5月. (キーワード) 原発性アルドステロン症・褐色細胞腫 / 脂質異常症・高尿酸血症 / 体重減少・体重増加

学術論文(審査論文):

1.	Taiki Hori, Ken-ichi Aihara, Takeshi Watanabe, Kaori Inaba, Keisuke Inaba, Yousuke Kaneko, Saki Kawata, Keisuke Kawahito, Hiroki Kita, Kazuma Shimizu, Minae Hosoki, Kensuke Mori, Teruyoshi Kageji, Hideyuki Uraoka and Shingen Nakamura : The Respiratory Adjusted Shock Index at Admission Is a Valuable Predictor of In-Hospital Outcomes for Elderly Emergency Patients with Medical Diseases at a Japanese Community General Hospital., Journal of Clinical Medicine, Vol.13, No.16, 2024. (要約) : The RASI is a simple indicator that can be used for predicting in-hospital outcomes in elderly emergency patients with medical diseases. Larger prospective studies based on this study are needed. (徳島大学機関リポジトリ) ● Metadata: 119610 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/jcm13164866 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39201007 ● Search Scopus @ Elsevier (PMID): 39201007 ● Search Scopus @ Elsevier (DOI): 10.3390/jcm13164866 (徳島大学機関リポジトリ: 119610, DOI: 10.3390/jcm13164866, PubMed: 39201007)
2.	Tomoyo Hara, Takeshi Watanabe, Hiroki Yamagami, Kosuke Miyataka, Saya Yasui, Takahito Asai, Yohsuke Kaneko, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Soichi Honda, Akira Kondo, Munehide Matsuhisa and Ken-ichi Aihara : Development of Liver Fibrosis Represented by the Fibrosis-4 Index Is a Specific Risk Factor for Tubular Injury in Individuals with Type 2 Diabetes, Biomedicines, Vol.12, No.8, 1789, 2024. (要約) Although hyperglycemia and hypertension are well-known risk factors for glomerular injury in individuals with type 2 diabetes (T2D), specific risk factors for tubular injury remain unclear. We aimed to clarify the differences between risk factors for glomerular injury and risk factors for tubular injury in individuals with T2D. We categorized 1243 subjects into four groups based on urinary biomarkers, including the albumin-to-creatinine ratio (uACR) and L-type fatty acid-binding protein-to-creatinine ratio (uL-ABPCR) as a normal (N) group (uACR < 30 mg/gCr and uL-FABPCR < 5 μg/gCr; n = 637), a glomerular specific injury (G) group (uACR ≥ 30 mg/gCr and uL-FABPCR < 5 μg/gCr; n = 248), a tubular specific injury (T) group (uACR < 30 mg/gCr and uL-FABPCR ≥ 5 μg/gCr; n = 90), and a dual injury (D) group (uACR ≥ 30 mg/gCr and uL-FABPCR ≥ 5 μg/gCr; n = 268). Logistic regression analysis referencing the N group revealed that BMI, current smoking, and hypertension were risk factors for the G group, creatinine (Cr) and Fibrosis-4 (FIB-4) index were risk factors for the T group, and BMI, hypertension, HbA1c, Cr, and duration of diabetes were risk factors for the D group. While hypertension was a distinct specific risk factor for glomerular injury, the FIB-4 index was a specific contributor to the prevalence of tubular injury. On the other hand, the logistic regression analysis revealed that the hepatic steatosis index (HSI) did not show any significant association with the G group, T group, or D group. Taken together, the development of liver fibrosis rather than liver steatosis is an inherent threat relating to tubular injury in individuals with T2D. (出版サイトへのリンク) ● Publication site (DOI): 10.3390/biomedicines12081789 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39200252 ● Summary page in Scopus @ Elsevier: 2-s2.0-85202596205 (DOI: 10.3390/biomedicines12081789, PubMed: 39200252, Elsevier: Scopus)
3.	Taiki Hori, Taro Shimizu, Hidenori ANDO, Naoto Okada, Hiroki Yamagami, Saya Yasui, Minae Hosoki, Akihiro Tojima, Toshiki Otoda, Tomoyuki Yuasa, Ken-ichi Aihara, Makoto Takishita, Sumiko Yoshida, Masahiro Abe, Tatsuhiro Ishida and Shingen Nakamura : Humoral immune response against SARS-CoV-2 and polyethylene glycol elicited by anti-SARS-CoV-2 mRNA vaccine, and effect of pre-existing anti-polyethylene glycol antibody in patients with hematological and autoimmune diseases., Heliyon, Vol.10, No.10, e31489, 2024. (要約) The effects of vaccination are modified by hematological and autoimmune diseases and/or treatment. Anti-SARS-CoV-2 mRNA vaccine contains polyethylene glycol (PEG), it is largely unknown whether PEG influences the effects of vaccination or induces a humoral response. This study examined whether anti-PEG antibodies before vaccination (pre-existing) influenced the acquisition of SARS-CoV-2 antibodies and evaluated the relationship between the development of anti-SARS-CoV-2 antibodies and anti-PEG antibodies after SARS-CoV-2 vaccination in hematological and autoimmune diseases. Anti-SARS-CoV-2 antibody IgG, anti-PEG IgG, and IgM titers were evaluated in patients with hematological and autoimmune diseases after the second dose of BNT162B2. Anti-PEG IgG and IgM titers were also measured before vaccination to examine changes after vaccination and the relationship with vaccine efficacy. In patients with hematological (n = 182) and autoimmune diseases (n = 96), anti-SARS-CoV-2 and anti-PEG antibody titers were evaluated after a median of 33 days from 2nd vaccination. The median anti-SARS-CoV-2 antibody titers were 1901 AU/mL and 3832 AU/mL in patients with hematological and autoimmune disease, respectively. Multiple regression analysis showed that age and days from 2nd vaccination were negatively associated with anti-SARS-CoV-2 antibody titers. Anti-CD20 antibody treatment was negatively correlated with anti-SARS-CoV-2 antibody titers in hematological disease, and C-reactive protein (CRP) was positively correlated with anti-SARS-CoV-2 antibody titers in autoimmune disease. Baseline anti-PEG antibody titers were significantly higher in patients with autoimmune disease but were not correlated with anti-SARS-CoV-2 antibody titers. Patients with increased anti-PEG IgG acquired higher anti-SARS-CoV-2 antibody titers in patients with autoimmune disease. Anti-SARS-CoV-2 antibody acquisition was suboptimal in patients with hematological disease, but both anti-SARS-CoV-2 antibody and anti-PEG IgG were acquired in patients with autoimmune disease, reflecting robust humoral immune response. Pre-existing anti-PEG antibody titers did not affect anti-SARS-CoV-2 antibody acquisition. (徳島大学機関リポジトリ) ● Metadata: 119625 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.heliyon.2024.e31489 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38813140 ● Search Scopus @ Elsevier (PMID): 38813140 ● Search Scopus @ Elsevier (DOI): 10.1016/j.heliyon.2024.e31489 (徳島大学機関リポジトリ: 119625, DOI: 10.1016/j.heliyon.2024.e31489, PubMed: 38813140)
4.	Taiki Hori, Ken-ichi Aihara, Koki Ishida, Kaori Inaba, Keisuke Inaba, Yousuke Kaneko, Keisuke Kawahito, Shoki Bekku, Minae Hosoki, Kensuke Mori, Kanako Itami, Masayo Katsuse, Yoshimi Hanaoka, Teruyoshi Kageji, Hideyuki Uraoka and Shingen Nakamura : Usefulness of Palliative Prognostic Index, Objective Prognostic Score, and Neutrophil-Lymphocyte Ratio/Albumin Ratio As Prognostic Indicators for Patients Without Cancer Receiving Home-Visit Palliative Care: A Pilot Study at a Community General Hospital., Palliative Medicine Reports, Vol.5, No.1, 142-149, 2024. (要約) < 0.001). The survival curves of the groups classified according to PPI, OPS, and NLR/Alb were significantly stratified. The predictive capacities of PPI, OPS, and NLR/Alb for death within 21 days were as follows: PPI (area under the curve [AUC]: 0.71; sensitivity: 59%; specificity: 68%), OPS (AUC: 0.73; sensitivity: 88%; specificity: 47%), and NLR/Alb (AUC: 0.72; sensitivity: 72%; specificity: 73%). (徳島大学機関リポジトリ) ● Metadata: 119250 (出版サイトへのリンク) ● Publication site (DOI): 10.1089/pmr.2023.0096 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38596695 ● Search Scopus @ Elsevier (PMID): 38596695 ● Search Scopus @ Elsevier (DOI): 10.1089/pmr.2023.0096 (徳島大学機関リポジトリ: 119250, DOI: 10.1089/pmr.2023.0096, PubMed: 38596695)
5.	Minae Hosoki, HORI Taiki, KANEKO Yohsuke, Kensuke Mori, Saya Yasui, Seijiro Tsuji, Hiroki Yamagami, Saki Kawata, Tomoyo Hara, Shiho Masuda, Yukari Mitsui, Kiyoe Kurahashi, Takeshi Harada, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : Causes of In-Hospital Death and Pharmaceutical Associations with Age of Death during a 10-Year Period (2011-2020) in Individuals with and without Diabetes at a Japanese Community General Hospital., Journal of Clinical Medicine, Vol.13, No.5, 1283, 2024. (要約) Since diabetes and its complications have been thought to exaggerate cardiorenal disease, resulting in a short lifespan, we investigated causes of death and lifespans in individuals with and without diabetes at a Japanese community general hospital during the period from 2011 to 2020. Causes of death and age of death in individuals with and those without diabetes were compared, and associations between medications used and age of death were statistically analyzed. A total of 2326 deaths were recorded during the 10-year period. There was no significant difference between the mean ages of death in individuals with and those without diabetes. Diabetic individuals had higher rates of hepato-pancreatic cancer and cardio-renal failure as causes of death. The prescription rates of antihypertensives, antiplatelets, and statins in diabetic individuals were larger than those in non-diabetic individuals. Furthermore, the use of sulfonyl urea or glinides and insulin was independently and inversely associated with the age of death. In conclusion, individuals with diabetes were treated with comprehensive pharmaceutical interventions and had life spans comparable to those of individuals without diabetes. This study's discovery of an inverse relationship between the use of insulin secretagogues or insulin and the age of death suggests that the prevention of life-threatening hypoglycemia is crucial for individuals with diabetes. (徳島大学機関リポジトリ) ● Metadata: 119252 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/jcm13051283 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38592103 ● Search Scopus @ Elsevier (PMID): 38592103 ● Search Scopus @ Elsevier (DOI): 10.3390/jcm13051283 (徳島大学機関リポジトリ: 119252, DOI: 10.3390/jcm13051283, PubMed: 38592103)
6.	Kimiko Sogabe, Shingen Nakamura, Yoshiki Higa, Hirokazu Miki, Asuka Oda, Tomoko Maruhashi, Ryohei Sumitani, Masahiro Oura, Mamiko Takahashi, Masafumi Nakamura, Yusaku Maeda, Tomoyo Hara, Hiroki Yamagami, Shiroh Fujii, Kumiko Kagawa, Shuji Ozaki, Kiyoe Kurahashi, Itsuro Endo, Ken-ichi Aihara, Emiko Nakaue, Masahiro Hiasa, Jumpei Teramachi, Takeshi Harada and Masahiro Abe : Acute accumulation of PIM2 and NRF2 and recovery of β5 subunit activity mitigate multiple myeloma cell susceptibility to proteasome inhibitors., International Journal of Hematology, Vol.119, No.3, 303-315, 2024. (要約) Resistance to proteasome inhibitors (PIs) has emerged as an important clinical issue. We investigated the mechanisms underlying multiple myeloma (MM) cell resistance to PIs. To mimic their pharmacokinetic/pharmacodynamic (PK/PD) profiles, MM cells were treated with bortezomib and carfilzomib for 1 h at concentrations up to 400 and 1,000 nM, respectively. Susceptibility to these PIs markedly varied among MM cell lines. Pulsatile treatments with PIs suppressed translation, as demonstrated by incorporation of puromycin at 24 h in PI-susceptible MM.1S cells, but not PI-resistant KMS-11 cells. Inhibition of β5 subunit activity decreased at 24 h in KMS-11 cells, even with the irreversible PI carfilzomib, but not under suppression of protein synthesis with cycloheximide. Furthermore, the proteasome-degradable pro-survival factors PIM2 and NRF2 acutely accumulated in MM cells subjected to pulsatile PI treatments. Accumulated NRF2 was trans-localized into the nucleus to induce the expression of its target gene, HMOX1, in MM cells. PIM and Akt inhibition restored the anti-MM effects of PIs, even against PI-resistant KMS-11 cells. Collectively, these results suggest that increased synthesis of β5 proteasome subunit and acute accumulation of PIM2 and NRF2 reduce the anti-MM effects of PIs. (キーワード) Humans / Proteasome Inhibitors / NF-E2-Related Factor 2 / Multiple Myeloma / Proteasome Endopeptidase Complex / Drug Resistance, Neoplasm / Cell Line, Tumor / Bortezomib / Antineoplastic Agents / Proto-Oncogene Proteins / Protein Serine-Threonine Kinases (徳島大学機関リポジトリ) ● Metadata: 119384 (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s12185-023-03705-9 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38245883 ● Search Scopus @ Elsevier (PMID): 38245883 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-023-03705-9 (徳島大学機関リポジトリ: 119384, DOI: 10.1007/s12185-023-03705-9, PubMed: 38245883)
7.	堀太貴, 中村信元, 粟飯原賢一 : Clinical Significance of Phase Angle and Extracellular Water-to-Total Body Water Ratio Measured by Bioelectrical Impedance Analysis, Journal of leukemia, Vol.12, 368, 2024年. (徳島大学機関リポジトリ) ● Metadata: 119624 (徳島大学機関リポジトリ: 119624)
8.	Hiroki Yamagami, Tomoyo Hara, Saya Yasui, Minae Hosoki, Taiki Hori, Yousuke Kaneko, Yukari Mitsui, Kiyoe Kurahashi, Takeshi Harada, Sumiko Yoshida, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Cross-Sectional and Longitudinal Associations between Skin Autofluorescence and Tubular Injury Defined by Urinary Excretion of Liver-Type Fatty Acid-Binding Protein in People with Type 2 Diabetes., Biomedicines, Vol.11, No.11, 3020, 2023. (要約) = 0.026). In conclusion, SAF is positively correlated with uL-FABP but not with uACR in people with T2D. Thus, there is a possibility that SAF can serve as a novel predictor for the development of diabetic tubular injury. (キーワード) skin autofluorescence / type 2 diabetes / diabetic kidney disease / albuminuria / tubular injury / L-FABP (徳島大学機関リポジトリ) ● Metadata: 119108 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/biomedicines11113020 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38002020 ● CiNii @ 国立情報学研究所 (CRID): 1870302167614368000 ● Summary page in Scopus @ Elsevier: 2-s2.0-85178346619 (徳島大学機関リポジトリ: 119108, DOI: 10.3390/biomedicines11113020, PubMed: 38002020, CiNii: 1870302167614368000, Elsevier: Scopus)
9.	Saya Yasui, Yousuke Kaneko, Hiroki Yamagami, Minae Hosoki, Taiki Hori, Akihiro Tani, Tomoyo Hara, Kiyoe Kurahashi, Takeshi Harada, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Hiroyasu Mori, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Takeshi Soeki and Ken-ichi Aihara : Dehydroepiandrosterone Sulfate, an Adrenal Androgen, Is Inversely Associated with Prevalence of Dynapenia in Male Individuals with Type 2 Diabetes., Metabolites, Vol.13, No.11, 1129, 2023. (要約) Dehydroepiandrosterone sulfate (DHEAS) is thought to be associated with life expectancy and anti-aging. Although skeletal muscle disorders are often found in diabetic people, the clinical significance of DHEAS in skeletal muscle remains unclear. Therefore, we aimed to determine whether DHEAS is associated with the development of skeletal muscle disorders in individuals with type 2 diabetes (T2D). A cross-sectional study was conducted in 361 individuals with T2D. Serum DHEAS levels, skeletal muscle mass index (SMI), handgrip strength (HS), and gait speed (GS) were measured in the participants. Pre-sarcopenia, sarcopenia, and dynapenia were defined according to the definitions of the AWGS 2019 criteria. DHEAS level was positively associated with HS but not with SMI or GS after adjustment of confounding factors. Multiple logistic regression analyses in total subjects showed that DHEAS level had an inverse association with the prevalence of dynapenia but not with the prevalence of pre-sarcopenia or sarcopenia. Furthermore, a significant association between DHEAS level and dynapenia was found in males but not in females. ROC curve analysis indicated that cutoff values of serum DHEAS for risk of dynapenia in males was 92.0 μg/dL. Therefore, in male individuals with T2D who have low serum levels of DHEAS, adequate exercise might be needed to prevent dynapenia. (徳島大学機関リポジトリ) ● Metadata: 119107 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/metabo13111129 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37999225 ● CiNii @ 国立情報学研究所 (CRID): 1870583643033891840 ● Summary page in Scopus @ Elsevier: 2-s2.0-85178271509 (徳島大学機関リポジトリ: 119107, DOI: 10.3390/metabo13111129, PubMed: 37999225, CiNii: 1870583643033891840, Elsevier: Scopus)
10.	Toshiki Otoda, Akiko Sekine, Ryoko Uemoto, Seijiro Tsuji, Tomoyo Hara, Motoyuki Tamaki, Tomoyuki Yuasa, Toshiaki Tamaki, Munehide Matsuhisa and Ken-ichi Aihara : Albuminuria and Serum Tumor Necrosis Factor Receptor Levels in Patients with Type 2 Diabetes on SGLT2 Inhibitors: A Prospective Study., Diabetes Therapy, Vol.15, No.1, 127-143, 2023. (要約) (interquartile range (IQR) 23.1-28.9), and the median HbA1c level was 7.3% (IQR 6.9-8.3). After SGLT2i administration, the uACR declined from 19.2 mg/gCr (IQR 7.1-48.7) to 13.3 mg/gCr (IQR 7.5-31.6), whereas the uL-FABPCR was not influenced. In univariate analysis, the change in log-transformed uACR due to SGLT2i administration showed a positive correlation with the change in serum TNFR1 level (R = 0.244, p < 0.01). Multivariate regression analysis, including confounding factors, showed that the changes in serum TNFR1 level were independently associated with the changes in the log-transformed uACR (independent t = 2.102, p < 0.05). (徳島大学機関リポジトリ) ● Metadata: 119109 (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s13300-023-01488-0 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37883001 ● CiNii @ 国立情報学研究所 (CRID): 1872272493157884672 ● Summary page in Scopus @ Elsevier: 2-s2.0-85174952372 (徳島大学機関リポジトリ: 119109, DOI: 10.1007/s13300-023-01488-0, PubMed: 37883001, CiNii: 1872272493157884672, Elsevier: Scopus)
11.	森博康, 谷口諭, 玉木悠, 野村友美, 鈴木麗子, 黒田暁生, 明比祐子, 倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 白神敦久, 田蒔基行, 天満仁, 長島伸光, 比木武, 松久宗英 : 2型糖尿病患者のPersonal Health Recordを用いたセルフモニタリングに自動支援メッセージが与える効果:探索的ランダム化比較試験, 日本糖尿病インフォマティクス学会誌, Vol.22, No.2, 7-18, 2023年.
12.	Shiho Masuda, Tomoyo Hara, Hiroki Yamagami, Yukari Mitsui, Kiyoe Kurahashi, Sumiko Yoshida, Takeshi Harada, Toshiki Otoda, Tomoyuki Yuasa, Shingen Nakamura, Akio Kuroda, Itsuro Endo, Toshio Matsumoto, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Vascular Endothelial Function Is Associated with eGFR Slope in Female and Non-Smoking Male Individuals with Cardiovascular Risk Factors: A Pilot Study on the Predictive Value of FMD for Renal Prognosis., Journal of Atherosclerosis and Thrombosis, 2023. (要約) In individuals with cardiovascular risk factors, evaluation of vascular endothelial function enables prediction of renal prognosis in females and non-smoking males. (徳島大学機関リポジトリ) ● Metadata: 118250 (出版サイトへのリンク) ● Publication site (DOI): 10.5551/jat.63987 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37081616 ● Search Scopus @ Elsevier (PMID): 37081616 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.63987 (徳島大学機関リポジトリ: 118250, DOI: 10.5551/jat.63987, PubMed: 37081616)
13.	Taiki Hori, Shingen Nakamura, Hiroki Yamagami, Saya Yasui, Minae Hosoki, Tomoyo Hara, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Sumiko Yoshida, Takeshi Harada, Akio Kuroda, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Phase angle and extracellular water-to-total body water ratio estimated by bioelectrical impedance analysis are associated with levels of hemoglobin and hematocrit in patients with diabetes., Heliyon, Vol.9, No.4, 2023. (要約) PhA and ECW/TBW but not SMI were associated with levels of Hgb and Hct in patients with diabetes. Therefore, aberrant values of PhA and ECW/TBW suggest a risk of anemia in diabetic patients. (徳島大学機関リポジトリ) ● Metadata: 118251 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.heliyon.2023.e14724 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37057050 ● Search Scopus @ Elsevier (PMID): 37057050 ● Search Scopus @ Elsevier (DOI): 10.1016/j.heliyon.2023.e14724 (徳島大学機関リポジトリ: 118251, DOI: 10.1016/j.heliyon.2023.e14724, PubMed: 37057050)
14.	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. (要約) Multiple regression analysis including confounding factors showed that plasma HCII activity independently contributed to decreases in FIB-4 index (p<0.001), NFS (p<0.001) and APRI (p=0.004). In addition, logistic regression analysis for the prevalence of advanced hepatic fibrosis defined by the cutoff points of the clinical scores showed that plasma HCII activity was the sole and common negative factor for prevalence of advanced hepatic fibrosis (FIB-4 index: p=0.002, NFS: p=0.026 and APRI: p=0.012). (徳島大学機関リポジトリ) ● Metadata: 118258 (出版サイトへのリンク) ● Publication site (DOI): 10.5551/jat.63752 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 118258, DOI: 10.5551/jat.63752, PubMed: 36244745)
15.	Shingen Nakamura, Motoki Sugasaki, Masayoshi Souri, Hirohito Akazawa, Maiko Sogawa, Taiki Hori, Hiroki Yamagami, Makoto Takishita, Ken-ichi Aihara, Masahiro Abe, Atsushi Yasumoto, Eriko Morishita and Akitada Ichinose : Autoimmune Acquired Factor XIII/13 Deficiency after SARS-CoV-2 mRNA Vaccination., Thrombosis and Haemostasis, 2022. (徳島大学機関リポジトリ) ● Metadata: 118345 (出版サイトへのリンク) ● Publication site (DOI): 10.1055/a-1863-7265 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35636450 ● Search Scopus @ Elsevier (PMID): 35636450 ● Search Scopus @ Elsevier (DOI): 10.1055/a-1863-7265 (徳島大学機関リポジトリ: 118345, DOI: 10.1055/a-1863-7265, PubMed: 35636450)
16.	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. (徳島大学機関リポジトリ) ● Metadata: 117134 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.phymed.2022.154213 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.1016/j.phymed.2022.154213 (徳島大学機関リポジトリ: 117134, DOI: 10.1016/j.phymed.2022.154213)
17.	Asami Okada, Misuzu Yamada-Yamashita, Yukari Tominaga, Kyoka Jo, Hiroyasu Mori, Reiko Suzuki, Masashi Ishizu, Motoyuki Tamaki, Yuko Akehi, Yuichi Takashi, Daisuke Koga, Eisuke Shimokita, Fuminori Tanihara, Kiyoe Kurahashi, Sumiko Yoshida, Yukari Mitsui, Shiho Masuda, Itsuro Endo, Ken-ichi Aihara, Shoji Kagami, Masahiro Abe, Kevin Ferreri, Yoshio Fujitani, Munehide Matsuhisa and Akio Kuroda : Novel method utilizing bisulfite conversion with dual amplification-refractory mutation system polymerase chain reaction to detect circulating pancreatic β-cell cfDNA., Journal of Diabetes Investigation, Vol.13, No.7, 1140-1148, 2022. (要約) We developed a novel method for detecting unmethylated insulin DNA in circulation that can be performed using a conventional real-time PCR system. This method would be useful for analyzing dynamic profiles of β-cells in human disease such as type 1 diabetes. (徳島大学機関リポジトリ) ● Metadata: 117206 (出版サイトへのリンク) ● Publication site (DOI): 10.1111/jdi.13806 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35396829 ● Search Scopus @ Elsevier (PMID): 35396829 ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.13806 (徳島大学機関リポジトリ: 117206, DOI: 10.1111/jdi.13806, PubMed: 35396829)
18.	Yukari Mitsui, Akio Kuroda, Masashi Ishizu, Hiroyasu Mori, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Yuko Akehi, Ken-ichi Aihara, Itsuro Endo, Masahiro Abe and Munehide Matsuhisa : Basal insulin requirement in patients with type 1 diabetes depends on the age and body mass index., Journal of Diabetes Investigation, Vol.13, No.2, 292-298, 2022. (要約) T (徳島大学機関リポジトリ) ● Metadata: 116546 (出版サイトへのリンク) ● Publication site (DOI): 10.1111/jdi.13547 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33740836 ● Search Scopus @ Elsevier (PMID): 33740836 ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.13547 (徳島大学機関リポジトリ: 116546, DOI: 10.1111/jdi.13547, PubMed: 33740836)
19.	Yukari Mitsui, Yuto Iizuka, Tomoaki Tanaka, Tomoyo Hara, Shiho Masuda, Yukiyo Ohnishi, Mai Kanai, Kiyoe Kurahashi, Sumiko Yoshida, Takeshi Kondo, Toshiko Kanezaki, Yasumi Shintani, Hiroki Yamagami, Hiroyuki Yamaguchi, Yuichi Fujinaka, Kana Morimoto, Atsuhisa Shirakami, Ken-ichi Aihara, Seiji Fukumoto, Masahiro Abe and Itsuro Endo : An attempt to create a treatment algorithm of central adrenal insufficiency using CRH test, DHEA-S and clinical evaluation., The Journal of Medical Investigation : JMI, Vol.69, No.3.4, 287-293, 2022. (要約) Objective : To examine diagnostic performance of corticotropin-releasing hormone (CRH) test combined with baseline dehydroepiandrosterone sulfate (DHEA-S) in patients with a suspect of central adrenal insufficiency. Methods : Patients (n=215) requiring daily or intermittent hydrocortisone replacement, or no replacement were retrospectively checked with their peak cortisol after CRH test and baseline DHEA-S. Results : None of 106 patients with the peak cortisol · 17.5 g /L after CRH test required replacement, and all 64 patients with the peak cortisol < 10.0 g /L required daily replacement. Among 8 patients with 10.0 g /L the peak cortisol < 17.5 g /L and baseline DHEA-S below the reference range, 6 patients required daily replacement and 1 patient was under intermittent replacement. Among 37 patients with 10.0 g /L the peak cortisol < 17.5 g /L and baseline DHEA-S within the reference range, 10 and 6 patients were under intermittent and daily replacement, respectively. Conclusions : No patients with the peak cortisol · 17.5 g /L required hydrocortisone replacement, and all patients with the peak cortisol below 10.0 g /L required daily replacement. Careful clinical evaluation was required to determine requirement for replacement in patients with 10.0 g /L the peak cortisol < 17.5 g /L even in combination with baseline DHEA-S. J. Med. Invest. 69 : 287-293, August, 2022. (キーワード) Adrenal Insufficiency / Adrenocorticotropic Hormone / Algorithms / Corticotropin-Releasing Hormone / Dehydroepiandrosterone Sulfate / Humans / Hydrocortisone / Retrospective Studies (徳島大学機関リポジトリ) ● Metadata: 117738 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.69.287 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36244782 ● CiNii @ 国立情報学研究所 (CRID): 1390575263318485248 ● Summary page in Scopus @ Elsevier: 2-s2.0-85139886801 (徳島大学機関リポジトリ: 117738, DOI: 10.2152/jmi.69.287, PubMed: 36244782, CiNii: 1390575263318485248, Elsevier: Scopus)
20.	岡田朝美, 山田美鈴, 森博康, 明比祐子, 倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 黒田暁生 : 循環血中遊離 DNA を用いた膵β細胞傷害の新規検出法の確立, 四国医学雑誌, Vol.77, No.5,6, 249-254, 2021年. (要約) In people with type1 diabetes(T1D), biomarkers that can sensitively and quantitatively evaluate injury of pancreatic beta cell are required in order to predict the onset of the disease at an early stage and to provide interventions to prevent the progression of the disease. We developed a new method for quantifying pancreatic beta cell-derived insulin DNA in circulation that combines bisulfite conversion and Amplification Refractory Mutation System(ARMS)PCR, which can be performed using a conventional real-time PCR system. We applied this method to T1D patients and healthy adults, both could be detected in about 30% of cases. The results in healthy adults indicate that this method may have sensitivity to detect the turnover of pancreatic beta cells at physiological conditions. In post-onset T1D patients, there were many negatives because the amount of residual pancreatic beta cells was extremely small. However, in some cases with a short duration of the disease, pancreatic beta cell-derived insulin DNA was detected in negative correlation between the duration of the disease, that suggested the residual pancreatic beta cells continue to be slowly destroyed. It was demonstrated that the time course of pathophysiology in T1D could be understood using this method. (キーワード) インスリン (insulin) / DNA methylation / RT-PCR / Type1 diabetes / cell-free DNA (徳島大学機関リポジトリ) ● Metadata: 117138 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1520573657290659200 (徳島大学機関リポジトリ: 117138, CiNii: 1520573657290659200)
21.	Tomoyuki Yuasa, Yasunori Takata, Nanako Aki, Kotaro Kunimi, Miki Satoh, Mari Nii, Yoshihiko Izumi, Toshiki Otoda, Seiichi Hashida, Haruhiko Osawa and Ken-ichi Aihara : Insulin receptor cleavage induced by estrogen impairs insulin signaling., BMJ Open Diabetes Research & Care, Vol.9, No.2, 2021. (要約) Soluble insulin receptor (sIR), which is the ectodomain of insulin receptor (IR), is present in human plasma. Plasma sIR levels are positively correlated with blood glucose levels and negatively correlated with insulin sensitivity. An in vitro model of IR cleavage shows that extracellular calpain 2 directly cleaves IR, which generates sIR, and sequential cleavage of the IR subunit by -secretase impairs insulin signaling in a glucose concentration-dependent manner. Nevertheless, sIR levels vary among subjects with normal glucose levels. We examined sIR levels of pregnant women throughout gestation. Using an in vitro model, we also investigated the molecular mechanisms of IR cleavage induced by estradiol. In pregnant women, sIR levels were positively correlated with estrogen levels and significantly increased at late pregnancy independent of glucose levels. Using an in vitro model, estrogen elicited IR cleavage and impaired cellular insulin signaling. Estradiol-induced IR cleavage was inhibited by targeting of calpain 2 and -secretase. Estrogen exerted these biological effects via G protein-coupled estrogen receptor, and its selective ligand upregulated calpain 2 expression and promoted exosome secretion, which significantly increased extracellular calpain 2. Simultaneous stimulation of estrogen and high glucose levels had a synergic effect on IR cleavage. Metformin prevented calpain 2 release in exosomes and restored insulin signaling impaired by estrogen. Estradiol-induced IR cleavage causes cellular insulin resistance, and its molecular mechanisms are shared with those by high glucose levels. sIR levels at late pregnancy are significantly elevated along with estrogen levels. Therefore, estradiol-induced IR cleavage is preserved in pregnant women and could be part of the etiology of insulin resistance in gestational diabetes mellitus and overt diabetes during pregnancy. (キーワード) Diabetes, Gestational / Estrogens / Female / Humans / Insulin / Insulin Resistance / Pregnancy / 可溶性インスリン受容体 (soluble insulin receptor) (徳島大学機関リポジトリ) ● Metadata: 118344 (出版サイトへのリンク) ● Publication site (DOI): 10.1136/bmjdrc-2021-002467 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34969688 ● Search Scopus @ Elsevier (PMID): 34969688 ● Search Scopus @ Elsevier (DOI): 10.1136/bmjdrc-2021-002467 (徳島大学機関リポジトリ: 118344, DOI: 10.1136/bmjdrc-2021-002467, PubMed: 34969688)
22.	Rie Tsutsumi, Yuki Yamasaki, Jiro Takeo, Hiroko Miyahara, Mayu Sebe, Masahiro Bando, Yousuke Tanba, Yuna Mishima, Kana Takeji, Nanako Ueshima, Masashi Kuroda, Saeko Masumoto, Nagakatsu Harada, Daiju Fukuda, Ryoko Yoshimoto, Yasuo M. Tsutsumi, Ken-ichi Aihara, Masataka Sata and Hiroshi Sakaue : Long-chain monounsaturated fatty acids improve endothelial function with altering microbial flora, Translational Research : The Journal of Laboratory and Clinical Medicine, Vol.237, 16-30, 2021. (要約) Fish oil-derived long-chain monounsaturated fatty acids (LCMUFAs) with a carbon chain length longer than 18 units ameliorate cardiovascular risk in mice. In this study, we investigated whether LCMUFAs could improve endothelial functions in mice and humans. In a double-blind, randomized, placebo-controlled, parallel-group, multi-center study, healthy subjects were randomly assigned to either an LCMUFA oil (saury oil) or a control oil (olive and tuna oils) group. Sixty subjects were enrolled and administrated each oil for 4 weeks. For the animal study, ApoE mice were fed a Western diet supplemented with 3% of either gadoleic acid (C20:1) or cetoleic acid (C22:1) for 12 weeks. Participants from the LCMUFA group showed improvements in endothelial function and a lower trimethylamine-N-oxide level, which is a predictor of coronary artery disease. C20:1 and C22:1 oils significantly improved atherosclerotic lesions and plasma levels of several inflammatory cytokines, including IL-6 and TNF-α. These beneficial effects were consistent with an improvement in the gut microbiota environment, as evident from the decreased ratio of Firmicutes and/ or Bacteroidetes, increase in the abundance of Akkermansia, and upregulation of short-chain fatty acid (SCFA)-induced glucagon-like peptide-1 (GLP-1) expression and serum GLP-1 level. These data suggest that LCMUFAs alter the microbiota environment that stimulate the production of SCFAs, resulting in the induction of GLP-1 secretion. Fish oil-derived long-chain monounsaturated fatty acids might thus help to protect against cardiovascular disease. (徳島大学機関リポジトリ) ● Metadata: 116689 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.trsl.2021.03.016 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33775867 ● Summary page in Scopus @ Elsevier: 2-s2.0-85114290883 (徳島大学機関リポジトリ: 116689, DOI: 10.1016/j.trsl.2021.03.016, PubMed: 33775867, Elsevier: Scopus)
23.	川原綾香, 倉橋清衛, 工藤千晶, 鎌田基夢, 加藤真介, 富岡有紀子, 辻本賀美, 安井沙耶, 遠藤ふうり, 桝田志保, 三井由加里, 吉田守美子, 粟飯原賢一, 遠藤逸朗, 福本誠二, 松久宗英, 安倍正博 : 歩行不能だったが，多職種の高度な連携と患者特性に配慮したケアにより自宅生活可能となった高度肥満症の一例, 四国医学雑誌, Vol.76, No.5-6, 317-322, 2021年. (要約) A 48-year-old man who weighed 216 kg was significantly overweight with a body mass index (BMI)of 75．6kg/m2, and was unable to walk due to disuse syndrome. Because of the psychological and social problems in the background, a psychological examination was performed and the staff took time to build a trusting relationship with the patient, taking into account his characteristics. With diet and rehabilitation, he was able to lose weight to 124kg and BMI 43．9kg/m2 over 600 days, and was able to walk with assistive devices and defecate by himself. The patient was discharged from our hospital after a series of multidisciplinary meetings with medical, nursing, welfare, and governmental agencies to create an environment for home recuperation. The reasons for the improvement to enable him to be discharged from the hospital were due to the multi-disciplinary meetings among the staff inside and outside the hospital, information sharing and advanced coordination, and smooth communication with the patient by taking into account his characteristics from a psychological standpoint. (キーワード) Sever obesity / 廃用症候群 (disuse syndrome) / Patient-specific care / Multidisciplinary team (徳島大学機関リポジトリ) ● Metadata: 115801 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1050583790041627392 (徳島大学機関リポジトリ: 115801, CiNii: 1050583790041627392)
24.	Yousuke Kaneko, Motoki Sugasaki, Naoto Okada, Mako Niimi, Saya Yasui, Taiki Hori, Ken-ichi Aihara, Makoto Takishita, Masahiro Abe and Shingen Nakamura : Artifactual prolongation of the activated partial thromboplastin time by amikacin or gentamicin with ellagic acid, but not silica activated reagent., International Journal of Laboratory Hematology, Vol.44, No.2, e72-e75, 2021. (キーワード) Amikacin / Anti-Bacterial Agents / Ellagic Acid / Gentamicins / Humans / Indicators and Reagents / Partial Thromboplastin Time / Silicon Dioxide (徳島大学機関リポジトリ) ● Metadata: 118369 (出版サイトへのリンク) ● Publication site (DOI): 10.1111/ijlh.13718 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34585530 ● Search Scopus @ Elsevier (PMID): 34585530 ● Search Scopus @ Elsevier (DOI): 10.1111/ijlh.13718 (徳島大学機関リポジトリ: 118369, DOI: 10.1111/ijlh.13718, PubMed: 34585530)
25.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 116545 (出版サイトへのリンク) ● Publication site (DOI): 10.1111/jdi.13602 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 116545, DOI: 10.1111/jdi.13602, PubMed: 34043882)
26.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 115399 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.kint.2020.10.041 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 115399, DOI: 10.1016/j.kint.2020.10.041, PubMed: 33307103)
27.	Masashi Ishizu, Hiroyasu Mori, Mami Ohishi, Akio Kuroda, Y Akehi, Sumiko Yoshida, Ken-ichi Aihara, M Aiba, T Kawano, Seiichi Hashida and Munehide Matsuhisa : Urinary adiponectin excretion is an early predictive marker of the decline of the renal function in patients with diabetes mellitus., Journal of Diabetes and its Complications, Vol.35, No.4, 107848, 2021. (要約) Since diabetes-associated kidney complication changes from diabetic nephropathy to diabetic kidney disease (DKD), more suitable biomarkers than urinary albumin are required. It has been hypothesized that urinary adiponectin (u-ADPN) is associated with the progression of DKD. We therefore evaluated the effectiveness of u-ADPN in predicting the decline of the renal function in patients with diabetes prior to end-stage renal disease. An ultrasensitive immune complex transfer enzyme immunoassay (ICT-EIA) was used to measure total and high molecular weight (HMW) adiponectin separately. We evaluated the relationships between the creatinine-adjusted urinary total-ADPN and HMW-ADPN, albumin (UACR) and liver-type fatty acid binding protein (L-FABP) at baseline and the 2-year change of the estimated glomerular filtration rate (ΔeGFR). This 2-year prospective observational study included 201 patients with diabetes. These patients were divided into three groups according to their ΔeGFR: ≤-10 mL/min/1.73m, >-10 and ≤0 mL/min/1.73m, and >0 mL/min/1.73m. Jonckheere-Terpstra test showed that lower ΔeGFR was associated with higher u-HMW-ADPN (p = 0.045). In logistic regression analysis, u-HMW-ADPN was associated with ΔeGFR after adjusted age, sex, and basal eGFR. Urinary HMW-ADPN could predict a declining renal function in patients with diabetes. (徳島大学機関リポジトリ) ● Metadata: 115675 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.jdiacomp.2021.107848 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33558151 ● Search Scopus @ Elsevier (PMID): 33558151 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jdiacomp.2021.107848 (徳島大学機関リポジトリ: 115675, DOI: 10.1016/j.jdiacomp.2021.107848, PubMed: 33558151)
28.	Akira Takashima, Shusuke Yagi, Koji Yamaguchi, Kiyoe Kurahashi, Yuko Kojima, Robert Zheng, Takayuki Ise, Kenya Kusunose, Sumiko Yoshida, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Ken-ichi Aihara, Masashi Akaike and Masataka Sata : Congenital Hypogonadotropic Hypogonadism with Early-Onset Coronary Artery Disease., The Journal of Medical Investigation : JMI, Vol.68, No.1.2, 189-191, 2021. (要約) The patient with congenital hypogonadotropic hypogonadism (HH) shows low serum levels of androgen, which is a group of sex hormones including testosterone, caused by the decreased gonadotropin release in the hypothalamus. Recent reports showed androgens exert protective effects against insulin resistance or atherosclerotic diseases, such as diabetes mellitus or coronary artery disease. However, whether the juvenile hypogonadism affects the diabetes or cardiovascular disease is unclear. We report a case of a middle-aged man with congenital HH who had severe coronary artery disease complicated with metabolic disorders. J. Med. Invest. 68 : 189-191, February, 2021. (徳島大学機関リポジトリ) ● Metadata: 116019 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.68.189 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33994469 ● Search Scopus @ Elsevier (PMID): 33994469 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.68.189 (徳島大学機関リポジトリ: 116019, DOI: 10.2152/jmi.68.189, PubMed: 33994469)
29.	桑村由美, 吉田守美子, 倉橋清衛, 澄川真珠子, 坂本英次郎, 黒田暁生, 粟飯原賢一, 船木真理, 湯本浩通, 上村浩一, 岡本美鈴, 大和光, 松久宗英, 遠藤逸朗, 岸田佐智 : 糖尿病患者の口腔保健行動アセスメントツールを用いた看護支援プログラムの評価, 糖尿病, Vol.63, No.Supplement, S117, 2020年. (キーワード) 糖尿病 (diabetes mellitus) / 口腔保健行動 (oral health behaviors) / アセスメント (assessment) / 看護支援
30.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 114409 (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s00125-020-05153-0 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32430665 ● Summary page in Scopus @ Elsevier: 2-s2.0-85085484596 (徳島大学機関リポジトリ: 114409, DOI: 10.1007/s00125-020-05153-0, PubMed: 32430665, Elsevier: Scopus)
31.	Yumi Kuwamura, Sumiko Yoshida, Kiyoe Kurahashi, Masuko Sumikawa, Eijiro Sakamoto, Ken-ichi Aihara, Hiromichi Yumoto, Akio Kuroda, Itsuro Endo, Toshiyuki Yasui and Sachi Kishida : Modified diabetes oral health assessment tool (M-DiOHAT©) for nurses and their association with efficacy beliefs and outcome expectancies in patients with diabetes, JNI : The Journal of Nursing Investigation, Vol.18, No.1, 13-26, 2020. (キーワード) 糖尿病 (diabetes mellitus) / アセスメント (assessment) / 看護 (nursing) / 口腔保健行動 (oral health behaviors) (徳島大学機関リポジトリ) ● Metadata: 114058 (出版サイトへのリンク) ● Publication site (DOI): 10.32273/jni.JNI_018_013 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.32273/jni.JNI_018_013 (徳島大学機関リポジトリ: 114058, DOI: 10.32273/jni.JNI_018_013)
32.	鶴尾美穂, 住友正治, 大島康志, 小松まち子, 鈴木麗子, 粟飯原賢一, 安藝菜奈子, 坂東智子, 高橋保子, 丸岡重代, 原田和代, 若槻真吾, 桜井えつ, 井野口卓, 白神敦久, 豊崎纏, 松久宗英, 宇都宮正登 : 第42回徳島医学会賞受賞論文糖尿病患者の在宅ケア向上をめざした徳島市糖尿病サポーター(TCDS)育成の試み, 四国医学雑誌, Vol.75, No.3, 97-102, 2019年. (要約) The Tokushima City Medical Association has cultivated the talented persons of nursing care profession by both the education of diabetes and the instruction of medical treatments to secure the quality of home care for increasing diabetic patients. They are certified to be the Tokushima City Certified Diabetes Supporter(TCDS). In Tokushima Prefecture, the rate of aging and the certification rate of care need are ranked high in Japan, and the medical measures should be provided for the aged diabetic patients utilizing team nursing care as well as team medical care, because many of these patients are obliged to receive home medical care owing to the introduction of community-based integrated care systems. Tokushima Prefecture kept the worst of age-adjusted diabetes mortality and also the worst of crude diabetes mortality in recent years. Therefore, the program for the TCDS was arranged by the staffs composed of board certified fellows of the Japan Diabetes Society, certified diabetes physicians of Tokushima, and Tokushima local certified diabetes educators (Tokushima LCDEs). The program includes the lectures of diabetes and medical treatments, the practical training, and the group work by the World Café system collaborated with the medical staffs across many different fields, using the dramatic skit presented by the medical doctors and the LCDE staffs after narrating the scenario for the blood glucose control of diabetic patients to be treated. The persons who have completed the training course are certified as the TCDS by The Tokushima City Medical Association. The workshop is held twice a year and the certification is renewed every three years without examination. In conclusion, it is suggested that the development of TCDS leads to the improvement of the ability of nursing care staffs to support diabetic treatments and the advancement of the quality of home medical care for the aged diabetic patients. (徳島大学機関リポジトリ) ● Metadata: 113809 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1050020697876183168 (徳島大学機関リポジトリ: 113809, CiNii: 1050020697876183168)
33.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 113746 (出版サイトへのリンク) ● Publication site (DOI): 10.1096/fj.201802724RR (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 113746, DOI: 10.1096/fj.201802724RR, PubMed: 31145863)
34.	Shusuke Yagi, Daisuke Kondo, Takayuki Ise, Daiju Fukuda, Koji Yamaguchi, Tetsuzo Wakatsuki, Yutaka Kawabata, Hiroyuki Ito, Yoshihito Saijo, Hiromitsu Seno, Kumiko Sutou, Rie Ueno, Takafumi Todoroki, Kenya Kusunose, Tomomi Matsuura, Takeshi Tobiume, Hirotsugu Yamada, Takeshi Soeki, Michio Shimabukuro, Ken-ichi Aihara, Masashi Akaike and Masataka Sata : Association of Decreased Docosahexaenoic Acid Level After Statin Therapy and Low Eicosapentaenoic Acid Level with In-Stent Restenosis in Patients with Acute Coronary Syndrome, Journal of Atherosclerosis and Thrombosis, Vol.26, No.3, 272-281, 2019. (要約) It is speculated that statin therapy modulates the synthesis of polyunsaturated fatty acids (PUFA), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). However, the data available on the effects of statin therapy on the serum levels of PUFA and the subsequent impact on in-stent restenosis (ISR) in patients with acute coronary syndrome (ACS) are limited. A total of 120 ACS patients who received emergent coronary stent implantation, follow-up coronary angiography to evaluate ISR, and new statin therapy were enrolled. We measured the serum levels of the PUFA and lipids at the onset of ACS and at the follow-up coronary angiography. The follow-up coronary angiography revealed 38 ISR cases. New statin therapy significantly reduced the serum levels of DHA and low-density lipoprotein cholesterol (LDL-C), while it did not affect EPA level. Single regression analysis revealed that a decreased serum level of LDL-C was associated with decreased DHA level. The multiple logistic regression analysis revealed that the decreased DHA level after statin therapy and low serum level of EPA on admission were determinants of prevalence of ISR. Statin therapy decreased the serum level of DHA with a parallel reduction in LDL-C level in patients with ACS. Decreased DHA level after statin therapy and low EPA level on admission are risk factors for ISR, indicating that in patients with ACS, decreased serum levels of DHA may be a residual target for the prevention of ISR. (キーワード) Acute Coronary Syndrome / Aged / Coronary Restenosis / Docosahexaenoic Acids / Eicosapentaenoic Acid / 女性 (female) / Follow-Up Studies / Humans / Hydroxymethylglutaryl-CoA Reductase Inhibitors / 男性 (male) / Prognosis / Retrospective Studies / Risk Factors / Stents (徳島大学機関リポジトリ) ● Metadata: 113220 (出版サイトへのリンク) ● Publication site (DOI): 10.5551/jat.44735 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30135329 ● Summary page in Scopus @ Elsevier: 2-s2.0-85062425735 (徳島大学機関リポジトリ: 113220, DOI: 10.5551/jat.44735, PubMed: 30135329, Elsevier: Scopus)
35.	Hiroyasu Mori, Akio Kuroda, Masashi Ishizu, Mami Ohishi, Yuichi Takashi, Yinhua Otsuka, Satoshi Taniguchi, Motoyuki Tamaki, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki, Yuko Akehi and Munehide Matsuhisa : Association of accumulated advanced glycation end-products with a high prevalence of sarcopenia and dynapenia in patients with type 2 diabetes., Journal of Diabetes Investigation, 2019. (要約) Advanced glycation end-products (AGEs), which are a major cause of diabetic vascular complications, accumulate in various tissues under chronic hyperglycemic conditions, as well as with aging in patients with diabetes. The loss of muscle mass and strength, so-called sarcopenia and dynapenia, has recently been recognized as a diabetic complication. However, the influence of accumulated AGEs on muscle mass and strength remains unclear. The present study aimed to evaluate the association of sarcopenia and dynapenia with accumulated AGEs in patients with type 2 diabetes. We recruited 166 patients with type 2 diabetes aged 30 years (mean age 63.2 ± 12.3 years; body mass index 26.3 ± 4.9 kg/m ; glycated hemoglobin 7.1 ± 1.1%). Skin autofluorescence as a marker of AGEs, limb skeletal muscle mass index, grip strength, knee extension strength and gait speed were assessed. Sarcopenia and dynapenia were observed in 7.2 and 13.9% of participants, respectively. Skin autofluorescence was significantly higher in patients with sarcopenia and dynapenia. Skin autofluorescence was the independent determinant for skeletal muscle mass index, grip strength, knee extension strength, sarcopenia and dynapenia. Accumulated AGEs could contribute to reduced muscle mass and strength, leading to sarcopenia and dynapenia in patients with type 2 diabetes. (徳島大学機関リポジトリ) ● Metadata: 114022 (出版サイトへのリンク) ● Publication site (DOI): 10.1111/jdi.13014 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30677242 ● Search Scopus @ Elsevier (PMID): 30677242 ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.13014 (徳島大学機関リポジトリ: 114022, DOI: 10.1111/jdi.13014, PubMed: 30677242)
36.	Ariunzaya Bat-Erdene, Shingen Nakamura, Asuka Oda, Masami Iwasa, Jumpei Teramachi, Mohannad Ashtar, Takeshi Harada, Hirokazu Miki, Hirofumi Tenshin, Masahiro Hiasa, Shiroh Fujii, Kimiko Sogabe, Masahiro Oura, Kengo Udaka, Kumiko Kagawa, Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Itsuro Endo and Masahiro Abe : Class 1 HDAC and HDAC6 inhibition inversely regulates CD38 induction in myeloma cells via interferon-α and ATRA., British Journal of Haematology, 2018. (徳島大学機関リポジトリ) ● Metadata: 113393 (出版サイトへのリンク) ● Publication site (DOI): 10.1111/bjh.15673 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30474853 ● Summary page in Scopus @ Elsevier: 2-s2.0-85057280798 (徳島大学機関リポジトリ: 113393, DOI: 10.1111/bjh.15673, PubMed: 30474853, Elsevier: Scopus)
37.	Shiroh Fujii, Shingen Nakamura, Asuka Oda, Hirokazu Miki, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Ariunzaya Bat-Erdene, Yusaku Maeda, Masahiro Oura, Mamiko Takahashi, Masami Iwasa, Itsuro Endo, Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Takeshi Harada, Kumiko Kagawa, Michiyasu Nakao, Shigeki Sano and Masahiro Abe : Unique anti-myeloma activity by thiazolidine-2,4-dione compounds with Pim inhibiting activity., British Journal of Haematology, Vol.180, No.2, 246-258, 2018. (要約) Proviral Integrations of Moloney virus 2 (PIM2) is overexpressed in multiple myeloma (MM) cells, and regarded as an important therapeutic target. Here, we aimed to validate the therapeutic efficacy of different types of PIM inhibitors against MM cells for their possible clinical application. Intriguingly, the thiazolidine-2,4-dione-family compounds SMI-16a and SMI-4a reduced PIM2 protein levels and impaired MM cell survival preferentially in acidic conditions, in contrast to other types of PIM inhibitors, including AZD1208, CX-6258 and PIM447. SMI-16a also suppressed the drug efflux function of breast cancer resistance protein, minimized the sizes of side populations and reduced in vitro colony-forming capacity and in vivo tumourigenic activity in MM cells, suggesting impairment of their clonogenic capacity. PIM2 is known to be subject to ubiquitination-independent proteasomal degradation. Consistent with this, the proteasome inhibitors bortezomib and carfilzomib increased PIM2 protein levels in MM cells without affecting its mRNA levels. However, SMI-16a mitigated the PIM2 protein increase and cooperatively enhanced anti-MM effects in combination with carfilzomib. Collectively, the thiazolidine-2,4-dione-family compounds SMI-16a and SMI-4a uniquely reduce PIM2 protein in MM cells, which may contribute to their profound efficacy in addition to their immediate kinase inhibition. Their combination with proteasome inhibitors is envisioned. (キーワード) Animals / Antineoplastic Agents / Cell Line, Tumor / Cell Survival / Cell Transformation, Neoplastic / Disease Models, Animal / Humans / Hydrogen-Ion Concentration / Mice / Multiple Myeloma / Proteasome Inhibitors / Protein-Serine-Threonine Kinases / Proteolysis / Proto-Oncogene Proteins / Thiazolidinediones (徳島大学機関リポジトリ) ● Metadata: 112752 (出版サイトへのリンク) ● Publication site (DOI): 10.1111/bjh.15033 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29327347 ● Summary page in Scopus @ Elsevier: 2-s2.0-85040344893 (徳島大学機関リポジトリ: 112752, DOI: 10.1111/bjh.15033, PubMed: 29327347, Elsevier: Scopus)
38.	Shusuke Yagi, Ken-ichi Aihara, Takeshi Kondo, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Daiju Fukuda, Yutaka Nakaya, Kin-Ichiro Suwaki, Takashi Takeji, Toshihiro Wada, Masdan Hotimah Salim, Saori Hama, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Takeshi Tobiume, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Munehide Matsuhisa, Michio Shimabukuro, Masashi Akaike and Masataka Sata : Predictors for the Treatment Effect of Sodium Glucose Co-transporter 2 Inhibitors in Patients with Type 2 Diabetes Mellitus., Advances in Therapy, Vol.35, No.1, 124-134, 2017. (要約) Predictors for the effect of sodium glucose co-transporter 2 (SGLT2) inhibitors at lowering hemoglobin A1c (HbA1c) levels in type 2 diabetes mellitus patients remain unclear. We therefore aimed to elucidate these predictors in type 2 diabetes patients after 3 months of SGLT2 treatment. A total of 302 consecutive type 2 diabetes patients who had been treated with SGLT2 inhibitors as monotherapy or add-on therapy to existing antidiabetic treatments were enrolled retrospectively. After excluding 27 patients whose HbA1c levels could not be evaluated 3 months after treatment, the glucose-lowering effects of SGLT2 inhibitors were assessed in 275 patients by measuring HbA1c levels before and 3 months after treatment. The predictors for changes in HbA1c levels after 3 months of treatment were evaluated. SGLT2 inhibitor treatment for 3 months decreased HbA1c levels from 7.8 ± 1.2% to 7.4 ± 1.0% (p < 0.0001). A multiple regression analysis showed that the independent determinants for SGLT2 inhibitor treatment effect included decreased HbA1c levels after 1 month of treatment, high baseline HbA1c levels, and a high estimated glomerular filtration rate (eGFR). We show that type 2 diabetes patients who received the greatest glucose-lowering effect with SGLT2 inhibitor treatment were those with preserved renal function (high baseline eGFR) and high baseline HbA1c levels. Moreover, SGLT2 inhibitor treatment efficacy could be predicted by the patients' initial response to treatment. (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s12325-017-0639-z (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29185199 ● Summary page in Scopus @ Elsevier: 2-s2.0-85035102977 (DOI: 10.1007/s12325-017-0639-z, PubMed: 29185199, Elsevier: Scopus)
39.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 112368 (出版サイトへのリンク) ● Publication site (DOI): 10.1038/s41598-017-11089-0 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 112368, DOI: 10.1038/s41598-017-11089-0, PubMed: 28878231)
40.	Kiyoe Kurahashi, Itsuro Endo, Takeshi Kondo, Kana Morimoto, Sumiko Yoshida, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa, Kohhei Nakajima, Yoshifumi Mizobuchi, Shinji Nagahiro, Masahiro Abe and Seiji Fukumoto : Remarkable Shrinkage of a Growth Hormone (GH)-secreting Macroadenoma Induced by Somatostatin Analogue Administration: A Case Report and Literature Review., Internal Medicine, Vol.56, No.18, 2455-2461, 2017. (要約) Acromegaly is caused by excessive growth hormone secretion, usually from pituitary adenomas. Somoatostatin analogues are widely used as primary or adjunctive therapy in the management of acromegaly. In this report, we present a case with remarkable shrinkage of a tumor after relatively short-term octreotide long-acting release (LAR) administration. During the 30-month follow-up after starting octreotide LAR, there was no recurrence of acromegaly with remarkable shrinkage of the tumor on pituitary magnetic resonance imaging. A literature review of the predictors for tumor shrinkage after the administration of somatostatin analogues in patients with acromegaly is also discussed in relation to this case. (徳島大学機関リポジトリ) ● Metadata: 114396 (出版サイトへのリンク) ● Publication site (DOI): 10.2169/internalmedicine.8223-16 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28824054 ● Summary page in Scopus @ Elsevier: 2-s2.0-85029653591 (徳島大学機関リポジトリ: 114396, DOI: 10.2169/internalmedicine.8223-16, PubMed: 28824054, Elsevier: Scopus)
41.	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. (要約) In Study 1, pitavastatin attenuated plaque formation and medial fibrosis of the aortic root with decreased macrophage infiltration in eNOS(-/-) ApoE(-/-) mice. PCR array analysis showed reductions in aortic gene expression of proatherogenic factors, including Ccl2 and Ccr2 in pitavastatin-treated double mutant mice. In addition, pitavastatin activated not only atherogenic p38MAPK and JNK but also anti-atherogenic ERK1/2 and ERK5 in the aorta of the double mutant mice. In Study 2, pitavastatin prolonged hind-limb survival after the surgery with increased BCL2-to-BAX protein ratio and inactivated JNK. Enhanced expression of anti-apoptotic genes, including Vegf, Api5, Atf5, Prdx2, and Dad1, was observed in the ischemic limb of pitavastatin-treated eNOS(-/-) mice. Furthermore, pitavastatin activated both aortic and skeletal muscle AMPK in the eNOS-deficient vascular injury models. (徳島大学機関リポジトリ) ● Metadata: 115483 (出版サイトへのリンク) ● Publication site (DOI): 10.5551/jat.37747 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 115483, DOI: 10.5551/jat.37747, PubMed: 28592707)
42.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 110925 (出版サイトへのリンク) ● Publication site (DOI): 10.5551/jat.37739 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 110925, DOI: 10.5551/jat.37739, PubMed: 28502917)
43.	Akio Kuroda, Tsuruo Miho, Aki Nanako, Takeshi Kondo, Oguro Yukari, Motoyuki Tamaki, Ken-ichi Aihara, Itsuro Endo, Toshio Matsumoto, Masahiro Abe and Munehide Matsuhisa : A Pirot study comparing the CGM-assessed glycemic profiles of patients with type 1 diabetes on insulin degludec and insulin glargine, Diabetology International, Vol.8, No.1, 112-115, 2017. (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s13340-016-0289-4 (文献検索サイトへのリンク) ● Summary page in Scopus @ Elsevier: 2-s2.0-85013200573 (DOI: 10.1007/s13340-016-0289-4, Elsevier: Scopus)
44.	Takeshi Kondo, Itsuro Endo, Yukari Ooguro, Kana Morimoto, Kiyoe Kurahashi, Sumiko Yoshida, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa, Masahiro Abe and Seiji Fukumoto : Suppression of the Hypothalamic-pituitary-adrenal Axis by Maximum Androgen Blockade in a Patient with Prostate Cancer., Internal Medicine, Vol.55, No.24, 3623-3626, 2016. (要約) A 78-year-old Japanese man showed suppression of the hypothalamic-pituitary-adrenal axis during maximum androgen blockade (MAB) therapy including chlormadinone acetate (CMA) for prostate cancer. After stopping the MAB therapy, both the basal ACTH level and the response to CRH recovered. While no reports have indicated that CMA suppresses the hypothalamic-pituitary-adrenal axis in patients with prostate cancer, CMA has been shown to inhibit this axis in animals. These observations suggest that we must monitor the hypothalamic-pituitary-adrenal axis in patients treated with CMA, especially under stressful conditions. (キーワード) Adrenal Glands / Adrenocorticotropic Hormone / Aged / Androgen Antagonists / Animals / Antineoplastic Agents / Chlormadinone Acetate / Corticotropin-Releasing Hormone / Diabetes Mellitus, Type 2 / Humans / Hypothalamo-Hypophyseal System / Male / Pituitary-Adrenal System / Prostatic Neoplasms / Treatment Outcome (徳島大学機関リポジトリ) ● Metadata: 114392 (出版サイトへのリンク) ● Publication site (DOI): 10.2169/internalmedicine.55.7359 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27980263 ● Summary page in Scopus @ Elsevier: 2-s2.0-85007140325 (徳島大学機関リポジトリ: 114392, DOI: 10.2169/internalmedicine.55.7359, PubMed: 27980263, Elsevier: Scopus)
45.	Ariunzaya Bat-Erdene, Hirokazu Miki, Asuko Oda, Shingen Nakamura, Jumpei Teramachi, Ryota Amachi, Hirofumi Tenshin, Masahiro Hiasa, Masami Iwasa, Takeshi Harada, Shiroh Fujii, Kimiko Sogabe, Kumiko Kagawa, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara and Masahiro Abe : Synergistic targeting of Sp1, a critical transcription factor for myeloma cell growth and survival, by panobinostat and proteasome inhibitors., Oncotarget, Vol.7, No.48, 79064-79075, 2016. (要約) Panobinostat, a pan-deacetylase inhibitor, synergistically elicits cytotoxic activity against myeloma (MM) cells in combination with the proteasome inhibitor bortezomib. Because precise mechanisms for panobinostat's anti-MM action still remain elusive, we aimed to clarify the mechanisms of anti-MM effects of panobinostat and its synergism with proteasome inhibitors. Although the transcription factor Sp1 was overexpressed in MM cells, the Sp1 inhibitor terameprocol induced MM cell death in parallel with reduction of IRF4 and cMyc. Panobinostat induced activation of caspase-8, which was inversely correlated with reduction of Sp1 protein levels in MM cells. The panobinostat-mediated effects were further potentiated to effectively induce MM cell death in combination with bortezomib or carfilzomib even at suboptimal concentrations as a single agent. Addition of the caspase-8 inhibitor z-IETD-FMK abolished the Sp1 reduction not only by panobinostat alone but also by its combination with bortezomib, suggesting caspase-8-mediated Sp1 degradation. The synergistic Sp1 reduction markedly suppressed Sp1-driven prosurvival factors, IRF4 and cMyc. Besides, the combinatory treatment reduced HDAC1, another Sp1 target, in MM cells, which may potentiate HDAC inhibition. Collectively, caspase-8-mediated post-translational Sp1 degradation appears to be among major mechanisms for synergistic anti-MM effects of panobinostat and proteasome inhibitors in combination. (徳島大学機関リポジトリ) ● Metadata: 109988 (出版サイトへのリンク) ● Publication site (DOI): 10.18632/oncotarget.12594 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27738323 ● Search Scopus @ Elsevier (PMID): 27738323 ● Search Scopus @ Elsevier (DOI): 10.18632/oncotarget.12594 (徳島大学機関リポジトリ: 109988, DOI: 10.18632/oncotarget.12594, PubMed: 27738323)
46.	Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, Takeshi Harada, Asuka Oda, Shingen Nakamura, Derek Hanson, Keiichiro Watanabe, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Masami Iwasa, Itsuro Endo, Takeshi Kondo, Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Yoshiaki Kuroda, Hideaki Horikawa, Eiji Tanaka, Masahiro Abe and Toshio Matsumoto : A vicious cycle between acid sensing and survival signaling in myeloma cells: acid-induced epigenetic alteration., Oncotarget, Vol.7, No.43, 70447-70461, 2016. (要約) Myeloma (MM) cells and osteoclasts are mutually interacted to enhance MM growth while creating acidic bone lesions. Here, we explored acid sensing of MM cells and its role in MM cell response to acidic conditions. Acidic conditions activated the PI3K-Akt signaling in MM cells while upregulating the pH sensor transient receptor potential cation channel subfamily V member 1 (TRPV1) in a manner inhibitable by PI3K inhibition. The acid-activated PI3K-Akt signaling facilitated the nuclear localization of the transcription factor Sp1 to trigger the expression of its target genes, including TRPV1 and HDAC1. Consistently, histone deacetylation was enhanced in MM cells in acidic conditions, while repressing a wide variety of genes, including DR4. Indeed, acidic conditions deacetylated histone H3K9 in a DR4 gene promoter and curtailed DR4 expression in MM cells. However, inhibition of HDAC as well as either Sp1 or PI3K was able to restore DR4 expression in MM cells suppressed in acidic conditions. These results collectively demonstrate that acid activates the TRPV1-PI3K-Akt-Sp1 signaling in MM cells while inducing HDAC-mediated gene repression, and suggest that a positive feedback loop between acid sensing and the PI3K-Akt signaling is formed in MM cells, leading to MM cell response to acidic bone lesions. (徳島大学機関リポジトリ) ● Metadata: 113048 (出版サイトへのリンク) ● Publication site (DOI): 10.18632/oncotarget.11927 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27626482 ● Search Scopus @ Elsevier (PMID): 27626482 ● Search Scopus @ Elsevier (DOI): 10.18632/oncotarget.11927 (徳島大学機関リポジトリ: 113048, DOI: 10.18632/oncotarget.11927, PubMed: 27626482)
47.	Takeshi Harada, Hirokazu Miki, Q Cui, A Oda, Ryota Amachi, Jumpei Teramachi, A Bat-Erdene, K Sogabe, M Iwasa, Shiroh Fujii, Shingen Nakamura, Kumiko Kagawa, Sumiko Yoshida, I Endo, Ken-ichi Aihara, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : Expansion of Th1-like V9V2T cells by new-generation IMiDs, lenalidomide and pomalidomide, in combination with zoledronic acid., Leukemia, Vol.31, No.1, 258-262, 2016. (出版サイトへのリンク) ● Publication site (DOI): 10.1038/leu.2016.273 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27698446 ● Search Scopus @ Elsevier (PMID): 27698446 ● Search Scopus @ Elsevier (DOI): 10.1038/leu.2016.273 (DOI: 10.1038/leu.2016.273, PubMed: 27698446)
48.	菅澤典子, 西雄千佳, 中山泰介, 黒部裕嗣, 宅見央子, 東口文治, 粟飯原賢一, 島袋充生, 佐田政隆, 北川哲也 : 糖転移ヘスペリジン/分散ヘスペレチンの動脈硬化病巣進展に対する抑制効果についての検討, 日本病態栄養学会誌, Vol.19, No.3, 351-360, 2016年. (キーワード) 糖転移ヘスペリジン / 分散ヘスペレチン / 動脈硬化 (atherosclerosis) / マクロファージ / ApoEノックアウトマウス
49.	Takeshi Kondo, Itsuro Endo, Ken-ichi Aihara, Ohnishi Yukiyo, Dong Bingzi, Oguro Yukari, Kiyoe Kurahashi, Sumiko Yoshida, Yuichi Fujinaka, Akio Kuroda, Munehide Matsuhisa, Seiji Fukumoto, Toshio Matsumoto and Masahiro Abe : Serum carboxy-terminal telopeptide of type I collagen levels are associated with carotid atherosclerosis in patients with cardiovascular risk factors., Endocrine Journal, Vol.63, No.4, 397-404, 2016. (要約) Carboxy-terminal telopeptide of type I collagen (ICTP) is generated through matrix metalloproteinase (MMP)-dependent type I collagen digestion, and has been widely utilized as a biomarker for bone turnover. The fact that atherosclerotic lesions are rich in both type I collagen and MMP-producing macrophages led to the hypothesis that serum ICTP concentrations may serve as a non-invasive clinical biomarker for atherosclerosis. Therefore, the association of serum ICTP concentrations with the maximum intima-media thickness (IMT) of carotid arteries, a surrogate index of systemic atherosclerosis, or brachial-ankle pulse wave velocity (baPWV) in patients with atherosclerotic risk factors was evaluated. A total of 52 male and 65 female (mean age: 62.8 yrs) patients without renal failure, malignancies or bone diseases known to affect serum ICTP concentrations were recruited. Patients with max IMTs ≥1.1 mm showed significantly higher serum ICTP concentrations compared with patients with max IMTs <1.1 mm (3.33 ± 0.97 vs 2.82 ± 0.65 ng/mL, p<0.05). Serum ICTP concentration was also positively correlated with max IMT (p<0.001) or baPWV values (p<0.05). Multivariate analyses also revealed that serum ICTP concentrations were correlated with max IMT (p<0.001; 95% CI 0.200 to 0.454). These results suggest that serum ICTP concentrations can be used as a non-invasive biomarker for systemic atherosclerosis. (徳島大学機関リポジトリ) ● Metadata: 109666 (出版サイトへのリンク) ● Publication site (DOI): 10.1507/endocrj.EJ15-0589 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26877258 ● Summary page in Scopus @ Elsevier: 2-s2.0-84964267287 (徳島大学機関リポジトリ: 109666, DOI: 10.1507/endocrj.EJ15-0589, PubMed: 26877258, Elsevier: Scopus)
50.	Yumi Kuwamura, Sumikawa Masuko, Tetsuya Tanioka, Toshihiko Nagata, Eijiro Sakamoto, Hiromi Murata, Munehide Matsuhisa, Ken-ichi Aihara, Daisuke Hinode, Hirokazu Uemura, Hirokazu Ito, Yuko Yasuhara and Rozzano De Castro Locsin : Development of the Diabetes Oral Health Assessment Tool © for Nurses, Health, Vol.7, No.12, 1710-1720, 2015. (キーワード) 糖尿病 (diabetes mellitus) / 口腔保健行動 (oral health behaviors) / Oral Status / Nursing Assessment / Diabetes Nurse Specialist (出版サイトへのリンク) ● Publication site (DOI): 10.4236/health.2015.712186 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.4236/health.2015.712186 (DOI: 10.4236/health.2015.712186)
51.	T Shigekiyo, E Sekimoto, H Shibata, Shuji Ozaki, T Okumura, H Fujinaga, H Shibata, Ken-ichi Aihara and Masashi Akaike : Factor VII Tokushima: the first case of factor VII Cys22Gly with the development of myocardial infarction in the proband receiving recombinant factor VIIa replacement therapy., Blood Coagulation & Fibrinolysis, Vol.26, No.8, 956-958, 2015. (要約) An 81-year-old man was referred to our department because of suspected factor VII (FVII) deficiency. His FVII activity was under 1%, whereas the FVII activity levels of his son and granddaughter were 65 and 109%, respectively. The nucleotide at position 3886 of his FVII gene was homozygous for G. A single T to G substitution results in the replacement of wild-type Cys at residue 22 by Gly. His son was heterozygous for G and T at position 3886, whereas his granddaughter was homozygous for wild-type T. These results suggest that he was homozygous for FVII Cys22Gly. He underwent radiofrequency ablation (RFA) for hepatocellular carcinoma, receiving 20 μg/kg of recombinant FVIIa prior to RFA and 10 μg/kg of recombinant FVIIa twice after RFA. He showed no bleeding tendency; however, a myocardial infarction was diagnosed and percutaneous coronary intervention was performed. (キーワード) Aged, 80 and over / Base Sequence / Blood Coagulation Tests / Coagulants / Factor VII Deficiency / Factor VIIa / Genotype / Heterozygote / Homozygote / Humans / Male / Molecular Sequence Data / Myocardial Infarction / Pedigree / Recombinant Proteins (出版サイトへのリンク) ● Publication site (DOI): 10.1097/MBC.0000000000000346 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26517065 ● Summary page in Scopus @ Elsevier: 2-s2.0-84947057797 (DOI: 10.1097/MBC.0000000000000346, PubMed: 26517065, Elsevier: Scopus)
52.	Shusuke Yagi, Ken-ichi Aihara, Daiju Fukuda, Akira Takashima, Mika Bando, Tomoya Hara, Sachiko Nishimoto, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Takeshi Tobiume, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Masashi Akaike and Masataka Sata : Reduced ratio of eicosapentaenoic acid and docosahexaenoic acid to arachidonic acid is associated with early onset of acute coronary syndrome., Nutrition Journal, Vol.14, No.1, 111, 2015. (要約) BACKGROUND: The hospitalization rate for acute coronary syndrome (ACS) for people aged 50 has remained stable over the past decade. Increased serum levels of n-3 polyunsaturated fatty acids (PUFAs), such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are associated with a decreased incidence of cardiovascular events and mortality in older patients; however, it is currently unknown whether reduced serum levels of n-3 PUFAs is also a risk factor for ACS in patients aged 50 years.METHODS AND RESULTS: We retrospectively reviewed 102 (male/ female 73/29) Japanese ACS patients whose serum levels of EPA/arachidonic acid (AA) and DHA/AA were evaluated on admission. The EPA/AA ratio was the lowest in patients aged 50 compared to patients aged 51-74 and 75. Pearson correlation analysis showed that early ACS onset was associated with low EPA/AA and DHA/AA ratios, and multiple regression analysis determined that decreased ratios of EPA/AA and DHA/AA, and male sex, current smoker status, increased body mass index and triglyceride levels, independently correlated with early ACS onset. Conversely, low-density and high-density lipoproteins, glycated hemoglobin, and hypertension did not correlate with early ACS onset. Subgroup analyses of male patients revealed that decreased ratios of EPA/AA and DHA/AA independently correlated with early ACS onset.CONCLUSION: Decreased EPA/AA and DHA/AA ratios may be risk factors for early onset of ACS, suggesting that reduced EPA/AA and DHA/AA may represent targets for preventing ACS in Japanese young people. (出版サイトへのリンク) ● Publication site (DOI): 10.1186/s12937-015-0102-4 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26514181 ● Summary page in Scopus @ Elsevier: 2-s2.0-84945959581 (DOI: 10.1186/s12937-015-0102-4, PubMed: 26514181, Elsevier: Scopus)
53.	Shusuke Yagi, Ken-ichi Aihara, Masashi Akaike, Daiju Fukuda, HM Salim, Masayoshi Ishida, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Toshio Matsumoto and Masataka Sata : Predictive factors for efficacy of dipeptidyl peptidase-4 inhibitors in patients with type 2 diabetes mellitus., Diabetes & Metabolism Journal, Vol.39, No.4, 342-347, 2015. (要約) BACKGROUND: Predictive factors for the efficacy of dipeptidyl peptidase-4 (DPP-4) inhibitors for lowering glycosylated hemoglobin (HbA1c) remain unclear in patients with type 2 diabetes mellitus. The aim of this study is therefore to clarify predictive factors of the efficacy of DPP-4 inhibitors for lowering HbA1c after 12 months of treatment.METHODS: A total of 191 consecutive type 2 diabetic patients (male sex 55%, mean age, 68.3±35.8 years), who had been treated with DPP-4 inhibitors for 12 months, were enrolled in this study and evaluated retrospectively.RESULTS: After 12 months of DPP-4 inhibitor treatment, random blood glucose level, and HbA1c level, decreased from 167±63 to 151±49 mg/dL (P<0.01), and from 7.5%±1.3% to 6.9%±0.9% (P<0.01) respectively, without severe side effects. Multiple regression analysis showed that predictors of DPP-4 inhibitor treatment efficacy in lowering HbA1c level after 12 months were a decrease in HbA1c level after 3 months of treatment, a high baseline HbA1c level, a low baseline body mass index, and the absence of coronary artery disease.CONCLUSION: Most suitable candidates for treatment with DPP-4 inhibitors are diabetics who are not obese and do not have coronary artery disease. In addition, long-term efficacy of DPP-4 inhibitors can be predicted by decrement of HbA1c after 3 months of treatment. (キーワード) Coronary artery disease / 糖尿病 (diabetes mellitus) / Dipeptidyl-peptidase IV inhibitors / Obese / Predictive factors (出版サイトへのリンク) ● Publication site (DOI): 10.4093/dmj.2015.39.4.342 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26301197 ● Summary page in Scopus @ Elsevier: 2-s2.0-84939780057 (DOI: 10.4093/dmj.2015.39.4.342, PubMed: 26301197, Elsevier: Scopus)
54.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 113751 (出版サイトへのリンク) ● Publication site (DOI): 10.1038/hr.2015.74 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26134126 ● Summary page in Scopus @ Elsevier: 2-s2.0-84946558014 (徳島大学機関リポジトリ: 113751, DOI: 10.1038/hr.2015.74, PubMed: 26134126, Elsevier: Scopus)
55.	Jin Temma, Munehide Matsuhisa, Toru Horie, Akio Kuroda, Hiroyasu Mori, Motoyuki Tamaki, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe and Toshio Matsumoto : Non-invasive Measurement of Skin Autofluorescence as a Beneficial Surrogate Marker for Atherosclerosis in Patients with Type 2 Diabetes, The Journal of Medical Investigation : JMI, Vol.62, No.3-4, 126-129, 2015. (要約) Advanced glycation end-products (AGEs) are thought to play a major role in the pathogenesis of diabetic vascular complications. Skin autofluorescence (AF) was recently reported to represent tissue AGEs accumulation with a non-invasive method. The aim of the present study was to evaluate association between AF value and diabetic vascular complications, such as retinopathy, nephropathy and cervical atherosclerosis using the carotid intima-media thickness (IMT), an established marker of cardiovascular disease in patients with type 2 diabetes. A total of 68 patients with type 2 diabetes were enrolled in a cross-sectional manner. AGEs accumulation was measured with AF reader. Clinical parameters were collected at the time of AF and IMT measurement. Max-IMT was correlated with age and AF (r=0.407, p=0.001), but not with HbA1c, GA, and pentosidine. Also, AF was not correlated with HbA1c, GA and pentosidine, but was correlated with age (r=0.560, p<0.001), duration of diabetes (r=0.256, p<0.05). Multivariate regression analysis revealed that AF, but not age, was an independent determinant of max-IMT. In conclusion, AF might be a beneficial surrogate marker for evaluating carotid atherosclerosis in patients with type 2 diabetes non-invasively. J. Med. Invest. 62: 126-129, August, 2015. (徳島大学機関リポジトリ) ● Metadata: 111266 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.62.126 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26399335 ● Summary page in Scopus @ Elsevier: 2-s2.0-84942054596 (徳島大学機関リポジトリ: 111266, DOI: 10.2152/jmi.62.126, PubMed: 26399335, Elsevier: Scopus)
56.	Shusuke Yagi, Ken-ichi Aihara, Daiju Fukuda, Akira Takashima, Tomoya Hara, Junko Hotsuchi, Takayuki Ise, Koji Yamaguchi, Takeshi Tobiume, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Masashi Akaike and Masataka Sata : Effects of docosahexaenoic acid on the endothelial function in patients with coronary artery disease., Journal of Atherosclerosis and Thrombosis, Vol.22, No.5, 447-454, 2015. (要約) AIM: The consumption of n-3 polyunsaturated fatty acids (PUFA), including docosahexaenoic acid DHA), reduces the incidence of cardiovascular events, and reduced serum levels of n-3 PUFA may be associated with an increased risk of cardiovascular events. However, controversy remains regarding which components of PUFA are associated with the endothelial function in patients with coronary artery disease (CAD). We therefore examined the associations between the n-3 and n-6 PUFA levels and CAD.METHODS: We retrospectively reviewed 160 consecutive Japanese patients with CAD whose endothelial function was measured according to the percent change in flow-mediated dilation (FMD) and the serum levels of n-3 PUFA, including eicosapentaenoic acid (EPA) and DHA, and n-6 PUFA, including arachidonic acid (AA) and dihomo-gamma-linolenic acid (DHLA).RESULTS: A single regression analysis showed no relationships between the FMD and the serum levels of PUFA, including EPA, DHA, AA and DHLA. In contrast, a multiple regression analysis showed that the DHA level was a positive (P0.01) and age was a negative (P0.001) contributor to an increased FMD; however, sex, body mass index, systolic and diastolic blood pressure, current/past smoking and the levels of HbA1c, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, EPA, AA and DHLA did not significantly affect the outcome.CONCLUSIONS: The serum level of DHA is associated with the endothelial function evaluated according to the FMD in patients with CAD, thus suggesting that a low serum level of DHA may be a predictive biomarker for endothelial dysfunction. (キーワード) Flow-mediated dilation / n-3 polyunsaturated fatty acids / Docosahexaenoic acid (出版サイトへのリンク) ● Publication site (DOI): 10.5551/jat.26914 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25342567 ● CiNii @ 国立情報学研究所 (CRID): 1390001204431540352 ● Summary page in Scopus @ Elsevier: 2-s2.0-84929412906 (DOI: 10.5551/jat.26914, PubMed: 25342567, CiNii: 1390001204431540352, Elsevier: Scopus)
57.	Shusuke Yagi, A Takashima, M Mitsugi, T Wada, Junko Hotsuchi, Ken-ichi Aihara, T Hara, Masayoshi Ishida, Daiju Fukuda, Takayuki Ise, Koji Yamaguchi, Takeshi Tobiume, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Masashi Akaike and Masataka Sata : Effect of combination tablets containing amlodipine 10 mg and irbesartan 100 mg on blood pressure and cardiovascular risk factors in patients with hypertension., Therapeutics and Clinical Risk Management, Vol.11, 83-88, 2015. (要約) Background: Hypertension is one of the major risk factors for cardiovascular and cerebrovascular disease and mortality. Patients who receive insufficient doses of antihypertensive agents or who are poorly adherent to multidrug treatment regimens often fail to achieve adequate blood pressure (BP) control. The aim of this study was to determine the efficacy of an angiotensin II receptor blocker (ARB) and calcium channel blocker (CCB) combination tablet containing a regular dose of irbesartan (100 mg) and a high dose of amlodipine (10 mg) with regard to lowering BP and other risk factors for cardiovascular disease.Methods: We retrospectively evaluated data from 68 patients with essential hypertension whose treatment regimen was changed either from combination treatment with an independent ARB and a low-dose or regular-dose CCB or from a combination tablet of ARB and a low-dose or regular-dose CCB to a combination tablet containing amlodipine 10 mg and irbesartan 100 mg, because of incomplete BP control. Previous treatments did not include irbesartan as the ARB.Results: The combination tablet decreased systolic and diastolic BP. In addition, it significantly decreased serum uric acid, low-density lipoprotein cholesterol, and increased high-density lipoprotein cholesterol levels, independent of the BP-lowering effect. Treatment with the combination tablet did not affect serum triglycerides, plasma glucose, glycated hemoglobin, serum potassium or creatinine levels, or the urinary albumin excretion rate.Conclusion: The combination tablet containing amlodipine 10 mg and irbesartan 100 mg had a greater BP-lowering effect than an ARB and a low-dose or regular-dose CCB. In addition, the combination tablet had more favorable effects on serum uric acid, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol levels in patients with hypertension. (キーワード) blood pressure / combination tablet / uric acid / low-density lipoprotein cholesterol / high-density lipoprotein cholesterol (出版サイトへのリンク) ● Publication site (DOI): 10.2147/TCRM.S72299 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25624765 ● Summary page in Scopus @ Elsevier: 2-s2.0-84921260560 (DOI: 10.2147/TCRM.S72299, PubMed: 25624765, Elsevier: Scopus)
58.	Shusuke Yagi, T Hara, R Ueno, Ken-ichi Aihara, Daiju Fukuda, A Takashima, Junko Hotsuchi, Takayuki Ise, Koji Yamaguchi, Takeshi Tobiume, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Masashi Akaike and Masataka Sata : Serum concentration of eicosapentaenoic acid is associated with cognitive function in patients with coronary artery disease., Nutrition Journal, Vol.13, No.1, 112, 2014. (要約) BACKGROUND: Recent studies have shown that intake of n-3 polyunsaturated fatty acids (PUFAs) is associated with reduced risk of cognitive impairment and coronary artery disease (CAD); however, it is currently unknown whether reduced serum n-3 PUFA is associated with cognitive impairment in patients with CAD.METHODS: We retrospectively evaluated cognitive function with the mini-mental state examination (MMSE), serum levels of PUFAs (including eicosapentaenoic acid [EPA], docosahexaenoic acid [DHA], dihomogammalinolenic acid [DGLA], and arachidonic acid [AA]), cardiovascular risk factors (hypertension, dyslipidemia, diabetes mellitus, cerebrovascular disease, and history of current/previous smoking), and parameters of cardiac function (left ventricular ejection fraction and brain natriuretic peptide levels) in 146 Japanese CAD patients. The associations between the MMSE scores and the other parameters were evaluated.RESULTS: Pearson correlation analysis showed that EPA (R =0.25, P <0.01), EPA/AA ratio (R =0.22, P =0.01), and left ventricular ejection fraction (R =0.15, P =0.04) were positively associated with MMSE score, and that age (R = -0.20, P <0.01) and brain natriuretic peptide levels (R = -0.28, P <0.01) were inversely associated with MMSE score. Multiple regression analysis showed that age (P <0.05) was negatively associated with MMSE score, while EPA (P <0.01) and EPA/AA ratio (P <0.05) were positively associated with MMSE score; however, sex; body mass index; left ventricular ejection fraction; levels of DHA, AA, and DGLA; DHA/AA ratio; brain natriuretic peptide; and presence of hypertension, dyslipidemia, diabetes mellitus, cerebrovascular disease, and history of current/previous smoking were statistically excluded.CONCLUSIONS: Serum EPA concentration is associated with cognitive function in patients with CAD, suggesting that a low serum EPA level is a risk factor for cognitive impairment independent of cardiac function, including left ventricular ejection fraction. This correlation potentially lends further support to a role of dietary n-3 PUFAs in preventing the cognitive decline in CAD patients. (キーワード) Aged / Arachidonic Acid / Cognition / Cognition Disorders / Coronary Disease / Eicosapentaenoic Acid / Fatty Acids, Omega-3 / Female / Humans / Japan / Male / Middle Aged / Retrospective Studies / Risk Factors / Stroke Volume (出版サイトへのリンク) ● Publication site (DOI): 10.1186/1475-2891-13-112 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25471307 ● Summary page in Scopus @ Elsevier: 2-s2.0-84926465688 (DOI: 10.1186/1475-2891-13-112, PubMed: 25471307, Elsevier: Scopus)
59.	Shusuke Yagi, M Fujimura, Masashi Akaike, Ken-ichi Aihara, Takashi Iwase, M Tada, Yuka Ueda, Takayuki Ise, Koji Yamaguchi, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Increase in serum triglyceride was associated with coronary plaque vulnerability in a patient with rheumatoid arthritis., Journal of Cardiology Cases, Vol.10, No.2, 54-57, 2014. (要約) Rates of morbidity and mortality from cardiovascular disease are high in patients with rheumatoid arthritis (RA); however, the mechanisms and biomarkers that reflect coronary plaque vulnerability have not yet been established. We present a case of acute coronary syndrome (ACS) presumably caused by exacerbation of chronic inflammation of RA, in which an abrupt increase in serum triglyceride was seen on the day of onset of ACS but not during effort angina. This case suggests that RA patients with an abrupt increase in triglyceride need intensive care including anti-platelet and statin therapy for the prevention of coronary plaque rupture.<Learning objective: Triglyceride might be a sensitive biomarker of activated macrophages and plaque vulnerability in patients with RA. RA patients with an abrupt increase in triglyceride might need intensive care including anti-platelet and statin therapy for the prevention of coronary plaque rupture.> (キーワード) Acute coronary syndrome / Triglyceride / Tumor necrosis factor- / Biomarker (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.jccase.2014.04.009 (文献検索サイトへのリンク) ● Summary page in Scopus @ Elsevier: 2-s2.0-84905378195 (DOI: 10.1016/j.jccase.2014.04.009, Elsevier: Scopus)
60.	Shusuke Yagi, Ken-ichi Aihara, Takeshi Kondo, Itsuro Endo, Junko Hotsuchi, Takayuki Ise, Takashi Iwase, Masashi Akaike, Toshio Matsumoto and Masataka Sata : High serum parathyroid hormone and calcium are risk factors for hypertension in Japanese patients., Endocrine Journal, Vol.61, No.7, 727-733, 2014. (要約) Excess parathyroid hormone (PTH), known as primary hyperparathyroidism (pHPT), results in hypercalcemia and bone loss. Recent studies have shown that PTH is associated with the occurrence of hypertension in Western countries; however, controversy remains regarding high serum levels of PTH and calcium as risk factors for hypertension in Japanese patients. We retrospectively enrolled 114 consecutive Japanese patients who visited our hospital for examination and treatment of hypercalcemia and/or hypertension with serum calcium levels ≥ 9.8 mg/dL. To estimate the prevalence of hypertension, the patients were categorized according to calcium levels into hypercalcemic (10.2-13.4 mg/dL) and normocalcemic (9.8-10.1 mg/dL) groups, which were further categorized into high PTH (50-440 pg/mL) and low PTH (8-49 pg/mL) groups. The prevalence of hypertension was higher in patients with hypercalcemia than in patients with normocalcemia in both the high and low PTH groups. The prevalence of hypertension was higher in patients with high serum PTH levels than in patients with low serum PTH levels in both the hypercalcemic and normocalcemic groups. Logistic multiple regression analysis determined that serum calcium (P < 0.05) and PTH (P < 0.01) levels were positive contributors to hypertension. In conclusion, high serum levels of PTH and calcium are risk factors for hypertension in Japanese patients. (キーワード) parathyroid hormone / カルシウム (calcium) / 高血圧 (hypertension) (出版サイトへのリンク) ● Publication site (DOI): 10.1507/endocrj.EJ14-0004 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24849536 ● CiNii @ 国立情報学研究所 (CRID): 1390001206300211712 ● Summary page in Scopus @ Elsevier: 2-s2.0-84905190698 (DOI: 10.1507/endocrj.EJ14-0004, PubMed: 24849536, CiNii: 1390001206300211712, Elsevier: Scopus)
61.	Masashi Akaike, Ken-ichi Aihara, Hiroaki Yanagawa, Takashi Iwase, Sumiko Yoshida, Sato Chiho, Saijo Tomoka, Hiroaki Mikasa, Kashiwada Yoshizaki, Yoshihisa Takaishi, Koichiro Tsuchiya, Toshiaki Tamaki, Toshio Matsumoto and Masataka Sata : Efficacy and safety of Citrus sudachi peel in obese adults:A randomized, double-blind, pilot study, Functional Foods in Health and Disease, Vol.4, No.6, 276-284, 2014. (出版サイトへのリンク) ● Publication site (DOI): 10.31989/ffhd.v4i7.5 (文献検索サイトへのリンク) ● Summary page in Scopus @ Elsevier: 2-s2.0-85054855286 (DOI: 10.31989/ffhd.v4i7.5, Elsevier: Scopus)
62.	Shusuke Yagi, Kadota Muneyuki, Ken-ichi Aihara, Nishikawa Koji, Hara Tomoya, Takayuki Ise, Yuka Ueda, Takashi Iwase, Masashi Akaike, Michio Shimabukuro, Shinsuke Katoh and Masataka Sata : Association of lower limb muscle mass and energy expenditure with visceral fat mass in healthy men, Diabetology & Metabolic Syndrome, Vol.6, No.1, 27, 2014. (要約) A high-calorie diet and physical inactivity, an imbalance between caloric intake and energy consumption, are major causes of metabolic syndrome (MetS), which manifests as accumulation of visceral fat and insulin resistance. However, the lifestyle-related factors associated with visceral fat mass in healthy men are not fully understood. We evaluated visceral fat area (VFA), skeletal muscle mass, caloric intake, and energy expenditure in 67 healthy male participants (mean age, 36.9 ± 8.8 years; body mass index 23.4 ± 2.5 kg/m2). Multiple regression analysis showed that the total skeletal muscle mass (P < 0.001) were negatively and age (P < 0.001) were positively associated with VFA. Lower limb muscle mass (P < 0.001) was strongly associated with VFA. However, total caloric intake, total energy expenditure, and energy expenditure during exercise were not associated with VFA. Skeletal muscle mass especially lower limb muscle mass negatively contributes to visceral fat mass in healthy men. Therefore, maintaining lower limb muscular fitness through daily activity may be a useful strategy for controlling visceral obesity and metabolic syndrome. (出版サイトへのリンク) ● Publication site (DOI): 10.1186/1758-5996-6-27 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24571923 ● Summary page in Scopus @ Elsevier: 2-s2.0-84896075201 (DOI: 10.1186/1758-5996-6-27, PubMed: 24571923, Elsevier: Scopus)
63.	Mizuho Kinouchi, Ken-ichi Aihara, Yuichi Fujinaka, Sumiko Yoshida, Yukari Ooguro, Kiyoe Kurahashi, Takeshi Kondo, Nanako Aki, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Toshio Matsumoto : Diabetic conditions differentially affect the endothelial function, arterial stiffness and carotid atherosclerosis., Journal of Atherosclerosis and Thrombosis, Vol.21, No.5, 486-500, 2014. (要約) Aim: The levels of fasting and postprandial plasma glucose, HbA1c and other risk factors for atherosclerosis have distinct effects in patients with and those without diabetes mellitus. The aim of this study was to determine the impact of diabetic surrogate markers on the endothelial function, arterial stiffness and carotid atherosclerosis in individuals with and without diabetes. Methods: A total of 320 Japanese subjects(mean age: 61.2±12.1 years) were recruited in this study. Demographic, clinical and laboratory parameters, including 75 g OGTT(155 subjects) results, were examined. The endothelial function was evaluated according to the flow-mediated vasodilation of the brachial artery(%FMD). In addition, arterial stiffness was evaluated according to the brachial-ankle pulse wave velocity(baPWV), and carotid atherosclerotic changes were estimated according to the maximum intima-media thickness(max-IMT) and resistive index of the common carotid artery(CCA-RI). A multiple regression analysis was performed to identify independent determinants of these vascular surrogate markers. Results: None of the glucose-related parameters were associated with the %FMD. In contrast, the presence of T2DM, the HbA1c level and an increased plasma glucose level at 60 minutes during 75 g OGTT were associated with an increased baPWV. The HbA1c level was also correlated with an increased max-IMT. The fasting plasma glucose(FPG) level and the presence of T2DM correlated with an increased CCA-RI. In the subjects with T2DM, the protective effects of high-density lipoprotein cholesterol(HDL-C) on the %FMD and baPWV were abolished. Conclusions: Various glucose metabolism parameters have different effects the degree of arterial stiffness and presence of carotid atherosclerosis, but not the endothelial function, suggesting that pharmacological intervention has the potential to preserve the endothelial function in diabetic individuals. In addition, the presence of T2DM blunts the vascular protective effects of HDL-C on the endothelial function and progression of arterial stiffness. (キーワード) Type 2 diabetes / Endothelial function / Arterial stiffness / Carotid atherosclerosis (徳島大学機関リポジトリ) ● Metadata: 106061 (出版サイトへのリンク) ● Publication site (DOI): 10.5551/jat.20834 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24401746 ● CiNii @ 国立情報学研究所 (CRID): 1390001204430842112 ● Summary page in Scopus @ Elsevier: 2-s2.0-84901494272 (徳島大学機関リポジトリ: 106061, DOI: 10.5551/jat.20834, PubMed: 24401746, CiNii: 1390001204430842112, Elsevier: Scopus)
64.	近藤剛史, 黒田暁生, 曽我部公子, 大黒由加里, 倉橋清衛, 田蒔基行, 木内美瑞穂, 吉田守美子, 安芸菜奈子, 遠藤逸朗, 粟飯原賢一, 藤中雄一, 松久宗英, 松本俊夫 : 術前後で持続血糖モニター(CGM)を比較しえたアドレナリン優位褐色細胞腫の1例, 糖尿病, Vol.57, No.9, 729-735, 2014年. (要約) 症例は78歳女性．2012年1月，25 mm大の左副腎腫瘍，尿メタネフリン高値，MIBGシンチからアドレナリン優位型褐色細胞腫と診断され，5月当科を紹介された．罹病期間9年の糖尿病があり内服加療をうけるも2010年頃よりHbA1cは悪化し，初診時8.5 %で，褐色細胞腫の周術期管理および血糖管理目的で当科入院した．入院後速やかにインスリン導入を行い，目標血糖値に達した際の持続血糖モニター(以下CGMと略す)の標準偏差(SD)は54であった．腹腔鏡下腫瘍摘除後は，一日総インスリン量が術前50単位から術後14単位に減少し，術後CGMでSDが24に改善した．また退院時はグリメピリド0.5 mg，シタグリプチン50 mgで管理可能となった．本例は，家族歴がなくやせ型で術後の血糖管理の改善からアドレナリン過剰が術前の病態の中心と考えられた． (キーワード) 褐色細胞腫 / アドレナリン / 糖尿病 / CGM(持続血糖モニター) (出版サイトへのリンク) ● Publication site (DOI): 10.11213/tonyobyo.57.729 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390001204908593792 ● Summary page in Scopus @ Elsevier: 2-s2.0-84908507898 (DOI: 10.11213/tonyobyo.57.729, CiNii: 1390001204908593792, Elsevier: Scopus)
65.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.1161/CIRCULATIONAHA.113.001533 (文献検索サイトへのリンク) ● 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)
66.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, Daiju Fukuda, Masayoshi Ishida, Takayuki Ise, Toshiyuki Niki, Yuka Ueda, Koji Yamaguchi, Takashi Iwase, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro and Masataka Sata : Pharmacology of Aldosterone and the Effects of Mineralocorticoid Receptor Blockade on Cardiovascular Systems., Acta Cardiologica Sinica, Vol.29, No.3, 201-207, 2013. (文献検索サイトへのリンク) ● Summary page in Scopus @ Elsevier: 2-s2.0-84878307366 (Elsevier: Scopus)
67.	Shuji Kato, Itsuro Endo, Mitsunori Fujimura, Rika Kuriwaka-Kido, Yuichi Fujinaka, Ken-ichi Aihara, Takashi Iwase, Daisuke Inoue, Masashi Akaike, Masahiro Abe and Toshio Matsumoto : Serum carboxy-terminal telopeptide of type I collagen (ICTP) as a surrogate marker for vulnerable plaques in atherosclerotic patients: A pilot study., Atherosclerosis, Vol.229, No.1, 182-185, 2013. (要約) Evaluation of atherosclerotic plaques depends on invasive intravascular ultrasonography (IVUS). Carboxy-terminal telopeptide of type I collagen (ICTP) is produced by matrix metalloproteinase (MMP)-dependent digestion of type I collagen. Because vulnerable plaques are rich in type I collagen and MMPs from macrophages, we examined the association between serum ICTP and coronary plaques in patients with coronary disease. We recruited 46 men and 17 women without renal failure or bone diseases affecting serum ICTP, who underwent coronary IVUS. Serum ICTP levels were higher in patients with coronary plaques containing more than 10% necrotic core area than in patients with less than 10% necrotic core area. A positive correlation was found between serum ICTP and necrotic core area. Only serum ICTP was positively correlated with necrotic core area by multivariate analysis (p < 0.05). These results suggest that serum ICTP can be used as a non-invasive marker of vulnerable plaques in atherosclerotic patients. (徳島大学機関リポジトリ) ● Metadata: 105936 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.atherosclerosis.2013.03.030 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23639859 ● Search Scopus @ Elsevier (PMID): 23639859 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2013.03.030 (徳島大学機関リポジトリ: 105936, DOI: 10.1016/j.atherosclerosis.2013.03.030, PubMed: 23639859)
68.	吉田守美子, 黒田暁生, 新居沙央里, 松本友里, 近藤絵里, 安藝菜奈子, 遠藤逸朗, 粟飯原賢一, 鈴木麗子, 松本俊夫, 松久宗英 : 新たなインスリンポンプParadigm 722によりカーボカウントのみで血糖管理が可能となった1型糖尿病の1例, 糖尿病, Vol.56, No.4, 240-245, 2013年. (要約) インスリンポンプParadigm712は，インスリン作用時間(AIT)が8時間の設定のため，十分な食後血糖補正インスリン投与を提案しないが，新しいParadigm 722はAITを2~8時間に設定できる．そこで，Paradigm 722の食後血糖補正インスリン量の妥当性を検証した．症例は1型糖尿病の50歳代女性．入院の上インスリンリスプロでParadigm 722を導入，食事スキップで基礎インスリンを設定し，糖質/インスリン比を各食前(11，15，13)g/Uとしたカーボカウントのもと，AITを3時間，インスリン効果値を60mg/dl/Uと設定した．退院前1週間の食後2時間血糖補正の際，150mg/dlを目標にインスリン効果値を用いた補正による自己算出インスリン量とポンプでの自動算出インスリン量とを比較した．食後高血糖に対する補正インスリンは，14回中7回で自己算出量よりも自動算出量が適切であった．Paradigm 722による食後補正インスリン自動算出法は，自己算出法と同等で，これを用いることで良好な血糖管理が簡便になった．(著者抄録) (キーワード) インスリン作用 / 持続皮下インスリン注入療法 / カーボカウント / 1型糖尿病 (出版サイトへのリンク) ● Publication site (DOI): 10.11213/tonyobyo.56.240 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390001204909103744 ● Summary page in Scopus @ Elsevier: 2-s2.0-84878045431 (DOI: 10.11213/tonyobyo.56.240, CiNii: 1390001204909103744, Elsevier: Scopus)
69.	Yoko Yamamoto, Tatsuya Yoshizawa, Toru Fukuda, Yuko Shirode-Fukuda, Taiyong Yu, Keisuke Sekine, Takashi Sato, Hirotaka Kawano, Ken-ichi Aihara, Yuko Nakamichi, Tomoyuki Watanabe, Masayo Shindo, Kazuki Inoue, Erina Inoue, Naoya Tsuji, Maiko Hoshino, Gerard Karsenty, Daniel Metzger, Pierre Chambon, Shigeaki Kato and Yuuki Imai : Vitamin D receptor in osteoblasts is a negative regulator of bone mass control., Endocrinology, Vol.154, No.3, 1008-1020, 2013. (要約) The physiological and beneficial actions of vitamin D in bone health have been experimentally and clinically proven in mammals. The active form of vitamin D [1,25(OH)(2)D(3)] binds and activates its specific nuclear receptor, the vitamin D receptor (VDR). Activated VDR prevents the release of calcium from its storage in bone to serum by stimulating intestinal calcium absorption and renal reabsorption. However, the direct action of VDR in bone tissue is poorly understood because serum Ca(2+) homeostasis is maintained through tightly regulated ion transport by the kidney, intestine, and bone. In addition, conventional genetic approaches using VDR knockout (VDR-KO, VDR(-/-)) mice could not identify VDR action in bone because of the animals' systemic defects in calcium metabolism. In this study, we report that systemic VDR heterozygous KO (VDR(+/L-)) mice generated with the Cre/loxP system as well as conventional VDR heterozygotes (VDR(+/-)) showed increased bone mass in radiological assessments. Because mineral metabolism parameters were unaltered in both types of mice, these bone phenotypes imply that skeletal VDR plays a role in bone mass regulation. To confirm this assumption, osteoblast-specific VDR-KO (VDR(Ob/Ob)) mice were generated with 2.3 kb 1(I)-collagen promoter-Cre transgenic mice. They showed a bone mass increase without any dysregulation of mineral metabolism. Although bone formation parameters were not affected in bone histomorphometry, bone resorption was obviously reduced in VDR(Ob/Ob) mice because of decreased expression of receptor activator of nuclear factor kappa-B ligand (an essential molecule in osteoclastogenesis) in VDR(Ob/Ob) osteoblasts. These findings establish that VDR in osteoblasts is a negative regulator of bone mass control. (キーワード) Animals / Bone Density / Bone Resorption / Bone and Bones / Calcium / Female / Gene Expression / Male / Mice / Mice, Inbred C57BL / Mice, Inbred CBA / Mice, Knockout / Mice, Transgenic / Osteoblasts / Osteoclasts / Receptors, Calcitriol / Rickets (出版サイトへのリンク) ● Publication site (DOI): 10.1210/en.2012-1542 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23389957 ● Search Scopus @ Elsevier (PMID): 23389957 ● Search Scopus @ Elsevier (DOI): 10.1210/en.2012-1542 (DOI: 10.1210/en.2012-1542, PubMed: 23389957)
70.	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. (要約) 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. (キーワード) 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 (徳島大学機関リポジトリ) ● Metadata: 113754 (出版サイトへのリンク) ● Publication site (DOI): 10.1097/FJC.0b013e318287d526 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 113754, DOI: 10.1097/FJC.0b013e318287d526, PubMed: 23364610)
71.	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. (要約) 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. (キーワード) Angiotensin II / Animals / Antioxidants / Aorta, Thoracic / カルシウム (calcium) / Cell Movement / Cell Proliferation / Fibrosis / Male / Mice / Mice, Inbred C57BL / Muscle, Smooth, Vascular / Nifedipine / Nitroso Compounds / 酸化ストレス (oxidative stress) / Rats / 活性酸素 (reactive oxygen species) (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s00210-012-0810-7 (文献検索サイトへのリンク) ● 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)
72.	Akio Kuroda, Tetsuyuki Yasuda, Mitsuyoshi Takahara, Fumie Sakamoto, Ryuichi Kasami, Kazuyuki Miyashita, Sumiko Yoshida, Eri Kondo, Ken-ichi Aihara, Itsuro Endo, Taka-Aki Matsuoka, Hideaki Kaneto, Toshio Matsumoto, Iichiro Shimomura and Munehide Matsuhisa : Carbohydrate-to-Insulin Ratio Is Estimated from 300-400 Divided by Total Daily Insulin Dose in Type 1 Diabetes Patients Who Use the Insulin Pump., Diabetes Technology & Therapeutics, Vol.14, No.11, 1077-1080, 2012. (要約) Abstract Background: To optimize insulin dose using insulin pump, basal and bolus insulin doses are widely calculated from total daily insulin dose (TDD). It is recommended that total daily basal insulin dose (TBD) is 50% of TDD and that the carbohydrate-to-insulin ratio (CIR) equals 500 divided by TDD. We recently reported that basal insulin requirement is approximately 30% of TDD. We therefore investigated CIR after adjustment of the proper basal insulin rate. Subjects and Methods: Forty-five Japanese patients with type 1 diabetes were investigated during several weeks of hospitalization. The patients were served standard diabetes meals (25-30 kcal/kg of ideal body weight). Each meal omission was done to confirm basal insulin rate. Target blood glucose level was set at 100 and 150 mg/dL before and 2 h after each meal, respectively. After the basal insulin rate was fixed and target blood glucose levels were achieved, TBD, CIR, TDD, and their products were determined. Results: Mean (±SD) blood glucose levels before and 2 h after meals were 121±47 and 150±61 mg/dL, respectively. TDD was 31.5±9.0 U, and TBD was 27.0±6.5% of TDD. CIR×TDD of breakfast was significantly lower than those of lunch and supper (288±73 vs. 408±92 and 387±83, respectively; P<0.01). Conclusions: CIR has diurnal variance and is estimated from the formula CIR=300/TDD at breakfast or CIR=400/TDD at lunch and supper in type 1 diabetes patients. These results indicate that the insulin dose has been underestimated by using previously established calculations. (出版サイトへのリンク) ● Publication site (DOI): 10.1089/dia.2012.0109 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23101953 ● Search Scopus @ Elsevier (PMID): 23101953 ● Search Scopus @ Elsevier (DOI): 10.1089/dia.2012.0109 (DOI: 10.1089/dia.2012.0109, PubMed: 23101953)
73.	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. (要約) 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. (キーワード) Heparin cofactor II (HCII) / vascular endothelial cells / 血管新生 (angiogenesis) (出版サイトへのリンク) ● Publication site (DOI): 10.1074/jbc.M112.353532 (文献検索サイトへのリンク) ● 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)
74.	Toshio Shigekiyo, Etsuko Sekimoto, Atsuhisa Shirakami, Hiroshi Yamaguchi, Hironobu Shibata, Shuji Ozaki, Masahiko Maegawa and Ken-ichi Aihara : Fibrinogen Tokushima II: a new case of congenital dysfibrinogenemia with a methionine-310 to threonine substitution., International Journal of Hematology, Vol.96, No.3, 395-397, 2012. (キーワード) Afibrinogenemia / Aged, 80 and over / Amino Acid Substitution / Base Sequence / Female / Fibrinogens, Abnormal / Humans / Mutation / Pedigree (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s12185-012-1148-0 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22836217 ● Search Scopus @ Elsevier (PMID): 22836217 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-012-1148-0 (DOI: 10.1007/s12185-012-1148-0, PubMed: 22836217)
75.	吉田守美子, 粟飯原賢一, 上田由佳, 伊勢孝之, 池田康将, 倉橋清衛, 木内美瑞穂, 遠藤逸朗, 藤中雄一, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 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年.
76.	Hirotsugu Kurobe, Ken-ichi Aihara, Higashida Mayuko, Hirata Yoichiro, Nishiya Masako, Matsuoka Yuki, Tamotsu Kanbara, Nakayama Taisuke, Hajime Kinoshita, Mikio Sugano, Eiki Fujimoto, Kurobe Ayako, Sugawara Noriko, Takashi Kitaichi, Masashi Akaike, Masataka Sata, Toshio Matsumoto and Tetsuya Kitagawa : Ezetimibe monotherapy ameliorates vascular function in patients with hypercholesterolemia through decreasing oxidative stress., Journal of Atherosclerosis and Thrombosis, Vol.18, No.12, 1080-1089, 2011. (要約) Ezetimibe, an inhibitor of cholesterol intestinal absorption, is a lipid lowering agent. However, anti-atherogenic effects of ezetimibe have not been fully elucidated. Therefore, the objective in this study was to clarify the vascular protective effects of ezetimibe in patients with hypercholesterolemia. Ezetimibe was administered to 20 patients with hypercholesterolemia (group E), and 20 age- and sex-matched patients with hypercholesterolemia were followed as controls (group C). Difference in metabolic profiles and cardiovascular surrogate markers before ezetimibe treatment and after 12 weeks of ezetimibe treatment were statistically evaluated. Ezetimibe treatment significantly reduced serum levels of low-density lipoprotein cholesterol (LDL-C) and malondialdehyde-modified low-density lipoprotein (MDA-LDL). In addition, the values of body mass index, body weight, waist circumference, plasma HbA1c and urinary albumin were significantly decreased in group E compared to those in group C. On the other hand, high-density lipoprotein cholesterol (HDL-C) and adiponectin levels were significantly increased in group E compared to those in group C. The values of brachial-ankle pulse wave velocity (ba-PWV), mean arterial blood pressure (m-ABP), and % of flow-mediated dilation (FMD) were significantly improved in group E. Furthermore, ultrasonic studies demonstrated amelioration of the vascular stiffness of common carotid arteries in group E but not in group C. These vascular protective effects of ezetimibe were statistically correlated with the decreased values of MDA-LDL and MDA-LDL-to-LDL-C ratio but not with those of LDL-C. Ezetimibe has a lipid lowering-independent vascular protective effect in patients with hypercholesterolemia through decreasing oxidative stress. (キーワード) Aged / Azetidines / Case-Control Studies / Endothelium, Vascular / Humans / Hypercholesterolemia / Lipids / Male / Middle Aged / 酸化ストレス (oxidative stress) (出版サイトへのリンク) ● Publication site (DOI): 10.5551/jat.9548 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22027560 ● Search Scopus @ Elsevier (PMID): 22027560 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.9548 (DOI: 10.5551/jat.9548, PubMed: 22027560)
77.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, Takashi Iwase, Kazue Ishikawa, Sumiko Yoshida, Yuka Sumitomo-Ueda, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Noriko Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Effect of low-dose (1 mg/day) pitavastatin on left ventricular diastolic function and albuminuria in patients with hyperlipidemia., The American Journal of Cardiology, Vol.107, No.11, 1644-1649, 2011. (要約) The aim of the present study was to evaluate the factors that modulate the protective action of statins on cardiorenal function, regardless of the lipid-lowering effect. To treat abnormal serum lipid profiles, low-dose pitavastatin (1.0 mg/day) was administered to 65 hyperlipidemic patients. The exclusion criteria included left ventricular ejection fraction <40% and apparent renal disease. Age- and gender-matched patients with hyperlipidemia (n = 40) served as the controls. After 12 to 16 weeks of pitavastatin treatment, pitavastatin had decreased low-density lipoprotein cholesterol (from 143.5 ± 31.4 to 98.2 ± 19.4 mg/dl, p <0.01), triglycerides (from 157.7 ± 57.2 to 140.5 ± 60.7 mg/dl, p <0.01), E/e' (from 10.8 ± 6.2 to 9.0 ± 4.5, p <0.05), a parameter of left ventricular diastolic function, and albuminuria (from 47.6 ± 55.9 to 28.5 ± 40.0 mg/g creatinine, p <0.01). Furthermore, pitavastatin decreased serum transforming growth factor-1 (from 709 ± 242 to 550 ± 299 pg/ml, p <0.01), urinary 8-hydroxy-2'-deoxyguanosine (from 6.6 ± 4.1 to 5.0 ± 3.1 g/g creatinine, p <0.01), an oxidative stress marker, and increased urinary nitrate and nitrite (from 22.5 ± 14.6 to 29.4 ± 27.6 nmol/g creatinine, p <0.05). No such changes were observed in the controls. Multiple regression analysis in the pitavastatin group revealed the effect of pitavastatin on cardiorenal function was associated with suppression of oxidative stress, but not on low-density lipoprotein cholesterol reduction. In conclusion, pitavastatin decreases E/e' and albuminuria, which is associated with suppression of oxidative stress. (キーワード) Aged / Albuminuria / Case-Control Studies / Cholesterol, LDL / Diastole / Female / Humans / Hydroxymethylglutaryl-CoA Reductase Inhibitors / Hyperlipidemias / Male / Middle Aged / Quinolines / Treatment Outcome / Triglycerides / Ventricular Function, Left (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.amjcard.2011.01.054 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21458773 ● Search Scopus @ Elsevier (PMID): 21458773 ● Search Scopus @ Elsevier (DOI): 10.1016/j.amjcard.2011.01.054 (DOI: 10.1016/j.amjcard.2011.01.054, PubMed: 21458773)
78.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, Takashi Iwase, Yuka Sumitomo-Ueda, Sumiko Yoshida, Toshio Matsumoto and Masataka Sata : Bosentan improves systemic sclerosis-related peripheral circulation insufficiency., International Journal of Cardiology, Vol.147, No.3, 472-475, 2011. (キーワード) Adult / Aged / Blood Circulation / Female / Humans / Middle Aged / Pain Measurement / Raynaud Disease / Scleroderma, Systemic / Sulfonamides (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.ijcard.2011.01.025 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21296436 ● Search Scopus @ Elsevier (PMID): 21296436 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ijcard.2011.01.025 (DOI: 10.1016/j.ijcard.2011.01.025, PubMed: 21296436)
79.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.atherosclerosis.2011.01.009 (文献検索サイトへのリンク) ● 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)
80.	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. (要約) 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. (キーワード) Adult / Blood Platelets / 細胞分化 (cell differentiation) / Cell Line, Tumor / Dyslipidemias / Female / Fenofibrate / 遺伝子発現 (gene expression) / Humans / 免疫組織化学 (immunohistochemistry) / Lipids / Male / Megakaryocytes / Middle Aged / PPAR alpha / Platelet-Derived Growth Factor / Pyrimidines / RNA, Messenger / Tetradecanoylphorbol Acetate (出版サイトへのリンク) ● Publication site (DOI): 10.5551/jat.5868 (文献検索サイトへのリンク) ● 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)
81.	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. (要約) 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. (キーワード) Aged / Cross-Sectional Studies / Female / Heparin Cofactor II / Humans / Male / Middle Aged / Risk Factors / Ventricular Dysfunction / Ventricular Remodeling (出版サイトへのリンク) ● Publication site (DOI): 10.1038/hr.2010.211 (文献検索サイトへのリンク) ● 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)
82.	Shusuke Yagi, Masashi Akaike, Takashi Iwase, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Sumiko Yoshida, Yuka Sumitomo-Ueda, Ken-ichi Aihara, Yoichiro Hirata, Munkhbaatar Dagvasumberel, Yoshio Taketani, Noriko Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Bosentan ameliorated exercise-induced pulmonary arterial hypertension complicated with systemic sclerosis., Internal Medicine, Vol.49, No.21, 2309-2312, 2010. (要約) Pulmonary arterial hypertension (PAH) is a frequent complication in patients with systemic sclerosis. Bosentan is used in patients with symptomatic PAH; however, it has not been established whether or not bosentan ameliorates the progression of PAH in patients with no PAH-related symptoms. We present a case of systemic sclerosis with no PAH-related symptoms in which bosentan ameliorated exercise-induced PAH evaluated by 6-minute walk stress echocardiography, brachial flow-mediated dilation, and skin temperature of hands and feet. The results suggest that administration of bosentan in patients with early-stage PAH ameliorates pulmonary arterial vasodilatation through improvement of endothelial function. (キーワード) Exercise / Exercise Test / Female / Humans / Hypertension, Pulmonary / Middle Aged / Scleroderma, Systemic / Sulfonamides (出版サイトへのリンク) ● Publication site (DOI): 10.2169/internalmedicine.49.3812 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21048365 ● CiNii @ 国立情報学研究所 (CRID): 1390282679847104768 ● Search Scopus @ Elsevier (PMID): 21048365 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.49.3812 (DOI: 10.2169/internalmedicine.49.3812, PubMed: 21048365, CiNii: 1390282679847104768)
83.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.1038/hr.2010.179 (文献検索サイトへのリンク) ● 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)
84.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1161/HYPERTENSIONAHA.110.152207 (文献検索サイトへのリンク) ● 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)
85.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.atherosclerosis.2010.05.011 (文献検索サイトへのリンク) ● 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)
86.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1210/me.2009-0402 (文献検索サイトへのリンク) ● 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)
87.	Shusuke Yagi, Masashi Akaike, Mitsunori Fujimura, Takehiko Kimura, Takeshi Nishiuchi, Takashi Iwase, Ken-ichi Aihara, Sumiko Yoshida, Yuka Sumitomo-Ueda, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoichiro Hirata, Munkhbaatar Dagvasumberel, Yoshio Taketani, Noriko Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Congenital ventricular aneurysm as an unexpected complication of monomorphic premature ventricular contractions., Internal Medicine, Vol.49, No.10, 907-912, 2010. (要約) Congenital ventricular diverticulum (CVD) in adults is a rare cardiac malformation, which includes fibrous type congenital ventricular aneurysm (CVA). CVA is often clinically asymptomatic and shows no abnormality in the electrocardiogram or chest X-ray. However, some cases of sudden death resulting from ventricular tachycardia, cardiac embolism or ventricular rupture have been reported. Therefore, physicians should perform further cardiac imaging studies to detect a CVA if ventricular arrhythmia originating from the left ventricle is observed. Here, we report two successfully followed cases of CVA which were diagnosed from premature ventricular contractions. (キーワード) congenital ventricular aneurysm / congenital ventricular diverticulum / ventricular arrythmia (出版サイトへのリンク) ● Publication site (DOI): 10.2169/internalmedicine.49.3008 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20467175 ● CiNii @ 国立情報学研究所 (CRID): 1390001204871212928 ● Search Scopus @ Elsevier (PMID): 20467175 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.49.3008 (DOI: 10.2169/internalmedicine.49.3008, PubMed: 20467175, CiNii: 1390001204871212928)
88.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1161/HYPERTENSIONAHA.109.146076 (文献検索サイトへのリンク) ● 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)
89.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, Takashi Iwase, Kazue Ishikawa, Sumiko Yoshida, Yuka Sumitomo-Ueda, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoichiro Hirata, Munkhbaatar Dagvasumberel, Yoshio Taketani, Noriko Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Ezetimibe ameliorates metabolic disorders and microalbuminuria in patients with hypercholesterolemia., Journal of Atherosclerosis and Thrombosis, Vol.17, No.2, 173-180, 2010. (要約) AIM: Ezetimibe, an inhibitor of Niemann-Pick C1-like 1 protein, has been shown to reduce the intestinal absorption of cholesterol. We investigated whether it also has beneficial effects on metabolic disorder and/or renal insufficiency in patients with hypercholesterolemia. METHODS: Ezetimibe was administered to 38 Japanese patients with hypercholesterolemia to obtain appropriate low-density lipoprotein cholesterol (LDL-chol) levels. Age- and sex-matched patients with hypercholesterolemia (n=38) were the controls. We evaluated the effects of ezetimibe before and 4 to 8 weeks after ezetimibe treatment. RESULTS: Ezetimibe significantly decreased LDL-chol levels and metabolic syndrome-related factors, including body weight, waist circumference, blood pressure; homeostasis model assessment insulin resistance (HOMA-IR), and urinary albumin excretion, were significantly reduced. In addition, it decreased the level of high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor (TNF)-alpha, the urinary excretion of 8-hydroxy-2'-deoxyguanosine, a parameter of oxidative stress, and increased the urinary excretion of nitrate and nitrite (NOx). In the controls we observed no such changes. Excepting the decrease in the serum TNF-alpha level, the effects of ezetimibe were not correlated with decreased LDL-chol levels. CONCLUSION: Ezetimibe ameliorated the status of metabolic syndrome and microalbuminuria, reduced inflammation and oxidative stress, and increased nitric oxide bioavailability in a LDL-chol reduction-dependent and -independent manner. (キーワード) Aged / Albuminuria / Anticholesteremic Agents / Azetidines / C-Reactive Protein / Case-Control Studies / Cholesterol, LDL / Deoxyguanosine / Female / Humans / Hypercholesterolemia / Male / Metabolic Diseases / Metabolic Syndrome X / Middle Aged / Nitrates / Nitrites / Oxidative Stress / Tumor Necrosis Factor-alpha (出版サイトへのリンク) ● Publication site (DOI): 10.5551/jat.2378 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20150722 ● Search Scopus @ Elsevier (PMID): 20150722 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.2378 (DOI: 10.5551/jat.2378, PubMed: 20150722)
90.	Hirotsugu Kurobe, Masahisa Urata, Masaki Ueno, Masaaki Ueki, Shiro Ono, Yuki Izawa-Ishizawa, Yayoi Fukuhara, Yu Lei, Adiratna Mat Ripen, Tamotsu Kanbara, Ken-ichi Aihara, Keisuke Ishizawa, Masashi Akaike, Frank J. Gonzalez, Toshiaki Tamaki, Yousuke Takahama, Masanori Yoshizumi, Tetsuya Kitagawa and Shuhei Tomita : Role of Hypoxia-Inducible Factor 1α in T Cells as a Negative Regulator in Development of Vascular Remodeling, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.30, No.2, 210-217, 2010. (要約) Recent studies have shown that the cellular immune response in the development of vascular remodeling modulates the resulting pathological alterations. We show that hypoxia-inducible factor 1 (Hif-1) (specifically expressed in T cells) is involved in the immune response to vascular remodeling that accompanies arteriosclerosis. To study the role of T cells in the development of vascular remodeling, femoral arterial injury induced by an external vascular polyethylene cuff was examined in mice lacking Hif-1 (specifically in T cells). We found that cuff placement caused prominent neointimal hyperplasia of the femoral artery in Hif-1- (T-cell)-deficient mice compared with that in control mice and that infiltration of inflammatory cells at the adventitia was markedly increased in the mutant mice. Studies to clarify the mechanism of augmented vascular remodeling in the mutant mice showed enhanced production of cytokines by activated T cells and augmented antibody production in response to a T-dependent antigen in the mutant mice. The results of this study revealed that Hif-1alpha in T cells plays a crucial role in vascular inflammation and remodeling in response to cuff injury as a negative regulator of T cell-mediated immune response. Potential new therapeutic strategies that target Hif-1alpha are described. (キーワード) Animals / Antibody Formation / Arteriosclerosis / Cell Hypoxia / Cell Proliferation / Chemokine CXCL12 / Chemotaxis, Leukocyte / 細胞質分裂 (cytokinesis) / Disease Models, Animal / Femoral Artery / Hyperplasia / Hypoxia-Inducible Factor 1, alpha Subunit / Immunity, Cellular / 免疫組織化学 (immunohistochemistry) / Lymphocyte Activation / 男性 (male) / Mice / ノックアウトマウス (knockout mice) / Nitroimidazoles / Receptors, Antigen, T-Cell / Tリンパ球 (T lymphocytes) / Thymus Gland / Time Factors / Tunica Intima (出版サイトへのリンク) ● Publication site (DOI): 10.1161/ATVBAHA.109.192666 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20007912 ● Search Scopus @ Elsevier (PMID): 20007912 ● Search Scopus @ Elsevier (DOI): 10.1161/ATVBAHA.109.192666 (DOI: 10.1161/ATVBAHA.109.192666, PubMed: 20007912)
91.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.1210/en.2009-0661 (文献検索サイトへのリンク) ● 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)
92.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.2143/AC.64.5.2042687 (文献検索サイトへのリンク) ● 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)
93.	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. (要約) 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. (キーワード) Aged / Aged, 80 and over / Cardiovascular Diseases / Female / Heparin Cofactor II / Humans / Male / Middle Aged / Peripheral Vascular Diseases / Prevalence / Protective Agents / Risk Factors (出版サイトへのリンク) ● Publication site (DOI): 10.5551/jat.E695 (文献検索サイトへのリンク) ● 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)
94.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1210/en.2008-1254 (文献検索サイトへのリンク) ● 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)
95.	粟飯原賢一, 赤池雅史, 池田康将, 上田由佳, 吉田守美子, 伊勢孝之, 八木秀介, 岩瀬俊, 近藤彰, 田村克也, 松本俊夫 : 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年. (要約) 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． (キーワード) 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
96.	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. (要約) 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. (キーワード) Adult / Alcoholism / Endocarditis, Bacterial / Gram-Positive Bacterial Infections / Heart Valve Prosthesis Implantation / Humans / Immunocompromised Host / Lactobacillus / Male / Mitral Valve Insufficiency (出版サイトへのリンク) ● Publication site (DOI): 10.2169/internalmedicine.47.0744 (文献検索サイトへのリンク) ● 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)
97.	赤池雅史, 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, 八木秀介, 池田康将, 岩瀬俊, 粟飯原賢一, 東博之 : 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年. (要約) 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． (キーワード) 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
98.	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. (要約) 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. (キーワード) 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 (出版サイトへのリンク) ● Publication site (DOI): 10.1161/CIRCRESAHA.107.163493 (文献検索サイトへのリンク) ● 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)
99.	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. (要約) 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. (キーワード) Amyloidosis / Cardiomyopathies / Combined Modality Therapy / Female / Heart / Humans / Melphalan / Middle Aged / Peripheral Blood Stem Cell Transplantation / Prognosis (出版サイトへのリンク) ● Publication site (DOI): 10.2169/internalmedicine.46.0142 (文献検索サイトへのリンク) ● 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)
100.	Toshio Shigekiyo, Junko Miyagi, Atsuhisa Shirakami, Hironobu Shibata, Kazuo Tsukai and Ken-ichi Aihara : Isolated high-molecular-weight kininogen deficiency: a novel frameshift mutation in exon 10, Blood, Vol.109, No.11, 5062-5063, 2007. (キーワード) Base Sequence / Blood Coagulation Disorders / DNA, Complementary / Exons / Family Health / Female / Frameshift Mutation / Humans / Japan / Kininogen, High-Molecular-Weight / Male / Molecular Sequence Data / Partial Thromboplastin Time / Phylogeny / Thrombosis (出版サイトへのリンク) ● Publication site (DOI): 10.1182/blood-2006-12-060616 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17522339 ● Search Scopus @ Elsevier (PMID): 17522339 ● Search Scopus @ Elsevier (DOI): 10.1182/blood-2006-12-060616 (DOI: 10.1182/blood-2006-12-060616, PubMed: 17522339)
101.	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. (要約) 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. (キーワード) 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 / ノックアウトマウス (knockout mice) / Pregnancy (出版サイトへのリンク) ● Publication site (DOI): 10.1172/JCI27095 (文献検索サイトへのリンク) ● 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)
102.	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. (要約) 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. (キーワード) Angiotensin II / Animals / 血圧 (blood pressure) / Cardiomegaly / DNA-Binding Proteins / 肺線維症 (pulmonary fibrosis) / Heart Rate / Male / Mice / Mice, Inbred C57BL / Mice, Inbred CBA / ノックアウトマウス (knockout mice) / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinase 7 / 心筋 (myocardium) / RNA, Messenger / Receptors, Androgen / Smad2 Protein / Trans-Activators / Transforming Growth Factor beta / Transforming Growth Factor beta1 / Ventricular Remodeling (出版サイトへのリンク) ● Publication site (DOI): 10.1074/jbc.M411694200 (文献検索サイトへのリンク) ● 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)
103.	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. (要約) 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. (キーワード) Antigens, CD13 / Aspirin / Cells, Cultured / Endothelial Cells / Endothelin-1 / Endothelium, Vascular / Enzyme Induction / Fibrinolytic Agents / Genes, Reporter / Humans / Leucine / Protease Inhibitors / RNA, Messenger / 活性酸素 (reactive oxygen species) / Subtraction Technique / Thrombin / Transcription, Genetic / Transfection / Umbilical Veins (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.atherosclerosis.2005.03.003 (文献検索サイトへのリンク) ● 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)
104.	Tomonori Yoshida, Hiroyuki Azuma, Ken-ichi Aihara, Mitsunori Fujimura, Masashi Akaike, Takao Mitsui and Toshio Matsumoto : Vascular smooth muscle cell proliferation is dependent upon upregulation of mitochondrial transcription factor A (mtTFA) expression in injured rat carotid artery, Atherosclerosis, Vol.178, No.1, 39-47, 2005. (要約) Consistent with the physiological response to increased energy demand in proliferating cells, the number of mitochondria is upregulated in synthetic states of vascular smooth muscle cells (VSMC) in atherosclerotic lesion. We hypothesized that mitochondrial transcription factor A (mtTFA), a prerequisite factor for the transcription and replication of mtDNA, may be upregulated in VSMC of injured rat carotid artery, and that inhibition of its expression can attenuate the intimal thickening. Changes of intimal thickening and mtTFA expression by a treatment with antisense oligodeoxynucleotides (ODN) for mtTFA were investigated in balloon-injured rat carotid artery model. The expression of mtTFA was upregulated as early as 3 h up to 7 days after balloon injury. Delivery of ansisense ODN for mtTFA from adventitia side to injured arterial wall caused a significant decrease in intima-to-media (I/M) ratio. Furthermore, the increase in immunoreactivity and mRNA expression of mtTFA in injured artery as well as the number of mitochondria in intimal VSMC was abrogated by antisense ODN treatment. These data demonstrate that expression of mtTFA is upregulated in intimal VSMC of injured rat carotid artery, and that suppression of mtTFA expression by antisense ODN can attenuate intimal thickening after balloon injury. (キーワード) Antisense oligodeoxynucleotide / Arterial injury / Intimal thickening / Dedifferentiation / Restenosis (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.atherosclerosis.2004.08.029 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15585199 ● Search Scopus @ Elsevier (PMID): 15585199 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2004.08.029 (DOI: 10.1016/j.atherosclerosis.2004.08.029, PubMed: 15585199)
105.	山口普史, 池田康将, 藤村光則, 森岡将臣, 橋詰俊二, 加藤みどり, 粟飯原賢一, 赤池雅史, 東博之, 松本俊夫, 稲山真美, 埴淵昌毅 : 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年. (要約) 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 (キーワード) 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
106.	荒瀬友子, 近藤彰, 谷田典子, 富永恵美子, 土井大介, 加藤修司, 川井尚臣, 粟飯原賢一, 大蔵雅夫, 桜井えつ, 田中恵子 : 「ホスピス徳島」における末期癌患者の傍腫瘍性神経症候群の発症頻度とその臨床的意義, 四国医学雑誌, Vol.60, No.3, 94-98, 2004年. (要約) 当ホスピスに入院した癌末期患者127名を対象に傍腫瘍性神経症候群について検討した.対象中,薬剤の関与がない精神神経症状を呈した症例は52例で,精神症状は意識障害が多く,神経障害は対麻痺が多かった.原因は代謝内分泌の異常によるもの,癌の神経系への浸潤が多かった.52例のうち,傍腫瘍性神経症候群(疑いを含む)は4例であった.1例は肺小細胞癌患者で傍腫瘍性神経症候群の典型例であり,既知の抗神経抗体であるHu抗体および抗VGCC抗体を有し多彩な神経症状を呈した.1例は肺癌に辺縁系脳炎を発症し,既知の抗神経抗体は陰性,抗原未同定の抗神経組織抗体陽性であった.残りの2例中1例は子宮癌患者で異常な躁状態を認め,既知の抗神経抗体は陰性,抗原未同定の抗神経組織抗体陽性であり,他の1例は膵臓癌末期に変動する意識障害があり既知の抗神経抗体は陰性,抗原未同定の抗神経組織抗体陰性で,非特異的抗体陽性であった.本研究における発生頻度は確診例3 (キーワード) 自己抗体 / 神経症状(病因,診断) / 発生率 / ホスピス / 免疫組織化学 (immunohistochemistry) / ウエスタンブロッティング / 末期患者 / 腫瘍随伴性多発性神経障害(診断,合併症) / 精神症状(病因,診断) / 癌患者 / ヒト (Homo sapiens) / 中年(45~64) / 高齢者(65~79) / 高齢者(80~) / 男 / 女 (徳島大学機関リポジトリ) ● Metadata: 101813 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1050302172854589568 (徳島大学機関リポジトリ: 101813, CiNii: 1050302172854589568)
107.	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. (要約) 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. (キーワード) FILTRATION PRESSURE METHOD / TISSUE-FACTOR / 1,25-DIHYDROXYVITAMIN D-3 / ANTITHROMBIN DEFICIENCY / WHOLE-BLOOD / EXPRESSION / 細胞 (cells) / AGGREGATION / 阻害 (inhibition) / ALOPECIA (出版サイトへのリンク) ● Publication site (DOI): 10.1074/jbc.M404865200 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15205460 ● CiNii @ 国立情報学研究所 (CRID): 1362262945661168512 ● Summary page in Scopus @ Elsevier: 2-s2.0-4143096123 (DOI: 10.1074/jbc.M404865200, PubMed: 15205460, CiNii: 1362262945661168512, Elsevier: Scopus)
108.	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. (要約) 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. (キーワード) Adult / Aged / Aged, 80 and over / 加齢 (aging) / Antithrombins / Cardiovascular Diseases / Carotid Artery Diseases / Female / Heparin Cofactor II / Humans / Male / Middle Aged / Regression Analysis / Risk Factors / Severity of Illness Index (出版サイトへのリンク) ● Publication site (DOI): 10.1161/01.CIR.0000129968.46095.F3 (文献検索サイトへのリンク) ● 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)
109.	Takashi Sato, Takahiro Matsumoto, Hirotaka Kawano, Tomoyuki Watanabe, Yoshikatsu Uematsu, Keisuke Sekine, Toru Fukuda, Ken-ichi Aihara, Andrée Krust, Takashi Yamada, Yuko Nakamichi, Yoko Yamamoto, Takashi Nakamura, Kimihiro Yoshimura, Tatsuya Yoshizawa, Daniel Metzger, Pierre Chambon and Shigeaki Kato : Brain masculinization requires androgen receptor function., Proceedings of the National Academy of Sciences of the United States of America, Vol.101, No.6, 1673-1678, 2004. (要約) Testicular testosterone produced during a critical perinatal period is thought to masculinize and defeminize the male brain from the inherent feminization program and induce male-typical behaviors in the adult. These actions of testosterone appear to be exerted not through its androgenic activity, but rather through its conversion by brain aromatase into estrogen, with the consequent activation of estrogen receptor (ER)-mediated signaling. Thus, the role of androgen receptor (AR) in perinatal brain masculinization underlying the expression of male-typical behaviors remains unclear because of the conversion of testosterone into estrogen in the brain. Here, we report a null AR mutation in mice generated by the Cre-loxP system. The AR-null mutation in males (AR(L-/Y)) resulted in the ablation of male-typical sexual and aggressive behaviors, whereas female AR-null homozygote (AR(L-/L-)) mice exhibited normal female sexual behaviors. Treatment with nonaromatizable androgen (5alpha-dihydrotestosterone, DHT) was ineffective in restoring the impaired male sexual behaviors, but it partially rescued impaired male aggressive behaviors in AR(L-/Y) mice. Impaired male-typical behaviors in ERalpha(-/-) mice were restored on DHT treatment. The role of AR function in brain masculinization at a limited perinatal stage was studied in AR(L-/L-) mice. Perinatal DHT treatment of females led to adult females sensitive to both 17beta-estradiol and DHT in the induction of male-typical behaviors. However, this female brain masculinization was abolished by AR inactivation. Our results suggested that perinatal brain masculinization requires AR function and that expression of male-typical behaviors in adults is mediated by both AR-dependent and -independent androgen signaling. (キーワード) Androgen Receptor Antagonists / Animals / Behavior, Animal / Brain / Female / Gene Expression Regulation, Enzymologic / Male / Mice / Mice, Inbred C57BL / Nitric Oxide Synthase / Nitric Oxide Synthase Type I / Pregnancy / Receptors, Androgen (出版サイトへのリンク) ● Publication site (DOI): 10.1073/pnas.0305303101 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14747651 ● Search Scopus @ Elsevier (PMID): 14747651 ● Search Scopus @ Elsevier (DOI): 10.1073/pnas.0305303101 (DOI: 10.1073/pnas.0305303101, PubMed: 14747651)
110.	Nobuyuki Takamori, Hiroyuki Azuma, Midori Kato, Shunji Hashizume, Ken-ichi Aihara, Masashi Akaike, Katsuya Tamura and Toshio Matsumoto : High plasma heparin cofactor II activity is associated with reduced incidence of in-stent restenosis after percutaneous coronary intervention, Circulation, Vol.109, No.4, 481-486, 2004. (要約) Thrombin plays an important role in the development of atherosclerosis and restenosis after percutaneous coronary intervention. Because heparin cofactor II (HCII) inhibits thrombin action in the presence of dermatan sulfate, which is abundantly present in arterial wall, HCII may affect vascular remodeling by modulating thrombin action. We hypothesized that patients with high plasma HCII activity may show a reduced incidence of in-stent restenosis (ISR). Sequential coronary arteries (n=166) with NIR stent (Boston Scientific Corp) implantation in 134 patients were evaluated before, immediately after, and at 6 months after percutaneous coronary intervention. Patients were divided into the following groups: high HCII (> or =110%, 45 lesions in 36 patients), normal HCII (> or =80% and <110%, 81 lesions in 66 patients), and low HCII (<80%, 40 lesions in 32 patients). Percent diameter stenosis at follow-up in the high-HCII group (18.7%) was significantly lower (P=0.046) than that in the normal-HCII group (30.3%) or the low-HCII group (29.0%). The ISR rate in the high-HCII group (6.7%) was significantly lower than that in the low-HCII group (30.0%) (P=0.0039). Furthermore, multivariate analysis demonstrated that high plasma HCII activity is an independent factor in reducing the incidence of angiographic restenosis (odds ratio, 0.953/1% increase of HCII; 95% CI, 0.911 to 0.998). The results demonstrate that HCII may have a hitherto unrecognized effect in inhibiting ISR. The effect of HCII may be mediated by inactivating thrombin in injured arteries, thereby inhibiting vascular smooth muscle cell migration and proliferation. (キーワード) cardiovascular diseases / angioplasty / atherosclerosis / thrombin / dermatan sulfate (出版サイトへのリンク) ● Publication site (DOI): 10.1161/01.CIR.0000109695.39671.37 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14744972 ● Search Scopus @ Elsevier (PMID): 14744972 ● Search Scopus @ Elsevier (DOI): 10.1161/01.CIR.0000109695.39671.37 (DOI: 10.1161/01.CIR.0000109695.39671.37, PubMed: 14744972)
111.	粟飯原賢一, 東博之, 赤池雅史, 藤村光則, 吉田智則, 橋詰俊二, 加藤みどり, 山口普史, 池田康将, 加藤茂明, 松本俊夫 : 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年. (キーワード) *Vitamin D(薬理学) 遺伝子発現血液凝固 Calcitriol Receptors Thrombomodulin マウス動物
112.	Hirotaka Kawano, Takashi Sato, Takashi Yamada, Takahiro Matsumoto, Keisuke Sekine, Tomoyuki Watanabe, Takashi Nakamura, Toru Fukuda, Kimihiro Yoshimura, Tatsuya Yoshizawa, Ken-ichi Aihara, Yoko Yamamoto, Yuko Nakamichi, Daniel Metzger, Pierre Chambon, Kozo Nakamura, Hiroshi Kawaguchi and Shigeaki Kato : Suppressive function of androgen receptor in bone resorption., Proceedings of the National Academy of Sciences of the United States of America, Vol.100, No.16, 9416-9421, 2003. (要約) As locally converted estrogen from testicular testosterone contributes to apparent androgen activity, the physiological significance of androgen receptor (AR) function in the beneficial effects of androgens on skeletal tissues has remained unclear. We show here that inactivation of AR in mice using a Cre-loxP system-mediated gene-targeting technique caused bone loss in males but not in females. Histomorphometric analyses of 8-week-old male AR knockout (ARKO) mice showed high bone turnover with increased bone resorption that resulted in reduced trabecular and cortical bone mass without affecting bone shape. Bone loss in orchidectomized male ARKO mice was only partially prevented by treatment with aromatizable testosterone. Analysis of primary osteoblasts and osteoclasts from ARKO mice revealed that AR function was required for the suppressive effects of androgens on osteoclastogenesis supporting activity of osteoblasts but not on osteoclasts. Furthermore, expression of the receptor activator of NF-kappaB ligand (RANKL) gene, which encodes a major osteoclastogenesis inducer, was found to be up-regulated in osteoblasts from AR-deficient mice. Our results indicate that AR function is indispensable for male-type bone formation and remodeling. (キーワード) Androgen-Insensitivity Syndrome / Animals / Bone Diseases, Metabolic / Bone Resorption / Carrier Proteins / Female / Male / Membrane Glycoproteins / Mice / ノックアウトマウス (knockout mice) / Mutation / Osteoblasts / Osteoclasts / RANK Ligand / Receptor Activator of Nuclear Factor-kappa B / Receptors, Androgen / Reverse Transcriptase Polymerase Chain Reaction / Sex Factors / Time Factors / Up-Regulation (出版サイトへのリンク) ● Publication site (DOI): 10.1073/pnas.1533500100 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12872002 ● Search Scopus @ Elsevier (PMID): 12872002 ● Search Scopus @ Elsevier (DOI): 10.1073/pnas.1533500100 (DOI: 10.1073/pnas.1533500100, PubMed: 12872002)
113.	山本陽子, 吉澤達也, 福田亨, 関根圭輔, 佐藤隆史, 河野博隆, 粟飯原賢一, 渡辺資之, 新道真代, 中村貴, 加藤茂明 : 組織特異的VDRKOマウスの作出と解析, ホルモンと臨床, Vol.51, 202-207, 2003年. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1573668925632518144 (CiNii: 1573668925632518144)
114.	佐藤隆史, 河野博隆, 松本高広, 関根圭輔, 福田亨, 渡辺資之, 粟飯原賢一, 山田高嗣, 山本陽子, 中道裕子, 新道真代, 川口浩, 加藤茂明 : 雌雄アンドロゲン受容体遺伝子欠損マウスの作出と解析, ホルモンと臨床, Vol.51, 238-242, 2003年. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1573105976563574528 (CiNii: 1573105976563574528)
115.	Yuko Nakamichi, Chisa Shukunami, Takashi Yamada, Ken-ichi Aihara, Hirotaka Kawano, Takashi Sato, Yuriko Nishizaki, Yoko Yamamoto, Masayo Shindo, Kimihiro Yoshimura, Takashi Nakamura, Naoyuki Takahashi, Hiroshi Kawaguchi, Yuji Hiraki and Shigeaki Kato : Chondromodulin I is a bone remodeling factor, Molecular and Cellular Biology, Vol.23, No.2, 636-644, 2003. (要約) Chondromodulin I (ChM-I) was supposed from its limited expression in cartilage and its functions in cultured chondrocytes as a major regulator in cartilage development. Here, we generated mice deficient in ChM-I by targeted disruption of the ChM-I gene. No overt abnormality was detected in endochondral bone formation during embryogenesis and cartilage development during growth stages of ChM-I(-/-) mice. However, a significant increase in bone mineral density with lowered bone resorption with respect to formation was unexpectedly found in adult ChM-I(-/-) mice. Thus, the present study established that ChM-I is a bone remodeling factor. (キーワード) Alleles / Animals / Animals, Newborn / Blotting, Northern / Blotting, Southern / Blotting, Western / Bone Development / Bone Marrow Cells / Cartilage / Cells, Cultured / Female / Homozygote / Intercellular Signaling Peptides and Proteins / Macrophages / Male / Membrane Proteins / Mice / Mice, Inbred C57BL / Mice, Transgenic / Models, Genetic / Osteoblasts / RNA, Messenger / Recombination, Genetic / Reverse Transcriptase Polymerase Chain Reaction (出版サイトへのリンク) ● Publication site (DOI): 10.1128/MCB.23.2.636-644.2003 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12509461 ● Search Scopus @ Elsevier (PMID): 12509461 ● Search Scopus @ Elsevier (DOI): 10.1128/MCB.23.2.636-644.2003 (DOI: 10.1128/MCB.23.2.636-644.2003, PubMed: 12509461)
116.	Masashi Akaike, Hiroyuki Azuma, Ayako Kagawa, Kazuya Matsumoto, Ikuro Hayashi, Katsuya Tamura, Takeshi Nishiuchi, Takahiko Iuchi, Nobuyuki Takamori, Ken-ichi Aihara, Tomonori Yoshida, Yasuhiko Kanagawa and Toshio Matsumoto : Effect of Aspirin Treatment on Serum Concentrations of Lipoprotein(a) in Patients with Atherosclerotic Diseases, Clinical Chemistry, Vol.48, No.9, 1454-1459, 2002. (要約) Increased serum lipoprotein(a) [Lp(a)] is an independent risk factor for atherosclerosis. We previously reported that aspirin reduced Lp(a) production by cultured hepatocytes via the reduction of apolipoprotein(a) [apo(a)] gene transcription. We evaluated both the effect of aspirin treatment (81 mg/day) on serum Lp(a) concentrations and the correlation between the degree of reduction in serum Lp(a) and the type of apo(a) isoform in 70 patients with coronary artery disease or cerebral infarction. Aspirin lowered serum Lp(a) concentrations to approximately 80% of the baseline values in patients with high Lp(a) concentrations (>300 mg/L). The percentage of decrease in serum Lp(a) was larger in patients with high Lp(a) than in patients with low Lp(a) (<300 mg/L), irrespective of apo(a) isoform size. The decreases in serum Lp(a) in high Lp(a) patients with both the high-molecular-weight and the low-molecular-weight isoforms were positively correlated with the baseline Lp(a) concentrations. Because the secretory efficiencies of apo(a) in the same isoform are likely to be similar, the difference in serum Lp(a) concentrations in patients having the same apo(a) isoform depends on the transcriptional activity of the apo(a) gene. These findings suggest that aspirin decreases serum Lp(a) concentrations via a decrease in apo(a) gene transcription more effectively in patients with high transcriptional activity of this gene. (キーワード) Arteriosclerosis / Aspirin / Cerebral Infarction / Coronary Disease / Female / Humans / Hypolipidemic Agents / Lipoprotein(a) / Male / Middle Aged / Protein Isoforms (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12194922 ● Search Scopus @ Elsevier (PMID): 12194922 (PubMed: 12194922)
117.	吉村公宏, 粟飯原賢一, 山田高嗣, 佐藤隆史, Metzger Daniel, Chambon Pierre, 加藤茂明 : ビタミンA・Dレセプター(RAR・VDR)の生体内クロストークの解析, ビタミン, Vol.76, No.3, 156-157, 2002年. (キーワード) 028 (出版サイトへのリンク) ● Publication site (DOI): 10.20632/vso.76.3_156_3 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390001205784283904 ● Search Scopus @ Elsevier (DOI): 10.20632/vso.76.3_156_3 (DOI: 10.20632/vso.76.3_156_3, CiNii: 1390001205784283904)
118.	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. (要約) 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. (キーワード) Spur cell anemia / Free cholesterol / Hepatosplenomegaly / Pentoxifylline / Cholestyramine (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11345202 ● Search Scopus @ Elsevier (PMID): 11345202 (PubMed: 11345202)
119.	Yasuhiko Kanagawa, Toshio Shigekiyo, Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : Molecular mechanism of type I congenital heparin cofactor (HC) II deficiency caused by a missense mutation at reactive P2 site: HC II Tokushima, Thrombosis and Haemostasis, Vol.85, No.1, 101-107, 2001. (要約) We found a 66-year-old Japanese patient with type I congenital heparin cofactor (HC) II deficiency manifesting multiple atherosclerotic lesions. To investigate the molecular pathogenesis of our patient, we performed sequencing analysis and expressed recombinant human wild-type and mutant HC II molecules in COS-1 and CHO-K1 cells. Sequencing analysis following amplification of each of all 5 exons and its flanking region showed a single C to T transition at nucleotide position 12,854 in exon 5, which changed a Pro443 codon (CCG) to Leu codon (CTG). Because this mutation generates a new Bhv I site, the Bbv I digestion pattern of the PCR-amplified exon 5 fragments from each family member was analyzed. In all cases, the patterns were consistent with the activities and antigen levels of plasma HC I1 in those members. Transient transfection, metabolic labeling and pulse-chase experiments followed by immunoprecipitation analysis showed that the recombinant mutant HC II molecules were secreted from COS-1 cells in reduced amounts compared with the wild-type, and that an enhanced intracellular association of the mutant molecules with a chaperone, GRP78/BiP, was observed in CHO-K1 cells. Northern blot analysis indicated that the mutant HC I1 mRNA was transcribed at a similar level as that of wild-type. Immunohistochemical staining of the transfected cells revealed that COS-1 cells expressing the mutant HC II molecules were stained mainly in the perinuclear area. We conclude that the impaired secretion of the mutant HC II molecules, due to intracellular degradation, is the molecular pathogenesis of type I congenital HC II deficiency caused by a Pro443 to Leu mutation at reactive P2 site. (キーワード) heparin cofactor II / thrombosis / thrombin / transfection / chaperone (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11204559 ● Summary page in Scopus @ Elsevier: 2-s2.0-0035171975 (PubMed: 11204559, Elsevier: Scopus)
120.	赤池雅史, 東博之, 香川礼香, 金川泰彦, 粟飯原賢一, 松山まどか, 井内貴彦, 高森信行, 吉田智則, 松本俊夫, 松本和也, 林郁郎, 田村克也, 西内健 : 高リポ蛋白(a)血症に及ぼすaspirinの影響, --- アポリポ蛋白(a)アイソフォームとの関連 ---, 四国医学雑誌, Vol.55, No.3, 109-114, 1999年. (キーワード) Lipoprotein(a) / Apolipoprotein(a) / Aspirin / Apo(a)Isoform / Lp(a) Phenotype (徳島大学機関リポジトリ) ● Metadata: 112143 (徳島大学機関リポジトリ: 112143)
121.	粟飯原賢一, 宮田雅代, 金崎淑子, 加藤修司, 玉木康民, 木村成昭, 武市俊彰, 藤本浩史, 増田和彦, 白神〓, 千葉仁志 : インスリン非依存性糖尿病を合併したコレステリルエステル転送蛋白完全欠損症の1例, 日本内科学会雑誌, Vol.86, No.7, 1251-1253, 1997年. (出版サイトへのリンク) ● Publication site (DOI): 10.2169/naika.86.1251 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390282681418180864 ● Search Scopus @ Elsevier (DOI): 10.2169/naika.86.1251 (DOI: 10.2169/naika.86.1251, CiNii: 1390282681418180864)

学術レター:

1.	Ken-ichi Aihara, Masaki Mogi, Rei Shibata, David Bishop-Bailey and P Muredach Reilly : Inflammation and vascular remodeling., International Journal of Vascular Medicine, Vol.2012, 2012. (出版サイトへのリンク) ● Publication site (DOI): 10.1155/2012/596796 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23209907 ● Search Scopus @ Elsevier (PMID): 23209907 ● Search Scopus @ Elsevier (DOI): 10.1155/2012/596796 (DOI: 10.1155/2012/596796, PubMed: 23209907)
2.	Ken-ichi Aihara, Masaki Mogi, Rei Shibata, David Bishop-Bailey and Xin L. Ma : Interactions between CKD and MetS and the Development of CVD., Cardiology Research and Practice, Vol.2011, 878065, 2011. (出版サイトへのリンク) ● Publication site (DOI): 10.4061/2011/878065 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21629800 ● Search Scopus @ Elsevier (PMID): 21629800 ● Search Scopus @ Elsevier (DOI): 10.4061/2011/878065 (DOI: 10.4061/2011/878065, PubMed: 21629800)

総説・解説:

1.	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. (出版サイトへのリンク) ● Publication site (DOI): 10.5551/jat.31047 (文献検索サイトへのリンク) ● 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)
2.	鈴木麗子, 大和光, 川添和義, 粟飯原賢一, 遠藤逸朗, 安芸菜奈子, 倉橋清衛, 松本俊夫, 黒田暁生, 松久宗英 : インスリン注射により生じた皮下硬血を有する患者の実態調査とその介入の有用性の検討, プラクティス, Vol.31, No.6, 815-821, 2014年.
3.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.1155/2012/162545 (文献検索サイトへのリンク) ● 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)
4.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Masashi Akaike and Toshio Matsumoto : Effects of androgens on cardiovascular remodeling., The Journal of Endocrinology, Apr. 2012. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.1530/JOE-12-0126 (文献検索サイトへのリンク) ● 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)
5.	粟飯原賢一 : 【メタボリックシンドロームと多臓器障害】メタボリックシンドロームを司るもの, 細胞, Vol.43, No.5, 162-163, 2011年. (要約) 腹囲の増大を基盤として，脂質異常，血圧異常，糖代謝異常などの複合代謝異常状態を呈するメタボリックシンドロームは，その罹患該当者が近年増加の一途をたどっている．メタボリックシンドロームは，心血管イベントの発症リスクを増大させることから，その病態把握と治療介入の必要性が強く求められている．これまで多くの研究者が，基礎医学および臨床医学の面からメタボリックシンドロームの病態制御機構の探索に取り組んでいるが，本特集では，アディポネクチン，レニン・アンジオテンシン系，高血圧症，慢性腎臓病・骨格筋の役割などの5つの視点からその病態基盤や臓器合併症の解明にせまる事とした．これらの分野の最新の知見を吸収し，理解を深めることが，メタボリックシンドロームひいては心血管病の予防に向けた臨床的な実践につながると期待している．(著者抄録) (キーワード) レニン-アンジオテンシン系 / 危険因子 / 高血圧 / 多臓器不全(予防) / 動脈硬化症-アテローム性 / 肥満 / 骨格筋 / *メタボリックシンドローム / Adiponectin / 慢性腎臓病 / 病態生理 / ヒト
6.	粟飯原賢一 : 遺伝子改変動物から学ぶ血栓症(第28回) ヘパリンコファクターII欠損マウスにおける心血管リモデリング解析, 血栓と循環, Vol.19, No.1, 6-10, 2011年. (キーワード) Heparin Cofactor II / 遺伝子改変動物 / ノックアウトマウス / 心室リモデリング / *血管リモデリング / マウス / 動物
7.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.4061/2011/175381 (文献検索サイトへのリンク) ● 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)
8.	Ken-ichi Aihara : Heparin cofactor II attenuates vascular remodeling in humans and mice., Circulation Journal, Vol.74, No.8, 1518-1523, Jul. 2010. (要約) Heparin cofactor II (HCII), a serine protease inhibitor (serpin), inactivates thrombin action in the subendothelial layer of the vascular wall. Because a congenitally HCII-deficient patient has been shown to have multiple atherosclerotic lesions, it is hypothesized that HCII plays a pivotal role in the development of vascular remodeling, including atherosclerosis. To clarify this issue, 3 clinical studies concerning plasma HCII activity and atherosclerosis were carried out, and results demonstrated that a higher incidence of in-stent restenosis after percutaneous coronary intervention, maximum carotid arterial plaque thickness, and prevalence of peripheral arterial disease occurred in subjects with low plasma HCII activity. Furthermore, HCII-deficient mice were generated by a gene targeting method to determine the mechanism of the vascular protective action of HCII. Because HCII(-/-) mice were embryonically lethal, we used HCII(+/-) mice and found that they manifested augmentation of intimal hyperplasia and increased thrombosis after cuff or wire injury to the femoral arteries. HCII(+/-) mice with vascular injury showed augmentation of inflammatory cytokines and chemokines and oxidative stress. These abnormal phenotypes of vascular remodeling observed in HCII(+/-) mice were almost restored by human HCII protein supplementation. HCII protects against vascular remodeling, including atherosclerosis, in both humans and mice, and plasma HCII activity might be a predictive biomarker and novel therapeutic target for the prevention of cardiovascular diseases. (キーワード) Animals / 動脈硬化 (atherosclerosis) / Heparin Cofactor II / Humans / ノックアウトマウス (knockout mice) / Receptor, PAR-1 / Thrombin / Vascular Diseases (出版サイトへのリンク) ● Publication site (DOI): 10.1253/circj.CJ-10-0577 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20671370 ● Search Scopus @ Elsevier (PMID): 20671370 ● Search Scopus @ Elsevier (DOI): 10.1253/circj.CJ-10-0577 (DOI: 10.1253/circj.CJ-10-0577, PubMed: 20671370)
9.	粟飯原賢一 : 2009年度井村臨床研究奨励賞受賞記念論文新規動脈硬化抑制因子としてのヘパリンコファクター2の臨床的意義および分子生物学的解析, 最新医学, Vol.65, No.7, 1679-1684, 2010年7月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1520573328498801152 (CiNii: 1520573328498801152)
10.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Heparin Cofactor II as a Novel Vascular Protective Factor Against Atherosclerosis., Journal of Atherosclerosis and Thrombosis, Vol.16, No.5, 523-531, Sep. 2009. (要約) Heparin cofactor II (HCII) specifically inhibits thrombin action at the site of vascular wall injury. We encountered a congenital HCII deficiency patient with advanced multiple atherosclerotic lesions. This patient led us to conduct clinical studies to examine the role of HCII against atherosclerosis. We found that the incidence of in-stent restenosis after percutaneous coronary intervention, severity of carotid atherosclerosis and prevalence of peripheral arterial disease are inversely associated with plasma HCII activity. In order to clarify the vascular protective action of HCII, we generated HCII- deficient mice by gene targeting. In contrast to a previous study, HCII(-/-) mice were embryonically lethal. In HCII(+/-) mice, accelerated intimal hyperplasia and frequent thrombosis were observed after cuff or wire injury of femoral arteries. The number of protease-activated receptor-1 (PAR-1) -positive cells and the gene expression levels of inflammatory cytokines and chemokines were increased in the thickened vascular walls of HCII(+/-) mice. The accelerated intimal hyperplasia in HCII+/- mice with vascular injury was attenuated by human HCII administration. Furthermore, HCII deficiency exaggerated aortic plaque formation with increased oxidative stress in apolipoprotein E(-/-) mice. These results demonstrate that HCII protects against thrombin-induced vascular remodeling in both humans and mice and suggest that HCII is a predictive biomarker and therapeutic target for atherosclerosis. (キーワード) Animals / 動脈硬化 (atherosclerosis) / Female / Heparin Cofactor II / Humans / ノックアウトマウス (knockout mice) / ノックアウトマウス (knockout mice) / Recombinant Proteins (出版サイトへのリンク) ● Publication site (DOI): 10.5551/jat.1552 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19729870 ● Search Scopus @ Elsevier (PMID): 19729870 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.1552 (DOI: 10.5551/jat.1552, PubMed: 19729870)
11.	粟飯原賢一 : 高脂血症・動脈硬化とメタボリックシンドローム (特集メタボリックシンドロームの克服に向けて), 四国医学雑誌, Vol.63, No.3, 101-103, 2007年8月. (要約) The cardiovascular disease has been increasingly recognized over the last decade. The metabolic syndrome is associated with increased risk for development of dyslipidemia leading to atherosclerosis. In addition to healthy lifestyle promotion, treatment of atherogenic dyslipidemia using lipid lowering agents such as fibrates and statins is useful. In fact, bezafibrate reduces the incidence of myocardial infarction in patients with metabolic syndrome during long-term follow-up. Early detection of atherosclerosis including endothelial dysfunction is very important strategy for preventing cardiovascular events in patients with metabolic syndrome. We attempt to establish multiphasic health testing system(Anti-Aging Medical Center : AAMC)using recently-developed devices for medical diagnosis in Tokushima University Hospital. (キーワード) cardiovascular disease / dyslipidemia / atherosclerosis / multiphasic health testing system (徳島大学機関リポジトリ) ● Metadata: 110179 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1050302172854181248 (徳島大学機関リポジトリ: 110179, CiNii: 1050302172854181248)
12.	粟飯原賢一, 東博之, 松本俊夫 : Vitamin D-vitamin D receptor system regulates antithrombogenicity in vivo., Clinical Calcium, Vol.16, No.7, 1173-1179, 2006年7月. (要約) Although it has been well documented that vitamin D receptor (VDR) activation influences the expression of various genes involved in calcium homeostasis and cell differentiation, the physiological role of VDR action in hemostasis remains unclear. We studied thrombogenicity in normocalcemic VDR knock-out (KO) mice on a high calcium diet in comparison with that in wild-type mice and that in hypocalcemic VDRKO mice fed a regular diet. Platelet aggregation was significantly enhanced in normocalcemic VDRKO mice. Aortic endothelial nitric-oxide (NO) synthase expression and urinary NOx excretion were reduced in hypocalcemic VDRKO mice but not in normocalcemic VDRKO mice. The gene expression of antithrombin in the liver and that of thrombomodulin in the aorta, liver and kidney were down-regulated in hypo- and normocalcemic VDRKO mice, whereas tissue factor gene 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 the vitamin D-VDR system plays a pivotal role in antithrombogenicity in vivo. (キーワード) Animals / Antithrombins / Blood Coagulation / Down-Regulation / Hypocalcemia / Lipopolysaccharides / Liver / ノックアウトマウス (knockout mice) / Mice, Knockout / 一酸化窒素 (nitric oxide) / Nitric Oxide Synthase Type III / Receptors, Calcitriol / Thrombomodulin / Thromboplastin / Vitamin D (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16816478 ● Search Scopus @ Elsevier (PMID): 16816478 (PubMed: 16816478)
13.	粟飯原賢一 : ビタミンD受容体を介した生体内血液凝固制御機構の解析, 日本血栓止血学会誌, Vol.17, No.1, 38-46, 2006年2月. (出版サイトへのリンク) ● Publication site (DOI): 10.2491/jjsth.17.38 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390001204445774720 ● Search Scopus @ Elsevier (DOI): 10.2491/jjsth.17.38 (DOI: 10.2491/jjsth.17.38, CiNii: 1390001204445774720)
14.	粟飯原賢一, 池田康将, 松本俊夫 : 【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, 循環器科, Vol.59, No.6, 579-584, 2006年. (キーワード) 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
15.	粟飯原賢一, 赤池雅史, 井上大輔, 東博之, 松本俊夫 : 副甲状腺機能亢進症, ホルモンと臨床, Vol.52, No.5, 93(483)-96(486), 2004年5月.

国際会議:

1.	Hiroki Yamagami, Tomoyo Hara, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Analysis of clinical factors involved in AGE accumulation in people with type 2 diabetes, IDF-WPR Congress 2023/15th Scientific Meeting of AASD, Jul. 2023.
2.	Yosuke Kaneko, Saya Yasui, Minae Hosoi, Akihiro Tani, Hiroki Yamagami, Hiroyasu Mori, Tomoyo Hara, Yukari Mitsui, Kiyoe Kurahashi, Sumiko Yoshida, Shingen Nakamura, Akio Kuroda, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo, Takeshi Soeki, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Dehydroepiandrosterone sulfate and skeletal muscle disorders in patients with type 2 diabetes, IDF-WPR Congress 2023/15th Scientific Meeting of AASD, Tokyo, Jul. 2023.
3.	Yumi Kuwamura, Kiyoe Kurahashi, Sumiko Yoshida, Hiromichi Yumoto, Maki Hosoki, Yukihiro Momota, Ken-ichi Aihara, Masuko Sumikawa, Hirokazu Uemura, Munehide Matsuhisa and Itsuro Endo : Evaluation of Nursing Educational Material on Oral Health Behavior of Persons with Diabetes: Part 3 -- Physicians' Survey, International Diabetes Federation Western Pacific Congress 2023 /15th Scientific Meeting of Asian Association for the study of Diabetes, Kyoto, Japan, Jul. 2023.
4.	Seijiro Tsuji, Kensuke Mori, Yosuke Kaneko, Saki Kawata, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : Association between serum dehydroepiandrosterone sulfate levels and annual eGFR changes in people with type 2 diabetes, IDF-WPR Congress 2023/15th Scientific Meeting of AASD, Jul. 2023.
5.	Tomoyo Hara, Hiroki Yamagami, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Clinical factors and glycemic control in Japanese people with type 2 diabetes treated with weekly Dulaglutide at a dose of 0.75 mg, IDF-WPR Congress 2023/15th Scientific Meeting of AASD, Jul. 2023.
6.	Minae Hosoki, Hiroki Yamagami, Taiki Hori, Saya Yasui, Tomoyo Hara, Kiyoe Kurahashi, Sumiko Yoshida, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo, Masahiro Abe and Ken-ichi Aihara : Pharmaceutical Influences on In-hospital Death in Patients with and Those without Diabetes at a Japanese General Hospital, The 29th Scientific Meeting of the International Society of Hypertension, Oct. 2022.
7.	Shiho Masuda, Tomoyo Hara, Hiroki Yamagami, Mitsui Yukari, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Shingen Nakamura, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Evaluation of Vascular Function for Prediction of Renal Prognosis in Japanese Patients with Lifestyle-Related Diseases, The 29th Scientific Meeting of the International Society of Hypertension, Oct. 2022.
8.	Akihiro Tani, Takeshi Soeki, Yuji Ozaki, Ken-ichi Aihara and Masataka Sata : Impact of Sarcopenia and Atrial Fibrillation on the Incidence of Heart Failure in Elderly Patients, The 29th Scientific Meeting of the International Society of Hypertension, Oct. 2022.
9.	Tomoyo Hara, Mitsui Yukari, Masuda Shiho, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Plasma heparin cofactor activity is inversely associated with the development NAFLD in patients with diabetes, American Diabetes Association 82nd Scientific Sessions, Jun. 2022.
10.	Hiroki Yamagami, Yasui Saya, Hosoki Minae, Hori Taiki, Tomoyo Hara, Kiyoe Kurahashi, Sumiko Yoshida, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo, Masahiro Abe and Ken-ichi Aihara : Skin autofluorescence is associated with tubular injury represented by urinary excretion of liver-type fatty acid-binding protein in patients with diabetes, American Diabetes Association 82nd Scientific Sessions, Jun. 2022.
11.	Ken-ichi Aihara, Yamagami Hiroki, Yasui Saya, Hosoki Minae, Hori Taiki, Shingen Nakamura, Toshiki Otoda and Tomoyuki Yuasa : Clinical Significance of Dehydroepiandrosterone Sulfate in Carotid Atherosclerosis and Nonalcoholic Fatty Liver Disease, ESMED Congress 2021, Nov. 2021.
12.	Tomoyo Hara, Mitsui Yukari, Masuda Shiho, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Heparin cofactor II prevents the development of albuminuria in patients with diabetes, EASD 2021 57th Annual Meeting, Sep. 2021.
13.	Tomoyo Hara, H Yamagami, Y Mitsui, S Masuda, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Plasma heparin cofactor activity is inversely associated with the development NAFLD in patients with diabetes, American Diabetes Association 80th Scientific Session, Chicago, Jun. 2020.
14.	Yumi Kuwamura, Sumiko Yoshida, Kiyoe Kurahashi, Masuko Sumikawa, Eijiro Sakamoto, Akio Kuroda, Hikari Yamato, Misuzu Okamoto, Hirokazu Uemura, Daisuke Hinode, Hiromichi Yumoto, Ken-ichi Aihara, Makoto Funaki, Munehide Matsuhisa, Itsuro Endo and Sachi Kishida : Oral health behaviors of outpatients with diabetes based on the Revised Diabetes Oral Health Assessment Tool for nurses, Journal of Diabetes Investigation, Vol.10, No.Supplement1, 26, Sendai-City, Miyagi Prefecture, May 2019. (キーワード) 口腔保健行動 (oral health behaviors) / diabetes nursing / アセスメント (assessment)
15.	Sumiko Yoshida, Ken-ichi Aihara and Masahiro Abe : Eicosapentaenoic acid administration ameliorates cardiac remodeling in humans and protects against Ang II-induced cardiovascular remodeling via attenuation of oxidative stress in mice., Endocrine Society's Annual Meeting 2019, Mar. 2019.
16.	Yumi Kuwamura, Sumiko Yoshida, Kiyoe Kurahashi, Masuko Sumikawa, Eijiro Sakamoto, Ken-ichi Aihara, Hiromichi Yumoto, Munehide Matsuhisa, Itsuro Endo, Toshiyuki Yasui and Sachi Kishida : The Relationship Between the Modified Diabetes Oral Health Assessment Tool© for Nurses, Self-Efficacy Scale, and Outcome Expectancy Scale for Self-Care of Patients with Periodontal Disease, 2nd Technological Competency as Caring in the Health Sciences 2018, 63, Aug. 2018. (キーワード) nurse / 糖尿病 (diabetes mellitus) / oral health / self-efficacy / outcome expectancy
17.	Akio Kuroda, Misuzu Yamada, Yukari Tominaga, Reiko Suzuki, Motoyuki Tamaki, Yuko Akehi, Yuichi Takashi, Daisuke Otsuka, Eisuke Shimokita, Fuminori Tanihara, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe, Kevin Ferreri and Munehide Matsuhisa : Detection of pancreatic beta cell DNA in the circulation using the amplification refractory mustation system PCR, American Diabetes Association 78th Scientific Sessions, Orlando, Jun. 2018.
18.	Munehide Matsuhisa, Hiroyasu Mori, Mami Ohishi, Masashi Ishizu, Reiko Suzuki, Ineko Takikawa, Satoshi Taniguchi, Motoyuki Tamaki, Yuko Akehi, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Akio Kuroda : The risk factors for rapid decline of renal function in Japanese patients with diabetes mellitus, American Diabetes Association 78th Scientific Sessions, Orlando, Jun. 2018.
19.	Sumiko Yoshida, Kiyoe Kurahashi, Akio Kuroda, Itsuro Endo, Ken-ichi Aihara, Seiji Fukumoto, Munehide Matsuhisa and Masahiro Abe : Changes of oxidative stress markers in patient of diabetes educational hospitalization., The Endocrine Society's Annual Meeting 2018, Chicago, Mar. 2018.
20.	Kana Morimoto, Masuda Shiho, Kiyoe Kurahashi, Motoyuki Tamaki, Takeshi Kondo, Sumiko Yoshida, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Akehi Yuko, Makoto Funaki, Seiji Fukumoto, Munehide Matsuhisa and Ken-ichi Aihara : Identification of clinical determinants for coefficient of variation of - intervals in patients with type 2 diabetes., International Conference on Diabetes and Its Complications 2017, Baltimore, Nov. 2017. (キーワード) 治療 (therapy) / 合併症
21.	Ken-ichi Aihara, Uemoto Ryoko, Ishikawa Kazue, Kana Morimoto, Kiyoe Kurahashi, Sumiko Yoshida, Tomoyuki Yuasa and Masahiro Abe : Heparin cofactor II, a serine protease inhibitor, is associated with albuminuria in humans and mice., International Conference on Diabetes and Its Complications 2017, Baltimore, Nov. 2017. (キーワード) heparin cofactor II / albuminuria
22.	Kana Morimoto, Takahashi Yuka, Yamashita Saori, Kazue Ishikawa, Uemoto Ryoko, Sumiko Yoshida, Tomoyuki Yuasa and Ken-ichi Aihara : Evaluation of Endothelial Function-associated Clinical Parameters and Whole Blood PCR Array Analysis in Patients with Lifestyle-related Diseases, 19th International Vascular Biology Meeting. Boston. USA, Nov. 2016.
23.	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.
24.	Kana Morimoto, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Analysis of sodium restriction-induced blood pressure reduction in hospitalized patients with type 2 diabetes mellitus, The 10th Congress of the Asian-Pacific Society of Atherosclerosis and Vascular Diseases, Tokyo, Jul. 2016.
25.	Akio Kuroda, J Temma, T Horie, Hiroyasu Mori, Motoyuki Tamaki, Ken-ichi Aihara and Munehide Matsuhisa : Noninvasive measurement of skin autofluorescence as a beneficial surrogate marker for atherosclerosis in patients with type 2 diabetes, American Diabetes Association 75th Scientific Sessions, 2015.
26.	Takeshi Kondo, Itsuro Endo, Ken-ichi Aihara, nishi Oh Yukiyo, Bingzi Dong, Kiyoe Kurahashi, Sumiko Yoshida, Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, Masahiro Abe, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Serum carboxy-terminal telopeptide of type I collagen, as a marker for systemic atherosclerosis, ANZBMS 2015 Annual Meeting, Hobart, Sep. 2015.
27.	Akio Kuroda, 鶴尾美穂, Takeshi Kondo, 安芸奈菜子, 大黒由加里, Itsuro Endo, Ken-ichi Aihara, Motoyuki Tamaki, Toshio Matsumoto and Munehide Matsuhisa : Comparison of insulin Glargine with Insulin Degludec in Type 1 Diabetes Patients., 第74回アメリカ糖尿病学会, Jun. 2014.
28.	Ken-ichi Aihara, Sumiko Yoshida, Uemoto Ryoko, Ishikawa Kazue and Toshio Matsumoto : Plasma Heparin Cofactor II Activities are Inversely Associated with Aberrant Glucose Metabolism in Humans and Mice, American Heart Associations Scientific Sessions 2013 Dallas, Texas, Nov. 2013.
29.	Akio Kuroda, Takeshi Kondo, Ken-ichi Aihara, Itsuro Endo, T Yasuda, H Kaneto, T Matsuoka, Toshio Matsumoto and Munehide Matsuhisa : The characteristics of type 1 diabetes patients who use insulin pump with square-wave bolus insulin., 73th America Diabetes Association (poster), Jun. 2013.
30.	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.
31.	Ken-ichi Aihara, Sumiko Yoshida, Ryoko Uemoto, Kazue Ishikawa and Toshio Matsumoto : Plasma Heparin Cofactor II Activities are Inversely Associated with Aberrant Glucose Metabolism in Humans and Mice., American Heart Association, Scientific Sessions 2013, Dallas, Jun. 2013.
32.	Ken-ichi Aihara, Sumiko Yoshida, Mizuho Kinouchi, Takeshi Kondo, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Toshio Matsumoto : Diabetes Spoils the Favorable Effect of HDL-Cholesterol on Endothelial Function in the Elderly with Cardiovascular Risk Factors, American Heart Association Scientific Sessions 2012, ロサンゼルス, Nov. 2012.
33.	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.
34.	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.
35.	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.
36.	Akio Kuroda, YASUDA TETSUYUKI, TAKAHARA MITSUYOSHI, SAKAMOTO FUMIE, KASAMI RYUUICHI, MIYASHITA KAZUYUKI, MATSUOKA TAKA-AKI, Sumiko Yoshida, KONDO ERI, Itsuro Endo, Ken-ichi Aihara, KANETO HIDEAKI, Toshio Matsumoto, SHIMOMURA IICHIRO and Munehide Matsuhisa : Carbohydrate-to-Insulin Ratio is Calculated to be 300-400 Divided by Total Daily Insulin Dose in Type 1 Diabetic Patients Who Are on Insulin Pump Therapy, American Diabetes Association 72nd Scieentific Sessions, Philadelphia, Jun. 2012.
37.	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.
38.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, Takayuki Ise, Toshiyuki Niki, Kenya Kusunose, Yuka Ueda, N. Tomita, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Ken-ichi Aihara, Tetsuzo Wakatsuki, Masafumi Harada and Masataka Sata : Detection of Cardiac Involvement in Patients with Sarcoidosis Using Cardiac Magnetic Resonance., AHA Scientific Sessions 2011, Orlando, Nov. 2011.
39.	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.
40.	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.
41.	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.
42.	Itsuro Endo, Toshio Matsumoto and Ken-ichi Aihara : Serum ICTP can be a surrogate marker of coronary unstable plaques, ASBMR annual meeting, Tronto, Canada, Oct. 2010.
43.	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.
44.	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.
45.	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.
46.	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.
47.	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.
48.	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.
49.	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.
50.	Ken-ichi Aihara, Sumiko Yoshida, Kurahashi Kiyoe, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka and Toshio Matsumoto : Increased serum triglyceride is associated with left ventricular diastolic dysfunction., 14th International Congress of Endocrinology, Kyoto, Mar. 2010.
51.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Mizuho Kinouchi and Itsuro Endo : Rosuvastatin exerts an LDL cholesterol reduction-independent protective effect against carotid atherosclerosis, 14th International Congress of Endocrinology, Kyoto, Mar. 2010.
52.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Mizuho Kinouchi and Itsuro Endo : Dehydroepiandrosterone sulfate is an endothelial function-indipendent anti-atherogenic factor, 14th International Congress of Endocrinology, Kyoto, Mar. 2010.
53.	Ken-ichi Aihara, Yuichi Fujinaka, Mizuho Kinouchi, Sumiko Yoshida, Yuka Ueda, Kurahashi Kiyoe, Itsuro Endo, Uemoto Ryoko, Shusuke Yagi, Takashi Iwase, Hirata Yoichiro, Suzuki Reiko, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Albuminuria is an independent aggravating factor for visceral fat obesity regardless of diabetes mellitus: a study using abdominal CT scan imaging, 14th International Congress of Endocrinology, Kyoto, Mar. 2010.
54.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, K Adachi, Y Sumitomo, Shusuke Yagi, T Niki, Kenya Kusunose, N Tomita, Y Hirata, Koji Yamaguchi, Kunihiko Koshiba, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Ken-ichi Aihara, Masafumi Harada, Hiromu Nishitani and Masataka Sata : Utility of Cardiac Magnetic Resonance for Detection of Cardiac Involvement in Female Carriers of Duchenne Muscular Dystrophy., 第74回日本循環器学会総会・学術集会, Mar. 2010.
55.	Ken-ichi Aihara, Yuichi Fujinaka, Mizuho Kinouchi, Sumiko Yoshida, Takashi Iwase, Masashi Akaike, Yuka Ueda, Kurahashi Kiyoe, Itsuro Endo, Uemoto Ryoko, Shusuke Yagi, Takashi Iwase, Hirata Yoichiro, Suzuki Reiko, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Albuminuria is an independent aggravating factor for visceral fat obesity regardless of diabetes mellitus: a study using abdominal CT scan imaging, 14th International Congress of Endocrinology, Kyoto, Japan, Mar. 2010.
56.	Ken-ichi Aihara, Sumiko Yoshida, Yuka Ueda, Uemoto Ryoko, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Rosuvastatin attenuates left ventricular mass even in subjects without cardiac hypertrophy, 14th International Congress of Endocrinology, Kyoto, Japan, Mar. 2010.
57.	Ken-ichi Aihara, Sumiko Yoshida, Kurahashi Kiyoe, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka and Toshio Matsumoto : Increased serum triglyceride is associated with left ventricular diastolic dysfunction, 14th International Congress of Endocrinology, Kyoto, Japan, Mar. 2010.
58.	Yuka Ueda, Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Shusuke Yagi, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Exacerbation of Angiotensin ll-induced Cardiac Remodeling through Enhancement of NADPH oxidase-TGF- 1 Pathway in Heparin Cofactor ll-Deficient Mice, Scientific Sessions 2009, American Heart Association, Florida, Nov. 2009.
59.	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.
60.	Ken-ichi Aihara, Mizuho Kinouchi, Yuichi Fujinaka, Sumiko Yoshida, Yuka Ueda, Kurahashi Kiyoe, Itsuro Endo, Uemoto Ryoko, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : Albuminuria is an independent aggravating factor for visceral fat obesity regardless of diabetes mellitus: a study using abdominal CT scan imaging, Scientific Sessions 2009, American Heart Association, Florida, Nov. 2009.
61.	Itsuro Endo, Onishi Yukiyo, Kido Rika, Kurahashi Kiyoe, Ito Yuuji, Yuichi Fujinaka, Ken-ichi Aihara, Sumiko Yoshida, Masahiro Abe, Fukumoto S and Toshio Matsumoto : A new calcilytic compound,JTT-305,inhibits enhanced signaling by activating mutations of calcium-sensing receptor in autosomal dominant hypocalcemia (ADH), ASBMR 31st Annual Meeting, Denver, Sep. 2009.
62.	Shusuke Yagi, Masashi Akaike, Takashi Iwase, Kenya Kusunose, T Niki, Y Hirata, Koji Yamaguchi, Kunihiko Koshiba, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, S Yoshida, Y Sumitomo, Ken-ichi Aihara, Toshio Matsumoto and Masataka Sata : Bosentan, an Endothelin Receptor Antagonist, Exerts Protective Actions against Systemic Sclerosis-related Peripheral Circulation Insufficiency., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
63.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, S Yoshida, Y Sumitomo, Kenya Kusunose, T Niki, Y Hirata, Koji Yamaguchi, Kunihiko Koshiba, Takashi Iwase, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Pitavastatin Exerts LDL Cholesterol Reduction-independent Protective Action for Cardiac and Renal Function in Patients with Dyslipidemia., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
64.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, S Yoshida, Y Sumitomo, Kenya Kusunose, T Niki, Y Hirata, Koji Yamaguchi, Kunihiko Koshiba, Takashi Iwase, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Plasma Aldosterone Concentration is Associated with Cognitive Impairement in Patients with Hypertension., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
65.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, K Adachi, Y Sumitomo, Shusuke Yagi, T Niki, Kenya Kusunose, N Sakamoto, Y Hirata, Koji Yamaguchi, Kunihiko Koshiba, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Ken-ichi Aihara, Masafumi Harada, Hiromu Nishitani and Masataka Sata : Early Detection of Myocardial Damage in Female Carriers of Duchenne Muscular Dystrophy - the Utility of Cardiac Magnetic Resonance., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
66.	Ken-ichi Aihara, Sumiko Yoshida, Takayuki Ise, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Kurahashi Kiyoe, Itsuro Endo, Yuichi Fujinaka, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Increased serum triglyceride but not LDL cholesterol is associated with left ventricular diastolic dysfunction., Scientific Sessions 2008, American Heart Association, New Orleans, Nov. 2008.
67.	Takayuki Ise, Ken-ichi Aihara, Sumiko Yoshida, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Ishikawa Kazue, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Plasma Heparin Cofactor II Activity Is Inversely Associated with Left Atrial Volume and Left Ventricular Diastolic Dysfunction., Scientific Sessions 2008, American Heart Association, New Orleans, Nov. 2008.
68.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Kurahashi Kiyoe, Itsuro Endo, Yuichi Fujinaka, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Dehydroepiandrosterone sulfate is an antivascular remodeling factor in elderly individuals., Scientific Sessions 2008, American Heart Association, New Orleans, Nov. 2008.
69.	Takashi Iwase, Hirotsugu Kurobe, Masashi Akaike, Shunji Nakano, Sumiko Yoshida, Sumitomo Yuka, Shusuke Yagi, Ken-ichi Aihara, Shuji Ozaki, Masahiro Abe, Natsuo Yasui, Toshio Matsumoto, Tetsuya Kitagawa and Masataka Sata : Erythropoietin administration with autologous blood donation - a novel strategy to enhance mobilization of circulating progenitor cells, American Heart Association Sessions 2008, New Orleans, Nov. 2008.
70.	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.
71.	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.
72.	Takashi Iwase, Masashi Akaike, Shunji Nakano, Takayuki Ise, Sumiko Yoshida, Sumitomo Yuka, Shusuke Yagi, Ken-ichi Aihara, Natsuo Yasui and Toshio Matsumoto : Single erythropoietin administration with autologous blood donation - a novel strategy to enhance mobilization of endothelial progenitor cells, 22nd Scientific Meeting of the International Society of Hypertension 2008, Berlin, Germany, Berlin, Jun. 2008.
73.	Sumitomo Yuka, Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : Acceleration of angiotensin II-induced cardiac remodeling through enhancement of oxidative stress in heparin cofactor II knockout mice, 22nd Scientific Meeting of the International Society of Hypertension 2008, Berlin, Germany, Berlin, Jun. 2008.
74.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : Dehydroepiandrosterone sulfate regulates carotid blood flow in elderly individuals, 22nd Scientific Meeting of the International Society of Hypertension 2008, Berlin, Germany, Berlin, Jun. 2008.
75.	Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : Serum Lipid Disorder is Associated with Left Ventricular Diastolic Dysfunction in Elderly Individuals, 22nd Scientific Meeting of the International Society of Hypertension 2008, Berlin, Germany, Berlin, Jun. 2008.
76.	Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : The active form of vitamin D, 1,25(OH)2D3, prevents vascular remodeling and glucose intolerance in elderly individuals, 22nd Scientific Meeting of the International Society of Hypertension 2008, Berlin, Germany, Berlin, Jun. 2008.
77.	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.
78.	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.
79.	Hirotsugu Kurobe, Yuki Izawa, Y Fukuhara, Tamotsu Kanbara, A Kurushima, Ken-ichi Aihara, Masashi Akaike, Masashi Kano, Takashi Kitaichi, Yutaka Masuda, Hiroyuki Azuma, Toshiaki Tamaki, Toshio Matsumoto, Tetsuya Kitagawa, Shuhei Tomita and Masanori Yoshizumi : HIF-ARNT transcriptional system in Tcells has a pivotal role in vascular inflammation and remodeling, XIL International Symposium on Atherosclerosis, Italy, Jun. 2006.
80.	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.
81.	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.
82.	Hirotsugu Kurobe, Yuki Izawa, Yayoi Fukuhara, Tamotsu Kanbara, Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma, Tetsuya Kitagawa, Toshiaki Tamaki, Toshio Matsumoto, Masaki Ueno, Shuhei Tomita and Masanori Yoshizumi : T Cell-specific HIF-1α-deficient Mice, but Not ARNT-deficient Mice, Exhibit Exacerbated Inflammation and Vascular Remodeling in Response to Cuff Injury, American Heart Association 2005 Scientifc Sessions, Dallas, Nov. 2005.
83.	Takamori Nobuyuki, Masashi Akaike, Ken-ichi Aihara, Hirono Akira, Yamaguchi Hiroshi, Hiroyuki Azuma, Tamura Katsuya and Toshio Matsumoto : Plasma Heparin Cofactor II Activities Predict Cardiovascular Risk in Patients with Coronary Heart Disease, American Heart Associations Scientific Sessions 2005, Dallas, USA, Nov. 2005.
84.	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.

国内講演発表:

1.	粟飯原賢一, 湯浅智之, 中村信元, 村井純平, 岡本恵暢, 金子遥祐, 森建介, 細木美苗, 堀太貴, 河田沙紀, 辻誠士郎, 安井沙耶, 山上紘規, 原倫世, 乙田敏城, 遠藤逸朗 : 来院時心肺停止・死亡転帰患者の臨床背景における糖尿病有無の影響に関する検討, 第24回日本内分泌学会四国支部学術集会, 2024年9月.
2.	原倫世, 横田海友, 清水一磨, 浅井孝仁, 山上紘規, 三井由加里, 桝田志保, 倉橋清衛, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 粟飯原賢一 : 心血管疾患リスクを有する患者における可溶型DPP-4/CD26と動脈硬化指標との連関解析, 第56回日本動脈硬化学会総会, 2024年7月.
3.	三宅南帆, 辻誠士郎, 河田沙紀, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 2型糖尿病患者の推定食塩摂取量と糖尿病性腎臓病指標の連関解析, 第67回日本糖尿病学会年次学術集会, 2024年5月.
4.	宮髙紘輔, 金子遥祐, 山口佑樹, 原倫世, 吉田守美子, 辻誠士郎, 乙田敏城, 湯浅智之, 粟飯原賢一 : 2型糖尿病患者におけるRed blood cell Distribution Width (RDW)と糖尿病性腎臓病バイオマーカーとの関連解析, 第67回日本糖尿病学会年次学術集会, 2024年5月.
5.	金子遥祐, 森建介, 細木美苗, 堀太貴, 辻誠士郎, 乙田敏城, 湯浅智之, 中村信元, 粟飯原賢一 : 2型糖尿病患者の年間HbA1c変動と肝線維化指標の連関解析, 第67回日本糖尿病学会年次学術集会, 2024年5月.
6.	辻誠士郎, 河田沙紀, 金子遥祐, 森建介, 細木美苗, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 2型糖尿病患者におけるdehydroepiandrosterone sulfate(DHEAS)と尿中アルブミン，尿中L型脂肪酸結合蛋白(L-FABP)との関連, 第67回日本糖尿病学会年次学術集会, 2024年5月.
7.	原倫世, 横田海友, 清水一磨, 浅井孝仁, 山上紘規, 三井由加里, 桝田志保, 倉橋清衛, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 粟飯原賢一 : 糖尿病患者における可溶型DPP-4/CD26と動脈硬化指標との関連, 第67日本糖尿病学会学術集会, 2024年5月.
8.	金子遥祐, 河田沙紀, 森建介, 細木美苗, 堀太貴, 辻誠士郎, 乙田敏城, 湯浅智之, 中村信元, 粟飯原賢一 : 赤血球のmean corpuscular volumeと代謝異常関連脂肪肝疾患の連関解析, 日本内分泌学会雑誌, Vol.100, No.1, 339, 2024年5月.
9.	粟飯原賢一, 三宅南帆, 辻誠士郎, 河田沙紀, 中村信元, 乙田敏城, 湯浅智之 : 2型糖尿病患者の糖尿病性腎臓病における推定食塩摂取量の意義, 日本内分泌学会雑誌, Vol.100, No.1, 348, 2024年5月.
10.	堀太貴, 石田晃基, 稲葉香織, 稲葉圭佑, 金子遙祐, 細木美苗, 森建, 粟飯原賢一, 中村信元 : 内科救急疾患患者におけるRespiratory adjusted shock indexの有用性, 第121回日本内科学会総会・講演会, 2024年4月.
11.	辻誠士郎, 河田沙紀, 村井純平, 乙田敏城, 湯浅智之, 中村信元, 滝下誠, 粟飯原賢一 : 2型糖尿病患者における年間腎機能変化とdehydroepiandrosterone sulfate(DHEAS)の連関解析, 第121回日本内科学会総会・講演会, 2024年4月.
12.	金子遥祐, 森建介, 堀太貴, 細木美苗, 辻誠士郎, 河田沙紀, 乙田敏城, 湯浅智之, 中村信元, 粟飯原賢一 : 代謝異常関連脂肪肝疾患におけるmean corpuscular volumeの意義, 第121回日本内科学会総会・講演会, 2024年4月.
13.	堀太貴, 粟飯原賢一, 石田晃基, 稲葉香織, 稲葉圭佑, 金子遥祐, 川人圭祐, 別宮彰起, 細木美苗, 森建介, 伊丹加奈子, 勝瀬昌代, 花岡賀美, 影治照喜, 浦岡秀行, 中村信元 : 非がん在宅療養患者における予後予測指標の有用性についての検討, 第268回徳島医学会学術集会, 2024年3月.
14.	三宅南帆, 辻誠士郎, 河田沙紀, 粟飯原賢一, 中村信元, 乙田敏城, 湯浅智之 : 2型糖尿病患者における推定塩分摂取量に関わる臨床因子の探索, 四国医学雑誌, Vol.79, No.5-6, 283-284, 2024年3月.
15.	堀太貴, 石田晃基, 稲葉香織, 稲葉圭佑, 金子遥祐, 川人圭祐, 細木美苗, 森建介, 粟飯原賢一, 中村信元 : 内科救急疾患患者におけるRespiratory adjusted shock indexの有用性, 日本内科学会雑誌, Vol.113, 195, 2024年2月. (キーワード) *救急疾患(予後) 脈拍呼吸数ヒト男女
16.	村井純平, 中村信元, 辻誠士郎, 粟飯原賢一, 滝下誠 : 造血器疾患患者へのチキサゲビマブ/シルガビマブ投与による抗SARS-CoV-2 IgG抗体価経時的変化と予防効果の検討, 日本内科学会雑誌, Vol.113, 158, 2024年2月. (キーワード) IgG 血液疾患(薬物療法) モノクローナル抗体(治療的利用,毒性・副作用) 配合製剤(治療的利用,毒性・副作用) 中和抗体(治療的利用,毒性・副作用) COVID-19(予防) 造血器疾患(薬物療法) Tixagevimab(治療的利用,毒性・副作用) Cilgavimab(治療的利用,毒性・副作用) *Cilgavimab-Tixagevimab(治療的利用,毒性・副作用) ヒト中年(45∼64) 高齢者(65∼79) 高齢者(80∼) 男女
17.	三宅南帆, 辻誠士郎, 河田沙紀, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 2型糖尿病患者の推定塩分摂取量に関わる臨床因子解析, 日本糖尿病学会中国四国地方会第61回総会, 2023年10月.
18.	辻誠士郎, 河田沙紀, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 当院糖尿病患者における高血圧治療の現況, 日本糖尿病学会中国四国地方会第61回総会, 2023年10月.
19.	原倫世, 清水一磨, 浅井孝仁, 吉田麻衣子, 山上紘規, 三井由加里, 倉橋清衛, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 粟飯原賢一 : 2型糖尿病患者の非アルコール性脂肪性肝疾患における尿中可溶性ウロキナーゼ型プラスミノーゲン活性化受容体の臨床的意義, 第38回日本糖尿病合併症学会, 2023年10月.
20.	堀太貴, 金子遥祐, 細木美苗, 森建介, 村井純平, 乙田敏城, 湯浅智之, 粟飯原賢一, 滝下誠, 中村信元 : 生活習慣病患者におけるヘモグロビン値と関連因子の検討, 日本血液学会学術集会, 689, 2023年10月. (キーワード) Hemoglobins 生活習慣病(診断,予後) ヒト中年(45∼64) 高齢者(65∼79) 男女
21.	原倫世, 山上紘規, 三井由加里, 倉橋清衛, 中村信元, 乙田敏城, 湯浅智之, 遠藤逸朗, 粟飯原賢一 : 2 型糖尿病患者における血圧・血糖管理目標達成下での腎糸球体・尿細管障害のリスク因子の検討, 第45回日本高血圧学会総会, 2023年9月.
22.	森建介, 金子遥祐, 辻誠士郎, 河田沙紀, 三宅南帆, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 2 型糖尿病患者の年間収縮期血圧変動に関連する臨床因子の解析, 第45回日本高血圧学会総会, 2023年9月.
23.	三宅南帆, 辻誠士郎, 河田沙紀, 原倫世, 山上紘規, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 2 型糖尿病患者における推定塩分摂取量に関連する臨床因子の検討, 第45回日本高血圧学会総会, 2023年9月.
24.	堀太貴, 石田晃基, 稲葉香織, 稲葉圭佑, 金子遙祐, 川人圭祐, 細木美苗, 森建介, 影治照喜, 浦岡秀行, 粟飯原賢一, 中村信元 : 非がん在宅療養患者の予後予測についての検討, Palliative Care Research, Vol.18, No.Suppl._Chugoku-Shikoku, S646, 2023年9月. (キーワード) Albumins 好中球白血球計数ターミナルケア予後リスク評価リンパ球計数在宅死 *臨床意思決定ルールヒト
25.	三宅南帆, 辻誠士郎, 河田沙紀, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 2型糖尿病患者における推定塩分摂取量に関わる臨床因子の探索, 第267回徳島医学会, 2023年8月.
26.	山上紘規, 原倫世, 答島悠貴, 浅井孝仁, 三井由加里, 倉橋清衛, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博, 粟飯原賢一 : 2型糖尿病患者のSkin autofluorscenceを規定する因子の検討, 第96回日本内分泌学会学術総会, 2023年6月.
27.	河田沙紀, 金子遥祐, 森建介, 辻誠士郎, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 運動習慣及び体組成が2型糖尿病患者受診時HbA1cに及ぼす影響の解析, 第96回日本内分泌学会学術総会, 2023年6月.
28.	森建介, 金子遥祐, 辻誠士郎, 河田沙紀, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 2型糖尿病患者における糖尿病治療薬の年間収縮期血圧変動への影響, 第96回日本内分泌学会学術集会, 2023年6月.
29.	辻誠士郎, 森建介, 金子遥祐, 河田沙紀, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 2型糖尿病患者における年間腎機能変化とdehydroepiandrosterone sulfate(DHEAS)の連関解析, 第96回日本内分泌学会学術総会, 2023年6月.
30.	答島悠貴, 原倫世, 浅井孝仁, 山上紘規, 三井由加里, 倉橋衛清, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 粟飯原賢一 : 当院におけるインスリングラルギン/リキシセナチド(iGlarLixi)導入症例の臨床背景および効果の検討, 第66回日本糖尿病学会年次学術集会, 2023年5月.
31.	山上紘規, 原倫世, 答島悠, 浅井孝, 三井由加里, 倉橋清衛, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博, 粟飯原賢一 : 2型糖尿病患者のAGEs蓄積に関わる臨床的因子の解析, 第66回日本糖尿病学会年次学術集会, 2023年5月.
32.	森建介, 河田沙紀, 金子遥祐, 辻誠士郎, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 2型糖尿病患者の年間収縮期血圧変動における糖尿病治療薬の影響, 第66回日本糖尿病学会年次学術集会, 2023年5月.
33.	答島悠貴, 原倫世, 浅井孝, 山上紘規, 三井由加里, 倉橋清衛, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 粟飯原賢一 : 当院におけるインスリングラルギン/リキシセナチド (iGlarLixi)導入症例の臨床背景および効果の検討, 第66回日本糖尿病学会年次学術集会, 2023年5月.
34.	金子遥祐, 河田沙紀, 森建, 辻誠士郎, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 2型糖尿病患者の年間HbA1c変動における糖尿病治療薬の影響, 第66回日本糖尿病学会年次学術集会, 2023年5月.
35.	原倫世, 答島悠貴, 浅井孝仁, 山上紘規, 三井由加里, 倉橋清衛, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 粟飯原賢一 : 糖尿病患者における腎糸球体および尿細管障害特異的なリスク因子の臨床的検討, 第66回日本糖尿病学会年次学術集会, 2023年5月.
36.	辻誠士郎, 森建介, 金子遥祐, 河田沙紀, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 2型糖尿病患者のeGFR slopeにおけるdehydroepiandrosterone sulfate(DHEAS)の意義, 第66回日本糖尿病学会年次学術集会, 2023年5月.
37.	河田沙紀, 金子遥祐, 森建介, 辻誠士郎, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 2型糖尿病患者の受診時HbA1cにおける運動習慣及び体組成の影響, 第66回日本糖尿病学会年次学術集会, 2023年5月.
38.	Akihiro Tani, Takeshi Soeki, 小崎裕司, Ken-ichi Aihara and Masataka Sata : Concomitant Sarcopenia and Atrial Fibrillation is Associated with Heart Failure in Elderly Patients, 第87回日本循環器学会学術集会, Mar. 2023.
39.	金子遥祐, 河田沙紀, 森建介, 辻誠士郎, 中村信元, 乙田敏城, 湯浅智之, 井上善雄, 粟飯原賢一 : 多発腹腔内リンパ節腫脹を契機に診断に至ったPSA正常進行前立腺癌の一例, 第266回徳島医学会学術集会, 2023年2月.
40.	森建介, 河田沙紀, 金子遥祐, 谷彰浩, 辻誠士郎, 中村信元, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : 高齢2型糖尿病患者におけるGNRIスコアと骨格筋異常病態の検討, 第266回徳島医学会学術集会, 2023年2月.
41.	河田沙紀, 金子遥祐, 森建介, 谷彰浩, 辻誠士郎, 湯浅智之, 乙田敏城, 中村信元, 戸田直紀, 粟飯原賢一 : 集学的治療にて救命し得た未治療糖尿病合併咽後膿瘍の1例, 第266回徳島医学会学術集会, 2023年2月.
42.	辻誠士郎, 中村信元, 河田沙紀, 金子遥祐, 森建介, 滝下誠, 祖川麻衣子, 粟飯原賢一 : 帯状疱疹後急速に汎発性帯状疱疹に移行した2例, 第127回日本内科学会四国地方会, 2022年12月.
43.	森建介, 河田沙紀, 金子遥祐, 谷彰浩, 辻誠士郎, 中村信元, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : 2型糖尿病患者の骨格筋異常におけるGNRIスコアの意義, 日本糖尿病学会中国四国地方会第60回総会, 2022年11月.
44.	原倫世, 倉橋清衛, 濱野裕章, 吉田守美子, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 粟飯原賢一 : デュラグルチド使用中患者の HbA1c管理に影響を与える因子の検討, 日本糖尿病学会中国四国地方会第60回総会, 2022年11月.
45.	河田沙紀, 金子遥祐, 森建介, 谷彰浩, 辻誠士郎, 湯浅智之, 乙田敏城, 戸田直紀, 粟飯原賢一 : 咽後膿瘍を発症した未治療糖尿病の1例, 日本糖尿病学会中国四国地方会第60回総会, 2022年11月.
46.	中村信元, 堀太貴, 谷彰浩, 細木美苗, 安井沙耶, 宮田好裕, 山上紘規, 滝下誠, 粟飯原賢一 : 新型コロナワクチン接種後にvaccine-induced immune thrombotic thrombocytopeniaを疑われた症例, 日本老年医学会雑誌, Vol.59, No.4, 594, 2022年10月.
47.	金子遥祐, 河田沙紀, 森建介, 辻誠士郎, 湯浅智之, 乙田敏城, 井上善雄, 粟飯原賢一 : 多発肺転移・腹腔内リンパ節腫脹を契機に診断に至ったPSA陰性の進行前立腺癌の一例, 日本内分泌学会第22回四国支部学術集会, 2022年9月.
48.	細木美苗, 山上紘規, 安井沙耶, 堀太貴, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 当院10年間における死亡患者の年齢・死因および併存合併症における糖尿病と治療薬剤の影響, 第22回日本糖尿病インフォマティクス学会年次学術集会, 2022年8月.
49.	米田健一, 金子遥祐, 河田沙紀, 森建介, 谷彰浩, 辻誠士郎, 湯浅智之, 乙田敏城, 中村信元, 粟飯原賢一 : SGLT2阻害薬内服中のシックデイ対応困難が契機となり，糖尿病性ケトアシドーシスを認めた認知症高齢2型糖尿病の1例, 第265回徳島医学会学術集会, 2022年7月.
50.	桝田志保, 原倫世, 三井由加里, 倉橋清衛, 吉田守美子, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 粟飯原賢一 : 生活習慣病患者のeGFR年間変化量予測における血管内皮機能の意義, 第54回日本動脈硬化学会総会・学術集会, 2022年7月.
51.	原倫世, 山上紘規, 三井由加里, 倉橋清衛, 吉田守美子, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 粟飯原賢一 : 糖尿病患者における血漿Heparin Cofactor II活性とNAFLD病態指標の連関解析, 第8回肝臓と糖尿病・代謝研究会, 2022年6月.
52.	堀太貴, 中村信元, 谷彰浩, 細木美苗, 安井沙耶, 宮田好裕, 山上紘規, 辻誠士郎, 粟飯原賢一, 滝下誠 : 初発時にヘルペスウイルス属の再活性化と中枢浸潤を伴い急速に悪化した成人T細胞白血病リンパ腫の1例, 第126回日本内科学会四国地方会, 2022年6月.
53.	Shingen Nakamura, HORI Taiki, Minae Hosoki, Saya Yasui, Hiroki Yamagami, 赤澤啓人, 滝下誠 and Ken-ichi Aihara : FXIII/13, 第126回日本内科学会四国地方会, Jun. 2022.
54.	中村信元, 堀太貴, 細木美苗, 安井沙耶, 山上紘規, 赤澤啓人, 滝下誠, 粟飯原賢一 : 新型コロナワクチン接種後に発覚した自己免疫性出血病FXIII/13, 第126回日本内科学会四国地方会, 2022年6月.
55.	中村信元, 堀太貴, 細木美苗, 安井沙耶, 山上紘規, 滝下誠, 答島章公, 粟飯原賢一 : 血液疾患，自己免疫疾患における新型コロナワクチン接種後の抗体獲得能の検討, 第96回日本感染症学会総会, 2022年5月.
56.	乙田敏城, 湯浅智之, 関根明子, 上元良子, 森博康, 原倫世, 田蒔基行, 玉置俊晃, 松久宗英, 粟飯原賢一 : SGLT2 阻害薬投与による蛋白尿減少および炎症抑制効果の検討, 第 65 回日本糖尿病学会年次学術集会, 2022年5月.
57.	山上紘規, 細木美苗, 堀太貴, 安井沙耶, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : Skin Autofluorescenceの糖尿病性腎臓病における臨床的意義の解析, 第65回日本糖尿病学会年次学術集会, 2022年5月.
58.	細木美苗, 山上紘規, 安井沙耶, 堀太貴, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 当院10年間における死亡患者の年齢・死因および併存合併症における糖尿病と治療薬剤の影響, 第65回日本糖尿病学会年次学術集会, 2022年5月.
59.	乙田敏城, 湯浅智之, 関根明子, 上元良子, 森博康, 原倫世, 田蒔基行, 玉置俊晃, 松久宗英, 粟飯原賢一 : SGLT2阻害薬投与による蛋白尿減少および炎症抑制効果の検討, 第65回日本糖尿病学会年次学術集会, 2022年5月.
60.	中村信元, 堀太貴, 中村昌史, 住谷龍平, 大浦雅博, 曽我部公子, 丸橋朋子, 高橋真美子, 藤井志朗, 三木浩和, 原田武志, 粟飯原賢一, 安倍正博 : 形質細胞異常症患者におけるSARS-CoV-2に対するmRNAワクチンの液性免疫応答の評価(Humoral response of the mRNA vaccine against SARS-CoV-2 in patients with plasma cell dyscrasia), International Journal of Myeloma, Vol.12, No.3, 199, 2022年5月. (キーワード) 予防接種単クローン性免疫グロブリン血症-良性(免疫学) 液性免疫アミロイドーシス-免疫グロブリン軽鎖(免疫学) *COVID-19ワクチン(治療的利用,薬理学)
61.	山上紘規, 中村信元, 谷彰浩, 細木美苗, 安井沙耶, 宮田好裕, 堀太貴, 答島章公, 粟飯原賢一, 滝下誠 : 自己免疫疾患における新型コロナワクチンによる抗体獲得能の検討, 第119回日本内科学会総会, 2022年4月.
62.	堀太貴, 中村信元, 谷彰浩, 細木美苗, 安井沙耶, 宮田好裕, 山上紘規, 答島章公, 粟飯原賢一, 滝下誠 : 血液疾患患者における新型コロナウイルスワクチン接種による抗体獲得能の検討, 第119回日本内科学会総会, 2022年4月.
63.	中村信元, 堀太貴, 細木美苗, 安井沙耶, 山上紘規, 答島章公, 滝下誠, 粟飯原賢一 : 血液疾患，自己免疫疾患における新型コロナワクチン接種後の抗体獲得能の検討, 感染症学雑誌, Vol.96, 130, 2022年3月. (キーワード) 血液疾患(薬物療法) ウイルス抗体自己免疫疾患(薬物療法) 予防接種 *COVID-19ワクチン(治療的利用) ヒト中年(45∼64) 高齢者(65∼79) 高齢者(80∼) 男女
64.	中村信元, 堀太貴, 細木美苗, 安井沙耶, 山上紘規, 滝下誠, 粟飯原賢一 : 新型コロナワクチン接種後にvaccine-induced immune thrombotic thrombocytopeniaを疑われた症例., 第33回日本老年病学会四国地方会, 2022年1月23日(Web開催), 2022年2月.
65.	山上紘規, 中村信元, 細木美苗, 堀太貴, 安井沙耶, 粟飯原賢一, 答島章公, 滝下誠 : 自己免疫疾患における新型コロナワクチンによる抗体獲得能の検討, 日本内科学会雑誌, Vol.111, No.Suppl., 218, 2022年2月. (キーワード) Azathioprine(治療的利用) Methotrexate(治療的利用) Steroids(治療的利用) 関節炎-乾癬性(薬物療法) 関節リウマチ(薬物療法) ウイルス抗体予防接種 Janus Kinase Inhibitors(治療的利用) COVID-19(予防,薬物療法) *COVID-19ワクチン(治療的利用) ヒト中年(45∼64) 高齢者(65∼79) 高齢者(80∼) 男女
66.	堀太貴, 中村信元, 谷彰浩, 細木美苗, 安井沙耶, 宮田好裕, 山上紘規, 答島章公, 粟飯原賢一, 滝下誠 : 血液疾患患者における新型コロナウイルスワクチン接種による抗体獲得能の検討, 日本内科学会雑誌, Vol.111, No.Suppl., 220, 2022年2月. (キーワード) コロナウイルス感染症(予防,薬物療法) ウイルスワクチン(治療的利用) 血液疾患ウイルス抗体肺炎-ウイルス性(予防,薬物療法) 予防接種 COVID-19(予防,薬物療法) *COVID-19ワクチン(治療的利用) ヒト成人(19∼44) 中年(45∼64) 高齢者(65∼79) 高齢者(80∼) 男女
67.	堀太貴, Shingen Nakamura, Akihiro Tani, Minae Hosoki, Saya Yasui, Hiroki Yamagami, Ken-ichi Aihara, Yuko Miyagami, Takeshi Oya and 滝下誠 : T1, 第125回日本内科学会四国地方会, Dec. 2021.
68.	堀太貴, 中村信元, 細木美苗, 安井沙耶, 山上紘規, 滝下誠, 粟飯原賢一 : 血管中心性に浸潤し急速な経過で死に至った末梢性T細胞リンパ腫の1剖検例, 第125回日本内科学会四国地方会, 2021年12月.
69.	乙田敏城, 湯浅智之, 関根明子, 上元良子, 森博康, 田蒔基行, 玉置俊晃, 松久宗英, 粟飯原賢一 : SGLT2阻害薬の投与が蛋白尿減少効果をもたらす要因の検討, 第6回日本糖尿病・生活習慣病ヒューマンデータ学会, 2021年12月.
70.	桝田志保, 原倫世, 三井由加里, 倉橋清衛, 吉田守美子, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 粟飯原賢一 : 生活習慣病患者におけるeGFR年間変化量と血管内皮機能の連関解析, 第6回日本糖尿病・生活習慣病ヒューマンデータ学会, 2021年12月.
71.	原倫世, 倉橋清衛, 吉田守美子, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 粟飯原賢一 : 糖尿病患者における血漿Heparin Cofactor II活性とNAFLD病態指標の連関, 第6回日本糖尿病・生活習慣病ヒューマンデータ学会, 2021年12月. (キーワード) ヘパリンコファクターII / NAFLD / 糖尿病 (diabetes)
72.	細木美苗, 山上紘規, 安井沙耶, 堀太貴, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 当院死亡患者の年齢・死因および併存合併症における糖尿病の影響, 第59回日本糖尿病学会中国四国地方会, 2021年10月.
73.	岡田朝美, 山田美鈴, 森博康, 明比祐子, 倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 黒田暁生 : 1型糖尿病患者における膵β細胞傷害の定量化の試み, 日本糖尿病学会中国四国地方会第59回総会, 2021年10月.
74.	細木美苗, 山上紘規, 安井沙耶, 堀太貴, 中村信元, 乙田敏城, 湯浅智之, 粟飯原賢一 : 糖尿病の有無からみた当院死亡患者の年齢・死因および併存合併症に関する検討, 第21回日本内分泌学会四国支部学術集会, 2021年9月.
75.	岡田朝美, 山田美鈴, 森博康, 明比祐子, 倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 黒田暁生 : 循環血中遊離DNAを用いた膵β細胞障害の新規検出法の確立, 第263回徳島医学会学術集会, 2021年8月.
76.	金子遥祐, 安井沙耶, 山上紘規, 堀太貴, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : 糖尿病患者における歩行速度規定臨床因子の解析, 第64回日本糖尿病学会年次学術集会, 2021年5月.
77.	粟飯原賢一, 堀太貴, 山上紘規, 安井沙耶, 金子遥祐, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 安倍正博 : 生体電気インピーダンス法による細胞外水分比および位相角と糖尿病患者における血中HbおよびHtレベルの連関解析, 第64回日本糖尿病学会年次学術集会, 2021年5月.
78.	山上紘規, 安井沙耶, 金子遥祐, 堀太貴, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : 糖尿病患者におけるDehydroepiandrosterone sulfate (DHEAS)の糖尿病性腎臓病進展および高血圧症罹患における意義, 第64回日本糖尿病学会年次学術集会, 2021年5月.
79.	安井沙耶, 山上紘規, 金子遥祐, 堀太貴, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : 糖尿病患者における非アルコール性脂肪肝疾患および骨格筋異常症におけるDehydroepiandrosterone sulfate (DHEAS)の意義, 第64回日本糖尿病学会年次学術集会, 2021年5月.
80.	原倫世, 平岡栞名, 細木美苗, 宮髙紘輔, 辻誠士郎, 三井由加里, 倉橋清衛, 吉田守美子, 乙田敏城, 湯浅智之, 遠藤逸朗, 粟飯原賢一 : 糖尿病患者のアルブミン尿増加に関わる臨床因子の横断および縦断解析, 第9回日本高血圧学会臨床高血圧フォーラム, 2021年5月.
81.	堀太貴, 中村信元, 金子遥祐, 安井沙耶, 山上紘規, 粟飯原賢一, 滝下誠 : 1, 第124回日本内科学会四国地方会, 2021年5月.
82.	堀太貴, 中村信元, 細木美苗, 安井沙耶, 山上紘規, 滝下誠, 粟飯原賢一 : 腫大リンパ節に著明なアミロイド沈着を認めたリンパ形質細胞性リンパ腫の1例, 第124回日本内科学会四国地方会, 2021年5月.
83.	金子遥祐, 湯浅智之, 添木武, 乙田敏城, 谷口達哉, 粟飯原賢一, 安井沙耶, 堀太貴, 山上紘規, 中村信元 : 糖尿病患者における歩行速度規定臨床因子の解析, 糖尿病, Vol.64, No.Suppl.1, III-133-4, 2021年5月.
84.	山上紘規, 安井沙耶, 金子遥祐, 堀太貴, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : 糖尿病患者におけるDehydroepiandrosterone sulfate(DHEAS)の糖尿病性腎臓病進展および高血圧症罹患における意義, 糖尿病, Vol.64, No.Suppl.1, P-35-6, 2021年5月.
85.	堀太貴, 山上紘規, 安井沙耶, 金子遥祐, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 安倍正博, 粟飯原賢一 : 生体電気インピーダンス法による細胞外水分比および位相角は糖尿病患者の血中HbおよびHtレベルを規定する, 第94回日本内分泌学会学術総会, 2021年4月.
86.	山上紘規, 安井沙耶, 金子遥祐, 堀太貴, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : Dehydroepiandrosterone sulfate (DHEAS)高値は糖尿病性腎臓病進展および高血圧症罹患のリスクとなる, 第94回日本内分泌学会学術総会, 2021年4月.
87.	原倫世, 倉橋清衛, 吉田守美子, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 粟飯原賢一 : 血漿Heparin Cofactor II活性とNAFLD病態指標の連関解析, 第94回日本内分泌学会学術総会, 2021年4月.
88.	金子遥祐, 安井沙耶, 山上紘規, 堀太貴, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : 生活習慣病患者の歩行速度は骨格筋量よりも筋力が規定する, 第94回日本内分泌学会学術総会, 2021年4月.
89.	金子遥祐, 安井沙耶, 山上紘規, 堀太貴, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : 生活習慣病患者の歩行速度は骨格筋量よりも筋力が規定する, 日本内分泌学会雑誌, Vol.97, No.1, 366, 2021年4月. (キーワード) 筋骨格系生理学的現象骨格筋身体組成筋力生活習慣病(診断) 歩行速度 *筋量ヒト男女
90.	山上紘規, 金子遥祐, 安井沙耶, 堀太貴, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : Dehydroepiandrosterone sulfate(DHEAS)高値は糖尿病性腎臓病進展および高血圧症罹患のリスクとなる, 日本内分泌学会雑誌, Vol.97, No.1, 340, 2021年4月. (キーワード) 高血圧(病因,診断) 糖尿病性腎症(病因,診断) *Dehydroepiandrosterone Sulfate(血液) ヒト男女
91.	安井沙耶, 山上紘規, 金子遥祐, 堀太貴, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : Dehydroepiandrosterone sulfate(DHEAS)は生活習慣病患者における非アルコール性脂肪肝疾患およびダイナペニアの発症抑制因子である, 日本内分泌学会雑誌, Vol.97, No.1, 287, 2021年4月. (キーワード) Dehydroepiandrosterone Sulfate(血液) 生活習慣病(診断,病因,合併症) *肝疾患-非アルコール性脂肪性(診断,病因,合併症) ヒト男女
92.	池田康将, 濱野裕章, 合田光寛, 福島圭穣, 岸誠司, 中馬真幸, 座間味義人, 宮本理人, 石澤啓介, 藤野裕道, 粟飯原賢一, 土屋浩一郎, 玉置俊晃 : シスプラチン起因性腎障害の予防薬の探索・同定, 第94回日本薬理学会年会, 2021年3月.
93.	安井沙耶, 山上紘規, 金子遥祐, 堀太貴, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : 当院生活習慣病患者における骨格筋量に影響を与える因子の検討, 日本内分泌学会雑誌, Vol.96, No.3, 822, 2021年1月. (キーワード) 筋骨格系生理学的現象 / 骨格筋 / 身体組成 / 生活習慣病(診断) / 筋量 / ヒト / 中年(45~64) / 高齢者(65~79) / 男 / 女
94.	山上紘規, 安井沙耶, 金子遥祐, 堀太貴, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : 当院生活習慣病患者における握力と歩行速度に影響を与える因子の検討, 日本内分泌学会雑誌, Vol.96, No.3, 822, 2021年1月. (キーワード) 加齢 / 握力 / 生活習慣病(診断) / 歩行速度 / 中年(45~64) / 高齢者(65~79) / 男 / 女
95.	細木美苗, 三井由加里, 平岡栞名, 宮髙紘輔, 辻誠士郎, 原倫世, 桝田志保, 倉橋清衛, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 福本誠二 : 顕性Cushing症候群を示し片側副腎切除を施行したBMAHの一例, 第30回臨床内分泌代謝update, 2020年11月.
96.	金子遥祐, 中村信元, 細木美苗, 安井沙耶, 山上紘規, 堀太貴, 滝下誠, 粟飯原賢一 : アミカシンによるAPTT偽延長を来したSerratia marcescens菌血症の1例, 第123回日本内科学会四国地方会, 2020年11月.
97.	石津将, 森博康, 明比祐子, 黒田暁生, 田蒔基行, 吉田守美子, 粟飯原賢一, 藍場元弘, 河野友晴, 橋田誠一, 松久宗英 : 糖尿病性腎症における尿アディポネクチンの意義(第2報), 日本糖尿病学会中国四国地方会第58総会, 2020年10月.
98.	吉田守美子, 工藤千晶, 辻本賀美, 安井沙耶, 遠藤ふうり, 桝田志保, 三井由加里, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 福本誠二, 安倍正博, 松久宗英 : 血糖管理入院でのテストステロン値の変化の検討, 第63回日本糖尿病学会年次学術集会, 2020年10月.
99.	金子遥祐, 安井沙耶, 堀太貴, 山上紘規, 乙田敏城, 湯浅智之, 粟飯原賢一 : インスリングラルギンU300とデュラグルチドの併用からインスリンデグルデク・リラグルチド配合製剤への変更後に著明な血糖コントロールの改善を見た1例, 第20回日本内分泌学会四国支部学術集会, 2020年9月.
100.	山上紘規, 安井沙耶, 金子遥祐, 堀太貴, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : 当院生活習慣病患者における握力と歩行速度に影響を与える因子の検討, 第20回日本内分泌学会四国支部学術集会, 2020年9月.
101.	安井沙耶, 山上紘規, 金子遥祐, 堀太貴, 中村信元, 谷口達哉, 乙田敏城, 湯浅智之, 添木武, 粟飯原賢一 : 当院生活習慣病患者における骨格筋量に影響を与える因子の検討, 第20回日本内分泌学会四国支部学術集会, 2020年9月.
102.	原倫世, 坂根容子, 仁木裕子, 中野美恵子, 乙田敏城, 湯浅智之, 粟飯原賢一 : 糖尿病性腎症重症化予防外来受診患者の1年後腎機能評価, 第117回日本内科学会総会, 2020年8月.
103.	川原綾香, 倉橋清衛, 工藤千晶, 鎌田基夢, 加藤真介, 富岡有紀子, 辻本賀美, 安井沙耶, 遠藤ふうり, 桝田志保, 三井由加里, 吉田守美子, 粟飯原賢一, 遠藤逸朗, 福本誠二, 松久宗英, 安倍正博 : 歩行不能だったが，多職種の高度な連携と患者特性に配慮したケアにより自宅生活可能となった高度肥満症の一例, 第261回徳島医学会学術集会, 2020年8月.
104.	平岡栞名, 三井由加里, 三木浩和, 佐藤正大, 東桃代, 遠藤ふうり, 宮髙紘輔, 辻誠士郎, 桝田志保, 倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 福本誠二, 松久宗英, 安倍正博 : 発熱・全身リンパ節腫脹で発症し，リンパ節生検で診断しえた結核性リンパ節炎の一例, 第261回徳島医学会学術集会, 2020年8月.
105.	原倫世, 倉橋清衛, 吉田守美子, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 粟飯原賢一 : NAFLD病態指標血漿Heparin Cofactor IIの連関, 第52回日本動脈硬化学会総会・学術集会, 2020年8月.
106.	吉田守美子, 工藤千晶, 辻本賀美, 安井沙耶, 遠藤ふうり, 桝田志保, 三井由香里, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 安倍正博, 福本誠二 : 糖尿病教育入院でのテストステロン値の変化の検討, 第93回日本内分泌学会学術総会, Vol.96, No.1, 287, 2020年7月.
107.	原倫世, 倉橋清衛, 吉田守美子, 乙田敏城, 湯浅智之, 黒田暁生, 遠藤逸朗, 松久宗英, 粟飯原賢一 : NAFLD病態指標Fib4-indexと血漿Heparin Cofactor Ⅱの連関, 第52回日本動脈硬化学会総会・学術集会, 2020年7月. (キーワード) NAFLD / Heparin Cofactor Ⅱ
108.	原倫世, 乙田敏城, 湯浅智之, 粟飯原賢一 : エンパグリフロジンの糖尿病性腎臓病に対する効果の検討, 第93回日本内分泌学会学術総会, 2020年6月.
109.	乙田敏城, 上元良子, 関根明子, 湯浅智之, 粟飯原賢一 : 血清suPAR値の糖尿病性腎臓病進展予測マーカーとしての有用性, 第62回日本糖尿病学会年次学術集会, 2020年5月.
110.	原倫世, 乙田敏城, 湯浅智之, 粟飯原賢一 : SGLT2阻害薬の糖尿病性腎臓病に対する効果の検討, 第63回日本糖尿病学会年次学術集会, 2020年5月.
111.	川原綾香, 倉橋清衛, 工藤千晶, 鎌田基夢, 加藤真介, 富岡有紀子, 辻本賀美, 安井沙耶, 遠藤ふうり, 桝田志保, 三井由加里, 吉田守美子, 粟飯原賢一, 遠藤逸朗, 福本誠二, 松久宗英, 安倍正博 : 歩行不能だったが，多職種の密な連携と患者特性に配慮したケアにより自宅生活可能となった高度肥満症の一例, 第260回徳島医学会学術集会大塚講堂, 2020年2月.
112.	原倫世, 乙田敏城, 湯浅智之, 粟飯原賢一 : 減塩指導中の糖尿病患者におけるeGFR年間変化量の因子解析, 日本糖尿病学中国四国地方会第57回総会, 2019年12月.
113.	原倫世, 乙田敏城, 湯浅智之, 粟飯原賢一 : SPIDDM様の経過をたどったIA-2抗体単独陽性の中年発症1型糖尿病の1例, 第57回日本糖尿病学会中四国地方会, 2019年12月.
114.	三井由加里, 黒田暁生, 石津将, 桝田志保, 倉橋清衛, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 松久宗英 : 頻回インスリン注射療法下の1型糖尿病患者における基礎インスリン比率の検討, 日本糖尿病学会中国四国地方会第57回総会, 2019年12月.
115.	大島康志, 安藝菜奈子, 鶴尾美穂, 住友正治, 小松まち子, 髙橋保子, 鈴木麗子, 粟飯原賢一, 宇都宮正登, 松久宗英 : 介護に携わる医療従事者を対象にした徳島市糖尿病サポーター研修受講者の意識調査, 日本糖尿病学会中国四国地方会第57回総会, 2019年12月.
116.	鶴尾美穂, 住友正治, 小松まち子, 大島康志, 坂東智子, 森博康, 石津将, 髙橋保子, 粟飯原賢一, 松久宗英, 宇都宮正登 : 徳島市医師会糖尿病腎症重症化予防パイロット事業後アンケート結果, 日本糖尿病学会中国四国地方会第57回総会, 2019年12月.
117.	三井由加里, 黒田暁生, 石津将, 倉橋清衛, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 松久宗英 : 頻回インスリン注射療法下の1型糖尿病患者における基礎インスリン比率の検討, 第19回日本先進糖尿病治療研究会・第17回1型糖尿病研究会, 2019年11月.
118.	石津将, 森博康, 大石真実, 鈴木麗子, 岡本美鈴, 明比祐子, 黒田暁生, 田蒔基行, 髙士祐一, 吉田守美子, 粟飯原賢一, 藍場元弘, 河野友晴, 橋田誠一, 松久宗英 : 糖尿病性腎臓病における尿中アディポネクチン排泄の臨床的意義, 第40回日本肥満学会・第37回日本肥満症治療学会, 2019年11月.
119.	原倫世, 吉田守美子, 乙田敏城, 湯浅智之, 粟飯原賢一 : 原発性アルドステロン症患者に対するエプレレノン投与後血管機能の年間変化, 第42回日本高血圧学会総会, 2019年10月.
120.	吉田守美子, 池田康将, 粟飯原賢一, 安倍正博 : 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, 2019年9月.
121.	八木秀介, 粟飯原賢一, 吉田守美子, 池田康将, 赤池雅史, 佐田政隆 : 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, 2019年9月.
122.	原倫世, 乙田敏城, 湯浅智之, 吉田守美子, 粟飯原賢一 : 生活習慣病患者における血管内皮機能の増悪群と改善群間における年間臨床指標に関する検討, 第19会日本内分泌学会四国支部学術集会, 2019年9月.
123.	辻本賀美, 三井由加里, 工藤千晶, 安井沙耶, 遠藤ふうり, 桝田志保, 倉橋清衛, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 福本誠二 : 勤務時間の影響で副腎皮質機能異常が疑われた2例, 日本内分泌学会第19回四国支部学術集会, 2019年9月.
124.	工藤千晶, 枡田志保, 辻本賀美, 安井沙耶, 遠藤ふうり, 三井由加里, 倉橋清衛, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 新谷保実, 福本誠二 : 両側副腎偶発腫瘍で発見された123I-MIBGシンチ陰性の褐色細胞腫の一例, 日本内分泌学会第19回四国支部学術集会, 2019年9月.
125.	石津将, 鶴尾美穂, 豊崎纏, 粟飯原賢一, 坂東智子, 住友正治, 古川浩, 宮本泰文, 小松まち子, 大島康志, 桜井えつ, 若槻真吾, 岡川和人, 林正, 松村光博, 小川紘一, 安岡正治, 細井恵美子, 丸岡重代, 西岡恵子, 髙橋保子, 森博康, 松久宗英, 宇都宮正登 : 徳島市医師会糖尿病腎症重症化予防パイロット事業の報告, 第19回日本糖尿病情報学会年次学術集会, 2019年8月.
126.	安井沙耶, 桝田志保, 吉田守美子, 辻本賀美, 工藤千晶, 遠藤ふうり, 三井由加里, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 松久宗英, 安倍正博, 福本誠二 : 成長ホルモン分泌不全症と甲状腺機能低下症を呈した小児がん経験者の一例, 第259回徳島医学会学術集会(令和元年度夏期), 2019年8月.
127.	原倫世, 遠藤ふうり, 桝田志保, 三井由加里, 倉橋清衛, 吉田守美子, 乙田敏城, 湯浅智之, 遠藤逸朗, 粟飯原賢一 : 原発性アルドステロン症におけるエプレレノンの血管機能への影響, 第51回日本動脈硬化学会総会・学術集会, 2019年7月.
128.	吉田守美子, 粟飯原賢一, 安倍正博 : 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37回内分泌代謝学サマーセミナー, 2019年7月.
129.	吉田守美子, 粟飯原賢一, 安倍正博 : 心血管病と性差 ∼アンドロゲンを中心に∼, 第61回日本老年医学会学術集会, 2019年6月.
130.	中野美恵子, 坂根容子, 仁木裕子, 山田多喜子, 原倫世, 乙田敏城, 湯浅智之, 粟飯原賢一 : 当院での糖尿病性腎症重症化予防の取り組み, 2. 第62回日本糖尿病学会年次学術集会, 2019年5月.
131.	湯浅智之, 安藝菜奈子, 國見幸太郎, 佐藤美紀, 新居真里, 和泉佳彦, 高田康徳, 乙田敏城, 大澤春彦, 橋田誠一, 粟飯原賢一 : インスリン受容体切断が妊娠期に果たすインスリン作用調節機構の可能性, 第62回日本糖尿病学会年次学術集会, 2019年5月.
132.	鶴尾美穂, 豊﨑纏, 小松まち子, 住友正治, 大島康志, 粟飯原賢一, 森博康, 石津将, 岡川和人, 小川絋一, 古川浩, 桜井えつ, 林正, 坂東智子, 細井恵美子, 松村光輝, 宮本泰文, 保岡正治, 高橋保子, 丸岡重代, 西岡恵子, 宇都宮正登, 松久宗英 : 徳島市医師会糖尿病腎症重症化予防パイロット事業の取組, 第62回日本糖尿病学会年次学術集会, 2019年5月.
133.	原倫世, 上元良子, 関根明子, 乙田敏城, 湯浅智之, 吉田守美子, 粟飯原賢一 : 糖尿病性腎症における血漿ヘパリンコファクターⅡ活性の臨床的意義, 第62回日本糖尿病学会年次学術集会, 2019年5月.
134.	石津将, 森博康, 大石真実, 鈴木麗子, 岡本美鈴, 明比祐子, 黒田暁生, 田蒔基行, 髙士祐一, 吉田守美子, 粟飯原賢一, 藍場元弘, 河野友晴, 橋田誠一, 松久宗英 : 糖尿病性腎臓病における尿中アディポネクチン排泄率の臨床的意義の検討, 第62回日本糖尿病学会年次学術集会, 2019年5月.
135.	宮高絋輔, 吉田守美子, 遠藤ふうり, 枡田志保, 三井由加里, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 福本誠二, 船木真理, 松立吉弘, 軒原浩, 西岡安彦, 安倍正博, 松久宗英 : 免疫チェックポイント阻害薬投与後に1型糖尿病を発症した2例, 第62回日本糖尿病学会年次学術集会, 2019年5月.
136.	原倫世, 上元良子, 関根明子, 乙田敏城, 湯浅智之, 吉田守美子, 粟飯原賢一 : 糖尿病性腎症における血漿ヘパリンコファクターII活性の臨床的意義, 第62回日本糖尿病学会年次学術集会, 2019年5月.
137.	金井麻衣, 松岡飛翔, 遠藤逸朗, 大西幸代, 髙士祐一, 倉橋清衛, 吉田守美子, 粟飯原賢一, 安倍正博, 福本誠二, 松本俊夫 : 鉄製剤投与によるFGF23関連低リン血症モデル作成の試み, 第92回日本内分泌学会学術総会, Vol.95, No.1, 422, 2019年5月.
138.	吉田守美子, 粟飯原賢一, 安倍正博 : 骨格筋アンドロゲン受容体と耐糖能異常の検討, 第92回日本内分泌学会総会, 2019年5月.
139.	鶴尾美穂, 住友正治, 大島康志, 小松まち子, 鈴木麗子, 粟飯原賢一, 安藝菜奈子, 坂東智子, 高橋保子, 丸岡重代, 原田和代, 若槻真吾, 桜井えつ, 井野口卓, 白神敦久, 豊崎纏, 松久宗英, 宇都宮正登 : 糖尿病患者の在宅ケア向上をめざした徳島市糖尿病サポーター(TCDS)育成の試み, 第258回徳島医学会学術集会ポスターセッション, 2019年2月.
140.	宮高紘輔, 遠藤ふうり, 三井由加里, 枡田志保, 倉橋清衛, 吉田守美子, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 福本誠二, 軒原浩, 西岡安彦, 安倍正博, 松久宗英 : 抗PD-1抗体投与後に1型糖尿病を発症した1例, 第258回徳島医学会学術集会ポスターセッション, 2019年2月.
141.	吉田守美子, 原倫世, 山口佑樹, 近藤剛史, 遠藤ふうり, 筒井康継, 桝田志保, 倉橋清衛, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 中島公平, 福本誠二 : 急速に腫瘍が増大し悪性転化が疑われたCushing病の1例, 第28回臨床内分泌代謝Update, 2018年11月.
142.	石津将, 森博康, 大石真実, 鈴木麗子, 明比祐子, 黒田暁生, 田蒔基行, 髙士祐一, 吉田守美子, 粟飯原賢一, 藍場元弘, 河野友晴, 橋田誠一, 松久宗英 : 糖尿病性腎臓病における尿アディポネクチンの意義, 日本糖尿病学会中国四国地方会第56回総会, 2018年10月.
143.	乙田敏城, 上元良子, 関根明子, 湯浅智之, 粟飯原賢一 : 糖尿病性腎臓病における血清suPAR の臨床的意義に関する検討, 本糖尿病学会中国四国地方会第56回総会, 2018年10月.
144.	原倫世, 吉田守美子, 細井美希, 遠藤ふうり, 筒井康継, 桝田志保, 倉橋清衛, 明比祐子, 遠藤逸朗, 粟飯原賢一, 中島公平, 坂東良美, 安倍正博, 福本誠二 : 脳内，副鼻腔，下垂体に炎症を認めステロイドが著効した1例, 第22回日本臨床内分泌病理学会学術総会, 2018年10月.
145.	乙田敏城, 田蒔基行, 髙士祐一, 森本佳奈, 湯浅智之, 松久宗英, 東博之, 粟飯原賢一 : 肥満合併2型糖尿病患者におけるSGLT2阻害薬の短期的臨床効果に関する検討, 第39回日本肥満学会, 2018年10月.
146.	倉橋清衛, 遠藤逸朗, 近藤剛史, 遠藤ふうり, 原倫世, 桝田志保, 吉田守美子, 明比祐子, 坂東良美, 粟飯原賢一, 安倍正博, 福本誠二 : ソマトスタチンアナログ製剤にて著明な縮小がみられたGH産生マクロアデノーマの1例, 第22回日本臨床内分泌病理学会, 2018年9月.
147.	倉橋清衛, 遠藤ふうり, 桝田志保, 吉田守美子, 黒田暁生, 粟飯原賢一, 福本誠二, 遠藤逸朗, 松久宗英 : 足趾上腕血圧比定値を契機に末梢動脈疾患を診断しえた，重症下肢軟部組織感染症を繰り返す2型糖尿病の一例, 第3回日本下肢救済・足病学会中国四国地方会学術集会, 2018年9月.
148.	桝田志保, 遠藤逸朗, 遠藤ふうり, 原倫世, 筒井康継, 倉橋清衛, 吉田守美子, 岸本大輝, 粟飯原賢一, 福本誠二 : hCG,FSH製剤の併用によりパートナーの妊娠が確認された低ゴナドトロピン性男性性腺機能低下症の2例, 第18回日本内分泌学会四国支部学術集会, 2018年9月.
149.	粟飯原賢一, 吉田守美子, 遠藤ふうり, 筒井康継, 原倫世, 桝田志保, 倉橋清衛, 乙田敏城, 湯浅智之, 遠藤逸朗, 森本佳奈, 黒田暁生, 明比祐子, 船木真理, 松久宗英, 福本誠二, 安倍正博 : 原発性アルドステロン症におけるミネラルコルチコイド受容体拮抗薬の血管機能への影響, 第18回日本内分泌学会四国支部学術集会, 2018年9月.
150.	森博康, 荒木迪子, 黒田暁生, 石津将, 髙士祐一, 谷口諭, 倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 田蒔基行, 明比祐子, 松久宗英 : 1型糖尿病患者の血清IGF-1とサルコペニア合併に関する横断的検証, 第18回日本内分泌学会四国支部学術集会, 2018年9月.
151.	本田壮一, 鈴記好博, 小原聡彦, 竹田勝則, 北市雅代, 小笠原卓, 清久泰司, 粟飯原賢一, 吉本勝彦 : 地域での内分泌診療∼高カルシウム血症の2症例より∼, 第18回日本内分泌学会四国支部学術集会, 2018年9月.
152.	山上紘規, 吉田守美子, 遠藤ふうり, 原倫世, 筒井康継, 桝田志保, 倉橋清衛, 明比祐子, 遠藤逸朗, 粟飯原賢一, 大崎裕亮, 梶龍兒, 髙士祐一, 安倍正博, 福本誠二 : 壊死性ミオパチーを合併したX連鎖性低リン血症性くる病・骨軟化症の一例, 第18回日本内分泌学会四国支部学術集会, 2018年9月.
153.	吉田守美子, 粟飯原賢一 : アンドロゲン受容体は骨格筋の糖取り込みに関与する, 第36回内分泌代謝学サマーセミナー, 2018年8月.
154.	吉田守美子, 原倫世, 桝田志保, 倉橋清衛, 黒田暁生, 遠藤逸朗, 粟飯原賢一, 安倍正博, 松久宗英 : 高齢者における糖尿病教育入院中の体組成の変化, 第60回日本老年医学会学術集会, 2018年6月.
155.	黒田暁生, 山田美鈴, 冨永ゆかり, 鈴木麗子, 田蒔基行, 明比祐子, 髙士祐一, 石津将, 古賀大輔, 井本逸勢, 倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 安倍正博, Kevin Ferreri, 松久宗英 : 膵β細胞特異的PCRによる膵β細胞死の検出, 第61回日本糖尿病学会年次学術集会, 2018年5月.
156.	吉田守美子, 原倫世, 細井美希, 山上紘規, 山口佑樹, 桝田志保, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 福本誠二, 安倍正博, 松久宗英 : 糖尿病教育入院における筋肉量の変化, 第61回日本糖尿病学会年次学術集会, 2018年5月.
157.	乙田敏城, 田蒔基行, 髙士祐一, 森本佳奈, 湯浅智之, 松久宗英, 東博之, 粟飯原賢一 : SGLT2阻害薬の糖代謝および各種代謝指標への短期的効果に関する検討, 第61回日本糖尿病学会年次学術集会, 2018年5月.
158.	山上紘規, 吉田守美子, 原倫世, 細井美希, 山口佑樹, 桝田志保, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 福本誠二, 安倍正博, 松立吉弘, 松久宗英 : 免疫チェックポイント阻害薬投与後に甲状腺機能異常と劇症1型糖尿病を発症した1例, 第61回日本糖尿病学会年次学術集会, 2018年5月.
159.	田蒔基行, 髙士祐一, 乙田敏城, 福本誠二, 黒田暁生, 明比祐子, 森博康, 谷口諭, 鈴木麗子, 山田美鈴, 石津将, 大石真実, 白神敦久, 粟飯原賢一, 船木真理, 松久宗英 : かかりつけ患者に対するSGLT2阻害薬の投与開始タイミングの特徴と投与開始後の体重・eGFR・ALT・脂質代謝の変化, 第61回日本糖尿病学会年次学術集会, 2018年5月.
160.	粟飯原賢一, 上元良子, 石川カズ江, 森本佳奈, 桝田志保, 山上綋規, 山口佑樹, 原倫世, 細井美希, 倉橋清衛, 吉田守美子, 乙田敏城, 湯浅智之, 黒田暁生, 明比祐子, 遠藤逸朗, 船木真理, 福本誠二, 松久宗英, 東博之, 安倍正博 : 生活習慣病患者の尿中酸化ストレス指標における糖尿病および薬物療法の影響, 第61回日本糖尿病学会年次学術集会, 2018年5月.
161.	粟飯原賢一, 吉田守美子 : 副腎アンドロゲンDHEASの高血圧有病率における影響, 第91回日本内分泌学会学術総会, 2018年4月.
162.	遠藤逸朗, Dong Bingzi, 大西幸代, 吉田守美子, 粟飯原賢一, 相澤慎一, 福本誠二, 安倍正博, 松本俊夫 : 常染色体優性低Ca血症1型モデルマウスにおける骨強度の低下, 第91回日本内分泌学会学術総会, 2018年4月.
163.	吉田守美子, 原倫世, 細井美希, 山上紘規, 山口佑樹, 桝田志保, 倉橋清衛, 黒田暁生, 遠藤逸朗, 粟飯原賢一, 船木真理, 福本誠二, 浜田大輔, 松久宗英, 安倍正博 : 待機的高リスク整形外科手術における血糖管理の効果, 第91回日本内分泌学会学術総会, 2018年4月.
164.	原倫世, 倉橋清衛, 森本佳奈, 細井美希, 山上紘規, 山口佑樹, 桝田志保, 吉田守美子, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 坂東良美, 福本誠二 : オクトレオチドが有効であったGH-TSH同時産生下垂体腺腫の一例, 第27回臨床内分泌代謝Update, 2017年11月.
165.	桝田志保, 明比祐子, 吉田守美子, 山上紘規, 山口佑樹, 細井美希, 原倫世, 倉橋清衛, 遠藤逸朗, 黒田暁生, 粟飯原賢一, 松久宗英, 船木真理, 福本誠ニ : 123I-MIBGシンチグラフィ陽性の副腎皮質腺腫の一例, 第27回臨床内分泌代謝Update抄録集, 2017年11月.
166.	細井美希, 森本佳奈, 近藤剛史, 山上紘規, 山口佑樹, 原倫世, 桝田志保, 倉橋清衛, 吉田守美子, 遠藤逸朗, 明比祐子, 黒田暁生, 粟飯原賢一, 松久宗英, 福本誠ニ : 多発性骨髄腫治療を契機にプランマー病と判明した一例, 第27回臨床内分泌代謝Update抄録集, 2017年11月.
167.	乙田敏城, 森本佳奈, 湯浅智之, 田蒔基行, 東博之, 粟飯原賢一 : SGLT2 阻害薬の短期臨床的効果に関する検討, 日本糖尿病学会中国四国地方会第55回総会, 2017年11月. (キーワード) 糖尿病 (diabetes mellitus) / 治療 (therapy)
168.	山口佑樹, 吉田守美子, 原倫世, 細井美希, 山上紘規, 桝田志保, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 福本誠ニ, 安倍正博, 柏原秀也, 吉川幸造, 松久宗英 : 高度肥満症に対するスリーブ状胃切除術の長期の耐糖能異常改善効果の検討, 日本糖尿病学会中国四国地方会第55回総会抄録集, 2017年11月.
169.	國方脩登, 吉田守美子, 原倫世, 細井美希, 山上紘規, 山口佑樹, 桝田志保, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 福本誠ニ, 安倍正博, 浜田大輔, 松久宗英 : 待機的整形外科手術の術後経過における糖尿病の影響, 日本糖尿病学会中国四国地方会第55回総会抄録集, 2017年11月.
170.	細井美希, 倉橋清衛, 原倫世, 山口佑樹, 山上紘規, 桝田志保, 吉田守美子, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 福本誠ニ, 松久宗英 : 低血糖脳症をきたしたACTH単独欠損症合併1型糖尿病の一例, 日本糖尿病学会中国四国地方会第55回総会抄録集, 2017年11月.
171.	山上紘規, 倉橋清衛, 原倫世, 細井美希, 山口佑樹, 桝田志保, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 福本誠二 : 副腎クリーゼと急性膵炎を発症した21‐水酸化酵素欠損症の1例, 第117回日本内科学会四国地方会, 2017年11月.
172.	森博康, 大石真実, 鈴木麗子, 黒田暁生, 谷口諭, 田蒔基行, 明比祐子, 倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 船木真理, 松久宗英 : 2型糖尿病患者における末梢神経障害の合併が骨格筋力の質的低下に及ぼす影響, 第32回日本糖尿病合併症学会, 2017年10月.
173.	粟飯原賢一, 吉田守美子 : 男女別高血圧症有病率における副腎アンドロゲン DHEASの関与, 第 40 回日本高血圧学会総会シンボジウム:性ホルモンによる血圧調節機構, 2017年10月.
174.	原倫世, 吉田守美子, 山上紘規, 山口佑樹, 細井美希, 桝田志保, 倉橋清衛, 遠藤逸朗, 明比祐子, 黒田暁生, 粟飯原賢一, 松久宗英, 船木真理, 福本誠二 : 抗パーキンソン病薬により頻回な失神と著明な血圧変動をきたした一例, 2017年10月20日-22日ひめぎんホール, 2017年10月.
175.	原倫世, 吉田守美子, 山上紘規, 山口佑樹, 細井美希, 桝田志保, 倉橋清衛, 遠藤逸朗, 明比祐子, 黒田暁生, 粟飯原賢一, 松久宗英, 船木真理, 福本誠二 : 抗パーキンソン病薬により頻回な失神と著明な血圧変動をきたした一例, 第40回日本高血圧学会総会, 2017年10月.
176.	山上紘規, 倉橋清衛, 山口佑樹, 細井美希, 原倫世, 桝田志保, 吉田守美子, 遠藤逸朗, 明比祐子, 黒田暁生, 粟飯原賢一, 松久宗英, 船木真理, 福本誠二 : バセドウ病とTSH産生下垂体腺腫の合併の一例, 第60回日本甲状腺学会学術集会, 2017年10月.
177.	細井美希, 吉田守美子, 山上紘規, 山口佑樹, 原倫世, 桝田志保, 倉橋清衛, 遠藤逸朗, 明比祐子, 黒田暁生, 粟飯原賢一, 松久宗英, 船木真理, 福本誠二 : 無セルロプラスミン血症に合併した甲状腺乳頭癌の一例, 第60回日本甲状腺学会学術集会, 2017年10月.
178.	池田康将, 堀ノ内裕也, 濱野裕章, 平山祐, 岸誠司, 石澤有紀, 今西正樹, 座間味義人, 武智研志, 宮本理人, 石澤啓介, 粟飯原賢一, 永澤秀子, 土屋浩一郎, 玉置俊晃 : 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, 2017年9月.
179.	桝田志保, 倉橋清衛, 近藤剛史, 細井美希, 山口佑樹, 原倫世, 山上紘規, 吉田守美子, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 船木真理, 福本誠ニ : デノスマブ投与により術後の血清Ca/P値を容易に管理しえた巨大異所性副甲状腺腺腫の一例, 第17回日本内分泌学会四国支部学術集会抄録集, 2017年9月.
180.	原倫世, 吉田守美子, 山口佑樹, 細井美希, 山上紘規, 桝田志保, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 船木真理, 福本誠ニ, 安倍正博 : 当院での免疫チェックポイント阻害薬による下垂体機能低下症の5例, 第17回日本内分泌学会四国支部学術集会抄録集, 2017年9月.
181.	山口佑樹, 吉田守美子, 細井美希, 山上紘規, 原倫世, 桝田志保, 倉橋清衛, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 船木真理, 福本誠二, 滝沢宏光 : 当院での免疫チェックポインント阻害薬による内分泌異常の発生と有害事象対策, 第255回徳島医学会学術集会(平成29年度夏期), 2017年8月.
182.	吉田守美子, 粟飯原賢一, 倉橋清衛, 遠藤逸朗, 安倍正博 : 骨格筋のアンドロゲン受容体と耐糖能異常, 第35回内分泌代謝学サマーセミナー, 2017年7月.
183.	粟飯原賢一, 森本佳奈, 上元良子, 石川カズ江, 乙田敏城, 吉田守美子, 湯浅智之, 東博之 : 生活習慣病患者における血管内皮機能の1年変化に影響を与える臨床指標の検討, 第50回日本動脈硬化学会総会・学術集会, 2017年7月.
184.	森本佳奈, 桝田志保, 倉橋清衛, 田蒔基行, 近藤剛史, 吉田守美子, 湯浅智之, 黒田暁生, 遠藤逸朗, 福本誠二, 松久宗英, 安倍正博, 東博之, 粟飯原賢一 : 生活習慣病患者における血管内皮機能制御に関わる臨床指標の検討, 第49回日本動脈硬化学会総会・学術集会, 2017年7月.
185.	西山美月, 倉橋清衛, 桝田志保, 近藤剛史, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 小松まち子, 福本誠二, 安倍正博 : 維持透析中に管理困難な高Ca血症を契機に診断されたサルコイドーシスの一例, 第116回日本内科学会四国地方会, 2017年5月.
186.	吉田守美子, 粟飯原賢一, 倉橋清衛, 近藤剛史, 森本佳奈, 田蒔基行, 湯浅智之, 黒田暁生, 明比祐子, 遠藤逸朗, 船木真理, 福本誠ニ, 松久宗英 : 糖尿病教育入院での酸化ストレスマーカーの変化の検討, 第60回日本糖尿病学会年次学術集会抄録集, 2017年5月.
187.	田蒔基行, 黒田暁生, 倉橋清衛, 粟飯原賢一, 倉橋清衛, 吉田守美子, 遠藤逸朗, 山口普史, 白神敦久, 松久宗英 : 課程用電気筋刺激装置(EMS)の10週間継続使用は運動障害を有する2型糖尿病患者の血糖コントロールを改善する, 第60回日本糖尿病学会年次学術集会抄録集, 2017年5月.
188.	森本佳奈, 桝田志保, 倉橋清衛, 田蒔基行, 近藤剛史, 吉田守美子, 湯浅智之, 黒田暁生, 明比祐子, 遠藤逸朗, 船木真理, 福本誠ニ, 松久宗英, 安倍正博, 粟飯原賢一 : 糖尿病患者における自律神経機能をアルブミン尿の相互関連および各病態に影響を及ぼす因子解析, 第60回日本糖尿病学会年次学術集会, 2017年5月.
189.	荒木迪子, 森博康, 黒田暁生, 鈴木麗子, 大石真実, 谷口諭, 田蒔基行, 明比祐子, 阪上浩, 倉橋清衛, 近藤剛史, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 船木真理, 松久宗英 : 1型糖尿病患者における血清IGF-1とサルコペニア罹患との関連, 第60回日本糖尿病学会年次学術集会, 2017年5月.
190.	森博康, 黒田暁生, 荒木迪子, 鈴木麗子, 大石真実, 谷口諭, 田蒔基行, 明比祐子, 倉橋清衛, 近藤剛史, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 船木真理, 松久宗英 : 2型糖尿病患者における皮下AGE蓄積が筋機能低下に及ぼす影響, 第60回日本糖尿病学会年次学術集会抄録集, 2017年5月.
191.	吉田守美子, 黒田暁生, 苛原稔, 倉橋清衛, 近藤剛史, 遠藤逸朗, 粟飯原賢一, 松久宗英 : 加重型妊娠高血圧腎症を来し集学的治療で分娩に至った糖尿病腎症の2症例, 第6回臨床高血圧フォーラム, 2017年5月.
192.	吉田守美子, 粟飯原賢一, 倉橋清衛, 近藤剛史, 遠藤逸朗, 湯浅智之, 福本誠二, 安倍正博 : 骨格筋におけるアンドロゲン受容体の耐糖能への影響, 第90回日本内分泌学会学術総会, 2017年4月.
193.	森本佳奈, 高橋優花, 山下沙織, 上元良子, 石川カズ江, 倉橋清衛, 近藤剛史, 吉田守美子, 黒田暁生, 遠藤逸朗, 湯浅智之, 松久宗英, 東博之, 安倍正博, 粟飯原賢一 : 生活習慣病患者の血管内皮機能に関わる因子の臨床的検討, 第90回日本内分泌学会学術集会抄録集, 2017年4月.
194.	森博康, 黒田暁生, 荒木迪子, 鈴木麗子, 大石真実, 谷口諭, 田蒔基行, 明比祐子, 倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 船木真理, 松久宗英 : 2型糖尿病患者におけるサルコペニアのリスク因子解析, 第51回日本成人病学会学術集会, 2017年1月.
195.	桝田志保, 吉田守美子, 倉橋清衛, 近藤剛史, 遠藤逸朗, 安倍正博, 黒田暁生, 松久宗英, 粟飯原賢一, 福本誠二 : メーグルコシダーゼ阻害薬による腸管気腫症の一例, 第115回日本内科学会四国地方会, 2016年11月.
196.	原倫世, 倉橋清衛, 近藤剛史, 吉田守美子, 遠藤逸朗, 黒田暁生, 松久宗英, 粟飯原賢一, 福本誠二 : イピリムマブ投与後に続発性副腎不全を発症した一例, 第115回日本内科学会四国地方会, 2016年11月.
197.	上田浩之, 遠藤逸朗, 近藤剛史, 倉橋清衛, 吉田守美子, 安倍正博, 黒田暁生, 松久宗英, 粟飯原賢一, 福本誠二 : デノスマブによる耐糖能改善, 第115回日本内科学会四国地方会, 2016年11月.
198.	近藤剛史, 遠藤逸朗, 明比祐子, 倉橋清衛, 田蒔基行, 吉田守美子, 黒田暁生, 粟飯原賢一, 松久宗英, 安倍正博, 福本誠二 : 免疫チェックポイント阻害剤で中枢性副腎不全を来した2例, 第26回臨床内分泌代謝Update, 2016年11月.
199.	岡本恵暢, 吉田守美子, 倉橋清衛, 近藤剛史, 森本佳奈, 田蒔基行, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 松久宗英, 福本誠二 : IGF-2産生神経内分泌癌による重症低血糖の一例, 第26回臨床内分泌代謝Update, 2016年11月.
200.	吉田守美子, 倉橋清衛, 近藤剛史, 森本佳奈, 田蒔基行, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 船木真理, 松久宗英, 福本誠二 : 当院のニボルマブおよびイピリムマブ投与21例の内分泌異常の検討, 第26回臨床内分泌代謝Update, 2016年11月.
201.	山下沙織, 吉田守美子, 高橋優花, 粟飯原賢一, 倉橋清衛, 近藤剛史, 森本佳奈, 田蒔基行, 湯浅智之, 黒田暁生, 明比祐子, 遠藤逸朗, 船木真理, 福本誠二, 松久宗英, 安倍正博 : 糖尿病教育入院における酸化ストレス減少に影響を及ぼす因子の検討, 日本糖尿病学会中国四国地方会第54回総会, 2016年11月.
202.	荒木迪子, 森博康, 黒田暁生, 鈴木麗子, 大石真実, 谷口諭, 田蒔基行, 明比祐子, 阪上浩, 倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 船木真理, 松久宗英 : 1型糖尿病患者の血清IGF-1がサルコペニア罹患に及ぼす影響, 日本糖尿病学会中国四国地方会第54回総会, 2016年11月.
203.	森博康, 黒田暁生, 荒木迪子, 鈴木麗子, 大石真実, 谷口諭, 田蒔基行, 明比祐子, 倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 船木真理, 松久宗英 : 2型糖尿病患者におけるAGE蓄積とサルコペニアとの関連の検討, 日本糖尿病学会中国四国地方会第54回総会, 2016年11月.
204.	荒瀬美晴, 近藤剛史, 黒田暁生, 倉橋清衛, 田蒔基行, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 福本誠二, 安倍正博, 松久宗英 : 術前後で持続血糖モニター(CGM)を比較したアドレナリン優位褐色細胞腫の二例, 日本糖尿病学会中国四国地方会第54回総会, 2016年11月.
205.	上田浩之, 近藤剛史, 黒田暁生, 倉橋清衛, 田蒔基行, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 福本誠二, 安倍正博, 松久宗英 : 基礎インスリンが不要であった膵性糖尿病の一例, 日本糖尿病学会中国四国地方会第54回総会, 2016年11月.
206.	森本佳奈, 桝田志保, 倉橋清衛, 田蒔基行, 近藤剛史, 吉田守美子, 湯浅智之, 黒田暁生, 明比祐子, 遠藤逸朗, 船木真理, 福本誠二, 松久宗英, 安倍正博, 粟飯原賢一 : 糖尿病患者における心電図R-R間隔変動係数に影響を及ぼす因子の検討, 日本糖尿病学会中国四国地方会第54回総会, 2016年11月.
207.	荒木迪子, 森博康, 黒田暁生, 鈴木麗子, 大石真実, 谷口諭, 田蒔基行, 明比祐子, 阪上浩, 倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 船木真理, 松久宗英 : 1型糖尿病患者の血清IGF-1がサルコペニア罹患に及ぼす影響, 第14回1型糖尿病研究会, 2016年11月.
208.	高橋優花, 山下沙織, 吉田守美子, 桝田志保, 森本佳奈, 倉橋清衛, 田蒔基行, 近藤剛史, 黒田暁生, 湯浅智之, 遠藤逸朗, 松久宗英, 福本誠二, 東博之, 安倍正博, 粟飯原賢一 : 生活習慣病患者における血管内皮機能正常群および低下群の臨床指標に関する検討, 第16回日本内分泌学会四国支部学術集会, 2016年9月.
209.	山上紘規, 倉橋清衛, 森本佳奈, 近藤剛史, 遠藤逸朗, 明比祐子, 吉田守美子, 黒田暁生, 粟飯原賢一, 松久宗英, 福本誠二, 安倍正博 : バセドウ病を合併したTSH産生下垂体腺腫の一例, 第16回日本内分泌学会四国支部学術集会, 2016年9月.
210.	遠藤ふうり, 倉橋清衛, 森本佳奈, 近藤剛史, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 黒田暁生, 明比祐子, 船木真理, 松久宗英, 福本誠二, 安倍正博 : 日和見感染を合併したACTH依存性Cushing症候群の1例, 第253回徳島医学会学術集会(平成28年度夏期), 2016年7月.
211.	八木秀介, 西條良仁, 高川由利子, 赤池雅史, 佐田政隆, 近藤剛史, 吉田守美子, 遠藤逸朗, 粟飯原賢一 : 左副腎に腫瘤を認めた両側性特発性アルドステロン症の1例, 日本内科学会第114回四国地方会, 2016年5月.
212.	布村俊幸, 吉田守美子, 森本佳奈, 倉橋清衛, 近藤剛史, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫, 安倍正博 : 副腎に接する神経線維腫を合併したレックリングハウゼン病の1例, 第114回日本内科学会四国地方会, 2016年5月.
213.	吉田守美子, 粟飯原賢一, 森本佳奈, 倉橋清衛, 近藤剛史, 田蒔基行, 黒田暁生, 遠藤逸朗, 明比祐子, 船木真理, 福本誠二, 松久宗英 : 当院検診受診者における筋肉量がメタボリックパラメーターに及ぼす影響の検討, 第59回日本糖尿病学会年次学術集会, 2016年5月.
214.	森本佳奈, 粟飯原賢一, 吉田守美子, 倉橋清衛, 近藤剛史, 田蒔基行, 黒田暁生, 遠藤逸朗, 船木真理, 福本誠二, 松久宗英, 安倍正博 : 減塩による2型糖尿病入院症例の降圧予測指標, 第59回日本糖尿病学会年次学術集会, 2016年5月.
215.	吉田守美子, 粟飯原賢一, 森本佳奈, 倉橋清衛, 近藤剛史, 田蒔基行, 黒田暁生, 遠藤逸朗, 明比祐子, 船木真理, 福本誠二, 松久宗英 : 当院検診受診者における筋肉量が高血圧に及ぼす影響の検討, 第5回臨床高血圧フォーラム, 2016年5月.
216.	森本佳奈, 粟飯原賢一, 吉田守美子, 倉橋清衛, 田蒔基行, 近藤剛史, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博 : 血糖管理入院症例における減塩降圧効果と関連する因子および降圧薬に関する検討, 第5回臨床高血圧フォーラム, 2016年5月.
217.	森本佳奈, 粟飯原賢一, 吉田守美子, 倉橋清衛, 近藤剛史, 田蒔基行, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博 : 2型糖尿病患者の塩分制限による降圧効果を規定する因子の検討, 第89回日本内分泌学会学術総会, 2016年4月.
218.	粟飯原賢一, 吉田守美子, 森本佳奈, 倉橋清衛, 近藤剛史, 田蒔基行, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博 : 心筋リモデリングおよび頸動脈硬化症におけるアンジオテンシンII受容体拮抗薬の効果検証, 第89回日本内分泌学会学術総会, 2016年4月.
219.	Shusuke Yagi, Ken-ichi Aihara, Daiju Fukuda, A Takashima, Mika Bando, T Hara, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Takeshi Tobiume, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Masashi Akaike and Masataka Sata : Reduced Ratio of Eicosapentaenoic Acid and Docosahexaenoic Acid to Arachidonic Acid is Associated with Early Onset of Acute Coronary Syndrome., 第80回日本循環器学会学術集会, Mar. 2016.
220.	Shusuke Yagi, Ken-ichi Aihara, Masashi Akaike, T Hara, Takayuki Ise, Daiju Fukuda, Michio Shimabukuro and Masataka Sata : Modulation of Tissue Thrombin Action is a Novel Therapeutic Approach for Prevention of Polyvascular Disease., 第80回日本循環器学会学術集会, Mar. 2016.
221.	山上紘規, 倉橋清衛, 森本佳奈, 近藤剛史, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 黒田暁生, 明比祐子, 船木真理, 松久宗英, 福本誠二, 安倍正博 : インターフェロンβ治療中に糖尿病ケトアシドーシスを契機とし，急性発症1A型糖尿病と診断された一例, 第252回徳島医学会学術集会長井記念ホール, 2016年2月.
222.	森本佳奈, 粟飯原賢一, 吉田守美子, 倉橋清衛, 田蒔基行, 近藤剛史, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博 : 2型糖尿病患者における血糖指標と減塩がもたらす血圧低下との連関, 第252回徳島医学会学術集会長井記念ホール, 2016年2月.
223.	林亜紀, 近藤剛史, 遠藤逸朗, 倉橋清衛, 吉田守美子, 福本誠二, 粟飯原賢一, 安倍正博 : オクトレオチドLARで画像上，下垂体腺腫が消失した先端巨大症の一例, 第113回日本内科学会四国地方会, 2015年12月.
224.	粟飯原賢一, 赤池雅史, 吉田守美子, 松本俊夫 : グルココルコイド過剰誘導酸化ストレスの臨床的評価とeNOSの有無におけるピタバスタチンの虚血臓器保護効果機構の差異, 平成27年度第1回班会議, 2015年12月.
225.	森本佳奈, 近藤剛史, 遠藤逸朗, 倉橋清衛, 田蒔基行, 吉田守美子, 黒田暁生, 松久宗英, 福本誠二, 粟飯原賢一, 安倍正博 : 著明な低カルシウム血症を来した胃癌の骨転移の一例, 第25回臨床内分泌Update, 2015年11月.
226.	小山広士, 近藤剛史, 森本佳奈, 遠藤逸朗, 倉橋清衛, 田蒔基行, 吉田守美子, 黒田暁生, 松久宗英, 福本誠二, 粟飯原賢一, 安倍正博 : ACTH，コルチゾール基礎値正常のACTH単独欠損症の一例, 第25回臨床内分泌Update, 2015年11月.
227.	近藤剛史, 遠藤逸朗, 森本佳奈, 倉橋清衛, 田蒔基行, 吉田守美子, 黒田暁生, 松久宗英, 福本誠二, 粟飯原賢一, 安倍正博 : テタニーで来院し，Gitelman症候群を疑った一例, 第25回臨床内分泌Update, 2015年11月.
228.	粟飯原賢一, 吉田守美子, 森本佳奈, 倉橋清衛, 近藤剛史, 田蒔基行, 黒田暁生, 明比祐子, 遠藤逸朗, 船木真理, 福本誠二, 松久宗英, 安倍正博 : 2型糖尿病患者の左室形態および機能における強化インスリン療法の効果, 日本糖尿病学会第53回中国四国地方会, 2015年10月.
229.	岡田祐輝, 近藤剛史, 森本佳奈, 倉橋清衛, 田蒔基行, 吉田守美子, 黒田暁生, 遠藤逸朗, 松久宗英, 福本誠二, 粟飯原賢一, 安倍正博 : 高CPR血症からグリメピリド誤内服を診断し得た遷延性低血糖の一例, 第53回日本糖尿病学会中国四国地方会米子コンベンションセンター, 2015年10月.
230.	粟飯原賢一, 吉田守美子, 森本佳奈, 倉橋清衛, 近藤剛史, 田蒔基行, 黒田暁生, 明比祐子, 遠藤逸朗, 船木真理, 福本誠二, 松久宗英, 安倍正博 : 2型糖尿病患者の左室形態および機能における強化インスリン療法の効果, 第53回日本糖尿病学会中国・四国地方会米子コンベンションセンター, 2015年10月.
231.	林亜紀, 吉田守美子, 黒田暁生, 七篠あつ子, 苛原稔, 鶴尾美穂, 森本佳奈, 倉橋清衛, 近藤剛史, 田蒔基行, 明比祐子, 遠藤逸朗, 船木真理, 松久宗英, 福本誠二, 粟飯原賢一, 安倍正博 : 分娩前に10g/日以上の蛋白尿を合併し，出産に至った糖尿病腎症の1例, 日本糖尿病学会中国四国地方会第53回総会, 2015年10月.
232.	谷口諭, 黒田暁生, 田蒔基行, 銀花, 森本佳奈, 倉橋清衛, 近藤剛史, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 松久宗英 : CGM iPRO2と人工膵臓STG-55との測定グルコース濃度の比較, 第53回日本糖尿病学会中国・四国地方会米子コンベンションセンター, 2015年10月.
233.	奥村仙示, 和田宵湖, 新井田裕樹, 柏原秀也, 西正暁, 吉川幸造, 森本佳奈, 倉橋清衛, 近藤剛史, 吉田守美子, 田蒔基行, 黒田暁生, 明比祐子, 遠藤逸朗, 粟飯原賢一, 島田光生, 松久宗英 : 本院の腹腔鏡下袖状胃切除術後1年で異なった経過を示した2症例の報告, 第53回糖尿病学会中四国大会, 2015年10月.
234.	森本佳奈, 粟飯原賢一, 吉田守美子, 倉橋清衛, 田蒔基行, 近藤剛史, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博 : 2型糖尿病入院患者における減塩血圧低下効果に影響を及ぼす血糖指標の検討, 第38日本高血圧学会総会, 2015年10月.
235.	粟飯原賢一, 吉田守美子, 森本佳奈, 倉橋清衛, 田蒔基行, 近藤剛史, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博 : 長期のアンジオテンシンII受容体拮抗薬基盤高血圧治療による心筋リモデリングおよび頸動脈硬化症への効果検証, 第38日本高血圧学会総会, 2015年10月.
236.	吉田守美子, 粟飯原賢一, Walsh Kenneth : Inslin-like peptide 6はアンジオテンシンII負荷による心筋線維化に関与する, 第38回日本高血圧学会総会, 2015年10月.
237.	森本佳奈, 近藤剛史, 遠藤逸朗, 倉橋清衛, 田蒔基行, 吉田守美子, 黒田暁生, 松久宗英, 福本誠二, 粟飯原賢一, 安倍正博 : 診断まで長時間を要したACTH分泌低下症の一例, 第15回日本内分泌学会四国支部学術集会高知大学, 2015年9月.
238.	加藤正樹, 森本佳奈, 粟飯原賢一, 吉田守美子, 倉橋清衛, 田蒔基行, 近藤剛史, 黒田暁生, 遠藤逸朗, 松久宗英, 福本誠二, 安倍正博 : 2型糖尿病患者の減塩療法による血圧低下に関連する因子の解析, 第15回日本内分泌学会四国支部学術集会, 2015年9月.
239.	森本佳奈, 粟飯原賢一, 吉田守美子, 倉橋清衛, 田蒔基行, 近藤剛史, 黒田暁生, 遠藤逸朗, 松久宗英, 安倍正博 : 2型糖尿病における血糖指標と減塩がもたらす血圧低下との連関, 第251回徳島医学会学術集会ポスター, 2015年8月.
240.	粟飯原賢一, 吉田守美子, 上元良子, 石川カズ江, 松本俊夫 : 内因性血清尿酸値およびフェブキソスタットによる頸動脈硬化への影響, 第47回日本動脈硬化学会総会・学術集会, 2015年7月.
241.	吉田守美子, 池田康将, 粟飯原賢一, 松本俊夫 : 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, 2015年7月.
242.	池田康将, 粟飯原賢一, 吉田守美子, 赤池雅史, 玉置俊晃, 松本俊夫 : 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」, 2015年5月.
243.	粟飯原賢一, 吉田守美子, 大黒由加里, 田蒔基行, 近藤剛史, 倉橋清衛, 黒田暁生, 遠藤逸朗, 松久宗英, 松本俊夫 : ARB基盤高血圧治療の長期心腎保護効果における糖尿病の影響, 第58回総会日本糖尿病学会年次学術集会, 2015年5月.
244.	桑村由美, 澄川真珠子, 村田裕美, 瀧川稲子, 大和光, 石田伸子, 菊井聡子, 濵田康弘, 飯藤大和, 安原由子, 日野出大輔, 上村浩一, 粟飯原賢一, 松久宗英, 谷岡哲也, 永田俊彦 : 多職種協働での糖尿病患者の口腔保健行動支援:口腔保健行動を査定するための査定シート案についての糖尿病看護の専門家の評価と実施状況, 糖尿病, Vol.58, No.supplement 1, S290, 2015年5月. (キーワード) 糖尿病 (diabetes) / 口腔保健行動 (oral health behaviors) / 看護 (nursing)
245.	粟飯原賢一, 吉田守美子, 大黒由加里, 倉橋清衛, 近藤剛史, 田蒔基行, 黒田暁生, 遠藤逸朗, 松久宗英, 松本俊夫 : 本態性高血圧患者におけるアンジオテンシンII受容体拮抗薬単独およびカルシウム拮抗薬併用による長期心筋保護効果の検証, 第88回日本内分泌学会学術総会, 2015年4月.
246.	近藤剛史, 遠藤逸朗, 大黒由加里, 倉橋清衛, 田蒔基行, 吉田守美子, 黒田暁生, 粟飯原賢一, 松久宗英, 松本俊夫 : 遠位尿細管性アシドーシスの確定診断としてアミノレバンRは有用である．, 第112回日本内科学会総会・講演会, 2015年4月.
247.	大黒由加里, 黒田暁生, 田蒔基行, 倉橋清衛, 近藤剛史, 安芸菜奈子, 遠藤逸朗, 粟飯原賢一, 松本俊夫, 松久宗英 : 皮下注射による強化インスリン療養中の1型糖尿病患者における基礎インスリン比率の検討, 第250回徳島医学会学術集会(大塚講堂), 2015年2月.
248.	黒田暁生, 近藤剛史, 安田哲行, 高原充佳, 粟飯原賢一, 遠藤逸朗, 金藤秀明, 下村伊一郎, 松本俊夫, 松久宗英 : インスリンポンプ療法での追加インスリン注入時間を規定する因子の検討, 第14回日本先進糖尿病治療研究会(あわぎんホール), 2014年12月.
249.	大黒由加里, 黒田暁生, 田蒔基行, 倉橋清衛, 近藤剛史, 安芸菜奈子, 遠藤逸朗, 粟飯原賢一, 松本俊夫, 松久宗英 : 皮下注射による強化インスリン療法1型糖尿病患者における基礎インスリン比率の検討, 第12回1型糖尿病研究会(イーグレ姫路), 2014年11月.
250.	荒木迪子, 田蒔基行, 黒田暁生, 大黒由加里, 倉橋清衛, 近藤剛史, 粟飯原賢一, 遠藤逸朗, 安芸菜奈子, 松本俊夫, 松久宗英 : 2型糖尿病患者におけるeGFRの妥当性について, 日本糖尿病学会中国四国地方会第52回総会, 2014年10月.
251.	粟飯原賢一, 吉田守美子, 大黒由加里, 倉橋清衛, 近藤剛史, 遠藤逸朗, 松本俊夫 : アンジオテンシン受容体拮抗薬およびカルシウム拮抗薬併用による心筋リモデリング抑制の長期効果, 第37日本高血圧学会総会, 2014年10月.
252.	八木秀介, 粟飯原賢一, 赤池雅史, 添木武, 佐田政隆 : 血清PTH濃度は高血圧の発症と関連する, 第37回日本高血圧学会総会, 2014年10月.
253.	田蒔基行, 荒木迪子, 野崎綾音, 大黒由加里, 倉橋清衛, 近藤剛史, 粟飯原賢一, 遠藤逸朗, 安芸菜奈子, 松本俊夫, 松久宗英, 黒田暁生 : 肥満2型糖尿病患者のeGFRは24hrCCrと比較して過小評価されている, 第29回日本糖尿病合併症学会, 2014年10月.
254.	森本佳奈, 粟飯原賢一, 大黒由加里, 倉橋清衛, 近藤剛史, 田蒔基行, 安藝菜奈子, 黒田暁生, 遠藤逸朗, 松久宗英, 松本俊夫 : 多剤併用降圧療法と臓器障害モニタリングにより長期にわたり心腎大血管障害の改善が得られた加速型高血圧-悪性高血圧の1例, 第14回日本内分泌学会四国支部学術集会, 2014年9月.
255.	東口文治, 菅澤典子, 中山泰介, 木下肇, 宅見央子, 粟飯原賢一, 黒部裕嗣, 北川哲也 : アポE 欠損マウスに対する分散ヘスペレチンの抗動脈硬化作用, 公益社団法人日本食品科学工学会第61回大会, 2014年8月.
256.	粟飯原賢一, 吉田守美子, 池田康将, 上元良子, 石川カズ江, 赤池雅史, 松本俊夫 : 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, 2014年7月.
257.	粟飯原賢一, 大黒由加里, 倉橋清衛, 近藤剛史, 木内美瑞穂, 遠藤逸朗, 松本俊夫, 田蒔基行, 黒田暁生, 松久宗英 : エゼチミブとコレスチミドの併用で脂質プロフィルが改善した多発性筋炎合併家族性高コレステロール血症へテロ接合体の一例, 第110回日本内科学会四国地方会, 2014年6月.
258.	森本佳奈, 粟飯原賢一, 大黒由加里, 倉橋清衛, 木内美瑞穂, 田蒔基行, 安藝菜奈子, 黒田暁生, 遠藤逸朗, 松久宗英, 松本俊夫 : 多剤併用降圧療法により長期的な心・腎・大血管障害の改善が得られた高レニン性高血圧症の1例, 第3回臨床高血圧フォーラム, 2014年5月.
259.	大黒由加里, 黒田暁生, 田蒔基行, 倉橋清衛, 近藤剛史, 木内美瑞穂, 近藤絵里, 吉田守美子, 安芸菜奈子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : 皮下注射による強化インスリン療法1型糖尿病患者における基礎インスリン比率の検討, 第57回日本糖尿病学会年次学術集会口演, 2014年5月.
260.	粟飯原賢一, 木内美瑞穂, 大黒由加里, 倉橋清衛, 近藤剛史, 安藝菜奈子, 黒田暁生, 遠藤逸朗, 松久宗英, 松本俊夫 : 生活習慣病治療薬が血管内皮機能に及ぼす影響の検証, 第111回日本内科学会講演会, 2014年4月.
261.	菅澤典子, 中山泰介, 黒部裕嗣, 宅見央子, 東口文治, 木下肇, 菅野幹雄, 神原保, 藤本鋭貴, 粟飯原賢一, 北市隆, 松本俊夫, 北川哲也 : 動脈硬化病巣進展に対する糖転移ヘスペリジンの抑制効果についての検討, 第44回日本心臓血管外科学会学術総会, 2014年2月.
262.	八木秀介, 粟飯原賢一, 赤池雅史, 松本幸子, 福田大受, 松浦朋美, 伊勢孝之, 山口浩司, 岩瀬俊, 山田博胤, 添木武, 若槻哲三, 島袋充生, 松本俊夫, 佐田政隆 : DPP-4阻害薬の血糖降下作用に対する有効性予測因子, 第248回徳島医学会学術集会, 2014年2月.
263.	森本佳奈, 粟飯原賢一, 大黒由加里, 倉橋清衛, 近藤剛史, 木内美瑞穂, 田蒔基行, 安芸菜奈子, 黒田暁生, 遠藤逸朗, 松久宗英, 松本俊夫 : 6年間にわたる多剤併用降圧療法が心・腎・大血管障害の改善に寄与した高レニン性高血圧症の1例, 第248回徳島医学会学術集会, 2014年2月.
264.	大黒由加里, 近藤剛史, 倉橋清衛, 安芸菜奈子, 黒田暁生, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : 下垂体の経時的な変化を捉えたシーハン症候群の一例, 第23回臨床内分泌代謝Update, 2014年1月.
265.	黒田暁生, 近藤剛史, 安田哲行, 高原充佳, 粟飯原賢一, 遠藤逸朗, 金藤秀明, 下村伊一郎, 松本俊夫, 松久宗英 : インスリンポンプ療法での追加インスリン注入時間を規定する因子の検討, 第13回日本先進糖尿病治療研究会, 2013年11月.
266.	大和光, 瀧川稲子, 松村晃子, 山田静恵, 谷佳子, 粟飯原賢一, 松本俊夫, 銀花, 黒田暁生, 松久宗英 : 徳島大学病院における糖尿病透析予防指導の有用性の検討, 日本糖尿病学会中国四国地方会第51回総会, 2013年11月.
267.	大黒由加里, 近藤剛史, 黒田暁生, 倉橋清衛, 木内美瑞穂, 安芸菜奈子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : 過剰基礎インスリン量が不適切な間食摂取に関連したインスリンポンプ使用1型糖尿病の2例, 日本糖尿病学会中国四国地方会第51回総会, 2013年11月.
268.	近藤剛史, 大黒由加里, 黒田暁生, 倉橋清衛, 木内美瑞穂, 安芸菜奈子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : テストステロン補充で速やかにインスリン抵抗性が改善した汎下垂体機能低下症合併糖尿病例, 日本糖尿病学会中国四国地方会第51回総会, 2013年11月.
269.	粟飯原賢一, 木内美瑞穂, 大黒由加里, 近藤剛史, 倉橋清衛, 安藝菜奈子, 黒田暁生, 遠藤逸朗, 松久宗英, 松本俊夫 : メタボリックシンドロームおよび糖尿病の有無が血管内皮機能に及ぼす影響, 日本糖尿病学会中国四国地方会第51回総会, 2013年11月.
270.	近藤剛史, 大黒由加里, 黒田暁生, 倉橋清衛, 木内美瑞穂, 安芸菜奈子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : テストステロン補充で速やかにインスリン抵抗性が改善した汎下垂体機能低下症合併糖尿病例, 日本糖尿病学会中国四国地方会第51回総会, 2013年11月.
271.	粟飯原賢一, 木内美瑞穂, 吉田守美子, 大黒由加里, 倉橋清衛, 近藤剛史, 安藝菜奈子, 黒田暁生, 遠藤逸朗, 松久宗英, 松本俊夫 : 糖代謝異常の血管機能評価に及ぼす効果, 第36回日本高血圧学会総会, 2013年10月.
272.	中山泰介, 菅澤典子, 黒部裕嗣, 木下肇, 菅野幹雄, 神原保, 藤本鋭貴, 北市隆, 粟飯原賢一, 宅見央子, 東口文治, 北川哲也 : ヘスペリジンの血管内皮治療への応用, 第66回日本胸部外科学会定期学術集会, 2013年10月.
273.	大黒由加里, 近藤剛史, 藤井志朗, 中村信元, 倉橋清衛, 黒田暁生, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : 著名な汎血球減少と肝筋逸脱酵素高値を呈した神経性食欲不振症の一例, 第13回日本内分泌学会四国支部学術集会, 2013年9月.
274.	近藤剛史, 岩佐昌美, 大黒由加里, 倉橋清衛, 黒田暁生, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : 不動が惹起した高カルシウム血症で頻回の意識障害を来たした一例, 第13回日本内分泌学会四国支部学術集会, 2013年9月.
275.	鈴木麗子, 大和光, 瀧川稲子, 粟飯原賢一, 遠藤逸朗, 安芸菜奈子, 倉橋清衛, 松本俊夫, 黒田暁生, 松久宗英 : フットケア外来におけるインスリン皮下硬結の実態調査と皮下硬血患者への介入の結果報告, 第13回日本糖尿病情報学会年次学術集会, 2013年8月.
276.	木内美瑞穂, 粟飯原賢一, 吉田守美子, 大黒由加里, 倉橋清衛, 近藤剛史, 安藝菜奈子, 黒田暁生, 遠藤逸朗, 松久宗英, 松本俊夫 : 臨床血管機能における糖代謝異常の影響の解析, 第247回徳島医学会学術集会, 2013年8月.
277.	粟飯原賢一, 木内美瑞穂, 吉田守美子, 岩佐昌美, 倉橋清衛, 近藤剛史, 安藝菜奈子, 黒田暁生, 遠藤逸朗, 松久宗英, 松本俊夫 : Evaluation for influence of diabetes on clinical vascular function, 第45回日本動脈硬化学会総会・学術集会, 2013年7月.
278.	粟飯原賢一, 松本俊夫, 松久宗英, 大和光 : 血管年齢を正確に知ってアンチエイジング!, 第13回日本抗加齢医学会総会, 2013年6月.
279.	粟飯原賢一 : 血管内皮機能から診たメタボリックシンドロームと糖尿病, 第13回日本抗加齢医学会総会シンポジウム12, 2013年6月.
280.	鈴木麗子, 瀧川稲子, 大和光, 木田菊恵, 粟飯原賢一, 遠藤逸朗, 安芸菜奈子, 倉橋清衛, 松本俊夫, 黒田暁生, 松久宗英 : フットケア外来におけるインスリン皮下硬結の実態調査と皮下硬結患者への介入の有用性検討, 第56回日本糖尿病学会年次学術集会, 2013年5月.
281.	黒田暁生, 鶴尾美穂, 粟飯原賢一, 遠藤逸朗, 安芸菜奈子, 吉田守美子, 近藤剛史, 松本俊夫, 松久宗英 : 1型糖尿病患者におけるインスリングラルギンからインスリンデグルデッグへの同量での切り替え:CGMSを用いた検討, 第56回日本糖尿病学会年次学術集会, 2013年5月.
282.	近藤剛史, 黒田暁生, 吉田守美子, 安芸菜奈子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : 頻回インスリン療法による厳格な血糖管理下におけるシダグリプチン併用のインスリン所要量現象効果の検討, 第56回日本糖尿病学会年次学術集会ポスター, 2013年5月.
283.	桑村由美, 松田宣子, 田村綾子, 市原多香子, 南川貴子, 大和光, 金澤昭代, 粟飯原賢一, 倉橋清衛, 吉田守美子, 吉岡昌美, 日野出大輔, 松久宗英, 黒田暁生 : 糖尿病患者の口腔保健行動に及ぼす影響要因の検討―第1報口腔保健行動に対する認識との関係から―, 第56回日本糖尿病学会年次学術集会, Vol.56, No.Supplement 1, S-167, 2013年5月.
284.	近藤剛史, 黒田暁生, 曽我部公子, 吉田守美子, 安藝菜奈子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : 術前後で持続血糖測定(CGM)を比較しえたアドレナリン優位褐色細胞腫の1例, 第56回日本糖尿病学会年次学術集会, 2013年5月.
285.	吉田守美子, 粟飯原賢一, 池田康将, 盛真友, 松本高広, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2013年4月.
286.	松本和久, 吉田守美子, 粟飯原賢一, 岩佐昌美, 近藤剛史, 倉橋清衛, 木内美瑞穂, 遠藤逸朗, 安芸菜奈子, 黒田暁生, 松久宗英, 松本俊夫 : 膵臓の鉄過剰沈着とインスリン分泌不全を呈した無セルロプラスミン血症合併糖尿病の1例, 第86回日本内分泌学会学術総会, 2013年4月.
287.	三橋威史, 粟飯原賢一, 吉田守美子, 上元良子, 石川カズ江, 松本俊夫 : 粥状動脈硬化モデルにおけるピタバスタチンの臓器保護効果の検討, 第86回日本内分泌学会学術総会, 2013年4月.
288.	松本和久, 粟飯原賢一, 吉田守美子, 木内美瑞穂, 近藤剛史, 倉橋清衛, 安藝菜奈子, 遠藤逸朗, 黒田暁生, 松久宗英, 松本俊夫 : 膵臓の鉄過剰沈着とインスリン分泌不全を呈した無セルロプラスミン血症合併糖尿病の1例, 第86回日本内分泌学会学術総会, 2013年4月.
289.	粟飯原賢一, 吉田守美子, 上元良子, 石川カズ江, 赤池雅史, 松本俊夫 : 重症下肢虚血壊死に対するピタバスタチンの組織保護効果に関する検討, 第86回日本内分泌学会学術総会, 2013年4月.
290.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, Takayuki Ise, Toshiyuki Niki, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Ken-ichi Aihara, Tetsuzo Wakatsuki, Yasuhiko Nishioka, Masafumi Harada and Masataka Sata : Differentiation of Left Ventricular Systolic Dysfunction Related to Cardiac Sarcoidosis and Other Heart Diseases Using contrast-enhanced Cardiovascular Magnetic Resonance., 第77回日本循環器学会学術集会, Mar. 2013.
291.	曽我部公子, 近藤剛史, 黒田暁生, 吉田守美子, 片岡菜奈子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : 術前後で持続血糖測定(CGM)を比較しえた褐色細胞腫の一例, 第22回臨床内分泌代謝Update, 2013年1月.
292.	牟田口惇, 近藤剛史, 遠藤逸朗, 吉田守美子, 片岡菜奈子, 黒田暁生, 粟飯原賢一, 松久宗英, 松本俊夫 : 尿細管性アシドーシスの診断にアミノレバンが有用であった一例, 第22回臨床内分泌代謝Update, 2013年1月.
293.	幸田舞子, 近藤剛史, 遠藤逸朗, 吉田守美子, 片岡菜奈子, 黒田暁生, 粟飯原賢一, 松久宗英, 松本俊夫 : 悪性症候群様の症状から診断されたACTH分泌低下症の一例, 第22回臨床内分泌代謝Update, 2013年1月.
294.	松崎苑美, 粟飯原賢一, 吉田守美子, 倉橋清衛, 近藤剛史, 遠藤逸朗, 松本俊夫, 片岡菜奈子, 黒田暁生, 松久宗英 : 血栓性微小血管障害症様の病態を示したメタボリックシンドロームの1例, 第107回日本内科学会四国地方会, 2012年12月.
295.	佐埜弘樹, 粟飯原賢一, 吉田守美子, 近藤剛史, 倉橋清衛, 遠藤逸朗, 松本俊夫, 黒田暁生, 松久宗英, 片岡菜奈子 : 正常MRI所見を示し，ADH放出障害が主因と考えられた中枢性尿崩症の1例, 日本内科学会第107回四国地方会, 2012年12月.
296.	黒田暁生, 新居沙央里, 吉田守美子, 近藤絵里, 遠藤逸朗, 粟飯原賢一, 松本友里, 片岡菜奈子, 松本俊夫, 松久宗英 : 新たなインスリンポンプParadigm722によってカーボカウントのみで血糖管理が可能となった1症例, 第12回日本先進糖尿病治療学会研究会, 2012年12月.
297.	黒田暁生, 高原充佳, 安田哲行, 松岡孝昭, 近藤剛史, 遠藤逸朗, 粟飯原賢一, 吉田守美子, 松本俊夫, 下村伊一郎, 金藤秀明, 松久宗英 : 日本人1型糖尿病患者における「500ルールとは?」, 第12回日本先進糖尿病治療研究会, 2012年12月.
298.	吉田守美子, 近藤剛史, 倉橋清衛, 遠藤逸朗, 粟飯原賢一, 高島啓, 山口浩司, 松本俊夫 : 難治性冠攣縮性狭心症を合併した無痛性甲状腺炎の1例, 第55回日本甲状腺学会学術集会, Vol.88, No.2, 516, 2012年11月. (キーワード) Thiamazole(治療的利用) Thyroxine(治療的利用) 狭心症-異型(合併症,薬物療法) 甲状腺炎-自己免疫性(合併症,画像診断,薬物療法) Nicorandil(治療的利用) *甲状腺炎-無痛性(合併症,画像診断,薬物療法) ヒト中年(45~64) 男
299.	幸田舞子, 近藤剛史, 黒田暁生, 吉田守美子, 安芸菜奈子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : シタグリプチン投与によりインスリン所要量の減少効果が得られた高齢2型糖尿病の一例, 日本糖尿病学会中国四国地方会第50回総会, 2012年11月.
300.	近藤剛史, 黒田暁生, 曽我部公子, 吉田守美子, 安芸菜奈子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : 術前後で持続血糖測定(CGM)を比較しえたアドレナリン優位褐色細胞腫の一例, 日本糖尿病学会中国四国地方会第50回総会, 2012年11月.
301.	近藤剛史, 黒田暁生, 曽我部公子, 吉田守美子, 安芸菜奈子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : アドレナリン優位の褐色細胞腫の術前後で持続血糖測定(CGM)により血糖変動を比較した一例, 日本糖尿病学会中国四国地方会第50回総会, 2012年11月.
302.	幸田舞子, 近藤剛史, 黒田暁生, 吉田守美子, 片岡菜奈子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : シタグリプチン投与によりインスリン所要量の減少効果が得られた高齢2型糖尿病の一例, 日本糖尿病学会中国四国地方会第50回総会, 2012年11月.
303.	岩佐昌美, 黒田暁生, 吉田守美子, 近藤剛史, 片岡菜奈子, 遠藤逸朗, 粟飯原賢一, 福島泰江, 松久宗英, 松本俊夫 : 血糖管理基準を満たすために分割食を必要としなかった2型糖尿病合併妊娠の1例, 日本糖尿病学会中国四国地方会第50回総会, 2012年11月.
304.	粟飯原賢一, 吉田守美子, 近藤絵里, 近藤剛史, 倉橋清衛, 遠藤逸朗, 松本俊夫 : 高尿酸血症は頸動脈プラークおよび血管抵抗を亢進させる, 第35回日本高血圧学会総会, 423, 2012年9月. (キーワード) 頸動脈疾患血管抵抗動脈硬化症-アテローム性高尿酸血症 *動脈硬化プラークヒト男女
305.	粟飯原賢一 : 心血管系組織恒常性維持におけるアンドロゲン受容体の意義, 第3回テストステロン研究会・教育講演, 2012年9月.
306.	白河綾, 粟飯原賢一, 吉田守美子, 倉橋清衛, 近藤剛史, 遠藤逸朗, 安藝菜奈子, 黒田暁生, 松久宗英, 松本俊夫 : 副腎不全症状を呈し，診断に苦慮した両側副腎B細胞リンパ腫の1例, 第12回日本内分泌学会四国支部学術集会, 2012年9月.
307.	粟飯原賢一, 吉田守美子, 松本俊夫 : シンポジウム11 心・血管病の性差:血管形態と機能解析からみた頸動脈硬化の性差と副腎アンドロゲンDHEASの抗動脈硬化作用, 第44回日本動脈硬化学会・学術総会/ヒルトン福岡シーホーク, 2012年7月.
308.	粟飯原賢一, 吉田守美子, 松本俊夫 : 血管形態と機能解析からみた頸動脈硬化の性差と副腎アンドロゲンDHEASの抗動脈硬化作用, 第44回日本動脈硬化学会総会・学術集会: シンポジウム11 心・血管病の性差, 2012年7月.
309.	吉田守美子, 粟飯原賢一, 木内美瑞穂, 近藤絵里, 遠藤逸朗, 松本俊夫 : Diabetes abolishes protective effect of HDL-cholesterol against endothelial dysfunction., 第44回日本動脈硬化学会総会・学術集会, 2012年7月.
310.	遠藤逸朗, 吉田守美子, 倉橋清衛, 木内美瑞穂, 片岡菜奈子, 近藤剛史, 近藤絵里, 粟飯原賢一, 松本俊夫, 黒田暁生, 松久宗英 : Werner症候群に伴う糖尿病の治療経過, 第106回日本内科学会四国地方会, 2012年6月.
311.	粟飯原賢一, 吉田守美子, 倉橋清衛, 近藤剛史, 近藤絵里, 片岡菜奈子, 遠藤逸朗, 黒田暁生, 松久宗英, 松本俊夫 : インクレチン関連薬を用いた周術期血糖管理の有用性, 第106回日本内科学会四国地方会, 2012年6月.
312.	吉田守美子, 粟飯原賢一, 池田康将, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2012年5月. (キーワード) 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
313.	粟飯原賢一, 吉田守美子, 赤池雅史, 松本俊夫 : 血管内皮機能制御における血圧関連指標の意義, 日本高血圧学会第1回臨床高血圧フォーラム, 2012年5月.
314.	大黒由加里, 粟飯原賢一, 吉田守美子, 近藤絵里, 近藤剛史, 倉橋清衛, 木内美瑞穂, 遠藤逸朗, 片岡菜奈子, 黒田暁生, 松久宗英, 松本俊夫 : 摂食障害による著明な低K血症を呈した視床下部性ACTH分泌低下症の1例, 第85回日本内分泌学会学術総会, 2012年4月.
315.	吉田守美子, 粟飯原賢一, 近藤絵里, 倉橋清衛, 近藤剛史, 木内美瑞穂, 遠藤逸朗, 松本俊夫, 片岡菜奈子, 黒田暁生, 松久宗英 : 糖尿病はHDLコレステロールによる血管内皮機改善効果を減弱させる, 第85回日本内分泌学会学術総会, 2012年4月.
316.	粟飯原賢一, 吉田守美子, 近藤絵里, 近藤剛史, 倉橋清衛, 木内美瑞穂, 遠藤逸朗, 片岡菜奈子, 黒田暁生, 松久宗英, 松本俊夫 : ヘパリンコファクターⅡは耐糖能制御因子である, 第85回日本内分泌学会学術総会, 2012年4月.
317.	吉田守美子, 藤中雄一, 粟飯原賢一, 鈴木麗子, 木内美瑞穂, 近藤絵里, 安藝菜奈子, 遠藤逸朗, 黒田暁生, 松久宗英, 松本俊夫 : 当院検診受診者における耐糖能異常の特徴, 第109回日本内科学会総会・講演会, 2012年4月.
318.	粟飯原賢一, 吉田守美子, 近藤絵里, 近藤剛史, 倉橋清衛, 遠藤逸朗, 松本俊夫 : 尿酸は形態および機能的頸動脈硬化症進展のリスク因子である, 第109回日本内科学会総会・講演会, 2012年4月.
319.	粟飯原賢一, 吉田守美子, 近藤絵里, 近藤剛史, 倉橋清衛, 遠藤逸朗, 松本俊夫 : 尿酸は形態および機能的頸動脈硬化症進展のリスク因子である, 第109回日本内科学会総会・講演会, 2012年4月. (キーワード) 危険因子頸動脈疾患(診断) 動脈硬化症(診断) *Uric Acid(血液) 頸動脈内膜中膜肥厚度ヒト
320.	立花綾香, 田岡志保, 荻野寛隆, 高橋真美子, 粟飯原賢一, 吉田守美子, 遠藤逸朗, 黒田暁生, 松久宗英, 福森智治, 松本俊夫 : 低血圧で推移したvon Hippel-Lindau 病・褐色細胞腫の1手術例, 第21回臨床内分泌代謝Update in Hamamatsu, 2012年1月.
321.	田岡志保, 立花綾香, 荻野寛隆, 高橋真美子, 粟飯原賢一, 吉田守美子, 近藤絵里, 倉橋清衛, 遠藤逸朗, 松本俊夫, 片岡菜奈子, 黒田暁生, 松久宗英 : 周術期血糖管理にリラグルチドが有用であった2型糖尿病患者の2例, 第21回臨床内分泌代謝Update in Hamamatsu, 2012年1月.
322.	黒田暁生, 新居沙央理, 吉田守美子, 近藤絵里, 遠藤逸朗, 粟飯原賢一, 松本友里, 片岡菜奈子, 松本俊夫, 松久宗英 : 新たなインスリンポンプParadigm722によってカーボカウントのみで血糖管理が可能となった1症例, 第11回日本先進糖尿病治療研究会, 2011年11月.
323.	新居沙央里, 黒田暁生, 吉田守美子, 近藤絵里, 遠藤逸朗, 粟飯原賢一, 松本友里, 片岡菜奈子, 松久宗英, 松本俊夫 : 新たなインスリンポンプParadigm722によりカーボカウントのみで血糖管理が可能となった1例, 日本糖尿病学会中国四国地方会第49回総会, 2011年11月.
324.	木内美瑞穂, 粟飯原賢一, 藤中雄一, 鈴木麗子, 吉田守美子, 近藤絵里, 遠藤逸朗, 黒田暁生, 松久宗英, 松本俊夫 : 内臓脂肪肥満とアルブミン尿の連関に関する検討, 日本糖尿病学会中国四国地方会第49回総会, 2011年11月.
325.	鈴木麗子, 大和光, 木田菊恵, 粟飯原賢一, 遠藤逸朗, 片岡菜奈子, 近藤絵里, 松本俊夫, 黒田暁生, 松久宗英 : フットケア外来におけるインスリン皮下硬結の実態調査, 日本糖尿病学会中国四国地方会第49回総会, 2011年11月.
326.	田岡志保, 粟飯原賢一, 吉田守美子, 近藤絵里, 遠藤逸朗, 松本俊夫 : 心血管リスク因子を有する成人の血管内皮機能制御因子に関する臨床的検討, 第34回日本高血圧学会総会, 2011年10月. (キーワード) HDL Cholesterol(血液) LDL Cholesterol(血液) 危険因子血管内皮心臓血管疾患(病因) ヒト中年(45~64) 高齢者(65~79) 男女
327.	粟飯原賢一, 吉田守美子, 松本俊夫 : 頸動脈エコー法による心血管リスク評価のための血管形態と機能解析, 第34回日本高血圧学会総会, 2011年10月.
328.	Ken-ichi Aihara, Sumiko Yoshida and Toshio Matsumoto : Evaluation for cardiovascular risk by multi-method carotid artery ultrasound examinations, 第34回日本高血圧学会総会パネルディスカッション: 非侵襲的血管指標の有用性と課題, Oct. 2011.
329.	吉田守美子, 粟飯原賢一, 上田由佳, 池田康将, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2011年10月.
330.	藤中雄一, 木内美瑞穂, 小杉知里, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 谷口寿章, 松本俊夫 : Wntシグナル抑制因子sFRP4の肥満・糖代謝との関連性についての検討, 第32回日本肥満学会, 2011年9月. (キーワード) シグナルトランスダクション癌原遺伝子蛋白質肥満糖代謝脂肪細胞分化 Wnt Proteins SFRP4 Protein ヒト
331.	粟飯原賢一, 藤中雄一, 鈴木麗子, 木内美瑞穂, 吉田守美子, 近藤絵里, 片岡菜奈子, 倉橋清衛, 遠藤逸朗, 黒田暁生, 松久宗英, 松本俊夫 : 慢性腎臓病と内臓脂肪蓄積病態の連関, 第32回日本肥満学会, 2011年9月.
332.	吉田守美子, 藤中雄一, 粟飯原賢一, 鈴木麗子, 木内美瑞穂, 近藤絵里, 片岡菜奈子, 倉橋清衛, 遠藤逸朗, 黒田暁生, 松久宗英, 松本俊夫 : メタボリックシンドローム検診受診者における耐糖能異常の検討, 第32回日本肥満学会, 2011年9月.
333.	吉田守美子, 粟飯原賢一, 池田康将, 松本俊夫 : 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, 2011年9月.
334.	粟飯原賢一, 吉田守美子, 近藤絵里, 倉橋清衛, 近藤剛史, 木内美瑞穂, 遠藤逸朗, 松本俊夫, 片岡菜奈子, 黒田暁生, 松久宗英 : 慢性腎臓病におけるエイコサペンタエン酸の意義に関する臨床的検討, 第11回日本内分泌学会四国支部学術集会, 2011年9月.
335.	粟飯原賢一, 吉田守美子, 上田由佳, 池田康将, 岩瀬俊, 久岡白陽花, 平田陽一郎, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2011年8月.
336.	吉田守美子, 粟飯原賢一, 伊勢孝之, 上田由佳, 池田康将, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2011年8月.
337.	赤池雅史, 土屋浩一郎, 柏田良樹, 高石喜久, 玉置俊晃, 岩瀬俊, 佐田政隆, 粟飯原賢一, 吉田守美子, 松本俊夫, 佐藤千穂, 西条伴香, 楊河宏章 : 生活習慣病関連リスクファクターに及ぼすスダチ果皮加工品の効果 ∼探索的臨床試験による検討∼, 第243回徳島医学会学術集会公開シンポジウム, 2011年7月.
338.	赤池雅史, 土屋浩一郎, 柏田良樹, 高石喜久, 玉置俊晃, 岩瀬俊, 佐田政隆, 粟飯原賢一, 吉田守実子, 松本俊夫, 佐藤千穂, 西条伴香, 楊河宏章 : 生活習慣病関連リスクファクターに及ぼすスダチ果皮加工品の効果-探索的臨床試験による検討-, 第243回徳島医学会学術集会, 2011年7月.
339.	粟飯原賢一 : アンドロゲン受容体を介した心血管ストレス防御機構, 第11回日本抗加齢医学会総会・分科会共催シンポジウム7「テストステロン医学の最前線」, 2011年5月.
340.	吉田守美子, 大政暁, 粟飯原賢一, 倉橋清衛, 近藤剛史, 片岡菜奈子, 遠藤逸朗, 藤中雄一, 松久宗英, 松本俊夫 : 強化インスリン療法からGLP-1アナログ製剤少量投与に変更し，良好な血糖コントロールが得られた1例, 第104回日本内科学会四国地方会, 2011年5月.
341.	粟飯原賢一 : テストステロン医学の最前線アンドロゲン受容体を介した心血管ストレス防御機構, 第11回日本抗加齢医学会総会, 110, 2011年5月. (キーワード) Androgen Receptors 心臓血管疾患(実験的) ストレス(実験的) 生物学的現象ノックアウトマウス *生体防御マウス動物
342.	津川愛, 粟飯原賢一, 吉田守美子, 遠藤逸朗, 藤中雄一, 松久宗英, 松本俊夫 : DPP-4阻害薬シタグリプチンの臨床効果の特徴に関する検討, 第84回日本内分泌学会学術総会, 2011年4月.
343.	原知也, 粟飯原賢一, 吉田守美子, 倉橋清衛, 近藤剛史, 木内美瑞穂, 片岡菜奈子, 遠藤逸朗, 藤中雄一, 松本俊夫 : 血清エイコサペンタエン酸/アラキドン酸比は心血管リスクを有する高齢者のCKDリスクマーカーである, 第84回日本内分泌学会学術総会, 2011年4月.
344.	粟飯原賢一, 吉田守美子, 池田康将, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2011年4月.
345.	藤中雄一, 倉橋清衛, 木内美瑞穂, 吉田守美子, 片岡菜奈子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : トリロスタン投与により内分泌学的な寛解状態が得られた異所性ACTH症候群一例, 第84回日本内分泌学会学術総会, 2011年4月.
346.	池田康将, 粟飯原賢一, 吉田守美子, 佐藤隆史, 赤池雅史, 玉置俊晃, 加藤茂明, 松本俊夫 : 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」, 2011年4月.
347.	安積麻衣, 粟飯原賢一, 吉田守美子, 倉橋清衛, 木内美瑞穂, 片岡菜奈子, 遠藤逸朗, 松本俊夫 : 2型糖尿病患者に対する強化インスリン療法は左室リモデリングを改善する, 第84回日本内分泌学会学術総会, 2011年4月.
348.	赤池雅史, 粟飯原賢一, 池田康将, 八木秀介, 石川カズ江, 吉田守美子, 上田由佳, 岩瀬俊, 佐田政隆, 松本俊夫 : 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, 2011年4月.
349.	吉田守美子, 粟飯原賢一, 上田由佳, 池田康将, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2011年4月.
350.	吉田守美子, 粟飯原賢一, 上田由佳, 池田康将, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2011年4月.
351.	黒部裕嗣, 粟飯原賢一, 平田陽一郎, 西矢昌子, 中山泰介, 元木達夫, 菅野幹雄, 神原保, 北市隆, 赤池雅史, 佐田政隆, 北川哲也, 松本俊夫 : エゼチミブ投与による脂質代謝および血管機能改善効果の検討, 第84回日本内分泌学会学術総会, 2011年4月.
352.	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.
353.	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.
354.	Takashi Iwase, Shoichiro Takao, Masashi Akaike, S. Bando, S. Hisaoka, Toshiyuki Niki, Kenya Kusunose, N Tomita, Y. Hirata, Yuka Ueda, Koji Yamaguchi, Yoshio Taketani, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Ken-ichi Aihara, M. Harada and Masataka Sata : Diagnostic Utility of Cardiac Magnetic Resonance for Prediction of Cardiac Events in Patients with Hypertrophic Cardiomyopathy., 第75回日本循環器学会総会・学術集会, Mar. 2011.
355.	池田康将, 田島壮一郎, 吉田守美子, 山野範子, 木平孝高, 石澤啓介, 粟飯原賢一, 冨田修平, 土屋浩一郎, 玉置俊晃 : 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, 2011年2月.
356.	近藤剛史, 遠藤逸朗, 粟飯原賢一, 藤中雄一, 松本俊夫 : hCG,FSH製剤の併用によりパートナーの妊娠が確認された低ゴナドトロピン性男性性腺機能低下症の一例, 第20回臨床内分泌Update, 2011年1月.
357.	門田宗之, 藤中雄一, 廣野友理, 倉橋清衛, 木内美瑞穂, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 松久宗英, 松本俊夫 : 低ナトリウム血症で発症したトルコ鞍部腫瘍の一例, 第20回臨床内分泌代謝Update, 2011年1月.
358.	吉田守美子, 粟飯原賢一, 上田由佳, 池田康将, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2010年12月.
359.	池田康将, 田島壮一郎, 吉田守美子, 山野範子, 木平孝高, 石澤啓介, 粟飯原賢一, 冨田修平, 土屋浩一郎, 玉置俊晃 : 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, 2010年12月.
360.	粟飯原賢一 : 心血管ストレスに対するアンドロゲン受容体系の役割, 第1回テストステロン研究会, 2010年11月.
361.	安積麻衣, 粟飯原賢一, 吉田守美子, 松本俊夫, 遠藤逸朗 : 糖尿病患者の心筋リモデリングおよび左室機能におけつ強化インスリン療法の効果, 第12回徳島臨床脈管研究会, 2010年11月.
362.	近藤剛史, 遠藤逸朗, 藤中雄一, 松本俊夫, 粟飯原賢一 : hCG, FSH製剤の併用によりパートナーの妊娠が確認された低ゴナドトロピン性男性性腺機能低下症の一例, 第16回徳島内分泌研究会, 2010年11月.
363.	遠藤逸朗, 粟飯原賢一, 藤中雄一, 松本俊夫 : hCG, FSH製剤の併用によりパートナーの妊娠が確認された低ゴナドトロピン性男性性腺機能低下症の一例, 第103回日本内科学会四国地方会, 2010年11月.
364.	黒部裕嗣, 粟飯原賢一, 西矢昌子, 佐藤光代, 西尾進, 中山泰介, 元木達夫, 菅野幹雄, 神原保, 北市隆, 松本俊夫, 北川哲也 : エゼチミブ投与による脂質代謝および血管機能改善効果の検討, 第51回日本脈管学会総会, Vol.50, No.Suppl., S153, 2010年10月. (キーワード) LDL Cholesterol(血液) 運動療法血管内皮血流速度脂質代謝食事療法ランダム化比較試験 Ezetimibe(治療的利用) *脈波伝播速度ヒト
365.	赤池雅史, 八木秀介, 粟飯原賢一, 石川カズ江, 池田康将, 吉田守美子, 上田由佳, 岩瀬俊, 松本俊夫, 佐田政隆 : 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, 2010年10月. (キーワード) 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
366.	安積麻衣, 粟飯原賢一, 吉田守美子, 倉橋清衛, 木内美瑞穂, 片岡菜奈子, 遠藤逸朗, 藤中雄一, 松本俊夫, 松久宗英 : 2型糖尿病患者の左室拡張障害に対する強化インスリン療法の効果, 第10回日本内分泌学会四国支部学術集会, 2010年9月.
367.	藤中雄一, 倉橋清衛, 吉田守美子, 木内美瑞穂, 片岡菜奈子, 遠藤逸朗, 粟飯原賢一, 松本俊夫, 斎藤美菜子, 福本大輔, 大島康志 : インスリングルリジンの少量投与が有効であった即時型インスリンアレルギーの一例, 第10回日本内分泌学会四国支部学術集会, 2010年9月.
368.	吉田守美子, 粟飯原賢一, 伊勢孝之, 上田由佳, 池田康将, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2010年7月.
369.	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.
370.	吉田守美子, 粟飯原賢一, 上田由佳, 池田康将, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2010年6月.
371.	吉田守美子, 倉橋清衛, 木内美瑞穂, 片岡菜奈子, 遠藤逸朗, 藤中雄一, 粟飯原賢一, 松本俊夫 : ピオグリタゾンが著効したWerner症候群の1例, 第102回日本内科学会四国地方会, 2010年5月.
372.	粟飯原賢一, 藤中雄一, 吉田守美子, 遠藤逸朗, 松本俊夫 : 血管内皮機能と頸動脈硬化症の連関に関する検討, 第102回日本内科学会四国地方会, 2010年5月.
373.	倉橋清衛, 木内美瑞穂, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 藤中雄一, 松本俊夫 : 抗副腎薬投与により内因性コルチゾールの低下とともにACTHの劇的な低下が得られた異所性ACTH症候群の一例, 第83回日本内分泌学会学術総会, Vol.86, No.1, 144, 2010年3月. (キーワード) ACTH Hydrocortisone Mitotane(治療的利用) 異所性ACTH産生症候群(薬物療法) *Trilostane(治療的利用) ヒト高齢者(65~79) 女
374.	粟飯原賢一, 吉田守美子, 倉橋清衛, 木内美瑞穂, 遠藤逸朗, 藤中雄一, 松本俊夫, 岩瀬俊, 赤池雅史, 佐田政隆 : ロスバスタチンによる心筋リモデリング抑制効果の検討, 第83回日本内分泌学会学術総会, 2010年3月.
375.	吉田守美子, 粟飯原賢一, 伊勢孝之, 上田由佳, 池田康将, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2010年3月.
376.	黒部裕嗣, 浦田将久, 福原弥生, 神原保, 粟飯原賢一, 赤池雅史, 高浜洋介, 玉置俊晃, 松本俊夫, 冨田修平, 北川哲也 : 血管リモデリング時の転写因子HIF-1αの役割 (第110回日本外科学会定期学術集会), 日本外科学会雑誌, Vol.111, No.2, 701, 2010年3月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1572543027394884480 (CiNii: 1572543027394884480)
377.	倉橋清衛, 粟飯原賢一, 吉田守美子, 遠藤逸朗, 松本俊夫 : 強化インスリン療法による2型糖尿病患者の左室リモデリングおよび拡張能改善効果に関する検討, 第240回徳島医学会学術集会, 2010年2月.
378.	阿部容子, 遠藤逸朗, 粟飯原賢一, 松本俊夫 : 重症低血糖昏睡および肺炎をきたした神経性食思不振症の救命症例, 第240回徳島医学会学術集会, 2010年2月.
379.	粟飯原賢一, 吉田守美子, 倉橋清衛, 木内美瑞穂, 遠藤逸朗, 藤中雄一, 松本俊夫 : 強化インスリン療法による血糖コントロールの改善により左室拡張能の改善がみられた3例, 第101回日本内科学会四国地方会, 2009年11月.
380.	吉田守美子, 倉橋清衛, 木内美瑞穂, 遠藤逸朗, 粟飯原賢一, 藤中雄一, 松本俊夫 : 家族内集積が疑われた緩徐進行1型糖尿病の一例, 第47回に本糖尿病学会中国四国地方会, 2009年11月.
381.	吉田守美子, 藤中雄一, 倉橋清衛, 木内美瑞穂, 遠藤逸朗, 粟飯原賢一, 松本俊夫 : SPIDDMが疑われる1型糖尿病の家族内集積例, 第47回日本糖尿病学会中国四国地方会, 2009年11月.
382.	藤中雄一, 粟飯原賢一, 鈴木麗子, 木内美瑞穂, 吉田守美子, 倉橋清衛, 遠藤逸朗, 松本俊夫 : メタボリックシンドローム検診における糖代謝異常の検討, 第47回日本糖尿病学会中国四国地方会, 2009年11月.
383.	吉田守美子, 粟飯原賢一, 伊勢孝之, 住友由佳, 松本俊夫, 八木秀介, 岩瀬俊, 赤池雅史, 山田博胤, 佐田政隆, 西尾進 : 副腎アンドロゲンDHEASの抗動脈硬化作用における性差の検討, 第32回日本高血圧学会学術集会, 2009年10月.
384.	粟飯原賢一, 藤中雄一, 木内美瑞穂, 吉田守美子, 鈴木麗子, 倉橋清衛, 遠藤逸朗, 八木秀介, 岩瀬俊, 平田陽一郎, 赤池雅史, 佐田政隆, 松本俊夫 : 内臓脂肪蓄積制御に関わる因子の臨床的検討, 第32回日本高血圧学会総会, 196, 2009年10月. (キーワード) LDL Cholesterol 危険因子 *腹腔内脂肪(X線診断) ヒト中年(45~64) 高齢者(65~79) 男女
385.	吉田守美子, 粟飯原賢一, 伊勢孝之, 上田由佳, 八木秀介, 岩瀬俊, 山田博胤, 赤池雅史, 佐田政隆, 松本俊夫 : 副腎アンドロゲンDHEASの抗動脈硬化作用における性差の検討, 第32回日本高血圧学会総会, 2009年10月.
386.	赤池雅史, 粟飯原賢一, 池田康将, 石川カズ江, 吉田守美子, 上田由佳, 八木秀介, 岩瀬俊, 松本俊夫, 佐田政隆 : 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, 2009年10月. (キーワード) Glucocorticoids 血管内皮細胞系 Mineralocorticoid Receptors 内皮細胞ヒト
387.	倉橋清衛, 遠藤逸朗, 粟飯原賢一, 藤中雄一, 松本俊夫, 渡部真也, 大森哲郎 : 脳波の徐波化を伴う重症低血糖昏睡を来たした神経性食思不振症の一例, 第9回日本内分泌学会四国支部学術集会, 2009年9月.
388.	西尾進, 楠瀬賢也, 山田博胤, 冨田紀子, 遠藤桂輔, 千葉ちひろ, 平岡葉月, 佐藤光代, 鈴木麗子, 粟飯原賢一, 藤中雄一, 佐田政隆 : 糖尿病の動脈硬化指標:%FMDを用いた検討, 第57回日本心臓病学会学術集会, 2009年9月.
389.	藤中雄一, 粟飯原賢一, 鈴木麗子, 木内美瑞穂, 吉田守美子, 倉橋清衛, 遠藤逸朗, 松本俊夫 : 当院メタボリックシンドローム検診における糖代謝異常の検討．, 第239回徳島医学会学術総会, 2009年8月.
390.	粟飯原賢一, 藤中雄一, 木内美瑞穂, 吉田守美子, 倉橋清衛, 遠藤逸朗, 上田由佳, 平田陽一郎, 八木秀介, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : Influence of lipid profile on endothelial function in subjects with cardiovascular risk factors, 第41回日本動脈硬化学会総会・学術集会, 2009年7月.
391.	吉田守美子, 粟飯原賢一, 上田由佳, 倉橋清衛, 木内美瑞穂, 遠藤逸朗, 藤中雄一, 八木秀介, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : Regular use of rosuvastatin attenuates carotid atherosclerosis regardless of LDL cholesterol lowering effect, 第41回日本動脈硬化学会総会・学術集会, 2009年7月.
392.	遠藤逸朗, 大西幸代, 木戸里佳, 倉橋清衛, 吉田守美子, 藤中雄一, 粟飯原賢一, 安倍正博, 福本誠二, 松本俊夫 : 新規calcilytics，JTT305は常染色体優性低Ca血症におけるCa感知受容体活性型変異シグナルを抑制する, 第27回日本骨代謝学会学術集会, 195, 2009年7月. (キーワード) シグナルトランスダクション染色体異常低カルシウム血症(薬物療法) 変異 *Calcium-Sensing Receptors(拮抗物質・阻害物質)
393.	倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 藤中雄一, 八木秀介, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 一酸化炭素中毒にて急性心筋梗塞を発症した2型糖尿病の1例, 第100回日本内科学会四国地方会, 2009年5月.
394.	遠藤逸朗, 藤村光則, 吉田守美子, 栗若里佳, 木戸慎介, 岩瀬俊, 井上大輔, 粟飯原賢一, 藤中雄一, 赤池雅史, 松本俊夫 : 冠動脈不安定プラーク予測因子としてのICTP, 第82回日本内分泌学会学術総会, Vol.85, No.1, 283, 2009年4月. (キーワード) 生物学的マーカー Peptide Fragments(血液) 冠状動脈硬化症(診断) 動脈硬化症-アテローム性(診断) Collagen Type I(血液) *ICTP (Collagen Type I C-Terminal Telopeptides)(血液) ヒト男女
395.	赤池雅史, 粟飯原賢一, 池田康将, 石川カズ江, 住友由佳, 吉田守美子, 八木秀介, 岩瀬俊, 松本俊夫, 佐田政隆 : 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, 2009年4月. (キーワード) 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
396.	吉田守美子, 粟飯原賢一, 西尾進, 倉橋清衛, 遠藤逸朗, 藤中雄一, 伊勢孝之, 住友由佳, 八木秀介, 岩瀬俊, 山田博胤, 赤池雅史, 佐田政隆, 松本俊夫 : 副腎アンドロゲンDHEASは血管内皮機能非依存的に頸動脈硬化を抑制する, 第82回日本内分泌学会学術総会, Vol.85, No.1, 366, 2009年4月. (キーワード) 頸動脈疾患血管内皮動脈硬化症 Dehydroepiandrosterone Sulfate(薬理学) ヒト男女
397.	粟飯原賢一, 藤中雄一, 吉田守美子, 鈴木麗子, 倉橋清衛, 遠藤逸朗, 松本俊夫 : 尿中アルブミンは内臓脂肪蓄積の強力な増悪因子である, 第82回日本内分泌学会学術総会, Vol.85, No.1, 337, 2009年4月. (キーワード) Albumins(尿) 危険因子腹腔内脂肪ヒト中年(45~64) 高齢者(65~79) 男女
398.	粟飯原賢一, 藤中雄一, 吉田守美子, 鈴木麗子, 倉橋清衛, 遠藤逸朗, 松本俊夫 : 内臓脂肪増大因子に関する臨床的検討, 第106回日本内科学会総会・講演会, Vol.98, No.Suppl., 233, 2009年4月. (キーワード) 危険因子心臓血管疾患(病因) メタボリックシンドローム(合併症) *腹腔内脂肪ヒト男女
399.	吉田守美子, 粟飯原賢一, 倉橋清衛, 遠藤逸朗, 藤中雄一, 住友由佳, 松本俊夫, 八木秀介, 岩瀬俊, 赤池雅史 : DHEASは血管内皮機能に依存せず動脈硬化を抑制する(頸動脈エコーを用いた臨床的検討), 第106回日本内科学会総会・講演会, Vol.98, No.Suppl., 139, 2009年4月. (キーワード) 頸動脈(超音波診断) 超音波診断動脈硬化症(超音波診断) Dehydroepiandrosterone Sulfate(薬理学,血液) ヒト男女
400.	粟飯原賢一, 吉田守美子, 倉橋清衛, 木内美瑞穂, 遠藤逸朗, 藤中雄一, 松本俊夫, 岩瀬俊, 赤池雅史, 佐田政隆 : ロスバスタチンによる心筋リモデリング抑制効果の検討, 第83回日本内分泌学会学術総会国立京都国際会館, 2009年3月.
401.	粟飯原賢一, 吉田守美子, 伊勢孝之, 住友由佳, 八木秀介, 岩瀬俊, 倉橋清衛, 遠藤逸朗, 藤中雄一, 赤池雅史, 佐田政隆, 松本俊夫 : Increased serum triglyceride but not LDL cholesterol is associated with left ventricular diastolic dysfunction., 第73回日本循環器学会総会・学術集会, 2009年3月.
402.	吉田守美子, 粟飯原賢一, 伊勢孝之, 住友由佳, 八木秀介, 岩瀬俊, 倉橋清衛, 遠藤逸朗, 藤中雄一, 赤池雅史, 佐田政隆, 松本俊夫 : Dehydroepiandrosterone sulfate is an antivascular remodeling factor, 第73回日本循環器学会総会・学術集会, 2009年3月.
403.	住友由佳, 粟飯原賢一, 伊勢孝之, 吉田守美子, 八木秀介, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : Heparin Cofactor II-deficient Mice Exert Exacerbation of Angiotensin II-induced Cardiac Remodeling through Enhancement of NADPH oxidase - TGF- 1 Pathway, 第73回日本循環器学会総会・学術集会, 2009年3月.
404.	赤池雅史, 粟飯原賢一, 池田康将, 石川カズ江, 吉田守美子, 住友由佳, 八木秀介, 岩瀬俊, 松本俊夫, 佐田政隆 : 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, 2009年3月.
405.	倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 藤中雄一, 松本俊夫 : 甲状腺機能低下症の経過中にGraves眼症を来した一例, 第19回臨床内分泌代謝Up date, 2009年3月.
406.	吉田守美子, 藤中雄一, 倉橋清衛, 遠藤逸朗, 粟飯原賢一, 松本俊夫, 松本真一, 大島康志 : 重症筋無力症を合併したグレーブス眼症の一例, 第19回臨床内分泌代謝Up date, 2009年3月.
407.	倉橋清衛, 遠藤逸朗, 吉田守美子, 粟飯原賢一, 藤中雄一, 松本俊夫 : PEG-IFN-α2bおよびリバビリン治療後に劇症1型糖尿病をふくむ多彩な自己免疫疾患を発症した2例, 第99回日本内科学会四国地方会, 2008年11月.
408.	遠藤逸朗, 藤村光則, 吉田守美子, 栗若里佳, 木戸慎介, 岩瀬俊, 井上大輔, 粟飯原賢一, 藤中雄一, 赤池雅史, 松本俊夫 : 冠動脈不安定プラーク予測因子としてのICTP, 第26回日本骨代謝学会学術集会, 194, 2008年10月. (キーワード) Peptide Fragments(血液) 冠状動脈硬化症 Collagen Type I(血液) ICTP (Collagen Type I C-Terminal Telopeptides)(血液) ヒト男女
409.	粟飯原賢一, 吉田守美子, 伊勢孝之, 住友由佳, 倉橋清衛, 遠藤逸朗, 藤中雄一, 松本俊夫, 八木秀介, 岩瀬俊, 赤池雅史, 佐田政隆 : 左室拡張能に対する脂質代謝異常の意義, 第31回日本高血圧学会総会, 2008年10月.
410.	吉田守美子, 粟飯原賢一, 伊勢孝之, 住友由佳, 松本俊夫, 八木秀介, 岩瀬俊, 赤池雅史, 佐田政隆 : 副腎アンドロゲンDHEASは頚動脈血流の制御因子である, 第31回日本高血圧学会学術集会, 2008年10月.
411.	住友由佳, 粟飯原賢一, 伊勢孝之, 吉田守美子, 松本俊夫, 八木秀介, 岩瀬俊, 添木武, 赤池雅史, 佐田政隆 : ヘパリンコファクターⅡは抗酸化ストレス作用を介してアンジオテンシンIIによる心房および心室のリモデリングを抑制する, 第31回日本高血圧学会総会, 2008年10月.
412.	赤池雅史, 八木秀介, 粟飯原賢一, 石川カズ江, 池田康将, 吉田守美子, 住友由佳, 岩瀬俊, 阿部純一, 松本俊夫, 佐田政隆 : 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, 2008年10月.
413.	吉田守美子, 粟飯原賢一, 伊勢孝之, 住友由佳, 松本俊夫, 八木秀介, 岩瀬俊, 赤池雅史, 佐田政隆 : 副腎アンドロゲンDHEASの血管への作用(頚動脈エコーを用いた臨床的検討), 第13回武田高血圧シンポジウム, 2008年10月.
414.	遠藤逸朗, 倉橋清衛, 吉田守美子, 粟飯原賢一, 藤中雄一, 松本俊夫 : IFN-α2bおよびリバビリン治療後に劇症1型糖尿病，下垂体機能低下症，尋常性乾癬を発症した1例, 第8回内分泌学会四国支部学術集会, 2008年9月.
415.	倉橋清衛, 遠藤逸朗, 吉田守美子, 粟飯原賢一, 藤中雄一, 松本俊夫 : 甲状腺乳頭癌を合併した原発性副甲状腺機能亢進症の一例, 第8回内分泌学会四国支部学術集会, 2008年9月.
416.	粟飯原賢一, 吉田守美子, 伊勢孝之, 住友由佳, 八木秀介, 岩瀬俊, 遠藤逸朗, 藤中雄一, 赤池雅史, 松本俊夫 : 脂質代謝異常による左室拡張障害の臨床的検討, 第40回日本動脈硬化学会総会, 249, 2008年7月. (キーワード) 脂質異常症(合併症) / 左心室機能障害(病因) / ヒト (Homo sapiens) / 男性 (male) / 女性 (female)
417.	吉田守美子, 粟飯原賢一, 伊勢孝之, 住友由佳, 八木秀介, 岩瀬俊, 遠藤逸朗, 藤中雄一, 赤池雅史, 松本俊夫 : 副腎アンドロゲンの頸動脈硬化抑制作用に関する検討, 第40回日本動脈硬化学会総会, 253, 2008年7月. (キーワード) Androgens(治療的利用) / 頸動脈疾患(予防) / 頸動脈疾患(予防) / 動脈硬化症(予防) / 副腎 / ヒト (Homo sapiens) / 男性 (male) / 女性 (female)
418.	八木秀介, 粟飯原賢一, 伊勢孝之, 吉田守美子, 住友由佳, 池田康将, 岩瀬俊, 添木武, 赤池雅史, 松本俊夫 : 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, 2008年7月. (キーワード) 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
419.	吉田守美子, 遠藤逸朗, 倉橋清衛, 木内美瑞穂, 粟飯原賢一, 藤中雄一, 松本俊夫 : カルバマゼピンでビタミンD欠乏と下垂体機能検査異常を呈した1例, 第98回日本内科学会四国地方会, 2008年6月.
420.	粟飯原賢一, 吉田守美子, 倉橋清衛, 木内美瑞穂, 遠藤逸朗, 藤中雄一, 松本俊夫 : インスリン強化療法導入による血糖コントロールの改善により左室機能障害の回復をみた糖尿病性心筋症の2例, 第98回日本内科学会四国地方会, 2008年6月.
421.	吉田守美子, 粟飯原賢一, 木内美瑞穂, 遠藤逸朗, 藤中雄一, 伊勢孝之, 住友由佳, 八木秀介, 岩瀬俊, 赤池雅史, 松本俊夫 : 頸動脈血行動態における副腎アンドロゲンの臨床的意義, 第81回日本内分泌学会学術総会, Vol.84, No.1, 202, 2008年5月. (キーワード) Androgens(血液) 頸動脈 *副腎血行力学ヒト成人(19~44) 男女
422.	粟飯原賢一, 吉田守美子, 伊勢孝之, 住友由佳, 八木秀介, 岩瀬俊, 木内美瑞穂, 遠藤逸朗, 藤中雄一, 赤池雅史, 松本俊夫 : 左室拡張能における脂質代謝異常の影響に関する検討, 第81回日本内分泌学会学術総会, Vol.84, No.1, 222, 2008年5月. (キーワード) 脂質異常症左心室機能ヒト成人(19~44) 男女
423.	近藤剛史, 小島直, 伊勢孝之, 木内美瑞穂, 吉田守美子, 栗若里佳, 遠藤逸朗, 粟飯原賢一, 藤中雄一, 松本俊夫 : 進行性の頭蓋骨陥凹と骨粗鬆症を来たした一例, 第81回日本内分泌学会学術総会, Vol.83, No.4, 834, 2008年5月. (キーワード) 骨粗鬆症(合併症) 骨発育異常(合併症) 鑑別診断頭蓋骨ヒト成人(19~44) 女
424.	三原正朋, 粟飯原賢一, 藤中雄一, 小杉知里, 木内美瑞穂, 赤池雅史, 松本俊夫 : トロンビンによるインスリン抵抗性制御機構の解析, 第52回日本糖尿病学会年次学術集会, Vol.51, No.Suppl.1, S-126, 2008年5月. (キーワード) Thrombin(治療的利用) インスリン抵抗性(薬物療法) 3T3-L1細胞マウス動物
425.	粟飯原賢一, 伊勢孝之, 吉田守美子, 住友由佳, 八木秀介, 岩瀬俊, 赤池雅史, 松本俊夫 : 1α 25 dihydroxyvitamin D3 is a protective factor against vascular remodeling and glucose tolerance in elderly individuals, 第72回日本循環器学会学術集会, 2008年3月.
426.	住友由佳, 粟飯原賢一, 伊勢孝之, 吉田守美子, 八木秀介, 岩瀬俊, 石川カズ江, 赤池雅史, 松本俊夫 : Angiotensin II-induced cardiac remodeling is exacerbated with increased oxidative stress in heparin cofactor II-deficient mice., 第72回日本循環器学会総会・学術集会, 2008年3月.
427.	赤池雅史, 八木秀介, 粟飯原賢一, 池田康将, 石川カズ江, 伊勢孝之, 吉田守美子, 住友由佳, 岩瀬俊, Abe Jun-ichi, 松本俊夫 : 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, 2008年3月.
428.	遠藤逸朗, 近藤剛史, 木内美瑞穂, 吉田守美子, 粟飯原賢一, 藤中雄一, 樫原茂, 松本俊夫 : IFN-α2bおよびリバビリン治療後に甲状腺機能異常と劇症1型類似の糖尿病を発症した1例, 第97回日本内科学会四国地方会, 2007年12月.
429.	近藤剛史, 粟飯原賢一, 伊勢孝之, 木内美瑞穂, 吉田守美子, 遠藤逸朗, 藤中雄一, 松本俊夫 : 心腎障害の改善にACE阻害薬とARBの併用が有効であった高レニン性高血圧症の1例, 第97回日本内科学会四国地方会, 2007年12月.
430.	重清俊雄, 宮城順子, 川内千徳, 白神敦久, 柴田泰伸, 塚井一夫, 粟飯原賢一 : 高分子キニノゲン単独欠乏症の日本人家系で認められたフレームシフト変異, 第30回日本血栓止血学会学術集会, Vol.18, No.5, 535, 2007年11月. (キーワード) フレームシフト変異 High-Molecular-Weight Kininogen *血液凝固蛋白質障害(遺伝学) ヒト中年(45~64) 女
431.	住友由佳, 粟飯原賢一, 伊勢孝之, 八木秀介, 岩瀬俊, 赤池雅史, 松本俊夫 : レニン・アンジオテンシン活性下におけるヘパリンコファクターIIの心筋リモデリングへの影響, 第30回日本高血圧学会総会, 170, 2007年10月. (キーワード) Angiotensins Heparin Cofactor II Renin 心室リモデリングマウス動物
432.	八木秀介, 粟飯原賢一, 池田康将, 伊勢孝之, 住友由佳, 岩瀬俊, 赤池雅史, 松本俊夫 : 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, 2007年10月. (キーワード) 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
433.	赤池雅史, 粟飯原賢一, 八木秀介, 池田康将, 石川カズ江, 住友由佳, 岩瀬俊, 松本俊夫 : 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, 2007年10月. (キーワード) 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
434.	粟飯原賢一, 池田康将, 八木秀介, 伊勢孝之, 住友由佳, 岩瀬俊, 赤池雅史, 松本俊夫 : 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, 2007年10月. (キーワード) 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
435.	粟飯原賢一, 吉田守美子, 近藤剛史, 栗若里佳, 木内美瑞穂, 遠藤逸朗, 藤中雄一, 八木秀介, 住友由佳, 赤池雅史, 松本俊夫 : 活性型ビタミンDは血漿アンチトロンビン活性の制御に関与する, 日本内分泌学会第7回四国支部学術集会, Vol.83, No.4, 834, 2007年9月. (キーワード) Antithrombins(血液) Calcitriol(治療的利用,薬理学) ヒト中年(45~64) 高齢者(65~79) 男女
436.	近藤剛史, 小島直, 伊勢孝之, 木内美瑞穂, 吉田守美子, 栗若里佳, 遠藤逸朗, 粟飯原賢一, 藤中雄一, 松本俊夫 : 進行性の頭蓋骨陥凹と骨粗鬆症を来たした一例, 日本内分泌学会第7回四国支部学術集会, Vol.83, No.4, 834, 2007年9月. (キーワード) 骨粗鬆症(合併症) 骨発育異常(合併症) 鑑別診断頭蓋骨ヒト成人(19~44) 女
437.	Ken-ichi Aihara : Heparin cofactor II is required for fetal development and protects against vascular remodeling, The 8th US-Japan-Asia Dialogue on Cardiovascular Diseases: Grand Rounds with the Cardiovascular Division of Brigham and Womens Hospital, Aug. 2007.
438.	粟飯原賢一, 池田康将, 八木秀介, 住友由佳, 岩瀬俊, 赤池雅史, 松本俊夫 : 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, 2007年7月. (キーワード) 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
439.	遠藤逸朗, 近藤剛史, 木内美瑞穂, 吉田守美子, 粟飯原賢一, 藤中雄一, 松本俊夫 : Carbamazepineで著明な骨量減少と下垂体検査異常を呈した一例, 第80回日本内分泌学会学術総会, Vol.83, No.3, 784, 2007年6月. (キーワード) Carbamazepine(毒性・副作用) 甲状腺機能低下症(化学的誘発,診断) *骨密度ヒト高齢者(65~79) 男
440.	遠藤逸朗, 近藤剛史, 重清友理, 木内美瑞穂, 粟飯原賢一, 藤中雄一, 井上大輔, 工藤英治, 福本誠二, 松本俊夫 : 低リン血症性骨軟化症を来した腫瘍合併の成人2症例, 第80回日本内分泌学会学術総会, Vol.83, No.1, 156, 2007年6月. (キーワード) 線維芽細胞増殖因子巨細胞腫(合併症,画像診断) 骨軟化症(合併症) MRI 低リン血症(合併症) 腫瘍性低リン血症性骨軟化症(合併症) 線維芽細胞増殖因子-23 ヒト中年(45~64) 高齢者(65~79) 男女
441.	粟飯原賢一, 池田康将, 八木秀介, 住友由佳, 岩瀬俊, 近藤剛史, 重清友理, 木内美瑞穂, 遠藤逸朗, 藤中雄一, 赤池雅史, 松本俊夫 : 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, 2007年6月. (キーワード) 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
442.	近藤剛史, 遠藤逸朗, 木内美瑞穂, 粟飯原賢一, 藤中雄一, 松本俊夫, 福本誠二, 遠藤健次, 上原久典, 髙尾正一郎 : 腫瘍性骨軟化症の1例, 第96回日本内科学会四国地方会, 2007年5月.
443.	岩瀬俊, 住友由佳, 八木秀介, 池田康将, 粟飯原賢一, 尾崎修治, 赤池雅史, 安倍正博, 松本俊夫, 北川哲也 : 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, 2007年4月. (キーワード) 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
444.	粟飯原賢一, 赤池雅史, 池田康将, 八木秀介, 住友由佳, 岩瀬俊, 東博之, 松本俊夫 : 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, 2007年4月. (キーワード) 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
445.	遠藤逸朗, 近藤剛史, 木内美瑞穂, 吉田守美子, 粟飯原賢一, 藤中雄一, 松本俊夫 : carbamazepineで著明な骨量減少と下垂体検査異常を呈した一例, 第17回臨床内分泌代謝Update, 2007年3月.
446.	八木秀介, 粟飯原賢一, 池田康将, 住友由佳, 岩瀬俊, 赤池雅史, 松本俊夫 : 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, 2007年2月. (キーワード) 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
447.	池田康将, 粟飯原賢一, 赤池雅史, 住友由佳, 八木秀介, 岩瀬俊, 東博之, 加藤茂明, 松本俊夫 : 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, 2007年2月. (キーワード) 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
448.	赤池雅史, 粟飯原賢一, 池田康将, 石川カズ江, 八木秀介, 住友由佳, 岩瀬俊, 松本俊夫 : 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, 2007年2月. (キーワード) 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
449.	粟飯原賢一, 池田康将, 八木秀介, 住友由佳, 岩瀬俊, 東博之, 加藤茂明, 赤池雅史, 松本俊夫 : 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, 2007年2月. (キーワード) 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
450.	多田真理枝, 住友由佳, 岩瀬俊, 粟飯原賢一, 赤池雅史, 東博之, 松本俊夫, 山田博胤 : 心不全症状を繰り返した心尖部肥大型心筋症の一例, 第89回日本循環器学会四国地方会, 2006年12月.
451.	Hirotsugu Kurobe, Yuki Izawa, Yayoi Fukumura, Tamotsu Kanbara, Atsushi Kurushima, Ken-ichi Aihara, Masashi Akaike, Masashi Kano, Takashi Kitaichi, Yutaka Masuda, Hiroyuki Azuma, Toshiaki Tamaki, Toshio Matsumoto, Tetsuya Kitagawa, Shuhei Tomita and Masanori Yoshizumi : HIF-ARNT transcriptional system in T cells has a pivotal role in vascular in flammation and remodeling., 第70回日本循環器学会学術総会, Mar. 2006.
452.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Hirotsugu Kurobe, Mitsunori Fujimura, Syusuke Yagi, Syunji Hashizume, Yasumasa Ikeda, Takashi Iwase, Nobuyuki Takamori, Tetsuya Kitagawa and Toshio Matsumoto : Plasma Heparin Cofactor II Activity is Inversely Associated with Prevalence of Peripheral Arterial Disease in Elderly individuals., 第70回日本循環器学会学術総会, Mar. 2006.
453.	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.
454.	黒部裕嗣, 冨田修平, 井澤有紀, 福原弥生, 神原保, 粟飯原賢一, 赤池雅史, 北川哲也, 松本俊夫, 吉栖正典, 玉置俊晃 : T細胞特異的HIF1αKOマイスではカフモデルにて血管リモデリングが促進される, 第15回日本循環薬理学会, 2005年11月.
455.	粟飯原賢一, 東博之, 赤池雅史, 黒部裕嗣, 藤村光則, 八木秀介, 橋詰俊二, 池田康将, 岩瀬俊, 北川哲也, 松本俊夫 : 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, 2005年11月.
456.	粟飯原賢一 : ビタミンD受容体を介した生体内血液凝固制御機構の解析, 平成17年度日本血栓止血学会学術奨励賞受賞講演, Vol.16, No.5, 473, 2005年10月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1573950400484637568 (CiNii: 1573950400484637568)
457.	粟飯原賢一, 東博之, 赤池雅史, 黒部裕嗣, 佐田政隆, 池田康将, 藤村光則, 橋詰俊二, 岩瀬俊, 八木秀介, 大水章正, 塚田稔, 北川哲也, 加藤茂明, 松本俊夫 : 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, 2005年10月.
458.	八木秀介, 粟飯原賢一, 赤池雅史, 藤村光則, 池田康将, 橋詰俊二, 東博之, 松本俊夫 : 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, 2005年7月. (キーワード) 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
459.	粟飯原賢一, 東博之, 赤池雅史, 池田康将, 藤村光則, 橋詰俊二, 大水正章, 塚田稔, 加藤茂明, 松本俊夫 : 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, 2005年7月. (キーワード) *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
460.	粟飯原賢一, 三原正朋, 池田康将, 八木秀介, 藤村光則, 橋詰俊二, 松下隆哉, 赤池雅史, 東博之, 松本俊夫 : 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, 2005年7月. (キーワード) 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
461.	池田康将, 粟飯原賢一, 赤池雅史, 八木秀介, 岩瀬俊, 橋詰俊二, 藤村光則, 東博之, 加藤茂明, 松本俊夫 : 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, 2005年7月. (キーワード) 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
462.	八木秀介, 粟飯原賢一, 赤池雅史, 池田康将, 岩瀬俊, 橋詰俊二, 藤村光則, 東博之, 松本俊夫 : 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, 2005年7月. (キーワード) 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
463.	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.
464.	粟飯原賢一, 東博之, 赤池雅史, 黒部裕嗣, 藤村光則, 八木秀介, 橋詰俊二, 池田康将, 北川哲也, 松本俊夫 : 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, 2005年4月. (キーワード) 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)
465.	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.
466.	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.
467.	池田康将, 粟飯原賢一, 赤池雅史, 藤村光則, 八木秀介, 橋詰俊二, 東博之, 加藤茂明, 松本俊夫 : 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年. (キーワード) Androgens Angiotensin II Androgen Receptors 心筋心室リモデリングマウス動物オス
468.	粟飯原賢一, 東博之, 赤池雅史, 池田康将, 藤村光則, 橋詰俊二, 八木秀介, 加藤茂明, 松本俊夫 : 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, 2004年11月.
469.	粟飯原賢一, 東博之, 赤池雅史, 藤村光則, 吉田智則, 橋詰俊二, 加藤みどり, 池田康将, 周藤俊樹, 加藤茂明, 松本俊夫 : 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, 2004年6月. (キーワード) 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
470.	池田康将, 粟飯原賢一, 赤池雅史, 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, 東博之, 加藤茂明, 松本俊夫 : 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, 2004年6月. (キーワード) 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
471.	山口普史, 七條加奈, 松下隆哉, 池田康将, 森岡将臣, 加藤みどり, 橋詰俊二, 藤村光則, 吉田智則, 粟飯原賢一, 井上大輔, 赤池雅史, 東博之, 松本俊夫 : 拡張型心筋症様病態を呈したCushing病の一例, 第83回日本循環器学会中国・四国合同地方会, Vol.68, No.0, 828, 2004年4月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1573387451866119936 (CiNii: 1573387451866119936)
472.	池田康将, 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, 粟飯原賢一, 赤池雅史, 東博之, 松本俊夫, 木村建彦, 西内健 : Torsade de pointesを合併した汎下垂体機能低下症の一例, 第83回日本循環器学会中国・四国合同地方会, Vol.68, No.0, 828, 2004年4月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1571135652052441728 (CiNii: 1571135652052441728)
473.	橋詰俊二, 池田康将, 加藤みどり, 山口普史, 吉田智則, 藤村光則, 粟飯原賢一, 赤池雅史, 東博之, 松本俊夫 : 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年. (キーワード) 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
474.	粟飯原賢一, 高森信行, 金川泰彦, 藤村光則, 加藤みどり, 橋詰俊二, 池田康将, 田村克也, 近藤彰, 赤池雅史, 東博之, 松本俊夫 : 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年. (キーワード) 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
475.	山口普史, 池田康将, 橋詰俊二, 加藤みどり, 吉田智則, 藤村光則, 粟飯原賢一, 赤池雅史, 東博之, 松本俊夫 : 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, 2003年11月. (キーワード) 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
476.	粟飯原賢一, 東博之, 赤池雅史, 高森信行, 金川泰彦, 藤村光則, 吉田智則, 橋詰俊二, 加藤みどり, 山口普史, 池田康将, 加藤修司, 荒瀬友子, 近藤彰, 松本俊夫 : 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, 2003年11月. (キーワード) 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
477.	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.
478.	Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma, Toshio Matsumoto, Michiko Yamashita, Yoshimura Kimihiro and Imagawa Jun-ichi : Elevated blood pressure with a cardiovascular remodeling in mice lacking vitamin D receptor, 第66回日本循環器学会総会・学術集会, Apr. 2002.
479.	前田朝美, 杉浦ちとせ, 田中英世, 粟飯原賢一, 江夏偉育, 児島俊也, 合地研吾 : 高力価第VIII因子インヒビターを認め,プロトロンビン複合体製剤とプレドニゾロン投与で緩解を得た高齢非血友病の一例, 第496回日本内科学会関東地方会, 20, 2001年12月. (キーワード) Prednisolone(治療的利用) Prothrombin(治療的利用) 血液凝固異常(薬物療法) 血液凝固第VIII因子高齢者ヒト高齢者(65~) 女
480.	高森信行, 橋詰俊二, 加藤みどり, 吉田智則, 粟飯原賢一, 松山まどか, 石川カズ江, 藤村光則, 金川泰彦, 赤池雅史 : ヘパリンコファクターIIと動脈硬化発症との関連性甲状腺機能異常症患者での解析, 第22回日本血栓止血学会学術集会, Vol.11, No.5, 485, 2000年11月. (キーワード) Heparin Cofactor II 動脈硬化症甲状腺機能正常患者症候群ヒト
481.	赤池雅史, 東博之, 香川礼香, 井内貴彦, 藤村光則, 橋詰俊二, 高森信行, 吉田智則, 粟飯原賢一, 金川泰彦, 松本俊夫, 松本和也, 林郁郎, 田村克也, 西内健 : 血中リポ蛋白(a)濃度に及ぼすアスピリンの影響 : アポリポ蛋白(a)アイソフォーム解析を用いた検討, 第64回日本循環器学会学術集会, Vol.64, No.0, 427, 2000年3月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1570291227165355136 (CiNii: 1570291227165355136)
482.	高森信行, 橋詰俊二, 金川泰彦, 粟飯原賢一, 吉田智則, 井内貴彦, 赤池雅史, 東博之, 松本俊夫 : ヘパリンコファクターIIと動脈硬化発症の関連性, 第21回日本血栓止血学会学術集会, Vol.10, No.5, 393, 1999年11月. (キーワード) Heparin Heparin Cofactor II(生理学) 動脈硬化症 Cofactor ヒト中年(45~64) 高齢者(65~) 男女
483.	金川泰彦, 粟飯原賢一, 高森信行, 吉田智則, 井内貴彦, 赤池雅史, 重清俊雄, 東博之, 松本俊夫 : Pro443からLeuへの変異を有する先天性ヘパリンコファクター(HC)II欠乏症の分子機構の解明, 第21回日本血栓止血学会学術集会, Vol.10, No.5, 355, 1999年11月. (キーワード) Heparin(欠損・欠乏) 血液蛋白質障害(発生学・遺伝学) 変異 Cofactor ヒト
484.	赤池雅史, 井内貴彦, 高森信行, 粟飯原賢一, 吉田智則, 金川泰彦, 遠藤逸朗, 三ツ井貴夫, 東博之, 重清俊雄, 松本俊夫 : 先天性ヘパリンコファクターII(HC II)欠乏症でみられた多発性動脈病変 : 動脈硬化症の進展におけるHCIIの臨床的意義の検討, 第63回日本循環器学会学術集会, Vol.63, No.1, 645, 1999年3月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1574231876839482624 (CiNii: 1574231876839482624)
485.	赤池雅史, 東博之, 高森信行, 松本和也, 林郁郎, 田村克也, 西内健, 粟飯原賢一, 金川泰彦, 井内貴彦 : 高リポ蛋白(a)血症に及ぼすアスピリンの影響アポリポ蛋白(a)アイソフォームとの関連, 動脈硬化, Vol.26, No.8, 137, 1999年. (キーワード) Aspirin 高リポ蛋白質血症(生化学) Lipoprotein(a) 蛋白質アイソフォームヒト
486.	赤池雅史, 井内貴彦, 高森信行, 粟飯原賢一, 吉田智則, 金川泰彦, 遠藤逸朗, 三ツ井貴夫, 東博之, 重清俊雄 : 先天性ヘパリンコファクターII(HC II)欠乏症でみられた多発性動脈病変動脈硬化症の進展におけるHCIIの臨床的意義の検討, Japanese Circulation Journal, Vol.63, No.Suppl.I, 645, 1999年. (キーワード) Heparin Cofactor II(欠損・欠乏) 動脈硬化症(先天性) ヒト
487.	赤池雅史, 東博之, 香川礼香, 金川泰彦, 粟飯原賢一, 井内貴彦, 高森信行, 吉田智則, 松本俊夫, 松本和也 : 高リポ蛋白(a)血症に及ぼすaspirinの影響アポリポ蛋白(a)アイソフォームとの関連, 四国医学雑誌, Vol.55, No.2, 82, 1999年. (キーワード) Apolipoproteins A Aspirin 高リポ蛋白質血症蛋白質アイソフォームヒト (徳島大学機関リポジトリ) ● Metadata: 112136 (徳島大学機関リポジトリ: 112136)
488.	赤池雅史, 東博之, 松本和也, 林郁郎, 田村克也, 西内健, 香川礼香, 金川泰彦, 粟飯原賢一, 井内貴彦 : 血中リポ蛋白(a)濃度に及ぼすアスピリンの影響アポ蛋白(a)アイソフォームとの関連, 日本内分泌学会雑誌, Vol.75, No.1, 175, 1999年. (キーワード) Aspirin Lipoprotein(a)(血液,薬物影響) Apoprotein(a) ヒト in vitro
489.	赤池雅史, 金川泰彦, 香川礼香, 吉田智則, 粟飯原賢一, 東博之, 松本俊夫, 松本和也 : 高Lp(a)血症に及ぼすaspirinの影響 Lp(a)アイソフォーム解析を用いた検討, 日本内科学会雑誌, Vol.88, 139, 1999年. (キーワード) Aspirin(薬理学) Lipoprotein(a)(血液,薬物影響,代謝性障害) ヒト
490.	金川泰彦, 重清俊雄, 粟飯原賢一, 松山まどか, 香川礼香, 宮本和正, 井内貴彦, 赤池雅史, 東博之, 松本俊夫 : 先天性ヘパリンコファクターII(HCII)欠乏症1家系の遺伝子解析, 第20回日本血栓止血学会学術集会, Vol.9, No.4, 315, 1998年11月. (キーワード) Heparin Cofactor II(欠損・欠乏) 血液蛋白質障害配列分析ヒト
491.	粟飯原賢一, 宮田雅代, 金崎淑子, 加藤修司, 玉木康民, 木村成昭, 武市俊彰, 藤本浩史, 増田和彦, 白神〓, 千葉仁志 : インスリン非依存性糖尿病を合併したコレステリルエステル転送蛋白完全欠損症の1例, 第74回日本内科学会四国地方会, 1996年6月.
492.	粟飯原賢一 : 医原性の嚥下性肺炎を来した2例, 第19回日本集中治療医学会学術集会, 1992年2月. (キーワード) ICU 医原病吸引術肺炎-嚥下性(化学的誘発) ヒト高齢者(65~) 男女

その他・研究会:

1.	遠藤ふうり, 吉田守美子, 辻本賀美, 工藤千晶, 安井沙耶, 桝田志保, 三井由香里, 倉橋清衛, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 福本誠二 : ソマトスタチンアナログ治療中に胆嚢癌を認めた先端巨大症の1例, 第29回臨床内分泌代謝Update in Kochi, 2019年11月.
2.	工藤千晶, 倉橋清衛, 辻本賀美, 安井沙耶, 遠藤ふうり, 三井由香里, 桝田志保, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 福本誠二 : ニボルマブ投与により3系統の内分泌障害を発症した2例, 第29回臨床内分泌代謝Update in Kochi, 2019年11月.
3.	辻本賀美, 三井由香里, 工藤千晶, 安井沙耶, 遠藤ふうり, 桝田志保, 倉橋清衛, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 福本誠二 : 免疫関連有害事象の末ロイド治療中ACTH分泌低下症を認めた1例, 第29回臨床内分泌代謝Update in Kochi, 2019年11月.
4.	三井由香里, 辻本賀美, 工藤千晶, 安井沙耶, 遠藤ふうり, 桝田志保, 倉橋清衛, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 福本誠二 : 治療拒否により甲状腺クリーゼを繰り返したバセドウ病の1例, 第29回臨床内分泌代謝Update in Kochi, 2019年11月.
5.	倉橋清衛, 青山万里子, 滝沢宏光, 遠藤ふうり, 三井由香里, 桝田志保, 吉田守美子, 明比祐子, 遠藤逸朗, 粟飯原賢一, 安倍正博, 福本誠二 : 薬物治療に抵抗性で，日和見感染も合併したバセドウ病の一例, 第29回臨床内分泌代謝Update in Kochi, 2019年11月.
6.	Hiroyasu Mori, Akio Kuroda, Michiko Araki, Reiko Suzuki, Mami Ohishi, Satoshi Taniguchi, Motoyuki Tamaki, Yuko Akehi, Hiroshi Sakaue, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Munehide Matsuhisa : Advanced glycation end-products are a risk for muscle weakness in patients with type2 diabetes., American Diabetes Association 78th Scientific Sessions, Jun. 2017.
7.	吉田守美子, 粟飯原賢一, 赤池雅史, 松本俊夫 : ステロイド性大腿骨頭壊死症予防に向けた，大量グルココルチコイドによる酸化ストレスおよび血管内皮機能の変化と，ピタバスタチンの臨床的有効性の検討, 特発性大腿骨頭壊死症の治療法確立と革新的予防法開発にむけた全国学術研究, 2016年8月.
8.	粟飯原賢一, 吉田守美子, 池田康将, 上元良子, 石川カズ江 : 雄性生体の動脈硬化形成におけるマクロファージ・アンドロゲン受容体の意義, 第6回テストステロン研究会, 2015年9月.
9.	粟飯原賢一, 赤池雅史, 吉田守美子, 松本俊夫 : グルココルコイド過剰誘導酸化ストレスの臨床的評価とeNOSの有無におけるピタバスタチンの虚血臓器保護効果機構の差異, 厚生労働科学研究費補助金平成27年度第1回班会議, 2015年8月.
10.	Akio Kuroda, Tenma Jin, Horie Toru, Hiroyasu Mori, Motoyuki Tamaki, Ken-ichi Aihara and Munehide Matsuhisa : Non-invasive measurement of skin autofluorescence as a beneficial surrogate marker for atherosclerosis in patients with type 2 diabetes., 第75回アメリカ糖尿病学会ポスター発表, Jun. 2015.
11.	粟飯原賢一, 吉田守美子, 池田康将, 上元良子, 石川カズ江, 松本俊夫 : 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, 2013年11月.
12.	粟飯原賢一 : 心血管システム恒常性維持におけるアンドロゲン受容体の意義, 新学術領域研究「性差構築の分子基盤」第5回領域会議招待講演, 2013年9月.
13.	粟飯原賢一, 吉田守美子, 池田康将, 赤池雅史, 加藤茂明, 松本俊夫 : 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, 2013年3月.
14.	粟飯原賢一, 赤池雅史, 吉田守美子, 松本俊夫 : Pitavastatinは血管内皮機能障害を背景にした重症虚血誘導組織壊死を抑制する, 厚生労働科学研究費補助金難治性疾患克服研究事業特発性大腿骨頭壊死症調査研究班平成24 年度第2回班会議, 2013年1月.
15.	近藤剛史, 遠藤逸朗, 吉田守美子, 粟飯原賢一, 松本俊夫 : 当院で経験したSITSHの2例, 第18回徳島内分泌研究会, 2012年11月.
16.	粟飯原賢一 : 心血管系組織恒常性維持におけるアンドロゲン受容体の意義, 第3回テストステロン研究会, 2012年9月.
17.	粟飯原賢一, 赤池雅史, 吉田守美子, 松本俊夫 : 血管内皮機能障害を背景にした重症虚血誘導組織壊死に対するpitavastatinの効果, 厚生労働科学研究費補助金難治性疾患克服研究事業特発性大腿骨頭壊死症調査研究班平成24 年度第1回班会議, 2012年8月.
18.	吉田守美子, 粟飯原賢一, 松本俊夫 : 心腎連関病態におけるEPA;エイコサペントエン酸の臨床的意義, 第10回徳島リスクファクター研究会, 2012年6月.
19.	吉田守美子, 粟飯原賢一, 池田康将, 赤池雅史, 加藤茂明, 松本俊夫 : 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, 2012年4月.
20.	粟飯原賢一, 赤池雅史, 吉田守美子, 松本俊夫 : 酸化ストレス抑制作用を介したグルココルチコイド誘発性血管内皮細胞障害治療, 厚生労働科学研究費補助金難治性疾患克服研究事業特発性大腿骨頭壊死症調査研究班平成23 年度第2回班会議, 2011年12月.
21.	吉田守美子, 近藤絵里, 倉橋清衛, 木内美瑞穂, 片岡菜奈子, 遠藤逸朗, 粟飯原賢一, 松本俊夫, 黒田暁生, 松久宗英 : 当科での1型糖尿病に対するインスリンポンプ療法導入経験, 第17回徳島内分泌研究会, 2011年11月.
22.	赤池雅史, 粟飯原賢一, 吉田守美子, 松本俊夫 : グルココルチコイド誘発性血管内皮細胞障害に対する酸化ストレス抑制の意義, 厚生労働科学研究費補助金難治性疾患克服研究事業特発性大腿骨頭壊死症調査研究班平成23 年度第1回班会議, 2011年8月.
23.	吉田守美子, 倉橋清衛, 近藤剛史, 片岡菜奈子, 遠藤逸朗, 粟飯原賢一, 藤中雄一, 松本俊夫 : 当院での原発性アルドステロン症に対するエプレレノンの効果, Meet the Specialist, 2011年3月.
24.	吉田守美子, 粟飯原賢一, 池田康将, 赤池雅史, 加藤茂明, 松本俊夫 : 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, 2011年3月.
25.	吉田守美子, 粟飯原賢一, 上田由佳, 池田康将, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2011年3月.
26.	吉田守美子, 粟飯原賢一, 上田由佳, 池田康将, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2011年1月.
27.	吉田守美子, 粟飯原賢一, 上田由佳, 池田康将, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2010年5月.
28.	粟飯原賢一 : アンチエイジング検診とFMD, 血管不全研究会・第8回学術集会, 2010年4月.
29.	粟飯原賢一, 吉田守美子, 池田康将, 赤池雅史, 加藤茂明, 松本俊夫 : 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, 2010年3月.
30.	粟飯原賢一 : 新規動脈硬化抑制因子としてのヘパリンコファクターIIの臨床的意義および分子生物学的解析, 平成21年度井村臨床研究奨励賞受賞講演, 2009年12月.
31.	吉田守美子, 粟飯原賢一, 上田由佳, 池田康将, 倉橋清衛, 木内美瑞穂, 遠藤逸朗, 藤中雄一, 岩瀬俊, 赤池雅史, 佐田政隆, 松本俊夫 : 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, 2009年11月.
32.	遠藤逸朗, 大西幸代, 木戸里佳, 倉橋清衛, 藤中雄一, 粟飯原賢一, 吉田守美子, 安倍正博, 福本誠二, 松本俊夫 : Ca感知受容体機能に及ぼすcalcilyticsの作用, 第3回瀬戸内フォーラム, 2009年8月.
33.	倉橋清衛, 中村信元, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 藤中雄一, 松本俊夫, 八木秀介, 岩瀬俊, 赤池雅史, 佐田政隆 : 一酸化炭素中毒を契機に発見された急性心筋梗塞の一例, 第9回徳島総合診療研究会, 2009年7月.
34.	粟飯原賢一, 藤中雄一, 木内美瑞穂, 鈴木麗子, 吉田守美子, 倉橋清衛, 遠藤逸朗, 松本俊夫 : 内蔵脂肪蓄積因子の臨床的検討ーメタボリックシンドローム検診から見えたことー, 第7回徳島リスクファクター研究会, 2009年6月.
35.	遠藤逸朗, 吉田守美子, 栗若里佳, 木戸慎介, 粟飯原賢一, 藤中雄一, 藤村光則, 松本俊夫 : 冠動脈不安定ブラーク予測因子としてのICTP, 第3回徳島Vascular Endocrinology conference, 2009年3月.
36.	粟飯原賢一 : 頸動脈硬化と糖尿病, 徳島市医師会糖尿病対策委員会シンポジウム, 2008年10月.
37.	粟飯原賢一 : 血管リモデリングにおけるヘパリンコファクターIIの分子機構, 第3回宮崎サイエンスキャンプ, 2007年12月.
38.	粟飯原賢一 : 基礎と臨床からみた心血管リモデリング (マウスからヒトへ，ヒトからマウスへ), 第71回徳島循環器疾患談話会, 2007年10月.
39.	粟飯原賢一, 東博之, 赤池雅史, 池田康将, 八木秀介, 住友由佳, 吉田守美子, 伊勢孝之, 岩瀬俊, 松本俊夫 : 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, 2007年9月.
40.	粟飯原賢一 : 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の臨床及び分子生物学的解析, Meet The Specialist, 2007年7月.

報告書:

1.	粟飯原賢一 : 2型糖尿病の発症およびその心腎血管障害の予測マーカーとしてのヘパリンコファクターIIの臨床的意義, 三井厚生記念財団第20回医学研究特別助成報告書, 2011年4月.
2.	粟飯原賢一 : ヘパリンコファクターIIの抗動脈硬化作用, 上原記念生命科学財団研究報告集, Vol.21, 472-474, 2007年. (要約) 著者等はこれまでに，血漿中のヘパリンコファクターII(HC II)活性が高い患者では冠動脈形成術後のステント再狭窄や頸動脈プラークの形成が抑制されることを報告してきたが，その分子機序は不明であった．そこで今回，HC II欠損マウスの血管傷害モデルを用いてHC IIが抗動脈硬化作用を示す機序について解析した．その結果，傷害血管に対する抗トロンビン作用が主要メカニズムであると考えられた． (キーワード) Heparin Cofactor II(薬理学,治療的利用) 血管疾患(実験的,病理学,薬物療法) 血管内皮動脈硬化症 Thrombin Receptors 酸化ストレスノックアウトマウス血管リモデリング腹腔内投与マウス動物

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

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 (研究課題/領域番号: 22K08033 )
糖尿病性腎症病態におけるヘパリンコファクターIIの臨床及び分子生物学的意義の解明 (研究課題/領域番号: 19K08680 )
アンドロゲン受容体を介した性差依存および非依存性心血管リモデリング制御機構の解明 (研究課題/領域番号: 25461389 )
骨格系の分子制御機構の解明とその異常による病態の治療法の開発 (研究課題/領域番号: 25293215 )
ヘパリンコファクターIIを用いた心筋梗塞後心臓リモデリングに対する新規治療法の開発 (研究課題/領域番号: 23591046 )
ヘパリンコファクターIIによる心リモデリングおよびインスリン抵抗性制御機構の解析 (研究課題/領域番号: 21591140 )
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による血管内皮障害機構の解明 (研究課題/領域番号: 21590955 )
骨格系の制御システムと脂肪・血管制御系との連関およびその異常に基づく病態の解明 (研究課題/領域番号: 20249050 )
血管内皮機能を標的としたグルココルチコイド誘発性血管障害に対する新規治療法の開発 (研究課題/領域番号: 19590866 )
ヘパリンコファクターIIの動脈硬化進展抑制に対するトランスレーショナルリサーチ (研究課題/領域番号: 18590816 )
BMK1/ERK5による新たな血管内皮機能制御機構の解明と動脈硬化症治療への応用 (研究課題/領域番号: 17590740 )
研究者番号（70372711）による検索

特任教授 : 粟飯原賢一

研究活動

個人のホームページ

専門分野

研究テーマ

著書・論文

著書:

学術論文(審査論文):

学術レター:

総説・解説:

国際会議:

国内講演発表:

その他・研究会:

報告書:

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

特任教授 : 粟飯原 賢一

研究活動

個人のホームページ

専門分野

研究テーマ

著書・論文

著書:

学術論文(審査論文):

学術レター:

総説・解説:

国際会議:

国内講演発表:

その他・研究会:

報告書:

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

特任教授 : 粟飯原賢一