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石川 かおり イシカワ カオリ

所属
医学部
附属病院
職名講師
Last Updated :2020/09/17

研究者基本情報

学歴

  •  - 2002年, 香川医科大学大学院 医学研究科, 医科系研究科
  •  - 1998年, 香川医科大学, 医学部

学位

  • 医学博士 (香川医科大学 2002.3), 香川医科大学

所属学協会

  • The japan society of ultrasonics in medicine
  • 日本高血圧学会
  • 日本不整脈心電学会
  • 日本心臓病学会
  • 日本循環器学会
  • 日本内科学会
  • 日本病院総合診療医学会
  • 日本肺高血圧・肺循環学会

経歴

  •   2004年,  - 2007年, 香川大学 医学部附属病院 循環器・腎臓・脳卒中内科, 助教
  •   2007年, - 香川大学医学部附属病院 検査部, 助教
  •   2003年,  - 2004年, 香川大学医学部附属病院, 医員
  •   2002年,  - 2003年, 香川医科大学医学部附属病院第二内科, 医員
  •   1998年,  - 2002年, 香川医科大学大学院医学系研究科博士課程, 大学院生
  •   1998年,  - 2002年, School of Medicine, Kagawa Medical University,, Graduated,

研究活動情報

研究分野

  • ライフサイエンス / 循環器内科学

研究キーワード

    PET, echocardioglaphy, pulmonary hypertension, heart failure, PET, echocardioglaphy, pulmonary hypertension, heart failure

論文

  • Development of a Novel Algorithm to Detect Atrial Fibrillation Using an Automated Blood Pressure Monitor With an Irregular Heartbeat Detector., Makoto Ishizawa, Takahisa Noma, Takahiro Izumi, Ryosuke Tani, Tomoko Inoue, Eriko Nasu, Atsushi Tobiume, Yusuke Hasui, Shota Yokoyama, Hideyuki Hamaya, Shohei Ishikawa, Keiji Matsunaga, Ryo Kawakami, Kumi Konishi, Yuichi Miyake, Kaori Ishikawa, Teppei Tsuji, Kazushi Murakami, Naoki Nishimoto, Hiroyuki Kitajima, Tetsuo Minamino, Circulation journal : official journal of the Japanese Circulation Society, Circulation journal : official journal of the Japanese Circulation Society, 83, (12) 2428 - 2433,   2019年11月25日, [査読有り]
  • 心房細動アブレーション時の心電図同期下心臓造影CTを用いた心アミロイドーシスのスクリーニング, 松永 圭司, 野間 貴久, 井上 朋子, 那須 栄里子, 石川 昇平, 河上 良, 三宅 祐一, 石澤 真, 石川 かおり, 村上 和司, 南野 哲男, 日本心臓病学会学術集会抄録, 日本心臓病学会学術集会抄録, 67回,   2019年09月, [査読有り]
  • 開心術後に冠攣縮増悪による薬物治療抵抗性の発作性房室ブロックが遷延し2度の心停止に至った関節リウマチの1症例, 井上 朋子, 野間 貴久, 那須 栄里子, 松永 圭司, 河上 良, 三宅 祐一, 石澤 真, 石川 かおり, 村上 和司, 南野 哲男, 日本心臓病学会学術集会抄録, 日本心臓病学会学術集会抄録, 67回,   2019年09月, [査読有り]
  • 甲状腺中毒症合併の急性冠症候群患者に対してヨード造影剤を使用し甲状腺クリーゼなく治療し得た1例, 綾井 健太, 松永 圭司, 蓮井 雄介, 石川 昇平, 萬谷 薫, 三宅 祐一, 石澤 真, 石川 かおり, 辻 哲平, 村上 和司, 野間 貴久, 南野 哲男, 心臓, 心臓, 51, (4) 453 - 457,   2019年04月, [査読有り]
  • 家族性高コレステロール血症患者の早期診断における遺伝子検査の有用性について, 石川 昇平, 松永 圭司, 萬谷 薫, 三宅 祐一, 石澤 真, 石川 かおり, 辻 哲平, 村上 和司, 野間 貴久, 南野 哲男, 日本循環器病予防学会誌, 日本循環器病予防学会誌, 54, (2) 118 - 118,   2019年04月, [査読有り]
  • 周産期心筋症のスクリーニング方法に関する検討 肺野エコーによる早期発見の可能性, 外山 和季, 松永 圭司, 三宅 祐一, 石澤 真, 辻 哲平, 石川 かおり, 村上 和司, 野間 貴久, 南野 哲男, 超音波医学, 超音波医学, 46, (Suppl.) S698 - S698,   2019年04月, [査読有り]
  • FDG-PET検査で評価した糖尿病を有するDCM患者における心筋glucose取り込み量の増加(Increase in Myocardial Glucose Uptake in the DCM Patients with Diabetes Mellitus Evaluated by FDG-PET Study), 飛梅 淳, 野間 貴久, 蓮井 雄介, 石川 昇平, 松永 圭司, 萬谷 薫, 三宅 祐一, 石澤 真, 石川 かおり, 辻 哲平, 村上 和司, 南野 哲男, 日本循環器学会学術集会抄録集, 日本循環器学会学術集会抄録集, 83回,   2019年03月, [査読有り]
  • 最適な状況下にあるオムロン血圧計は一般的な心臓患者における心房細動を高精度で検出できる(The Omron Blood Pressure Monitor under the Optimized Condition can Detect Atrial Fibrillation with High Accuracy in General Cardiac Patients), 石澤 真, 野間 貴久, 那須 栄里子, 飛梅 淳, 蓮井 雄介, 横山 聖太, 濱谷 英幸, 石川 昇平, 松永 圭司, 萬谷 薫, 三宅 祐一, 石川 かおり, 辻 哲平, 村上 和司, 南野 哲男, 日本循環器学会学術集会抄録集, 日本循環器学会学術集会抄録集, 83回,   2019年03月, [査読有り]
  • 右上傍気管リンパ節の18F-fluoro-2-deoxy-D-glucose PET取込みは心サルコイドーシスにおける完全房室ブロックを予測する(18F-fluoro-2-deoxy-D-glucose Positron Emission Tomography Uptake in the Right Superior Paratracheal Lymph Node Predicts a Complete Atrioventricular Block in Cardiac Sarcoidosis), 松永 圭司, 谷 良介, 那須 栄里子, 飛梅 淳, 蓮井 雄介, 濱谷 英幸, 萬谷 薫, 横山 聖太, 石川 昇平, 三宅 祐一, 石澤 真, 辻 哲平, 石川 かおり, 村上 和司, 野間 貴久, 南野 哲男, 日本循環器学会学術集会抄録集, 日本循環器学会学術集会抄録集, 83回,   2019年03月, [査読有り]
  • 高齢者に対するPoint of Care Ultrasoundのための座位心エコーの正常値に関する検討, 舛形 尚, 谷内田 達夫, 石川 かおり, 高田 忠幸, 岡田 宏基, 千田 彰一, 日本病院総合診療医学会雑誌, 日本病院総合診療医学会雑誌, 14, (6) 651 - 651,   2018年11月, [査読有り]
  • 地域ICTの利活用による多施設共同臨床試験の仕組みの構築, 野間 貴久, 松永 圭司, 石川 昇平, 三宅 祐一, 石澤 真, 石川 かおり, 辻 哲平, 村上 和司, 南野 哲男, 日本心臓病学会学術集会抄録, 日本心臓病学会学術集会抄録, 66回,   2018年09月, [査読有り]
  • マウスではマクロファージ枯渇のアポトーシス阻害剤はアポトーシスを促すことでM1マクロファージを減少させ、心筋梗塞後心破裂を抑制した(Apoptosis Inhibitor of Macrophage Depletion Decreased M1 Macrophage by Promoting Apoptosis and Suppressed Cardiac Rupture after Myocardial Infarction in Mice), 石川 昇平, 野間 貴久, 和泉 高宏, 谷 良介, 飛梅 淳, 横山 聖太, 松永 圭司, 三宅 祐一, 石澤 真, 石川 かおり, 辻 哲平, 村上 和司, 南野 哲男, 日本循環器学会学術集会抄録集, 日本循環器学会学術集会抄録集, 82回,   2018年03月, [査読有り]
  • 導出18誘導心電図を用いた副伝導路の特定 2症例報告(Identification of the Accessory Pathways Using Synthesized 18 Lead Electrocardiography: A Report of Two Cases), 松永 圭司, 石澤 真, 和泉 高広, 谷 良介, 井上 朋子, 飛梅 淳, 蓮井 雄介, 横山 聖太, 石川 昇平, 萬谷 薫, 三宅 祐一, 石川 かおり, 辻 哲平, 村上 和司, 野間 貴久, 南野 哲男, 日本循環器学会学術集会抄録集, 日本循環器学会学術集会抄録集, 82回,   2018年03月, [査読有り]
  • Apoptosis inhibitor of macrophage depletion decreased M1 macrophage accumulation and the incidence of cardiac rupture after myocardial infarction in mice, Shohei Ishikawa, Takahisa Noma, Hai Ying Fu, Takashi Matsuzaki, Makoto Ishizawa, Kaori Ishikawa, Kazushi Murakami, Naoki Nishimoto, Akira Nishiyama, Tetsuo Minamino, PLOS ONE, PLOS ONE, 12,   2017年11月, [査読有り]
  • 慢性心不全患者の心臓交感神経系に対するARBの効果, 石川 昇平, 野間 貴久, 和泉 高広, 谷 良介, 井上 朋子, 飛梅 淳, 蓮井 雄介, 松永 圭司, 萬谷 薫, 三宅 祐一, 石澤 真, 石川 かおり, 辻 哲平, 村上 和司, 南野 哲男, 香川県医師会誌, 香川県医師会誌, 70, (特別) 46 - 46,   2017年10月, [査読有り]
  • 左鎖骨周囲に悪性リンパ腫を合併した不整脈源性右室心筋症に対してS-ICD植え込み術を施行した1例, 谷 良介, 松永 圭司, 和泉 高弘, 井上 朋子, 飛梅 淳, 横山 聖太, 蓮井 雄介, 萬谷 薫, 石川 昇平, 三宅 祐一, 石澤 真, 辻 哲平, 石川 かおり, 村上 和司, 野間 貴久, 南野 哲男, 香川県医師会誌, 香川県医師会誌, 70, (特別) 52 - 52,   2017年10月, [査読有り]
  • Role of the Low-Density Lipoprotein-Cholesterol/ High-Density Lipoprotein-Cholesterol Ratio in Predicting Serial Changes in the Lipid Component of Coronary Plaque, Ryo Kawakami, Ichiro Matsumoto, Motoi Shiomi, Mizuki Kurozumi, Yuichi Miyake, Makoto Ishizawa, Kaori Ishikawa, Kazushi Murakami, Takahisa Noma, Yuichiro Takagi, Naoki Nishimoto, Tetsuo Minamino, CIRCULATION JOURNAL, CIRCULATION JOURNAL, 81, (10) 1439 - +,   2017年10月, [査読有り]
  • 発作性心房細動患者において心房抗頻拍ペーシング治療が奏効する患者の臨床症状(Clinical Manifestations of the Responder to Atrial Anti-Tachycardia Pacing in the Patients with Paroxysmal Atrial Fibrillation), 野間 貴久, 石澤 真, 武内 将起, 井上 朋子, 松永 圭司, 三宅 祐一, 石川 かおり, 村上 和司, 南野 哲男, 日本循環器学会学術集会抄録集, 日本循環器学会学術集会抄録集, 81回,   2017年03月, [査読有り]
  • Apotosis inhibitor of macrophage(AIM)の枯渇により心筋梗塞後のM1型マクロファージ集積および心破裂が軽減される(Depletion of Apoptosis Inhibitor of Macrophage(AIM) Alleviates M1 Macrophage Recruitment and Cardiac Rupture after Myocardial Infarction), 石川 昇平, 野間 貴久, 井上 朋子, 林 夕起子, 宮井 翔平, 横山 聖太, 松永 圭司, 小西 久美, 高畠 渉, 萬谷 薫, 三宅 祐一, 石澤 真, 石川 かおり, 村上 和司, 南野 哲男, 日本循環器学会学術集会抄録集, 日本循環器学会学術集会抄録集, 81回,   2017年03月, [査読有り]
  • 特徴的な拡張期僧帽弁前尖運動を呈した大動脈弁閉鎖不全症の一例, 三宅 祐一, 大森 浩二, 水川 瑞紀, 大原 美奈子, 竹内 浩人, 大下 哲, 四宮 かおり, 藤田 憲弘, 河野 雅和, Circulation Journal, Circulation Journal, 70, (Suppl.III) 1153 - 1153,   2006年10月, [査読有り]
  • 筋強直性ジストロフィに合併した心不全に対する両心室ペーシング, 水川 瑞紀, 大森 浩二, 藤田 憲弘, 三宅 祐一, 竹内 浩人, 四宮 かおり, 河野 雅和, 横山 雄一郎, 鈴木 健夫, 山下 洋一, 前田 肇, 心臓, 心臓, 38, (6) 629 - 634,   2006年06月, [査読有り]
  • 下肢痛を初発症状とした拡張型心筋症の一例, 水川 瑞紀, 藤田 憲弘, 三宅 祐一, 大原 美奈子, 竹内 浩人, 四宮 かおり, 大下 哲, 大森 浩二, 河野 雅和, 横山 雄一郎, 鈴木 健夫, 山下 洋一, 前田 肇, Circulation Journal, Circulation Journal, 70, (Suppl.II) 1060 - 1060,   2006年04月, [査読有り]
  • サルコイドーシスの診断・治療における18F-FDG-PETの有用性, 四宮 かおり, 岩藤 泰慶, 瀧波 裕之, 三宅 祐一, 伊原 かすみ, 吉田 潤史, 藤田 憲弘, 大森 浩二, 河野 雅和, 日本内科学会雑誌, 日本内科学会雑誌, 95, (Suppl.) 232 - 232,   2006年02月, [査読有り]
  • 心房中隔欠損症術後肺高血圧症に対するフローランの使用経験, 四宮 かおり, 三宅 祐一, 大原 美奈子, 竹内 浩人, 大下 哲, 藤田 憲弘, 大森 浩二, 河野 雅和, Progress in Medicine, Progress in Medicine, 26, (1) 284 - 288,   2006年01月, [査読有り]
  • HEART's Original [症例] 筋強直性ジストロフィに合併した心不全に対する両心室ペーシング, 水川 瑞紀, 山下 洋一, 前田 肇, 大森 浩二, 藤田 憲弘, 三宅 祐一, 竹内 浩人, 四宮 かおり, 河野 雅和, 横山 雄一郎, 鈴木 健夫, 心臓, 心臓, 38, (6) 629 - 634,   2006年, [査読有り]
  • 右室ペーシングによる左室壁運動非同期性と右室流出路ペーシングによるその回避-心筋組織ドプラ法を用いた検討, 吉田 潤史, 大森 浩二, 四宮 かおり, 水川 瑞紀, 三宅 祐一, 藤田 憲弘, 竹内 浩人, 大下 哲, 大原 美奈子, 滝波 裕之, 石澤 真, 河野 雅和, 香川県医師会誌, 香川県医師会誌, 58, (特別) 51 - 51,   2005年10月, [査読有り]
  • 心筋組織ドプラ法を用いた右室心尖部ペーシング症例の左室壁運動に関する検討, 吉田 潤史, 大森 浩二, 四宮 かおり, 水川 瑞紀, 三宅 祐一, 藤田 憲弘, 難波 経立, 石澤 真, 河野 雅和, 竹内 浩人, Circulation Journal, Circulation Journal, 69, (Suppl.III) 940 - 940,   2005年10月, [査読有り]
  • 右室ペーシングによる左室壁運動非同期性と高位中隔ペーシングによるその回避 心筋組織ドプラ法を用いた検討, 吉田 潤史, 大森 浩二, 四宮 かおり, 水川 瑞紀, 三宅 祐一, 藤田 憲弘, 竹内 浩人, 難波 経立, 石澤 真, 河野 雅和, Journal of Cardiology, Journal of Cardiology, 46, (Suppl.I) 337 - 337,   2005年08月, [査読有り]

Misc

  • Intracoronary Administration of Nicorandil During Direct Coronary Stenting Complements Restoration of Regional Perfusion at Subacute Phase of Myocardial Infarction: A Demonstration With O-15 Water Pet, Wataru Takabatake, Yasuyoshi Iwado, Kaori Ishikawa, Yuka Miyauchi, Kumi Tada, Kazushi Murakami, Takahisa Noma, Koji Ohmori, Yosihiro Nisiyama, Masakazu Kohno, CIRCULATION, 126, (21),   2012年11月
  • Correlation of arterial stiffness to left ventricular function in patients with reduced ejection fraction, Sanae Noguchi, Hisashi Masugata, Shoichi Senda, Kaori Ishikawa, Hiromi Nakaishi, Ayu Tada, Toshihiro Inage, Tatsushi Kajikawa, Michio Inukai, Takashi Himoto, Naohisa Hosomi, Kazushi Murakami, Takahisa Noma, Masakazu Kohno, Hiroki Okada, Fuminori Goda, Koji Murao, Tohoku Journal of Experimental Medicine, 225, (3), 145 - 151,   2011年
    Heart failure has been divided into heart failure with preserved left ventricular (LV) ejection fraction (EF) and heart failure with reduced EF, because the patho-physiologies of the two conditions are different. Cardio-ankle vascular index (CAVI) is a new indicator of arterial stiffness, and the most conspicuous feature of CAVI is its independence of blood pressure at the time of measurement. Arterial stiffness has been considered to increase LV afterload, which requires special care to avoid the onset of heart failure. We compared the correlation of arterial stiffness as assessed by CAVI to LV function in 44 hypertensive patients with preserved EF (EF: 71 ± 7%) and 31 patients with reduced EF (48 ± 8%). All of patients with reduced EF had history of both hypertension and myocardial infarction. Using Doppler echocardiography, LV diastolic and systolic function was evaluated by measuring peak early diastolic mitral annular velocity (e') and global LV peak systolic longitudinal strain (GPSLS), respectively. In patients with preserved EF, CAVI was correlated with e' (r = -0.313, p = 0.038), but not with GPSLS (r = 0.207). By contrast, CAVI was correlated with GPSLS (r = 0.604, p < 0.001) as well as e' (r = -0.393, p = 0.029) in patients with reduced EF. Thus, patients with reduced EF showed a closer correlation of arterial stiffness to LV function compared with patients with preserved EF. Therefore, hypertensive patients with reduced EF require a stricter regimen for treating arterial stiffness than their counterparts with preserved EF. © 2011 Tohoku University Medical Press.
  • Positron emission tomographic demonstration of myocardial oxidative metabolism in a case of left ventricular restoration after cardiac resynchronization therapy, Kenji Kitaizumi, Kazushi Yukiiri, Hisashi Masugata, Kaori Shinomiya, Minako Ohara, Hiroyuki Takinami, Yasuyoshi Iwado, Junji Yoshida, Takahisa Noma, Koji Ohmori, Yoichi Yamashita, Taiko Horii, Shoich Senda, Masakazu Kohno, Circulation Journal, 72, (11), 1900 - 1903,   2008年
    A 65-year-old man with a history of coronary artery bypass grafting was admitted because of severe heart failure. Echocardiography showed diffuse severe hypokinesis of the left ventricle (ejection fraction 25%) and severe mitral regurgitation caused by tethering of the leaflet secondary to left ventricular (LV) dilation. He underwent mitral valve annuloplasty and LV papillary muscle imbrication, but postoperative sustained ventricular tachycardia developed and echocardiography showed ventricular dyssynchrony with a long septal-to-posterior wall motion delay (> 130 ms). Cardiac resynchronization therapy (CRT) was performed using a biventricular pacing system with an implantable cardioverter defibrillator, but biventricular pacing prolonged the QRS duration from 130 to 160ms, so 11C-acetate positron emission tomography was performed to evaluate the CRT. During biventricular pacing, myocardial oxidative consumption decreased by 15% and cardiac efficiency increased by 33%. The plasma brain natriuretic peptide level, which was 9,500 pg/ml preoperatively, decreased to 173 pg/ml just before discharge from hospital.
  • Differential impact of atorvastatin vs pravastatin on progressive insulin resistance and left ventricular diastolic dysfunction in a rat model of type II diabetes, Yan Chen, Koji Ohmori, Mizuki Mizukawa, Junji Yoshida, Yu Zeng, Ling Zhang, Kaori Shinomiya, Hiroaki Kosaka, Masakazu Kohno, CIRCULATION JOURNAL, 71, (1), 144 - 152,   2007年01月
    Background Controversy exists regarding the effects of statin therapy on progressive insulin resistance (IR) and its consequences, in the present study a rat model of spontaneously developing type II diabetes mellitus (DM) was used to examine the impact of atorvastatin (AS) vs pravastatin (PS). Methods and Results The Otsuka Long-Evans Tokushima Fatty rats were either untreated or treated with 100mg/kg per day of AS or PS from 6 weeks of age for 24 weeks. AS achieved much greater lipid lowering than PS. Serial oral glucose tolerance tests revealed new-onset diabetes was delayed by PS only. The untreated rats exhibited a progressive decrease in plasma adiponectin, increases in plasma leptin and tumor necrosis factor-a, and reduction of plasma nitric oxide (NO), which were limited more by PS than AS. PS, but not AS, enhanced adiponectin mRNA expression in white adipose tissue at 30 weeks. Cardiac endothelial NO synthase expression was upregulated, and overexpression of both transforming growth factor-beta 1 and monocyte chemoattractant protein-1 mRNA was limited more by PS than AS. Coronary perivascular fibrosis at 30 weeks was suppressed only by PS, which was accompanied by preserved left ventricular diastolic function assessed with Doppler echocardiography. Conclusions The moderate lipid lowering by PS, but not the intensive lipid lowering by AS, prevented new-onset DM and diastolic dysfunction in a rat model of IR, and this was associated with preferable adipocytokine profiles and cardiac redox states.
  • 42)特徴的な拡張期僧帽弁前尖運動を呈した大動脈弁閉鎖不全症の一例(第88回日本循環器学会中国・四国合同地方会), 三宅 祐一, 大森 浩二, 水川 瑞紀, 大原 美奈子, 竹内 浩人, 大下 哲, 四宮 かおり, 藤田 憲弘, 河野 雅和, Circulation journal : official journal of the Japanese Circulation Society, 70, (0), 1153 - 1153,   2006年10月20日
  • 81)下肢痛を初発症状とした拡張型心筋症の一例(第87回日本循環器学会中国・四国合同地方会), 水川 瑞紀, 藤田 憲弘, 三宅 祐一, 大原 美奈子, 竹内 浩人, 四宮 かおり, 大下 哲, 大森 浩二, 河野 雅和, 横山 雄一郎, 鈴木 健夫, 山下 洋一, 前田 肇, Circulation journal : official journal of the Japanese Circulation Society, 70, (0), 1060 - 1060,   2006年04月20日
  • 心膜心筋炎で発症した特発性好酸球増加症候群の1例, 三宅 祐一, 四宮 かおり, 水川 瑞紀, 大原 美奈子, 竹内 浩人, 大下 哲, 藤田 憲弘, 清元 秀泰, 大森 浩二, 河野 雅和, 日本内科学会雑誌, 95, (10), 2093 - 2095,   2006年
  • 筋強直性ジストロフィーに合併した心不全の治療に両心室ペーシングが有効であった一例(第86回日本循環器学会四国地方会), 水川 瑞紀, 藤田 憲弘, 石原 靖大, 伊原 かすみ, 三宅 祐一, 難波 経立, 四宮 かおり, 大森 浩二, 河野 雅和, 竹内 浩人, 横山 雄一郎, 鈴木 健夫, 山下 洋一, 前田 肇, Circulation journal : official journal of the Japanese Circulation Society, 69, (0), 938 - 938,   2005年10月20日
  • 心筋組織ドプラ法を用いた右室心尖部ペーシング症例の左室壁運動に関する検討(第86回日本循環器学会四国地方会), 吉田 潤史, 大森 浩二, 四宮 かおり, 水川 瑞紀, 三宅 祐一, 藤田 憲弘, 難波 経立, 石澤 真, 河野 雅和, 竹内 浩人, Circulation journal : official journal of the Japanese Circulation Society, 69, (0), 940 - 940,   2005年10月20日
  • ペーシング不全を呈した症例のFluorodeoxyglucose-Positron Emission Tomography所見, 岩藤 泰慶, 四宮 かおり, 大森 浩二, 河野 雅和, 千田 彰一, Journal of Cardiology, 45, (4), 173-175,   2005年04月, [査読有り]
  • 献腎移植後9年目に感染性心内膜炎を発症した1例, 乾 政志, 佃 文夫, 合田 裕美, 田岡 利宜也, 島田 治, 桑田 善弘, 筧 善行, 四宮 かおり, 伊原 かすみ, 清元 秀泰, 河野 雅和, 沼田 明, 中山 正吾, 腎移植血管外科, 17, (2), 177 - 180,   2005年
  • 拡張型心筋症に対するCarvedilolによるβ遮断薬療法の心筋血流予備能改善効果について, 瀧波 裕之, 岩藤 泰慶, 伊原 かすみ, 石澤 真, 四宮 かおり, 野間 貴久, 大森 浩二, 水重 克文, 西山 佳宏, 大川 元臣, 千田 彰一, 河野 雅和, 香川県医師会誌, 57, (特別), 71 - 71,   2004年10月
  • Plasma adrenomedullin and carotid atherosclerosis in atherothrombotic ischemic stroke, N Hosomi, H Ohyama, T Takahashi, K Shinomiya, T Naya, CR Ban, K Osaka, M Kohno, JA Koziol, JOURNAL OF HYPERTENSION, 22, (10), 1945 - 1951,   2004年10月
    Objective Adrenomedullin is known to exert anti-atherosclerotic actions by inhibiting proliferation and migration of smooth muscle cells in vitro. Here we examine the relationship between the plasma concentration of adrenomedullin and ultrasonographic characteristics of carotid arteries both in ischemic stroke and in the absence of cerebrovascular disease. Methods We studied 61 patients with atherothrombotic ischemic stroke in the chronic phase and 50 patients without any cerebrovascular disease. Intima-media thickness and vascular lumen diameters were evaluated by carotid ultrasonography. Plasma mature-adrenomedullin was determined by radioimmunoassay. Results Plasma mature-adrenomedullin in the patients with atherothrombotic ischemic stroke in the chronic phase (2.01 +/- 0.58 fmol/ml) was significantly higher than that in the patients without any cerebrovascular disease (1.24 +/- 0.18 fmol/ml, P< 0.001). With multiple regression analysis, plasma mature-adrenomedullin was found to be predicted by: stroke status (atherothrombotic ischemic stroke versus no cerebrovascular disease), diabetes status (yes/no), left ventricular ejection fraction, internal carotid artery intima-media thickness, and common carotid artery pressure strain elastic modulus (R-2 = 0.79; F-5,F-105 = 85.39, P < 0.0001). Conclusion Plasma mature-adrenomedullin showed significantly positive associations with carotid atherosclerosis and atherothrombotic ischemic stroke, independent of systolic blood pressure.
  • Treatment of acute myocardial infarction by hepatocyte growth factor gene transfer, Kondo, I, K Ohmori, A Oshita, H Takeuchi, S Fuke, K Shinomiya, T Noma, T Namba, M Kohno, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 44, (3), 644 - 653,   2004年08月, [査読有り]
    OBJECTIVES We examined whether ultrasonic microbubble destruction (US/MB) enables therapeutic myocardial gene transfer of hepatocyte growth factor (HGF) for acute myocardial infarction (MI). BACKGROUND Hepatocyte growth factor gene transfer provides cardioprotective effects in MI, which requires direct intramyocardial injection or special vectors. Although US/MB was used in myocardial gene transfer, its feasibility in transfer of a therapeutic gene with non-viral vector remains unknown. METHODS In a rat model of acute MI, naked plasmid (pVax1) encoding human HGF (1,500 mug) was infused into the left ventricular (LV) chamber during US/MB (HGF-US/MB) or insonation only (HGF-US) or alone (HGF-alone), while control MI rats received empty pVaxl during US/MB (pVax1-US/MB). For US/MB, transthoracic intermittent insonation with a diagnostic transducer (1.3 MHz) was performed for 2 min at a peak negative pressure of -2,160 kPa during intravenous 20% Optison. RESULTS Baseline risk area was comparable among the groups. Immunohistology seven days after treatment revealed significant myocardial expression of HGF protein only in HGF-US/MB. At three weeks, LV weight in HGF-US/MB (0.89 +/- 0.03 g) was significantly lower than those in HGF-alone (1.09 +/- 0.08 g), HGF-US (1.04 +/- 0.07 g), and pVax1-US/MB (1.04 +/- +/- 0.05 g). Moreover, scar size was significantly smaller (16 +/- 6% vs. 39 +/- 5%, 41 +/- 6%, and 40 +/- 4% of total myocardial circumferential length, respectively), while capillary density (49 +/- 8 vs. 34 +/- 5, 37 +/- 6, and 36 +/- 4 capitlaries/high-power field, respectively) and arterial density (37 +/- 7 vs. 15 +/- 9, 18 +/- 4, and 14 +/- 11 arterioles/high-power field, respectively) in the risk area were higher in HGF-US/MB than the other groups. CONCLUSIONS Ultrasound-mediated microbubble destruction may enable myocardial HGF gene transfer with systemic administration of naked plasmid, which enhances angiogenesis, Emits infarction size, and prevents LV remodeling after MI. (C) 2004 by the American College of Cardiology Foundation.
  • Effects of pravastatin on progression of glucose intolerance and cardiovascular remodeling in a type Ⅱ diabetes model., YU,Y, OHMORI,K, CHEN,Y, SATO,C, KIYOMOTO,H, SHINOMIYA,K, TAKEUCHI,H, MIZUSHIGE,K, KOHNO,M, J Am Coll Cardiol, 44, (4), 904 - 913,   2004年08月, [査読有り]
  • Treatment of acute myocardial infarction by hepatocyte growth factor gene transfer, Kondo, I, K Ohmori, A Oshita, H Takeuchi, S Fuke, K Shinomiya, T Noma, T Namba, M Kohno, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 44, (3), 644 - 653,   2004年08月, [査読有り]
    OBJECTIVES We examined whether ultrasonic microbubble destruction (US/MB) enables therapeutic myocardial gene transfer of hepatocyte growth factor (HGF) for acute myocardial infarction (MI). BACKGROUND Hepatocyte growth factor gene transfer provides cardioprotective effects in MI, which requires direct intramyocardial injection or special vectors. Although US/MB was used in myocardial gene transfer, its feasibility in transfer of a therapeutic gene with non-viral vector remains unknown. METHODS In a rat model of acute MI, naked plasmid (pVax1) encoding human HGF (1,500 mug) was infused into the left ventricular (LV) chamber during US/MB (HGF-US/MB) or insonation only (HGF-US) or alone (HGF-alone), while control MI rats received empty pVaxl during US/MB (pVax1-US/MB). For US/MB, transthoracic intermittent insonation with a diagnostic transducer (1.3 MHz) was performed for 2 min at a peak negative pressure of -2,160 kPa during intravenous 20% Optison. RESULTS Baseline risk area was comparable among the groups. Immunohistology seven days after treatment revealed significant myocardial expression of HGF protein only in HGF-US/MB. At three weeks, LV weight in HGF-US/MB (0.89 +/- 0.03 g) was significantly lower than those in HGF-alone (1.09 +/- 0.08 g), HGF-US (1.04 +/- 0.07 g), and pVax1-US/MB (1.04 +/- +/- 0.05 g). Moreover, scar size was significantly smaller (16 +/- 6% vs. 39 +/- 5%, 41 +/- 6%, and 40 +/- 4% of total myocardial circumferential length, respectively), while capillary density (49 +/- 8 vs. 34 +/- 5, 37 +/- 6, and 36 +/- 4 capitlaries/high-power field, respectively) and arterial density (37 +/- 7 vs. 15 +/- 9, 18 +/- 4, and 14 +/- 11 arterioles/high-power field, respectively) in the risk area were higher in HGF-US/MB than the other groups. CONCLUSIONS Ultrasound-mediated microbubble destruction may enable myocardial HGF gene transfer with systemic administration of naked plasmid, which enhances angiogenesis, Emits infarction size, and prevents LV remodeling after MI. (C) 2004 by the American College of Cardiology Foundation.
  • Effect of pravastatin on progression of glucose intolerance and cardiovascular remodeling in a type Ⅱdiabetes model., Yu Y, 大森 浩二, Chen Y, Sato C, 清元 秀泰, 四宮 かおり, 竹内 浩人, 水重 克文, 河野 雅和, J Am Coll Cardiol. 44: 904-913; 2004., 44, (4), 904 - 913,   2004年08月
  • Effects of pravastatin on progression of glucose intolerance and cardiovascular remodeling in a type II diabetes model, Y Yu, K Ohmori, Y Chen, CB Sato, H Kiyomoto, K Shinomiya, H Takeuchi, K Mizushige, M Kohno, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 44, (4), 904 - 913,   2004年08月
    OBJECTIVES We examined the effects of early treatment with a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor pravastatin on the progression of glucose intolerance and cardiovascular remodeling in a model of spontaneously developing type II diabetes mellitus (DM), the Otsuka Long-Evans Tokushima Fatty (OLETF) rats. BACKGROUND Clinical trials showed that pravastatin prevented new-onset DM in hypercholesterolemic patients, and that it was effective in prevention of cardiovascular events in diabetics. METHODS The OLETF rats were treated with pravastatin (100 mg/kg/day) from 5 weeks of age and compared with age-matched untreated OLETF rats and normal Long-Evans Tokushima Otsuka (LETO) rats on serial oral glucose tolerance tests (OGTT) and Doppler echocardiography and on histopathological/biochemical analyses of the heart at 30 weeks. RESULTS The OGTT revealed that 40% and 89% of untreated OLETF rats were diabetic at 20 and 30 weeks, respectively, but 0% and only 30%, respectively, were diabetic in the treated OLETF. Left ventricular diastolic function was found impaired from 20 weeks in untreated OLETF but remained normal in the treated-OLETF. The wall-to-lumen ratio and perivascular fibrosis of coronary arteries were increased in untreated-OLETF but were limited in the treated-OLETF at 30 weeks. Moreover, cardiac expressions of a fibrogenic growth factor, transforming growth factor-beta1 (TGF-beta1), and a proinflammatory chemokine, monocyte chemoattractant protein-1 (MCP-1), were increased in untreated-OLETF. However, in the treated-OLETF, overexpressions of TGF-beta1 and MCP-1 were attenuated, which was associated with overexpression of endothelial nitric oxide synthase (eNOS) (2.5-fold of control LETO). CONCLUSIONS Early pravastatin treatment prevented cardiovascular remodeling in the spontaneous DM model by retarding the progression of glucose intolerance, overexpressing cardiac eNOS, and inhibiting overexpressions of fibrogenic/proinflammatory cytokines. (C) 2004 by the American College of Cardiology Foundation.
  • Leukocyte-targeted myocardial contrast echocardiography can assess the degree of acute allograft rejection in a rat cardiac transplantation model, Kondo, I, K Ohmori, A Oshita, H Takeuchi, J Yoshida, K Shinomiya, S Fuke, T Suzuki, K Mizushige, M Kohno, CIRCULATION, 109, (8), 1056 - 1061,   2004年03月, [査読有り]
    Background - Repetitive endomyocardial biopsies are necessary to monitor the effects of immunosuppressants after cardiac transplantation. Contrast ultrasound with microbubble targeting of leukocytes detects acute leukocyte infiltration. We examined whether leukocyte- targeted myocardial contrast echocardiography ( MCE) could provide for the quantitative assessment of acute cardiac rejection. Methods and Results - Hearts from Brown Norway rats or Lewis rats were transplanted into other Brown Norway rats. Isografts and groups of allografts either untreated or treated with cyclosporin A ( CsA) at a low dose ( 3 mg . kg(-1) . d(-1)) or high dose (10 mg . kg(-1) . d(-1)) from 3 days before transplantation were compared at posttransplantation day 3. Echocardiography- derived left ventricular wall thickening was comparable among the 4 groups. Myocardial blood flow assessed with MCE, relating pulsing intervals with signal intensity ( SI), was slightly decreased only in untreated allografts. However, myocardial SI ( in gray levels) obtained after a 10- minute period allowing microbubble - leukocyte interactions after contrast injection exhibited a clear gradient in these groups ( 12 +/- 2 in untreated allografts, 9 +/- 5 in allografts treated with low- dose CsA, 6 +/- 3 in allografts treated with high- dose CsA, and 2 +/- 1 in isografts, P < 0.001). The pattern of difference in SI among the groups agreed well with that in ED- 1 - positive cell ( macrophage) count ( 25 +/- 7, 12 +/- 4, 5 +/- 3, and 1 +/- 0 cells per high- power field, respectively, P < 0.001), which correlated with CD3- positive cell ( T lymphocyte) count ( 33 +/- 5, 22 +/- 5, 9 +/- 4, and 1 +/- 0 cells per high- power field, respectively, P < 0.001). Conclusions - Leukocyte- targeted MCE can noninvasively assess the degree of rejection in transplanted hearts by directly revealing the magnitude of intramyocardial infiltration of macrophages and T lymphocytes.
  • Leukocyte-targeted myocardial contrast echocardiography can assess the degree of acute allograft rejection in a rat cardiac transplantation model, Kondo, I, K Ohmori, A Oshita, H Takeuchi, J Yoshida, K Shinomiya, S Fuke, T Suzuki, K Mizushige, M Kohno, CIRCULATION, 109, (8), 1056 - 1061,   2004年03月
    Background - Repetitive endomyocardial biopsies are necessary to monitor the effects of immunosuppressants after cardiac transplantation. Contrast ultrasound with microbubble targeting of leukocytes detects acute leukocyte infiltration. We examined whether leukocyte- targeted myocardial contrast echocardiography ( MCE) could provide for the quantitative assessment of acute cardiac rejection. Methods and Results - Hearts from Brown Norway rats or Lewis rats were transplanted into other Brown Norway rats. Isografts and groups of allografts either untreated or treated with cyclosporin A ( CsA) at a low dose ( 3 mg . kg(-1) . d(-1)) or high dose (10 mg . kg(-1) . d(-1)) from 3 days before transplantation were compared at posttransplantation day 3. Echocardiography- derived left ventricular wall thickening was comparable among the 4 groups. Myocardial blood flow assessed with MCE, relating pulsing intervals with signal intensity ( SI), was slightly decreased only in untreated allografts. However, myocardial SI ( in gray levels) obtained after a 10- minute period allowing microbubble - leukocyte interactions after contrast injection exhibited a clear gradient in these groups ( 12 +/- 2 in untreated allografts, 9 +/- 5 in allografts treated with low- dose CsA, 6 +/- 3 in allografts treated with high- dose CsA, and 2 +/- 1 in isografts, P < 0.001). The pattern of difference in SI among the groups agreed well with that in ED- 1 - positive cell ( macrophage) count ( 25 +/- 7, 12 +/- 4, 5 +/- 3, and 1 +/- 0 cells per high- power field, respectively, P < 0.001), which correlated with CD3- positive cell ( T lymphocyte) count ( 33 +/- 5, 22 +/- 5, 9 +/- 4, and 1 +/- 0 cells per high- power field, respectively, P < 0.001). Conclusions - Leukocyte- targeted MCE can noninvasively assess the degree of rejection in transplanted hearts by directly revealing the magnitude of intramyocardial infiltration of macrophages and T lymphocytes.
  • Antioxidant effect of a new calcium antagonist, azelnidipine, in cultured human arterial endothelial cells, K Shinomiya, K Mizushige, M Fukunaga, H Masugata, K Ohmori, M Kohno, S Senda, JOURNAL OF INTERNATIONAL MEDICAL RESEARCH, 32, (2), 170 - 175,   2004年03月
    Azelnidipine is a novel dihydropyridine-type calcium antagonist with long-acting anti-hypertensive action and a low reported incidence of tachycardia. We aimed to evaluate its antioxidant activity in cultured human arterial endothelial cells under oxidative stress. Endothelial cells were exposed to 1 mM H2O2 and treated with 100 muM alpha-tocopherol, I nM, 10 nM or 100 nM azelnidipine, 100 nM nifedipine or 100 nM amlodipine. After 3 h, the cell number and level of lipid peroxidation were evaluated by measuring the total protein and 8-iso-PGF(2alpha) concentrations, respectively. The total protein concentration was similar with each treatment. Inhibition of 8-iso-PGF(2alpha) was greatest with 10 nM azelnidipine (compared with the other drugs); the difference between 10 nM and 100 nM azelnidipine was not significant. We conclude that azelnidipine has a potent antioxidative effect that could be of significant clinical benefit when combined with its long-lasting anti-hypertensive action and low incidence of tachycardia.
  • Leukocyte-targeted myocardial contrast echocardiography can assess the degree of acute allograft rejection in a rat cardiac transplantation model, Kondo, I, K Ohmori, A Oshita, H Takeuchi, J Yoshida, K Shinomiya, S Fuke, T Suzuki, K Mizushige, M Kohno, CIRCULATION, 109, (8), 1056 - 1061,   2004年03月
    Background - Repetitive endomyocardial biopsies are necessary to monitor the effects of immunosuppressants after cardiac transplantation. Contrast ultrasound with microbubble targeting of leukocytes detects acute leukocyte infiltration. We examined whether leukocyte- targeted myocardial contrast echocardiography ( MCE) could provide for the quantitative assessment of acute cardiac rejection. Methods and Results - Hearts from Brown Norway rats or Lewis rats were transplanted into other Brown Norway rats. Isografts and groups of allografts either untreated or treated with cyclosporin A ( CsA) at a low dose ( 3 mg . kg(-1) . d(-1)) or high dose (10 mg . kg(-1) . d(-1)) from 3 days before transplantation were compared at posttransplantation day 3. Echocardiography- derived left ventricular wall thickening was comparable among the 4 groups. Myocardial blood flow assessed with MCE, relating pulsing intervals with signal intensity ( SI), was slightly decreased only in untreated allografts. However, myocardial SI ( in gray levels) obtained after a 10- minute period allowing microbubble - leukocyte interactions after contrast injection exhibited a clear gradient in these groups ( 12 +/- 2 in untreated allografts, 9 +/- 5 in allografts treated with low- dose CsA, 6 +/- 3 in allografts treated with high- dose CsA, and 2 +/- 1 in isografts, P < 0.001). The pattern of difference in SI among the groups agreed well with that in ED- 1 - positive cell ( macrophage) count ( 25 +/- 7, 12 +/- 4, 5 +/- 3, and 1 +/- 0 cells per high- power field, respectively, P < 0.001), which correlated with CD3- positive cell ( T lymphocyte) count ( 33 +/- 5, 22 +/- 5, 9 +/- 4, and 1 +/- 0 cells per high- power field, respectively, P < 0.001). Conclusions - Leukocyte- targeted MCE can noninvasively assess the degree of rejection in transplanted hearts by directly revealing the magnitude of intramyocardial infiltration of macrophages and T lymphocytes.
  • Antioxidant effect of a new calcium antagonist, azelnidipine, in cultured human arterial endothelial cells, K Shinomiya, K Mizushige, M Fukunaga, H Masugata, K Ohmori, M Kohno, S Senda, JOURNAL OF INTERNATIONAL MEDICAL RESEARCH, 32, (2), 170 - 175,   2004年03月
    Azelnidipine is a novel dihydropyridine-type calcium antagonist with long-acting anti-hypertensive action and a low reported incidence of tachycardia. We aimed to evaluate its antioxidant activity in cultured human arterial endothelial cells under oxidative stress. Endothelial cells were exposed to 1 mM H2O2 and treated with 100 muM alpha-tocopherol, I nM, 10 nM or 100 nM azelnidipine, 100 nM nifedipine or 100 nM amlodipine. After 3 h, the cell number and level of lipid peroxidation were evaluated by measuring the total protein and 8-iso-PGF(2alpha) concentrations, respectively. The total protein concentration was similar with each treatment. Inhibition of 8-iso-PGF(2alpha) was greatest with 10 nM azelnidipine (compared with the other drugs); the difference between 10 nM and 100 nM azelnidipine was not significant. We conclude that azelnidipine has a potent antioxidative effect that could be of significant clinical benefit when combined with its long-lasting anti-hypertensive action and low incidence of tachycardia.
  • Fundamental Lesson 読み方やっぱりこわい感染性心内膜炎, 四宮かおり, 大森浩二, SHINOMIYA,Kaori, OHMORI,Koji, 心エコー, 6, (4), 322-331,   2004年
  • Usefulness of brain natriuretic peptide as a marker for separating cardiac and noncardiac causes of syncope, K Tanimoto, K Yukiiri, K Mizushige, Y Takagi, H Masugata, K Shinomiya, N Hosomi, T Takahashi, K Ohmori, M Kohho, AMERICAN JOURNAL OF CARDIOLOGY, 93, (2), 228 - 230,   2004年01月
    We retrospectively evaluated the feasibility of measuring brain natriuretic peptide to identify cardiac syncope in 148 consecutive patients with syncope. Sixty-one patients with cardiac syncope were identified. A cut-off value of 40 pg/ml was used to determine the cardiac causes of syncope; the sensitivity and specificity for identification. of cardiac syncope were 82% and 92%, respectively. Thus, measurement of brain natriuretic peptide concentrations may help confirm cardiac causes of syncope, and merits consideration for incorporation into the algorithm used to diagnose syncope. (C) 2004 by Excerpta Medica, Inc.
  • Potentiation of C-type natriuretic peptide with ultrasound and microbubbles to prevent neointimal formation after vascular injury in rats, H Takeuchi, K Ohmori, Kondo, I, A Oshita, K Shinomiya, Y Yu, Y Takagi, K Mizushige, K Kangawa, M Kohno, CARDIOVASCULAR RESEARCH, 58, (1), 231 - 238,   2003年04月
    Objectives: Long-term intravenous infusion of high-dose C-type natriuretic peptide (CNP) is known to prevent neointimal formation after vascular injury. Ultrasound (US) irradiation during microbubbles (MBs) infusion (US/MBs) has been used for local delivery of bioactive agents. We examined whether short-term infusion of CNP could also inhibit neointimal development and whether combined US/MBs treatment at the beginning of the CNP infusion could enhance its effect. Methods: In the rat carotid artery-balloon injury model, the intima/media area (I/M) ratio 14 days after injury was compared among various short-term post-injury treatments. For combined US/MBs, a commercial echocardiograph (1.8 MHz, mechanical index 1.0) and albumin-coated octafluoropropane gas MBs were used. Results: Infusion of high-dose CNP (1.0 mug/kg/min) immediately after injury for only 24 h successfully reduced the I/M ratio (0.18+/-0.05) to 18% of the ratio in control rats (1.00+/-0.13) that underwent only balloon injury. Although low-dose CNP (0.1 mug/kg/min for 24 h) alone was not effective in reducing the I/M ratio (0.83+/-0.18), combined US/MBs treatment for the first 80 min of the infusion markedly reduced the I/M ratio (0.17+/-0.07), which persisted until 28 days after injury (0.16+/-0.04). Conclusions: The effects of CNP on the events occurring early after arterial injury may be important in preventing subsequent neointimal development. Thus, intravenous infusion of CNP with US/MBs at its initiation may provide a clinically feasible anti-restenosis therapy applicable immediately after vascular interventions. (C) 2003 European Society of Cardiology. Published by Elsevier Science B.V. All rights reserved.
  • Potentiation of C-type natriuretic peptide with ultrasound and microbubbles to prevent neointimal formation after vascular injury in rats, H Takeuchi, K Ohmori, Kondo, I, A Oshita, K Shinomiya, Y Yu, Y Takagi, K Mizushige, K Kangawa, M Kohno, CARDIOVASCULAR RESEARCH, 58, (1), 231 - 238,   2003年04月
    Objectives: Long-term intravenous infusion of high-dose C-type natriuretic peptide (CNP) is known to prevent neointimal formation after vascular injury. Ultrasound (US) irradiation during microbubbles (MBs) infusion (US/MBs) has been used for local delivery of bioactive agents. We examined whether short-term infusion of CNP could also inhibit neointimal development and whether combined US/MBs treatment at the beginning of the CNP infusion could enhance its effect. Methods: In the rat carotid artery-balloon injury model, the intima/media area (I/M) ratio 14 days after injury was compared among various short-term post-injury treatments. For combined US/MBs, a commercial echocardiograph (1.8 MHz, mechanical index 1.0) and albumin-coated octafluoropropane gas MBs were used. Results: Infusion of high-dose CNP (1.0 mug/kg/min) immediately after injury for only 24 h successfully reduced the I/M ratio (0.18+/-0.05) to 18% of the ratio in control rats (1.00+/-0.13) that underwent only balloon injury. Although low-dose CNP (0.1 mug/kg/min for 24 h) alone was not effective in reducing the I/M ratio (0.83+/-0.18), combined US/MBs treatment for the first 80 min of the infusion markedly reduced the I/M ratio (0.17+/-0.07), which persisted until 28 days after injury (0.16+/-0.04). Conclusions: The effects of CNP on the events occurring early after arterial injury may be important in preventing subsequent neointimal development. Thus, intravenous infusion of CNP with US/MBs at its initiation may provide a clinically feasible anti-restenosis therapy applicable immediately after vascular interventions. (C) 2003 European Society of Cardiology. Published by Elsevier Science B.V. All rights reserved.
  • Hepatocyte growth factorのヒト由来培養内皮細胞の遊走と増殖に及ぼす効果, 岡部 裕介, 四宮 かおり, 津嶋 明子, 大森 浩二, 清元 秀泰, 河野 雅和, 循環器科, 53, (2), 163 - 167,   2003年
  • Inhibition of migration and proliferation of rat vascular smooth muscle cells by a new HMG-CoA reductase inhibitor, Pitavastatin, Masakazu Kohno, Kaori Shinomiya, Satomi Abe, Takahisa Noma, Isao Kondo, Akira Oshita, Hiroto Takeuchi, Yuichiro Takagi, Kazushi Yukiiri, Katsufumi Mizushige, Koji Ohmori, Hypertension Research, 25, (2), 279 - 285,   2002年
    The migration and proliferation of vascular smooth muscle cells (SMCs) are known to play roles in the pathogenesis of atherosclerosis. Therapy with a reductase inhibitor of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA)("statin") produces significant alterations in various SMC functions. The objectives of the present study were to determine whether pitavastatin, a new chemically synthesized and powerful statin, can affect angiotensin II (Ang II)- and platelet-derived growth factor (PDGF)-induced migration and proliferation of cultured rat vascular SMCs. The effect of pitavastatin on cell viability was also examined in these cells. Migration was evaluated by the Boyden's chamber method using microchemotaxis chambers. As expected, Ang II and PDGF BB potently stimulated cell migration in a concentration-dependent manner. Pitavastatin significantly inhibited Ang II (10-6mol/l)-induced migration at the concentrations of 10-8 and 10-7 mol/l. Pitavastatin also inhibited PDGF BB (1 ng/ml)-induced migration at concentrations between 10-9 and 10-8 mol/l in a relatively concentration-dependent manner. This statin modestly but significantly inhibited Ang II (10-6 mol/l)- and PDGF BB (1 ng/ml)-induced DNA synthesis at concentrations between 10-9 and 10-7 mol/l. In addition, pitavastatin clearly inhibited Ang II (10-6 mol/l)- and PDGF BB (1ng/ml)-induced increases of cell number at concentrations between 10-9 and 10-7mol/l. Pitavastatin did not affect lactate dehydrogenase release from these cells at the concentrations used in this experiment. In a trypan blue exclusion test, dead cells stained with trypan blue were not found 24 h after treatment with 10-9, 10-8 or 10-7 mol/l of pitavastatin. These findings suggest that pitavastatin suppresses the migration and proliferation stimulated by Ang II and PDGF BB without affecting cell viability. Pitavastatin may exert an anti-atherogenic effect, in part, through these mechanisms.
  • A role of oxidative stress-generated eicosanoid in the progression of arteriosclerosis in type 2 diabetes mellitus model rats, K Shinomiya, M Fukunaga, H Kiyomoto, K Mizushige, T Tsuji, T Noma, K Ohmori, M Kohno, S Senda, HYPERTENSION RESEARCH, 25, (1), 91 - 98,   2002年01月
    Diabetes mellitus (DM) is a well-established risk factor of cardiovascular diseases. We investigated the mechanism of the progression of arteriosclerosis in DM, focusing on the role of oxidative stress and insulin resistance in vivo. Male Otsuka Long-Evans Tokushima Fatty (OLETF) rats, an experimental model of type 2 DM, were assigned to 3 groups, based on supplementation with vitamin E (VE) or troglitazone (TR), a VE-derived agent which improves insulin-resistance. At 36 weeks, plasma and aortic tissue 8-iso-PGF(2alpha) contents, a vascular proliferating eicosanoid produced in vivo by oxidative stress, were measured by EIA. TGF-beta(1) and TGF-beta(1) receptor II were immunohistochemically analyzed. Histopathologically, medial area and the nuclear number of smooth muscle cells of the aorta were measured. The tissue 8-iso-PGF(2alpha) content (pg/g tissue) was significantly decreased by either VE or TR in the aorta (untreated-OLETF, 15,332 +/- 3,254 vs. TR-treated-OLETF, 7,092 +/- 1,992 or VE-treated-OLETF, 5,394 +/- 836, both p < 0.01), but that in plasma decreased by only VE. VE and TR improved the increased the level of the actual medial area and the number of smooth muscle cells. The expression of TGF-β(1) was reduced, but TGF-β(1) receptor II was not. 8-iso-PGF(2α) may play an important role in the progression of arteriosclerosis. Antioxidant treatment may promise significant clinical benefits in the early diabetic stage.
  • Inhibition of migration and proliferation of rat vascular smooth muscle cells by a new HMG-CoA reductase inhibitor, Pitavastatin, Masakazu Kohno, Kaori Shinomiya, Satomi Abe, Takahisa Noma, Isao Kondo, Akira Oshita, Hiroto Takeuchi, Yuichiro Takagi, Kazushi Yukiiri, Katsufumi Mizushige, Koji Ohmori, Hypertension Research, 25, (2), 279 - 285,   2002年
    The migration and proliferation of vascular smooth muscle cells (SMCs) are known to play roles in the pathogenesis of atherosclerosis. Therapy with a reductase inhibitor of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA)("statin") produces significant alterations in various SMC functions. The objectives of the present study were to determine whether pitavastatin, a new chemically synthesized and powerful statin, can affect angiotensin II (Ang II)- and platelet-derived growth factor (PDGF)-induced migration and proliferation of cultured rat vascular SMCs. The effect of pitavastatin on cell viability was also examined in these cells. Migration was evaluated by the Boyden's chamber method using microchemotaxis chambers. As expected, Ang II and PDGF BB potently stimulated cell migration in a concentration-dependent manner. Pitavastatin significantly inhibited Ang II (10-6mol/l)-induced migration at the concentrations of 10-8 and 10-7 mol/l. Pitavastatin also inhibited PDGF BB (1 ng/ml)-induced migration at concentrations between 10-9 and 10-8 mol/l in a relatively concentration-dependent manner. This statin modestly but significantly inhibited Ang II (10-6 mol/l)- and PDGF BB (1 ng/ml)-induced DNA synthesis at concentrations between 10-9 and 10-7 mol/l. In addition, pitavastatin clearly inhibited Ang II (10-6 mol/l)- and PDGF BB (1ng/ml)-induced increases of cell number at concentrations between 10-9 and 10-7mol/l. Pitavastatin did not affect lactate dehydrogenase release from these cells at the concentrations used in this experiment. In a trypan blue exclusion test, dead cells stained with trypan blue were not found 24 h after treatment with 10-9, 10-8 or 10-7 mol/l of pitavastatin. These findings suggest that pitavastatin suppresses the migration and proliferation stimulated by Ang II and PDGF BB without affecting cell viability. Pitavastatin may exert an anti-atherogenic effect, in part, through these mechanisms.
  • A role of oxidative stress-generated eicosanoid in the progression of arteriosclerosis in type 2 diabetes mellitus model rats, K Shinomiya, M Fukunaga, H Kiyomoto, K Mizushige, T Tsuji, T Noma, K Ohmori, M Kohno, S Senda, HYPERTENSION RESEARCH, 25, (1), 91 - 98,   2002年01月
    Diabetes mellitus (DM) is a well-established risk factor of cardiovascular diseases. We investigated the mechanism of the progression of arteriosclerosis in DM, focusing on the role of oxidative stress and insulin resistance in vivo. Male Otsuka Long-Evans Tokushima Fatty (OLETF) rats, an experimental model of type 2 DM, were assigned to 3 groups, based on supplementation with vitamin E (VE) or troglitazone (TR), a VE-derived agent which improves insulin-resistance. At 36 weeks, plasma and aortic tissue 8-iso-PGF(2alpha) contents, a vascular proliferating eicosanoid produced in vivo by oxidative stress, were measured by EIA. TGF-beta(1) and TGF-beta(1) receptor II were immunohistochemically analyzed. Histopathologically, medial area and the nuclear number of smooth muscle cells of the aorta were measured. The tissue 8-iso-PGF(2alpha) content (pg/g tissue) was significantly decreased by either VE or TR in the aorta (untreated-OLETF, 15,332 +/- 3,254 vs. TR-treated-OLETF, 7,092 +/- 1,992 or VE-treated-OLETF, 5,394 +/- 836, both p < 0.01), but that in plasma decreased by only VE. VE and TR improved the increased the level of the actual medial area and the number of smooth muscle cells. The expression of TGF-β(1) was reduced, but TGF-β(1) receptor II was not. 8-iso-PGF(2α) may play an important role in the progression of arteriosclerosis. Antioxidant treatment may promise significant clinical benefits in the early diabetic stage.
  • Association of plasma adrenomedullin with carotid atherosclerosis in chronic ischemic stroke, K Shinomiya, K Ohmori, H Ohyama, N Hosomi, T Takahashi, K Osaka, M Kohno, PEPTIDES, 22, (11), 1873 - 1880,   2001年11月
    Adrenomedullin is a potent vasodilator peptide exerting anti-atherosclerotic actions in vitro. We investigated the impact of the severity of atherosclerosis on plasma mature-adrenomedullin (m-AM) levels in 38 patients with chronic ischemic stroke. The variables of carotid artery atherosclerosis assessed using ultrasound measurement, blood pressure, and risk factors were related to m-AM levels. Severe atherosclerosis was associated with a further elevation of the increased m-AM level in patients with high systolic blood pressure. Even in patients with fewer risk factors, the presence of severe atherosclerosis was associated with an increased m-AM level. Thus, atherosclerosis elevates m-AM independent of the blood pressure level or presence of risk factors. (C) 2001 Elsevier Science Inc. All rights reserved.
  • Association of plasma adrenomedullin with carotid atherosclerosis in chronic ischemic stroke, K Shinomiya, K Ohmori, H Ohyama, N Hosomi, T Takahashi, K Osaka, M Kohno, PEPTIDES, 22, (11), 1873 - 1880,   2001年11月
    Adrenomedullin is a potent vasodilator peptide exerting anti-atherosclerotic actions in vitro. We investigated the impact of the severity of atherosclerosis on plasma mature-adrenomedullin (m-AM) levels in 38 patients with chronic ischemic stroke. The variables of carotid artery atherosclerosis assessed using ultrasound measurement, blood pressure, and risk factors were related to m-AM levels. Severe atherosclerosis was associated with a further elevation of the increased m-AM level in patients with high systolic blood pressure. Even in patients with fewer risk factors, the presence of severe atherosclerosis was associated with an increased m-AM level. Thus, atherosclerosis elevates m-AM independent of the blood pressure level or presence of risk factors. (C) 2001 Elsevier Science Inc. All rights reserved.
  • Hepatocyte Growth FactorならびにBasic Fibroblast Growth Factorのエンドセリン産生に及ぼす効果 培養ラット平滑筋細胞での検討, 河野 雅和, 大森 浩二, 四宮 かおり, 福井 敏樹, 安倍 里美, 野間 貴久, 近藤 功, 大下 哲, 村上 和司, 難波 経立, 青山 徹, 清元 秀泰, 雪入 一志, 高木 雄一郎, 藤田 憲弘, 舛形 尚, 辻 哲平, 和田 佳宏, 水重 克文, Progress in Medicine, 21, (9), 2249 - 2252,   2001年
  • Treatment of acute myocardial infarction by hepatocyte growth factor gene transfer., Kondo I, Ohmori K, Oshita A, Takeuchi H, Fuke S, Shinomiya K, Noma T, Namba T, Kohno M, J Am Coll Cardiol. 44(3): 644-653, 2004.
  • Treatment of acute myocardial infarction by hepatocyte growth factor gene transfer., Kondo I, Ohmori K, Oshita A, Takeuchi H, Fuke S, Shinomiya K, Noma T, Namba T, Kohno M, J Am Coll Cardiol. 44(3): 644-653, 2004.

書籍等出版物

  • 超音波医学, (社)日本超音波医学会,   2011年
  • 日本内科学会雑誌・(今月の症例)多彩な血管合併症を有した多発性嚢胞腎に対する生体腎移植の1例, 日本内科学会,   2008年
  • 心筋シンチグラフィーと心筋PET, 日本臨床,   2007年
  • 微細気泡の最新技術・マイクロバブル・ナノバブルの生成・特性から食品・農業・環境浄化・医療への応用まで, 株式会社 エヌ・ティー・エス,   2006年

講演・口頭発表等

  • カルチノイド症候群の一例, 日本超音波学会第20回四国地方会,   2010年
  • 心室中隔-大動脈角度が僧帽弁輪速度に及ぼす影響, 第18回日本超音波医学会 四国地方会学術集会,   2008年
  • 心室中隔-大動脈角度が僧帽弁輪速度に及ぼす影響, 第41回 中四国医学検査学会,   2008年
  • Cardiac Expression of Redox-Sensitive Mediators Correlates with Plasma NO Endproducts but not with Cardiac eNOS Content in an NIDDM Model, 第69回日本循環器学会学術集会,   2005年
  • Cardiac Expression of Redox-Sensitive Mediators Correlates with Plasma NO Endproducts but not with Cardiac eNOS Content in an NIDDM Model, 第69回日本循環器学会学術集会,   2005年
  • 心疾患に伴う心原性塞栓の2例., 第23回香川心エコー研究会,   2004年
  • 脳梗塞再発予防としての抗凝固療法に難渋した僧帽弁狭窄症による二次性心房細動による心原性脳塞栓症の一例., 第6回中国四国脳卒中研究会,   2004年
  • ARTERIOGENESIS FOLLOWS ANGIOGENESIS INDUCED BY ULTRASONIC MICROBUBBLE DESTRUCTION IN ISCHEMIC LIMB AND PARALLELS ITS FUNCTIONAL IMPROVEMENT: EVIDENCE FOR THE POSITIVE NET OUTCOME, 第6回国際造影超音波シンポジウム,   2004年
  • Treatment of Ischemic Limbs Based on Local Recruitment of VEGF-producing Inflammatory Cells with Ultrasonic Microbubble Destruction, 4TH INTERNATIONAL SYMPOSIUM ON THERAPEUTIC ULTRASOUND,   2004年
  • Effects of Statins on Progression of Glucose Intolerance and Diastolic Dysfunction in a Model of Type-2 Diabetes Mellitus, 第8回日本心不全学会学術集会,   2004年
  • ARTERIOGENESIS FOLLOWS ANGIOGENESIS INDUCED BY ULTRASONIC MICROBUBBLE DESTRUCTION IN ISCHEMIC LIMB AND PARALLELS ITS FUNCTIONAL IMPROVEMENT: EVIDENCE FOR THE POSITIVE NET OUTCOME, 第6回国際造影超音波シンポジウム,   2004年
  • Treatment of Ischemic Limbs Based on Local Recruitment of VEGF-producing Inflammatory Cells with Ultrasonic Microbubble Destruction, 4TH INTERNATIONAL SYMPOSIUM ON THERAPEUTIC ULTRASOUND,   2004年
  • Effects of Statins on Progression of Glucose Intolerance and Diastolic Dysfunction in a Model of Type-2 Diabetes Mellitus, 第8回日本心不全学会学術集会,   2004年

受賞

  • 日本高血圧と動脈硬化研究会 優秀賞 (2002)
  • 日本高血圧と動脈硬化研究会 優秀賞 (2002)

競争的資金

  • 1. 酸化ストレスと循環器疾患 2 循環ペプチドの抗動脈硬化作用について
  • 1. Oxidative stress and cardiovascular diseases 2. Anti-atherosclerosis effect of cardiovascular peptides