コンテンツメニュー

Yoshimura Koichi

Affiliate Master Yamaguchi University

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山口医学 Volume 39 Issue 2 pp. 229 - 233
published_at 1990-04
Creators : Fujioka Kentarou Nakamura Takashi Yoshimura Kouichi Takenaka Hiroaki Ohara Masaki Zempo Nobuya Esato Kensuke Publishers : 山口大学医学会
山口医学 Volume 53 Issue 6 pp. 303 - 310
published_at 2004-12-31
Creators : Dairaku Koji Furutani Akira Nomura Shinji Ito Hiroshi Mikamo Akihito Akiyama Norio Yoshimura Kouichi Tsuruta Ryosuke Kasaoka Shunji Okabayashi Kiyoshi Publishers : 山口大学医学会
山口医学 Volume 42 Issue 3 pp. 225 - 230
published_at 1993-06
Creators : Kouchi Yasuhiro Furutani Akira Akiyama Norio Yoshimura Kohichi Seyama Atsushi Akimoto Fumikazu Fujioka Kentarou Esato Kensuke Publishers : 山口大学医学会
山口医学 Volume 46 Issue 4 pp. 237 - 244
published_at 1997-08
Creators : Dairaku Koji Morikage Noriyasu Toyota Shuji Yoshimura Koichi Kuga Takayuki Fujioka Kentaro Kato Tomoe Fujimura Yoshihiko Zempo Nobuya Esato Kensuke Publishers : 山口大学医学会
Atherosclerosis Volume 217 Issue 2 pp. 350 - 357
published_at 2011-08
Creators : Kaneko Hidehiro Anzai Toshihisa Morisawa Maho Kohno Takashi Nagai Toshiyuki Anzai Atsushi Takahashi Toshiyuki Shimoda Masayuki Sasaki Aya Maekawa Yuichiro Yoshimura Koichi Aoki Hiroki Tsubota Kazuo Yoshikawa Tsutomu Okada Yasunori Ogawa Satoshi Fukuda Keiichi Publishers : Elsevier | Elsevier Science Ireland
Cardiovascular research Volume 89 Issue 1 pp. 79 - 88
published_at 2011-01-01
Creators : Aoyama Hidekazu Ikeda Yasuhiro Miyazaki Yosuke Yoshimura Koichi Nishino Shizuka Yamamoto Takeshi Yano Masafumi Inui Makoto Aoki Hiroki Matsuzaki Masunori Publishers : British Medical Association | Elsevier Science
Cardiovascular Research Volume 91 Issue 2 pp. 358 - 367
published_at 2011-07-15
Creators : Kaneko Hidehiro Anzai Toshihisa Takahashi Toshiyuki Kohno Takashi Shimoda Masayuki Sasaki Aya Shimizu Hideyuki Nagai Toshiyuki Maekawa Yuichiro Yoshimura Koichi Aoki Hiroki Yoshikawa Tsutomu Okada Yasunori Yozu Ryohei Ogawa Satoshi Fukuda Keiichi Publishers : British Medical Association | Elsevier Science
Arteriosclerosis, thrombosis, and vascular biology Volume 32 Issue 6 pp. 1410 - 1417
published_at 2012-06
Creators : Tsuruda Toshihiro Hatakeyama Kinta Nagamachi Shigeki Sekita Yoko Sakamoto Sumiharu Endo George J. Nishimura Masanori Matsuyama Masakazu Yoshimura Koichi Sato Yuko Onitsuka Toshio Imamura Takuroh Asada Yujiro Kitamura Kazuo Publishers : American Heart Association
International Journal of Vascular Medicine Volume 2012 pp. 648167 -
published_at 2012-08-21
Creators : Yoshimura Koichi Aoki Hiroki Publishers : Hindawi Publishing Corporation
Atherosclerosis Volume 218 Issue 2 pp. 285 - 286
published_at 2011-10
Creators : Yoshimura Koichi Ikeda Yasuhiro Aoki Hiroki Publishers : Elsevier | Elsevier Science Ireland
日本外科学会雑誌 Volume 113 Issue 臨時増刊号2 pp. 338 - 338
published_at 2012-03-05
Creators : 長澤 綾子 吉村 耕一 鈴木 亮 藏澄 宏之 池永 茂 美甘 章仁 濱野 公一 Publishers : 日本外科学会
PLoS ONE Volume 8 Issue 11 pp. e79753 -
published_at 2013
Creators : Yamashita Osamu Yoshimura Koichi Nagasawa Ayako Ueda Koshiro Morikage Noriyasu Ikeda Yasuhiro Hamano Kimikazu Publishers : Public Library of Science
Background: Angiotensin II (AngII) increases reactive oxygen species (ROS) and induces glomerular sclerosis. Toll-like receptor 4 (TLR4)-mediated inflammation enhances the renal impairment in renal inflammatory diseases. The relationship between TLR4 and AngII-induced glomerular sclerosis is unknown.Methods: Mice lacking TLR4 function (Tlr4^{lps-d}) and wild-type (WT) mice were randomized into groups treated with AngII, norepinephrine (NE) or a sub-depressor dose of the AngII receptor blocker irbesartan along with AngII for 2 weeks. We then assessed the expressions of NADPH oxidase and monocyte chemoattractant protein-1 (MCP-1) and the inflammatory cell recruitment in the glomeruli. We also evaluated the mesangial matrix proliferation and ROS.Results: AngII and NE equally increased the systolic blood pressure compared to the control mice (p<0.05). In the WT mice treated with AngII, we observed glomerular sclerosis, an increase in NADPH oxidase, MCP-1 and the infiltration of macrophages as well as ROS content in the glomeruli compared to the control mice (p<0.05), whereas the Tlr4^{lps-d} mice showed little effects of AngII on these indices. In addition, the sub-depressor-dose irbesartan treatment reversed these changes. NE had little effects on these indices. Conclusions: TLR4 plays an important role in AngII-induced oxidative stress, inflammation and glomerular sclerosis through the AT1 receptor.
Creators : Okamoto Tadashi Umemoto Seiji Yoshimura Koichi Sakumura Toshihiro Murata Tomoaki Fukai Tohru Yano Masafumi Matsuzaki Masanori Publishers : Yamaguchi University School of Medicine
Aberrant increases in protein phosphatase 1(PP1) activity have been shown to be associated with inefficient sarcoplasmic reticulum Ca^{2+} cycling, leading to cardiac dysfunction in the failing heart. In the present study, we investigated whether BNP promoter-inducible suppression of PP1β would ameliorate progression of pressure overload-induced heart failure in mice, a clinically relevant animal model. An Adeno-associated virus 9 (AAV9) vector encoding PP1βshRNA and a negative control (NC) shRNA driven by a brain natriuretic peptide (BNP) promoter with an emerald green fluorescent protein expression (EmGFP) cassette were used to test the hypothesis. AAV9 vectors (AAV9-BNP-EmGFP-PP1βshRNA and AAV9-BNP-EmGFP-NCshRNA) were introduced into the in vivo heart via the tail vein injection (4x10^{11} GC/mice) in 8-week-old C57BL6J mice, followed by transverse aortic constriction (TAC) 2 weeks after the AAV9 vector injection. Post TAC cardiac function was sequentially assessed every 2 week by echocardiography, followed by hemodynamic assessment at 1 month. AAV9-BNP-EmGFP-PP1βshRNA treatment suppressed myocardial PP1β expression by 15% compared with the NCshRNA group (p<0.001). The fractional shortening (%FS) of the left ventricle in the PP1βshRNA-treated group was significantly larger than the NCshRNA-treated group (21%±1.0% vs. 15%±0.01, p<0.01). The ratios of heart weight (HW) / body weight (BW) and lung weight (LW) / BW in the PP1βshRNA group were significantly smaller than those of the NCshRNA group (HW/BW: 9.20±0.49 vs. 10.6±0.45 mg/g
Creators : Shiraishi Kozo Ikeda Yasuhiro Miyazaki Yosuke Fujimoto Shizuka N. Yoshimura Koichi Miura Toshiro Matsuzaki Masanori Yano Masafumi Publishers : Yamaguchi University School of Medicine