Zobrazeno 1 - 10
of 14
pro vyhledávání: '"Seiji Matsuhisa"'
Autor:
Yukiko Kuga, Yasunori Nishida, Seiji Matsuhisa, Hideshi Ishii, Yusuke Nishida, Kazuya Ueda, Hiroshi Ueda, Kojiro Yoshimura, Naohiro Yoshida, Motoyoshi Maenaka
Publikováno v:
Journal of the American College of Cardiology. 75:1454
Autor:
Koichiro Asawa, Mitsuru Tsujimoto, Hiroshi Ueda, Atsumichi Kido, Yukiko Kuga, Seiji Matsuhisa, Naohiro Yoshida, Yasunori Nishida, Kazuya Ueda, Shoichi Shinohara, Yasushi Sasaki, Masaki Yamasaki
Publikováno v:
American heart journal. 173
Background Patients with established coronary artery disease are at increased risk for future ischemic events and require secondary prevention for systemic vascular disease. We performed a randomized clinical trial to evaluate the impact of cilostazo
Autor:
Toshiji Iwasaka, Hajime Otani, Reiji Hattori, Hiroji Imamura, Hiroshi Kamihata, Shiori Kyoi, Yuzo Akita, Seiji Matsuhisa, Ayako Hamano, Hiroyoshi Fujiwara
Publikováno v:
Cardiovascular Research. 70:354-363
Objective Dystrophin is a sarcolemmal membrane protein that prevents the myocyte from oncosis induced by physical stress. Because ischemic preconditioning (IPC) protects mitochondria and prevents oncosis during reperfusion, we hypothesized that dystr
Autor:
Koichi Yamada, Hisako Tsuji, Koji Kurimoto, Satoshi Tokunaga, Norihito Inami, Seiji Matsuhisa, Hirofumi Maeba, Toshiji Iwasaka
Publikováno v:
International Journal of Cardiology. 108:309-313
Background After a myocardial infarction, a higher prevalence of coronary vasospastic response has been reported in the Japanese population than in the Caucasian population. Beta-blockers may exacerbate coronary vasospasm. However, beta-blockers are
Autor:
Kimiko Tatsumi, Toshiji Iwasaka, Hiroshi Kamihata, Seiji Matsuhisa, Shiori Kyoi, Hiroyoshi Fujiwara, Yuzo Akita, Hiroji Imamura, Hajime Otani, Chiharu Enoki
Publikováno v:
Cardiovascular Research. 69:888-898
Objective: p38 MAP kinase (p38 MAPK) and c-Jun NH2-terminal kinase (JNK) have been implicated in the pathophysiology of heart failure. We investigated the effects of chronic treatment with p38 MAPK and JNK inhibitors on the development of heart failu
Autor:
Yukiko Kuga, Yasushi Sasaki, Kenji Natsuyama, Hiroshi Ueda, Atsumichi Kido, Kazuya Ueda, Koichiro Asawa, Kojiro Yoshimura, Naohiro Yoshida, Yasunori Nishida, Kazushige Yamaguchi, Seiji Matsuhisa, Masahiro Yamasaki
Publikováno v:
Journal of the American College of Cardiology. 61(10)
Autor:
Akira Moriguchi, Koji Yamashita, Toshiji Iwasaka, Yuzo Akita, Toru Okazaki, Seiji Matsuhisa, Hajime Otani, Daisuke Sato
Publikováno v:
Antioxidantsredox signaling. 10(12)
Oxidative stress mediated by activation of angiotensin II type-1 receptor (AT(1)R) plays a crucial role in the progression of heart failure. We investigated the effect of N-acetylcysteine (NAC) and an AT(1)R blocker on oxidative stress and left ventr
Autor:
Toru Okazaki, Koji Yamashita, Yuzo Akita, Akira Moriguchi, Hiroji Imamura, Seiji Matsuhisa, Daisuke Sato, Toshiji Iwasaka, Hajime Otani
Publikováno v:
American journal of physiology. Heart and circulatory physiology. 294(6)
Oxidative stress is involved in the tolerance to ischemia-reperfusion (I/R) injury. Because angiotensin II type 1 receptor blockers (ARBs) inhibit oxidative stress, there is concern that ARBs abolish the tolerance to I/R injury. Dahl salt-sensitive (
Autor:
Reiji Hattori, Shiori Kyoi, Yutaka Kimura, Toshiji Iwasaka, Chiharu Enoki, Hiroshi Kamihata, Seiji Matsuhisa, Hiroji Imamura, Hajime Otani, Yuzo Akita
Publikováno v:
American journal of physiology. Heart and circulatory physiology. 292(5)
We investigated the mechanism of exercise-induced late cardioprotection against ischemia-reperfusion (I/R) injury. C57BL/6 mice received treadmill exercise (60 min/day) for 7 days at a work rate of 60–70% maximal oxygen uptake. Exercise transiently
Autor:
Hiroshi Kamihata, Shiori Kyoi, Yuzo Akita, Seiji Matsuhisa, Hiroji Imamura, Kimiko Tatsumi, Chiharu Enoki, Reiji Hattori, Toshiji Iwasaka, Hajime Otani
Publikováno v:
Antioxidantsredox signaling. 8(7-8)
We investigated the role of oxidative/nitrosative stress in the tolerance to ischemia/reperfusion (I/R) injury in BIO14.6 cardiomyopathy hamster hearts at 6 weeks of age. These hearts showed no significant morphologic change and left ventricular (LV)