Zobrazeno 1 - 10
of 15
pro vyhledávání: '"Tomoko Kanome"'
Autor:
Seiji Shioda, Akira Miyazaki, Tomoko Kanome, Haruaki Kageyama, Shigeko Arita, Takuya Watanabe, Shigeki Hongo
Publikováno v:
American Journal of Physiology-Endocrinology and Metabolism. 297:E474-E482
Leptin is an adipose tissue-derived hormone implicated in atherosclerosis and macrophage foam cell formation. The current study was conducted to examine the effect of leptin on cholesteryl ester accumulation in human monocytes/macrophages. Exogenousl
Autor:
Takuya Watanabe, Tetsuo Sakai, Shinji Koba, Tomoko Kanome, Kae Nishio, Kiyoshi Nose, Akira Miyazaki, Shigeki Hongo, Masayoshi Shichiri, Hidekazu Ota, Kengo Sato, Takashi Katagiri, Youichi Kobayashi, Taka-aki Matsuyama
Publikováno v:
Circulation. 117:638-648
Background— Human salusins, related bioactive polypeptides with mitogenic effects on vascular smooth muscle cells and fibroblasts and roles in hemodynamic homeostasis, may be involved in the origin of coronary atherosclerosis. Macrophage foam cell
Publikováno v:
Hypertension Research. 31:1801-1810
Angiotensin II (Ang II) is known to accelerate the progression of macrophage-driven atherosclerotic lesions. Acyl-CoA:cholesterol acyltransferase-1 (ACAT1) converts intracellular free cholesterol into cholesterol ester (CE) for storage in lipid dropl
Publikováno v:
Current Hypertension Reviews. 2:237-246
Human urotensin II (U-II), the most potent vasoconstrictor peptide identified to date, and its receptor (UT) are involved in etiology of hypertension. In hypertensive patients, U-II induces vasoconstriction in forearm brachial artery infusion studies
Autor:
Takuya Watanabe, Akira Miyazaki, Tomoko Kanome, Syuusuke Kodate, Mitsuru Adachi, Tsutomu Hirano, Toshiaki Suguro
Publikováno v:
Atherosclerosis. 186:275-281
Acyl-coenzyme A:cholesterol acyltransferase-1 (ACAT-1) converts intracellular free cholesterol into cholesterol ester for storage in lipid droplets and plays an important role in the formation of macrophage-derived foam cells in atherosclerotic lesio
Publikováno v:
Vascular Disease Prevention. 3:91-98
Autor:
Tomoko Kanome, Shinji Koba, Akira Miyazaki, Claude R. Benedict, Takashi Katagiri, Rajbabu Pakara, Shigeki Hongo, Takuya Watanabe, Keiko Takahashi
Publikováno v:
Hypertension Research. 29:821-831
Human urotensin-II (U-II) is the most potent vasoactive peptide identified to date, and may be involved in hypertension and atherosclerosis. We investigated the effects of the interactions between U-II or other vasoactive agents and mildly oxidized l
Autor:
Syuusuke Kodate, Toshiaki Suguro, Tamio Hagiwara, Akira Miyazaki, Tomoko Kanome, Shigeki Hongo, Mitsuru Adachi, Yu-Ichiro Sakamoto, Takuya Watanabe, Tsutomu Hirano
Publikováno v:
Hypertension. 46:738-744
Human urotensin II (U-II), the most potent vasoconstrictor peptide identified to date, and its receptor (UT) are involved in hypertension and atherosclerosis. Acyl-coenzyme A:cholesterol acyltransferase-1 (ACAT-1) converts intracellular free choleste
Autor:
Sojiro, Kusumoto, Tomohide, Sugiyama, Koichi, Ando, Takamichi, Hosaka, Hiroo, Ishida, Takao, Shirai, Toshimitsu, Yamaoka, Kentaro, Okuda, Takashi, Hirose, Tsukasa, Ohnishi, Fumiko, Inoue, Tomoko, Kanome, Tsuyoki, Kadofuku, Nagahiro, Saijo, Mitsuru, Adachii, Tohru, Ohmori
Publikováno v:
Anticancer research. 29(6)
Tumor cells that have acquired resistance to gefitinib may complicate the future treatment of patients with non-small cell lung cancer (NSCLC). To investigate the mechanisms of acquired resistance, an acquired gefitinib-resistant cell line, PC-9/ZD20
Publikováno v:
New Trends in the Molecular and Biological Basis for Clinical Oncology ISBN: 9784431886624
Non-small cell lung cancer cells expressed mutant EGFR are more sensitive to gefitinib (Iressa) than that expressed wild type EGFR. To elucidate the mechanism of the hypersensitivity to gefitinib in the mutant EGFR, we explored the difference of EGFR
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::81cd1468230d0c09f8838ef0cd6c1cd6
https://doi.org/10.1007/978-4-431-88663-1_14
https://doi.org/10.1007/978-4-431-88663-1_14