H
Hiromitsu Watanabe
Researcher at Hiroshima University
Publications - 160
Citations - 3568
Hiromitsu Watanabe is an academic researcher from Hiroshima University. The author has contributed to research in topics: Intestinal metaplasia & Stomach. The author has an hindex of 28, co-authored 160 publications receiving 3378 citations. Previous affiliations of Hiromitsu Watanabe include University of Wisconsin-Madison.
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Comparative study of the endocrine-disrupting activity of bisphenol A and 19 related compounds.
Shigeyuki Kitamura,Tomoharu Suzuki,Seigo Sanoh,Ryuki Kohta,Norimasa Jinno,Kazumi Sugihara,Shin'ichi Yoshihara,Nariaki Fujimoto,Hiromitsu Watanabe,Shigeru Ohta +9 more
TL;DR: The results suggest that the 4-hydroxyl group of the A- phenyl ring and the B-phenyl ring of BPA derivatives are required for these hormonal activities, and substituents at the 3,5-positions of the phenyl rings and the bridging alkyl moiety markedly influence the activities.
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Inhibitory effects of silk protein, sericin on UVB-induced acute damage and tumor promotion by reducing oxidative stress in the skin of hairless mouse
TL;DR: The results suggest that sericin possesses photoprotective effect against UVB-induced acute damage and tumor promotion by reducing oxidative stress, COX-2 and cell proliferation in mouse skin.
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High fat diet enhances colonic cell proliferation and carcinogenesis in rats by elevating serum leptin.
TL;DR: The results suggest that the enhancement of colon cell proliferation and carcinogenesis by high fat diet is mediated through elevating serum leptin.
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Supplemental Silk Protein, Sericin, Suppresses Colon Tumorigenesis in 1,2-Dimethylhydrazine-Treated Mice by Reducing Oxidative Stress and Cell Proliferation
TL;DR: It is suggested that dietary sericin suppresses the development of colon tumors by reducing oxidative stress, cell proliferation, and nitric oxide production.
Journal Article
Vascular endothelial growth factor inhibits apoptotic death in hematopoietic cells after exposure to chemotherapeutic drugs by inducing MCL1 acting as an antiapoptotic factor.
Osamu Katoh,Toshiaki Takahashi,Tetsuya Oguri,Ken Kuramoto,Keiichiro Mihara,Masao Kobayashi,Shitau Hirata,Hiromitsu Watanabe +7 more
TL;DR: It is shown that VEGF also inhibits apoptotic cell death that is induced by exposure to the chemotherapeutic drugs etoposide and doxorubicin and the expression level of MCL1, a member of the BCL2 family, was increased by V EGF.