『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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EID=130827EID:130827, Map:0, LastModified:2018年3月20日(火) 16:40:26, Operator:[三木 ちひろ], Avail:TRUE, Censor:0, Owner:[赤池 雅史], Read:継承, Write:継承, Delete:継承.
種別 (必須): 学術論文 (審査論文) [継承]
言語 (必須): 英語 [継承]
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著者 (必須): 1. (英) Iuchi Takahiko (日) (読)
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2.赤池 雅史 ([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.社会医学系.医療教育学])
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3.三ツ井 貴夫
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4. (英) Ohshima Yasushi (日) (読)
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5. (英) Shintani Yasumi (日) (読)
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6.東 博之
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7.松本 俊夫
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題名 (必須): (英) Glucocorticoid Excess Induces Superoxide Production in Vascular Endothelial Cells and Elicits Vascular Endothelial Dysfunction  (日)    [継承]
副題 (任意):
要約 (任意): (英) Glucocorticoid (GC) excess often elicits serious adverse effects on the vascular system, such as hypertension and atherosclerosis, and effective prophylaxis for these complications is limited. We sought to reveal the mechanism underlying GC-induced vascular complications. Responses in forearm blood flow to reactive hyperemia in 20 GC-treated patients were significantly decreased to 43+/-8.9% (mean+/-SEM) from the values obtained before GC therapy (130+/-14%). An administration of vitamin C almost normalized blood flow responses. In human umbilical vein endothelial cells (HUVECs), production of hydrogen peroxide was increased up to 166.5+/-3.3% of control values by 10(-7) mol/L dexamethasone (DEX) treatment (P<0.01). Concomitant with DEX-induced hydrogen peroxide production, intracellular amounts of peroxynitrite significantly increased and those of nitric oxide (NO) decreased, respectively (P<0.01). Immunoblotting analysis using anti-nitrotyrosine antibody showed that peroxynitrite formation was increased in DEX-treated HUVECs. Using inhibitors against metabolic pathways for generation of reactive oxygen species (ROS), we identified that the major production sources of ROS by DEX treatment were mitochondrial electron transport chain, NAD(P)H oxidase, and xanthine oxidase. These findings suggest that GC excess causes overproduction of ROS and thereby perturbs NO availability in the vascular endothelium, leading to vascular complications in patients with GC excess.  (日)    [継承]
キーワード (推奨): 1. (英) Glucocorticoid (日) (読) [継承]
2. (英) reactive oxygen species (日) (読) [継承]
3. (英) nitric oxide (日) (読) [継承]
4. (英) vascular endothelial function (日) (読) [継承]
発行所 (推奨): American Heart Association [継承]
誌名 (必須): Circulation Research ([American Heart Association])
(pISSN: 0009-7330, eISSN: 1524-4571)

ISSN (任意): 0009-7330
ISSN: 0009-7330 (pISSN: 0009-7330, eISSN: 1524-4571)
Title: Circulation research
Title(ISO): Circ. Res.
Publisher: American Heart Association
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
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年月日 (必須): 西暦 2003年 1月 10日 (平成 15年 1月 10日) [継承]
URL (任意): http://circres.ahajournals.org/cgi/content/abstract/92/1/81 [継承]
DOI (任意): 10.1161/01.RES.0000050588.35034.3C    (→Scopusで検索) [継承]
PMID (任意): 12522124    (→Scopusで検索) [継承]
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WOS (任意): 000180367200015 [継承]
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備考 (任意): 1.(英) Article.Affiliation: Department of Medicine and Bioregulatory Sciences, University of Tokushima Graduate School of Medicine, Tokushima, Japan.  (日)    [継承]
2.(英) Article.PublicationTypeList.PublicationType: Clinical Trial  (日)    [継承]
3.(英) Article.PublicationTypeList.PublicationType: Journal Article  (日)    [継承]
4.(英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't  (日)    [継承]

標準的な表示

和文冊子 ● Takahiko Iuchi, Masashi Akaike, Takao Mitsui, Yasushi Ohshima, Yasumi Shintani, Hiroyuki Azuma and Toshio Matsumoto : Glucocorticoid Excess Induces Superoxide Production in Vascular Endothelial Cells and Elicits Vascular Endothelial Dysfunction, Circulation Research, Vol.92, No.1, 81-87, 2003.
欧文冊子 ● Takahiko Iuchi, Masashi Akaike, Takao Mitsui, Yasushi Ohshima, Yasumi Shintani, Hiroyuki Azuma and Toshio Matsumoto : Glucocorticoid Excess Induces Superoxide Production in Vascular Endothelial Cells and Elicits Vascular Endothelial Dysfunction, Circulation Research, Vol.92, No.1, 81-87, 2003.

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