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このアイテムへのリンクには次のURLをご利用ください:http://hdl.handle.net/11094/2966
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pdf
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17607_論文
pdf
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論文/Dissertation
論文情報
タイトル
Vascular endothelial dysfunction resulting from L-arginine deficiency in a patient with lysinuric protein intolerance
別タイトル
L-アルギニン欠乏状態における血管内皮機能異常~リジン尿性蛋白不耐症患者における検討
タイトル (ヨミ)
L-アルギニン ケツボウジョウタイ ニオケル ケッカンナイヒ キノウイジョウ~リジン ニョウセイタンパク フタイショウカンジャ ニオケル ケントウ
著者
鎌田, 佳宏
鎌田, 佳宏
著者 (ヨミ)
カマダ, ヨシヒロ
内容
Kamada, Yoshihiro; Nagaretani, Hiroyuki; Tamura, Shinji; Ohama, Tohru; Maruyama, Takao; Hiraoka, Hisatoyo; Yamashita, Shizuya; Yamada, Akira; Kiso, Shinichi; Inui, Yoshiaki; Ito, Nobuyuki; Kayanoki, Yoshiro; Kawata, Sumio; Matsuzawa, Yuji. Vascular endothelial dysfunction resulting from L-arginine deficiency in a patient with lysinuric protein intolerance. Journal of Clinical Investigation. 2001. 108(5). p.717-724.
抄録
Although L-arginine is the only substrate for nitric oxide (NO) production, no studies have yet been reported on the effect of an L-arginine deficiency on vascular function in humans. Lysinuric protein intolerance (LPI) is a rare autosomal recessive defect of dibasic amino acid transport caused by mutations in the SLC7A7 gene, resulting in an L-arginine deficiency. Vascular endothelial function was examined in an LPI patient who was shown to be a compound heterozygote for two mutations in the gene (5.3-kbp Alu-mediated deletion, IVS3+1G→Α). The lumen diameter of the brachial artery was measured in this patient and in healthy controls at rest, during reactive hyperemia (endothelium-dependent vasodilation [EDV]), and after sublingual nitroglycerin administration (endothelium-independent vasodilation [EIV]) using ultrasonography. Both EDV and NOx concentrations were markedly reduced in the patient compared with those for the controls. They became normal after an L-arginine infusion. EIV was not significantly different between the patient and controls. Positron emission tomography of the heart and a treadmill test revealed ischemic changes in the patient, which were improved by the L-arginine infusion. Thus, in the LPI patient, L-arginine deficiency caused vascular endothelial dysfunction via a decrease in NO production.
著者所属研究科
医学系
専攻
生体制御医学
学位名
博士(医学)
学位授与年月日
2003-03-25
学位授与機関
大阪大学
学位授与番号
14401甲第08973号
学位記番号
17607
URL
http://hdl.handle.net/11094/2966
関連情報 (references)
http://www.jci.org/articles/view/11260
言語
英語
カテゴリ
博士論文 本文あり / 医学系研究科 / 2002年度
博士論文 / 医学系研究科 / 2002年度
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博士論文 本文あり
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dcmi資源タイプ
text
DC.title
Vascular endothelial dysfunction resulting from L-arginine deficiency in a patient with lysinuric protein intolerance
DCTERMS.alternative
L-アルギニン欠乏状態における血管内皮機能異常~リジン尿性蛋白不耐症患者における検討
DC.creator
鎌田, 佳宏
DC.language" scheme="DCTERMS.RFC1766
英語
DC.identifier" scheme="DCTERMS.URI
http://hdl.handle.net/11094/2966
DC.description
Kamada, Yoshihiro; Nagaretani, Hiroyuki; Tamura, Shinji; Ohama, Tohru; Maruyama, Takao; Hiraoka, Hisatoyo; Yamashita, Shizuya; Yamada, Akira; Kiso, Shinichi; Inui, Yoshiaki; Ito, Nobuyuki; Kayanoki, Yoshiro; Kawata, Sumio; Matsuzawa, Yuji. Vascular endothelial dysfunction resulting from L-arginine deficiency in a patient with lysinuric protein intolerance. Journal of Clinical Investigation. 2001. 108(5). p.717-724.
DCTERMS.abstract
Although L-arginine is the only substrate for nitric oxide (NO) production, no studies have yet been reported on the effect of an L-arginine deficiency on vascular function in humans. Lysinuric protein intolerance (LPI) is a rare autosomal recessive defect of dibasic amino acid transport caused by mutations in the SLC7A7 gene, resulting in an L-arginine deficiency. Vascular endothelial function was examined in an LPI patient who was shown to be a compound heterozygote for two mutations in the gene (5.3-kbp Alu-mediated deletion, IVS3+1G→Α). The lumen diameter of the brachial artery was measured in this patient and in healthy controls at rest, during reactive hyperemia (endothelium-dependent vasodilation [EDV]), and after sublingual nitroglycerin administration (endothelium-independent vasodilation [EIV]) using ultrasonography. Both EDV and NOx concentrations were markedly reduced in the patient compared with those for the controls. They became normal after an L-arginine infusion. EIV was not significantly different between the patient and controls. Positron emission tomography of the heart and a treadmill test revealed ischemic changes in the patient, which were improved by the L-arginine infusion. Thus, in the LPI patient, L-arginine deficiency caused vascular endothelial dysfunction via a decrease in NO production.
DCTERMS.issued" scheme="DCTERMS.W3CDTF
2003-03-25
citation_title
Vascular endothelial dysfunction resulting from L-arginine deficiency in a patient with lysinuric protein intolerance
citation_author
鎌田, 佳宏
citation_language
英語
citation_public_url
http://hdl.handle.net/11094/2966
citation_date
2003-03-25