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  1. 0 資料タイプ別
  2. 03 紀要論文
  1. 250 大学院医歯学総合研究科(医)
  2. 20 紀要
  3. 02 新潟医学会雑誌
  4. 第113巻第11・12号

^<123>I-BMIPPの心臓への集積欠損を呈する心疾患症例におけるCD36遺伝子の解析

http://hdl.handle.net/10191/46953
http://hdl.handle.net/10191/46953
f4c12787-c407-45c2-ac10-54c4a2967224
名前 / ファイル ライセンス アクション
113(11-12)_526-536.pdf 113(11-12)_526-536.pdf (2.4 MB)
Item type 紀要論文 / Departmental Bulletin Paper(1)
公開日 2017-03-03
タイトル
タイトル ^<123>I-BMIPPの心臓への集積欠損を呈する心疾患症例におけるCD36遺伝子の解析
タイトル
言語 en
タイトル ^<123>I-BMIPPの心臓への集積欠損を呈する心疾患症例におけるCD36遺伝子の解析
言語
言語 jpn
キーワード
主題Scheme Other
主題 ^<123>I-BMIPP myocardial scintigraphy
キーワード
主題Scheme Other
主題 CD36
キーワード
主題Scheme Other
主題 hypertrophic cardiomyopathy
キーワード
主題Scheme Other
主題 gene abnormality
キーワード
主題Scheme Other
主題 ^<123>I-BMIPP心筋シンチグラフィー
キーワード
主題Scheme Other
主題 肥大型心筋症
キーワード
主題Scheme Other
主題 遺伝子異常
資源タイプ
資源 http://purl.org/coar/resource_type/c_6501
タイプ departmental bulletin paper
その他のタイトル
その他のタイトル Analysis of Molecular Defects of the CD36 Gene in Patients Showing a Loss of Accumulation of ^<123>I-BMIPP in Hearts.
著者 小川, 祐輔

× 小川, 祐輔

WEKO 176646

小川, 祐輔

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著者別名
識別子 176647
識別子Scheme WEKO
姓名 Ogawa, Yusuke
抄録
内容記述タイプ Abstract
内容記述 Recently, ^<123>I-β-methyl-iodophenyl pentadecanoic acid (BMIPP) has been used in myocardial scintigraphy to evaluate fatty acid metabolism and myocardial viability. Some investigators reported absence of BMIPP-accumulation in the hearts of few patients with heart diseases. The mechanism and clinical significance of absence of BMIPP-accumulation in heart are not known. CD36, glycoprotein IV expressed in platelet membrane, is a receptor for collagen, thrombospondin, oxidised LDL and long-chain fatty acids. CD36 may play a role in platelet aggregation as well as in formation and progression of arteriosclerosis, and in myocardial fatty acid metabolism. The expression and genetic abnormality of CD36 were investigated in this study in relation to myocardial accumulation of BMIPP. There are two types of platelet CD36 deficiency; types I and II , associated with the absence and presence of CD36 on monocytes, respectively. In 200 patients with various heart diseases in this study, 24 cases revealed CD36 deficiency including 8 type I and 16 type II. No myocardial BMIPP-accumulations were observed in all 8 type I cases, while significant accumulation was seen in all type II cases. Genetic analysis of CD36 was carried in 3 of 8 cases with type I deficiency. Deletions of 52 base inn exon 4 and 70 base in exon 9 were documented in mRNA of CD36 in all 3 cases by means of sequence analysis after RT-PCR. Genomic DNA of CD36 was also analyzed by using a PCR-direct sequence method, and there were two types of point mutation, namely, ^<970>T→C/Ile-Thr (one of 3 cases) and ^<478>C→T/Pro→Ser (other 2 cases). The point mutation at ^<478>T was previously reported by other researchers. This is the first report to show the alternative splicing in exons 4 and 9 and the point mutation at ^<970> C. CD36 deficiency may contribute the pathogenesis of heart diseases and arteriosclerosis through abnormal fatty acid metabolism.
書誌情報 新潟医学会雑誌
en : 新潟医学会雑誌

巻 113, 号 11-12, p. 526-536, 発行日 1999-12
出版者
出版者 新潟医学会
ISSN
収録物識別子タイプ ISSN
収録物識別子 00290440
書誌レコードID
収録物識別子タイプ NCID
収録物識別子 AN00182415
著者版フラグ
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