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2002 Fiscal Year Final Research Report Summary

The etiological role of enterovirus infection in dilated cardiomyopathy patients -the study about degeneration of dystrophin dilated cardiomyopathy-

Research Project

Project/Area Number 13670758
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Circulatory organs internal medicine
Research InstitutionOsaka Medical College

Principal Investigator

UKIMURA Akira  Osaka Medical College Faculty of Medicine Research Associate, 医学部, 助手 (50257862)

Co-Investigator(Kenkyū-buntansha) KITAURA Yasushi  Osaka Medical College Faculty of Medicine Professor, 医学部, 教授 (50084950)
DEGUCHI Hirofumi  Osaka Medical College Faculty of Medicine Assistant Professor, 医学部, 助教授 (90131341)
Project Period (FY) 2001 – 2002
KeywordsDilated vardiomyopathy / dystropin / enterovirus / protease 2A / cytokine
Research Abstract

Enteroviruses have been implicated in the pathogenesis of idiopathic dilated cardiomyopathy, however the mechanisms of this pathology is unknown. It is reported that coxsackievirus protease 2A cleaves dystrophin. There is increasing evidence that inflammatory cytokines play an important role in the development of heart failure. To evaluate the pathological role of coxsackievirus in DCM, we analyzed the degeration of dystrophin by western blot of dystrophin, and the relative quantity of cytokine mRNA expression in hearts from DCM patients by quantitative PCR. We used heart tissues resected from DCM patients at the time of elective partial ventriculectomy (PLV). We tried to amplify the full-length enterovirus gebome from the hearts of DCM patients to analyze the mutation of enterovirus genome.
it was not clear whether enterovirus in hearts of DCM patients cleaves dystropin by western blot analysis. We succeeded 31 end-long-length PCR(4kb) of enterovirus cDNA which codes protease 2A from the heart of a DCM patient. The number of IL-10-positive DCM cases was significantly smaller than normal controls (p=0.0036). One (10%) of ten DCM patients with IL-10 mRNA expression died after PLV, and ten (45%) of twenty-two DCM patients without IL-10 mRNA expression died. We suggest that patients with heart failure deteriorate in DCM cases without IL-10 mRNA expression in the myocardium.

  • Research Products

    (7 results)

All Other

All Publications (7 results)

  • [Publications] Ukimura A, Terasaki F, Deguchi H, Kitaura Y et al.: "Quantitative analysis of cytokine mRNA expression in hearts from patients with non-ischemic dilated cardiomyopathy (DCM)"J Card Surg.. 18(in press). (2003)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] 浮村 聡, 出口寛文, 北浦 泰 他: "拡張型心筋症患者心筋からのエンテロウイルスゲノム全長の検索"厚生労働省特定疾患特発性心筋症調査研究班 平成14年度報告集 班長 北畠. (印刷中). (2003)

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      「研究成果報告書概要(和文)」より
  • [Publications] 浮村 聡, 北浦 泰: "エクセルナース[感染症編]内科系病棟-循環器科"メデイカルレビュー社. 15 (2002)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Ukimura A, Terasaki F, Fujioka S, Deguchi H, Kitaura Y, Isomura T, and Suma H: "Quantitative analysis of cytokine mRNA expression in hearts from patients with non-ischemic dilated cardiomyopathy (DCM)"J Card Surg. in press. (2003)

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      「研究成果報告書概要(欧文)」より
  • [Publications] Ukimura A, Terasaki F, Fujioka S, Deguchi H, Kitaura Y, Isomura T, and Suma H: "The quantitative analysis of cytokine mRNA expression in the myocardium of non-ischemic dilated cardiomyopathy (DCM)"Circ J. vol. 67 sup. 262 (2003)

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      「研究成果報告書概要(欧文)」より
  • [Publications] Terasaki F, Ukimura A, Shimomura H, Toukou H, Kanzaki Y, Okabe M, Fujioka S, Kitaura Y, Horii T, T Isomura T, H Suma: "Enhanced expression of helper Tcell type 1 cytokines in myocardium from patients with active sarcoidosis"Circ J. vol. 66 sup. 602 (2002)

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      「研究成果報告書概要(欧文)」より
  • [Publications] Terasaki F, Shimomura H, Toukou H, Kanzaki Y, Fujioka S, Ukimura A, Kitaura Y, Horii T, T Isomura T, H Suma: "Soluble nterleukin-2 Receptor and Th2 Cytokines Are Sensitive Markers of Disease Activity in Cardiac Sarcoidosis"Circ J. vol. 66 sup. 33 (2002)

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      「研究成果報告書概要(欧文)」より

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Published: 2004-04-14  

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