| Project/Area Number |
09670840
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | JIKEI UNIVERSITY SCHOOL OF MEDICINE |
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Principal Investigator |
FUJISAWA Kohji JIKEI UNIVERSITY SCHOOL OF MEDICINE,DEPARTMENT OF PADIATRICS,ASSOCIATE PROFESSOR, 医学部, 講師 (10130197)
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| Co-Investigator(Kenkyū-buntansha) |
DEGUCHI Yasushi JIKEI UNIVERSITY SCHOOL OF MEDICINE,DEPARTMENT OF PADIATRICS,ASSISTANT PROFESSOR, 医学部, 助手 (80246420)
IYORI Hideaki JIKEI UNIVERSITY SCHOOL OF MEDICINE,DEPARTMENT OF PADIATRICS,ASSISTANT PROFESSOR, 医学部, 助手 (90213256)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | ITP / autoantibody / TPO / c-mplligand / GPllb / llla / c-mpligand / GPllb / llla / c-mplligand |
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| Research Abstract |
To further identify pathophysiology of idiopathic thrombocytopenic purpura. TPO-depen-dent megakaryocytopoiesis of cord blood mononuclear cells(CBMC) in the exsistence or absence of patients' plasma which contains anti GPllb/llla autoantibody was analyzed under liquid-phase culture system. The degree of megakaryopoiesis was evaluated by quantitating platelet-specific antigen such as GPllb/llla in cultured CBMC subsequently solubilized. Platelet-associated or plasma anti GPllb/llla autoantibody and serum TPO values were also analyzed by established ELISA system. Add of TPO revealed extensive enhancement on platelet specific antigen (GPllb/llla) of CBMC in the presence of 5% serum from normal individuals, whereas marked decrease of GPllb/lllain supematant of solubilized CBMC was noted concomitant with a drop in number of cells morphologically identified as megakaryocytes when cultured in the existence of serum from ITP patients positive with anti GPllb/llla autoantibody. These inhibitory effcts of ITP serum were dependent on the concentration of TPO added. Furthermore, Protein A-affinity-purified lgG fraction of ITP serum showed dose-dependent suppression on the growth and development of CBMC to megakaryocyte and platelet, suggesting that an antibody activity against platelet-specific antigen or TPO=receptor interaction may account for these inhibition on TPO-dependent hematopoiesis. This suppression on megakaryocytopoiesis by patients' lgG was detected independent from antiplatelet autoantibody values or circulating TPO levels in evaluable patients. These data suggest that there may be detectable antibody activity against TPO=receptor interaction such as anti-TPO antibody in selected patients with ITP, which plays some role on the pathogenesis of thrombocytopenia of this disorder.
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