| Project/Area Number |
15K09664
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Nara Medical University |
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Principal Investigator |
Yada Koji 奈良県立医科大学, 医学部, 助教 (30635785)
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| Co-Investigator(Kenkyū-buntansha) |
野上 恵嗣 奈良県立医科大学, 医学部, 准教授 (50326328)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | インヒビター / 血友病 / 第VIII因子 / 活性化・不活性化 / 活性化第VII因子 / 第X因子 |
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| Outline of Final Research Achievements |
Development of an anti-factor(F) VIII allo-antibody (inhibitor), making hemostatic effect unstable during FVIII replacement therapy, is one of the serious events for hemophilia A patients. Bypassing agents such as rFVIIa, APCC and pdFVIIa/FX are generally considered to facilitate the hemostatic effect by enhancing the extrinsic coagulation pathway not by the intrinsic one. We have recently reported that FVIIa, an extrinsic factor included in the bypassing agents, could contribute to the hemostatic enhancement by activating FVIII with tissue factor in the early phase of coagulation. In this study, we have confirmed the crosstalk between FVIIa/TF and FVIII under the near physiological condition in the whole blood. We further investigated the function of self-FVIII in the mild hemophilia A with inhibitor, and confirmed that the change in binding to each component of FXase complex caused the variety of hemostatic function.
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