| Project/Area Number |
04670370
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
内科学一般
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| Research Institution | Hokkaido University |
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Principal Investigator |
KOIKE Takao Hokkaido Univ.Dep.Medicine, Professor, 医学部, 教授 (80146795)
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| Co-Investigator(Kenkyū-buntansha) |
SUMITA Takayuki Chiba Univ.Dep.Medicine, Assistant, 医学部, 助手 (00183054)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1993: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1992: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Anticardiolipin antibodies / beta2-glycoprotein I / Thrombosis / SLE / Oxygene atom / β_2ーグリコプロテインI |
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| Research Abstract |
Anticardiolipin antibodies (aCL) are found in sera of patients with systemic lupus erythematosus (SLE) and related connective tissue diseades. The term, antiphospholipid syndrome, has been proposed to explain the association of aCL and variety of clinical features, including arterial and venous thromboembolic events, recurrent fetal loss and thrombocytopenia.
We investigated the role of aCL on the development of thromboembolic manifestations in patients with collagen diseases and obtained the following results.
1) beta2-glycoprotein I (beta2-GPI) is essential for the detection of aCL.
2) beta2-GPI is a glycoprotein, migrates with an apparent molecular mass of 50KD and forms a unique structure termed "Sushi" domains.
3) aCL recognize altered structure of beta2-GPI, but not CL itself.
4) A new EIA system for the detection of aCL without CL has been established.
Besed on these findings, we concluded that aCL recognize beta2-GPI structure altered by interacting with negatively changed phospholipids or an oxygene modified solid-phase surface.
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