English  |  正體中文  |  简体中文  |  Items with full text/Total items : 54367/62174 (87%)
Visitors : 13685587      Online Users : 51
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTHU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    National Tsing Hua University Institutional Repository > 生命科學院  > 生命科學系 > 期刊論文 >  ACTIVATION OF HUMAN PLATELETS BY THE RABBIT ANTICARDIOLIPIN ANTIBODIES


    Please use this identifier to cite or link to this item: http://nthur.lib.nthu.edu.tw/dspace/handle/987654321/48357


    Title: ACTIVATION OF HUMAN PLATELETS BY THE RABBIT ANTICARDIOLIPIN ANTIBODIES
    Authors: LIN, YL;WANG, CT
    教師: 王成德
    Date: 1992
    Publisher: American Society of Hematology
    Relation: BLOOD,American Society of Hematology,Volume 80,Issue 12,DEC 15 1992,Pages 3135-3143
    Keywords: SYSTEMIC LUPUS-ERYTHEMATOSUS
    ANTI-CARDIOLIPIN ANTIBODIES
    MEMBRANE-PROTEIN
    Abstract: Affinity purified anticardiolipin antibodies (ACLA) raised in rabbits showed cross-reactivities with various negatively charged phospholipids as shown by both the solid phase enzyme-linked immunosorbent assay (ELISA) and inhibition studies. In ELISA, ACLA showed strong cross-reactivity to both sphingomyelin (SM) and phosphatidylethanolamine (PE), but the inhibition studies showed that ACLA failed to bind the aqueous suspensions of SM, PE, and PEIPC (1:l). ACLA bound to resting gel-filtered human platelets (GFP) as shown by both inhibition study and flow cytofluorometric analysis. Western blotting procedure showed that ACLA strongly cross-reacted to an 80-Kd plasma membrane protein. ACLA activated platelet response in a concentration-dependent manner. At less than 10 pg/mL, ACLA induced both platelet shape change to spiculate irregular forms as shown by scanning electron microscopy and the phosphorylation of 20-Kd protein. ACLA at more than 10 bg/mL caused platelet aggregation and secretion. The aggregation was inhibited by EDTA; aspirin; antimycin A plus 2-deoxyglucose; PGE,; and the F(ab‘)z fragment of ACLA. It was not inhibited by monoclonal antibody to Fc receptor (MoAb FcR2). The biochemical events of ACLA-induced platelet response involved the elevation of (1) thromboxane A2 formation, (2) cytosolic free calcium ion concentration ([Ca2+]i), and (3) 47-Kd protein phosphorylation. In addition, the subaggregatory concentration of ACLA showed synergistic platelet activation with that concentration of thrombin, collagen, and epinephrine. The study showed the mechanism involved in ACLA-induced platelet responses.
    URI: http://bloodjournal.hematologylibrary.org/cgi/content/abstract/80/12/3135
    http://www.hematology.org/
    http://nthur.lib.nthu.edu.tw/dspace/handle/987654321/48357
    Appears in Collections:[生命科學系] 期刊論文

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML843View/Open


    在NTHUR中所有的資料項目都受到原著作權保護,僅提供學術研究及教育使用,敬請尊重著作權人之權益。若須利用於商業或營利,請先取得著作權人授權。
    若發現本網站收錄之內容有侵害著作權人權益之情事,請權利人通知本網站管理者(smluo@lib.nthu.edu.tw),管理者將立即採取移除該內容等補救措施。

    SFX Query

    與系統管理員聯絡

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback