Author
Heddy Zola
Other affiliations: University of Sydney
Bio: Heddy Zola is an academic researcher from Flinders Medical Centre. The author has contributed to research in topics: Glycoprotein Ib & Glycoprotein IX. The author has an hindex of 2, co-authored 2 publications receiving 256 citations. Previous affiliations of Heddy Zola include University of Sydney.
Papers
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TL;DR: The combined results suggest that the apparent genetic absence of multiple proteins in Bernard-Soulier platelets is due, in part, to the presence in normal platelets of a tight membrane complex between glycoprotein Ib and at least one of the other absent glycoproteins.
172 citations
TL;DR: The combined evidence is consistent with quinine/quinidine-dependent antibody-platelet interaction occurring by way of a FVIII/vWF- independent, Fc receptor-independent mechanism that probably involves binding of antibody to glycop Protein Ib or the beta-subunit of glycoprotein Ib or both.
87 citations
Cited by
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TL;DR: A new assay is described that takes advantage of monoclonal antibodies against major platelet membrane constituents (glycoproteins IIb/IIIa and Ib and HLA class I molecule) to investigate selectively platelet reactive antibodies against epitopes on different glycoprotein.
870 citations
TL;DR: In 1948, Bernard and SOULIER described a young male patient with a severe bleeding disorder that was characterized by a prolonged bleeding time, thrombocytopenia, and extremely large platelets.
493 citations
TL;DR: A defect of the platelet plasma membrane glycoprotein composition is reported in a patient whose platelets are totally unresponsive to collagen, contributing significantly to present concepts of platelet function.
Abstract: The interaction of blood platelets with collagen is generally considered to be of primary importance in the arrest of bleeding and to have a role in the pathogenesis of thrombosis and atherosclerosis. Following damage to the vascular endothelium, circulating platelets come into contact with exposed collagen fibrils in the subendothelium and spread along it; this is followed by the secretion of several biologically active substances and by aggregation of platelets. The glycoproteins of the platelet plasma membrane have an important role in the mechanisms underlying these processes. So far, two specific defects of platelet function in patients with a bleeding disorder are known to be associated with a glycoprotein defect and the study of these patients has contributed significantly to present concepts of platelet function. The glycoprotein (GP) IIB-III complex, absent or deleted in the aggregation-defective Glanzmann's thrombasthenia, has been identified as the platelet fibrinogen receptor. GPIb, which is absent in the adhesion-defective Bernard-Soulier syndrome, has been identified as the von Willebrand factor receptor on platelets. We now report a defect of the platelet plasma membrane glycoprotein composition in a patient whose platelets are totally unresponsive to collagen.
491 citations
TL;DR: Observations indicate that the generation of procoagulant platelet-derived microparticles in vivo is a plausible explanation for the thrombotic complications observed in some patients with heparin-inducedThrombocytopenia.
467 citations
TL;DR: The objectives of this review have been to summarize the recent research on inherited defects involving abnormal platelet function and to illustrate how studies of hemorrhagic syndromes have led to an increased understanding of the molecular events involved in platelet adhesion and aggregation.
Abstract: EARLY in this century, it was clearly demonstrated that blood platelets are essential for hemostasis,1 and shortly thereafter the first report appeared demonstrating that a congenital hemorrhagic disease can result from abnormal platelet function.2 Since that time, descriptions of many additional disorders have greatly added to our understanding of the role of platelets in normal hemostasis.3 4 5 6 Analytical techniques developed during the past decade have helped both to identify the molecular abnormalities causing these disorders and to define the mechanisms of platelet-vessel-wall interactions. It has been demonstrated that platelet function requires the presence of specific receptors on the platelet surface that . . .
363 citations