2000
DOI: 10.1080/09537100075715
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Glycoprotein IIb-IIIa-liposomes bind fibrinogen but do not undergo fibrinogen-mediated aggregation

Abstract: This manuscri pt has been reproduced from the microfilm master. UMI films the text directly from the original or copy submitted. Thus, some thesis and dissertation copies are in typewriter face, while others may be from any type of computer printer.The quality of this reproduction is dependent upon the quality of the copy submitted. Broken or indistinct print, cobred or poor quality illustrations and photographs, print bleedthrough, substandard margins, and improper alignment can adversely affect reproduction.… Show more

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Cited by 4 publications
(3 citation statements)
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“…Fusion could explain the lack of enhanced platelet aggregation with or without ADP shown by RGD liposomes (Rybak and Renzulli, 1993) and GPIIbIIIa-loaded liposomes (Sloan et al, 2000). Similarly, it could offer an alternative explanation for the effectiveness and localization of synthetic phospholipids that promote procoagulant activity on damaged vessels (Galan et al, 1998), the clot accumulation of plasminogen-bearing liposomes (Heeremans et al, 1998) and the improved thrombolysis of streptokinasecontaining liposomes (Perkins et al, 1997).…”
Section: Discussionmentioning
confidence: 93%
“…Fusion could explain the lack of enhanced platelet aggregation with or without ADP shown by RGD liposomes (Rybak and Renzulli, 1993) and GPIIbIIIa-loaded liposomes (Sloan et al, 2000). Similarly, it could offer an alternative explanation for the effectiveness and localization of synthetic phospholipids that promote procoagulant activity on damaged vessels (Galan et al, 1998), the clot accumulation of plasminogen-bearing liposomes (Heeremans et al, 1998) and the improved thrombolysis of streptokinasecontaining liposomes (Perkins et al, 1997).…”
Section: Discussionmentioning
confidence: 93%
“…It was shown before that GPIIb/IIIa can be activated and can bind fibrinogen without aggregation necessarily occurring. 16,25 FITC-fibrinogen binding to platelets activated by echicetin-IgM was examined by flow cytometric analysis and was significantly increased on activated platelets (Figure 4).…”
Section: Discussionmentioning
confidence: 99%
“…Fibrinogen (Factor I) is a 340 kDa plasma glycoprotein. , When cleaved by thrombin as a result of clotting activation, it forms fibrin monomers that aggregate into an insoluble, cross-linked polymer structure. Fibrinogen is involved in primary hemostasis, platelet aggregation, and leukocyte−endothelial cell interactions . Fibrinogen concentration (and associated changes in whole blood viscosity) has been reported to be associated with the risk of cardiovascular heart disease, recurrent stroke, myocardial infarction, venous thrombosis, , disseminated intravascular coagulation (DIC), systemic fibrinolysis, pancreatitis, and severe hepatic dysfunction.…”
mentioning
confidence: 99%