Two monoclonal antibodies-one that blocks ristocetininduced platelet binding of von Willebrand factor to glycoprotein lb and one that blocks adenosine diphosphateinduced binding of fibrinogen to the glycoprotein llb/Illa complex-were used to assess the binding site(s) for von Willebrand factor when platelets are stimulated with thrombin or adenosine diphosphate (ADP). Neither agonist induced bi...

ischemic stroke accounts for about 87 percent of all cases. it occurs as a result of an obstruction within a vessel of the brain and sudden loss of blood circulation to the corresponding area resulting in the loss of brain function. it is caused by thrombotic or embolic occlusion of an artery and is more common than hemorrhagic stroke. we know that most of the injuries after an acute ischemic s...

Platelet activation in blood flow under high, overcritical shear rates is initiated by Von Willebrand factor. Despite the large amount of experimental data that have been obtained, the value of the critical shear rate, above which von Willebrand factor starts to activate platelets, is still controversial. Here, we recommend a theoretical approach to elucidate how the critical blood shear rate i...

5006 The Journal of Clinical Investigation http://www.jci.org Volume 123 Number 12 December 2013 1998;91(12):4397–4418. 5. Ruggeri ZM, Pareti FI, Mannucci PM, Ciavarella N, Zimmerman TS. Heightened interaction between platelets and Factor VIII/von Willebrand factor in a new subtype of von Willebrand’s disease. N Engl J Med. 1980;302(19):1047–1051. 6. Ware J, et al. Identification of a point mut...

The abnormal multimeric composition of plasma von Willebrand factor in type IIB von Willebrand's disease is transiently corrected after infusion of 1-deamino-[8-D-arginine]-vasopressin. However, the larger multimers released into the circulation disappear more rapidly in these patients than in type I von Willebrand's disease or normals. We demonstrate that the larger multimers of normal von Wil...

The agglutination of human platelets by ristocetin and von Willebrand factor was inhibited by aggregated immunoglobulin (Ig)G and by Fc fragments of IgG, but not by Fab, F(ab')(2) or pFc fragments of IgG. Because this inhibition occurred with formalin-fixed platelets as well as with normal platelets, a generalized aggregation of fluid membrane components by Fc fragments was not responsible for ...

Ristocetin will induce the agglutination of platelets in the presence of von Willebrand factor. In previous studies, an electrostatic mechanism was proposed for this phenomenon wherein first the platelet's surface charge is reduced by the binding of ristocetin and then the von Willebrand factor acts as a bridge between platelets. To test this hypothesis, the effects of ristocetin and von Willeb...

We have studied the modifications in the multimeric composition of plasma factor VIII/von Willebrand factor and the bleeding time response following administration of 1-Deamino-[8-D-arginine]-Vasopressin (DDAVP) to patients with different subtypes of von Willebrand's disease. In type I, all multimers were present in plasma in the resting state, though they were decreased in concentration. Admin...

The characteristics of the intact factor VIll/von Willebrand factor protein binding to human platelets was compared to 2-mercaptoethanol-treated factor VIll/von Willebrand factor protein and to fractions of plasma factor VIll/von Willebrand factor protein that elute after the void volume. These studies indicate that the factor VIlI/von Willebrand factor protein larger size oligomers bind prefer...

A form of von Willebrand’s disease has been described with enhanced ristocetin-induced platelet aggregation and anodal migration of the factor VIll/von Willebrand factor protein (type lIb). We studied two families with this form of von Willebrand s disease and macrothrombocytopenia. We have found that these platelets bind more of the normal and intermediate-sized multimers of the factor VIll/vo...