Platelet aggregation activating factor

The receptors for Factor Vlll/von Willebrand factor that are present on human platelets are directly proportional to the extent of ristocetin-induced platelet aggregating activity. Factor Vlll-related protein aggregates are multimers of pairs of basic sub-unit chains. Further studies support the hypothesis that the underlying defect in von Willebrand type II disease may be incomplete assembly of Factor Vlll/von Willebrand factor monomer molecules into oligomers at the quaternary level of molecular organization. In von Willebrand Type I disease reduced synthesis of the Factor Vlll/von Willebrand factor sub-unit or of primary polymers (mol. wt. 1.0 x 10 ) may be the defect. When prepared from lipid-poor plasma the size heterogeneity ranges from 6.0 x 10 to 2.0 x 10 . ... 

Monteagudo J, Pereira A, Roig S, et al. Investigation of plasma von Willebrand factor and circulating platelet aggregating activity in mitomycin C-related hemolytic-uremic syndrome. Am J Hematol 33 46-9,1990. 

A. H. Morita, D. A. Uchida, S. J. Taussig, S. C. Chou, and Y. Hokama. Chromatographic fractionation and characterization of the active platelet aggregation inhibitory factor from bromelain. Arch. Int. Pharmacodyn. 259 340 (1979). 

No changes in INR (a standardized scale used to report the results of blood coagulation tests), platelet aggregation, clotting factor activity, or plasma levels of warfarin, were observed in healthy volunteers orally administered two garlic tablets (each the equivalent of 2 g fresh garlic) daily for two weeks (Abdul et al. 2008). 

The preparation and the assay of the components of fibrinolysis and thrombolysis have been reviewed." The amino-acid sequences at the NH2-terminus, molecular weights, and amino-acid compositions of human prothrombin, factors IX and X, and a new plasma protein have been compared." Desialylation of human plasma factor VIII decreased its ristocetin-induced platelet-aggregation activity and facilitated its clearance by hepatocytes, but its procoagulant activity was not affected." " Experiments in vivo have confirmed the view that the inhibi-... 

Platelet activating factor (PAF) was first identified by its ability (at low levels) to cause platelet aggregation and dilation of blood vessels, but it is now known to be a potent mediator in inflammation, allergic responses, and shock. PAF effects are observed at tissue concentrations as low as 10 M. PAF causes a dramatic inflammation of air passages and induces asthma-like symptoms in laboratory animals. Toxic-shock syndrome occurs when fragments of destroyed bacteria act as toxins and induce the synthesis of PAF. This results in a drop in blood pressure and a reduced... 

The formation of a platelet aggregate requires the recruitment of additional platelets from the blood stream to the injured vessel wall. This process is executed through a variety of diffusible mediators which act through G-protein-coupled receptors. The main mediators involved in this process are adenosine diphosphate (ADP), thromboxane A2 (TXA2), and thrombin (factor Ila). These mediators of the second phase of platelet activation are formed in different ways. While ADP is secreted from platelets by exocytosis, the release of TXA2 follows its new formation in activated platelets. Thrombin can be formed on the surface of activated platelets (see Fig. 2). 

Platelet-activating Factor Platelet Aggregation Inhibitors Platelet-derived Growth Factor Receptor Platelet Inhibitors Platelets... 

Activated platelets, besides forming a platelet aggregate, are required, via newly expressed anionic phospholipids on the membrane surface, for acceleration of the activation of factors X and II in the coagulation cascade (Figure 51—1). 

Inhibits platelet aggregation by increasing levels of cAMP Binds protein C, which is then cleaved by thrombin to yield activated protein C this in combination with protein S degrades factors Va and Villa, limiting their actions Activates plasminogen to plas-min, which digests fibrin the action of t-PA is opposed by plasminogen activator inhibitor- (PAI-1)... 

Platelet-activating factor A mediator of platelet aggregation and inflammation that is produced in response to stimuli, such as white blood cells. 

P2Y receptors that are found on endothelial cells elicit a Ca2+-dependent release of endothelium-dependent relaxing factor (EDRF) and vasodilation. A secondary activation of a Ca2+-sensitive phospholipase A2 increases the synthesis of endothelial prostacyclin, which limits the extent of intravascular platelet aggregation following vascular damage and platelet stimulation. The P2Y-mediated vasodilation opposes a vasoconstriction evoked by P2X receptors located on vascular smooth muscle cells. The latter elicit an endothelial-independent excitation (i.e. constriction). P2Y receptors are also found on adrenal chromaffin cells and platelets, where they modulate catecholamine release and aggregation respectively. 

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