Hemostatic system factors

Functional Properties and Structures of the Hemostatic System Factors (Proteins)... 

Tumorigenic responses, 25 222-223 Tumor necrosis factor (TNF) role in hemostatic system, 4 89 Tumors, hydrazine-related, 23 590—591 Tunable diode lasers (TDLs), 23 143 Tunable diode laser systems, 23 138 Tunable optical properties, windows with, 23 25... 

The first reason is theoretical. The demonstrated effects of the new substances and combinations on lipids and carbohydrates do not have any major relevance to the thromboembolic process. The latter is linked primarily to changes in the hemostatic system and blood coagulation, involving platelet aggregation, coagulation factors, fibrinogen concentrations, and blood viscosity. 

Pharmacologic inhibitors of thrombin. Thrombin is a key enzyme in the hemostatic system in that it leads to the formation of fibrin strands and is a potent stimulus for platelet activation. Thrombin inhibitors, factor Xa inhibitors, and antiplatelet drugs act at different points in the hemostatic system to regulate the amount of thrombin that is generated. 

A particularly well studied example of functional amyloid is provided by Curli assembly (53). Curli amyloids are assembled by bacteria such as Escherichia coli and Salmonella. Once assembled on the extracellular surface, Curli amyloid fibers function as natural ceU adhesion molecules that link together bacterial cells into robust cellular networks of biofilms. Other examples of functional amyloids include the silk fibers observed commonly in spider webs the Chorion proteins of egg shells Factor XII, which is an activator of the hemostatic system and other naturally produced adhesives and materials (54). 

Kuroiwa M, Okamura T, Kanaji T, Okamura S, Harada M, Niho Y. Effects of granulocyte colony-stunulatmg factor on the hemostatic system in healthy volunteers. Int J Hematol 1996 63(4) 311-16. 

Proteinase inhibitors (proteins) that circulate in plasma inactivate the hemostatic system proteinases after they have essentially completed their proteolyses. With two exceptions, o 2-niacroglobulin and tissue factor pathway inhibitor, all of the inhibitors of the procoagulant, anticoagulant, and fibrinolytic proteinases are SERPINS... 

Von Willebrand Factor Von Willebrand factor (vWF) is a multisubunit protein that serves both to anchor the platelets to the subendothelium and as a carrier protein for factor VIII in the plasma. The circulating vWF is the largest protein of the hemostatic system. It is made of protomeric units which themselves are dimers of the 250,000-Da vWF polypeptide chain. The vWF gene product is a single polypeptide chain that associates to form the dimeric protomer. Disulfide bonds link the two vWF monomer chains in the protomer. The 500,000-Da dimeric protomers further associate to form the more than 20,000,000-Da vWF molecules present in the circulation. Recognition sites are present on the von Willebrand factor... 

Because inactivation of factors Va and Villa by activated protein C promotes the dissociation of the pro-teinases, cofactor protein inactivation complements the action of the proteinase inhibitors. This eliminates the protection that the proteinases have when bound to their cofactor proteins and substrates. Inactivation of proteinases by SERPINS occurs via a common mechanism that involves a Michaelis complex between the proteinase and the inhibitor (Figure 36-16). This mechanism applies to all serine proteinases of the hemostatic system, i.e., the procoagulant, anticoagulant, and fibrinolytic subsystem proteinases. 

Factors in addition to sickling may be responsible for the pathogenesis of a number of the clinical manifestations associated with SCD. Obstruction of blood flow to the spleen by sickle cells can result in functional asplenia, defined as the loss of splenic function with an intact spleen. These patients may also have deficient opsonization. Impaired splenic function increases susceptibility to infection by encapsulated organisms, particularly pneumococcal disease. Coagulation abnormalities in SCD may be the result of continuous activation of the hemostatic system or disorganization of the membrane layer. " ... 

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