Platelets second

Ceramic matrix composites are candidate materials for high temperature stmctural appHcations. Ceramic matrices with properties of high strength, hardness, and thermal and chemical stabiUty coupled with low density are reinforced with ceramic second phases that impart the high toughness and damage tolerance which is required of such stmctural materials. The varieties of reinforcements include particles, platelets, whiskers and continuous fibers. Placement of reinforcements within the matrix determines the isotropy of the composite properties. 

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). 

Primary hemostasis is the first phase of hemostasis consisting of platelet plug formation at the site of injury. It occurs within seconds and stops blood loss from capillaries, arterioles, and venules. Secondary hemostasis, in contrast, requires several minutes to be complete and involves the formation of fibrin through the coagulation cascade. 

The chemical engineering approach began with an analysis of the biochemistry of platelet metabolism. Like many cells, platelets consume glucose by two pathways, an oxidative pathway and an anaerobic pathway. The oxidative pathway produces carbon dioxide, which makes the solution containing the platelets more acidic (lower pH) and promotes anaerobic metabolism. This second metabolic pathway produces large amounts of lactic acid, further lowering pH. The drop in pH from both pathways kills the platelets. 

Maroni, M., Colombi, A., Gilioli, R., Bleecker, M.L., Villa, L., and Foa, V. (1985) Reference values for lymphocyte and platelet NTE activity in American and Italian populations, in Proceedings of the Second International Symposium on Neu-robehavioural Methods in Occupational and Environmental Health, Copenhagen, August 6-9, 1985. 

H, receptors also can stimulate the activity of phospholipase A2 (PLA2), with the subsequent release of arachido-nate and its metabolites. In platelets, this response does not require activation of the phosphoinositide cycle and is inhibited by pertussis toxin, suggesting a second, distinct Gj/o-protein-mediated transduction mechanism. In cells transfected with the H, receptor, PLA2 activation is partially inhibited by pertussis toxin, also suggesting at least two transduction systems [30,34],... 

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