Platelet activating factor activity

Franklin RA, Tordai A, Mazer B, Terada N, Lucas J, Gelfand EW. 1995. Platelet activating factor activates MAPK and increases in intracellular calcium via... 

Platelet activating factor Activates platelets and white blood cells ... 

Young s modulus for [CERAMICS - PffiCHANICAL PROPERTIES AND BEHAVIOR] (Vol 5) Platelet-activating factor QAE) antagonists... 

The synthetic utihty of the above transformations stems from the fact that many monoesters obtained as a result of hydrolysis may be converted to pharmaceutically important intermediates. For example, the optically active glycerol derivative (27) is a key intermediate in the production of P-blockers. Akyl derivative (25) may be converted into (5)-paraconic acid [4694-66-0] ((5)-5-oxo-3-tetrahydrofurancarboxyhc acid) that is a starting material for the synthesis of (3R)-A-factor. The unsaturated chiral cycHc monoacetate (31) is an optically active synthon for prostaglandins, and the monoester (29) is used for the synthesis of platelet activating factor (PAF) antagonists. 

Platelet Activating Factor A Potent Glyceroether Mediator... 

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... 

FIGURE 25.24 Platelet activating factor, formed from Talkyl-2-lysophosphatidylcholine by acetylation at C-2, is degraded by the action of acetylhydrolase. 

Various 1.4-benzodiazepines with a five-membered heteroaromatic ring fused to the 1,2-bond, such as 17, where A represents a heteroaromatic ring, have been prepared by such methods and tested for activity on the central nervous system, as cholecystokinin antagonists and as antagonists of platelet activating factors.245... 

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). 

The antiinflammatory effects of statins likely result from their ability to inhibit the formation of mevalonic acid. Downstream products of this molecule include not only the end product, cholesterol, but also several isoprenoid intermediates that covalently modify ( pre-nylate ) certain key intracellular signaling molecules. Statin treatment reduces leukocyte adhesion, accumulation of macrophages, MMPs, tissue factor, and other proinflammatory mediators. By acting on the MHC class II transactivator (CIITA), statins also interfere with antigen presentation and subsequent T-cell activation. Statin treatment can also limit platelet activation in some assays as well. All these results support the concept that in addition to their favorable effect on the lipid profile, statins can also exert an array of antiinflammatory and immunomodulatory actions. 

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

These cells respond to a number of different chemoattractants which have specific and distinct receptors on the membrane surface (for recent reviews see Refs. 3 and 4). Such chemoattractants include N-formylpeptides, which are bacterial peptides, and mediators of inflammation such as leukotriene B4, C5a, and platelet activating factor. 

Basophils Release Platelet-Activating Factor Instead of Histamine to Induce IgG-Mediated Systemic Anaphylaxis... 

Lie WJ, Homburg CH, Kuijpers TW, Knol EF, Mul FR Roos D, Tool AT Regulation and kinetics of platelet-activating factor and leukotriene C4 synthesis by activated human basophils. Clin Exp Allergy 2003 33 1125-1134. 

Vadas P, Gold M, Perelman B, Liss GM, Lack G, Blyth T Simons FE, Simons JK, Cass D, Yeung J Platelet-activating factor, PAF acetylhydrolase, and severe anaphylaxis. N Engl J Med 2008 358 28-35. 

---