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Ischemia platelet-activating factor

Ischemia and seizures increase platelet-activating factor content in the brain 580... [Pg.575]

Panetta, T., MarcheselH, V. L., Braquet, P., Spinnewyn, B. and Bazan, N. G. Effects of a platelet-activating factor antagonist (BN52021) on free fatty acids, diacylglycerols, polyphosphoinositides and blood flow in the gerbil brain Inhibition of ischemia-reperfusion induced cerebral injury. Biochem. Biophys. Res. Commun. 149 580-587,1987. [Pg.589]

Shigematsu S, Ishida S, Hara M, Takahashi N, Yoshimatsu H, Sakata T, Korthuis RJ. 2003. Resveratrol, a red wine constituent polyphenol, prevents superoxide-dependent inflammatory responses induced by ischemia/reperfusion, platelet-activating factor, or oxidants. Free Radic Biol Med 34 810-817. [Pg.328]

A platelet-activating factor, l-0-alkyl-2-(R)acetyl-sn-glyceryl-3-phosphocholine, is released in the presence of shock and ischemia. The platelet-activating factor antagonist can protect the heart and brain against ischemic injury. [Pg.42]

Hinman JD, Peters A, Cabral H, Rosene DL, Hollander W, Rasband MN, Abraham CR (2006) Age-related molecular reoiganization at the node of Ranvier. J Comp Neurol 495 351-362 Ho MC, Lo AC, KuriharaH, Yu AC, Chung SS, Chung SK (2001) EndotheUn-l protects astrocytes from hypoxic/ischemic injury. EASEB J 15 618-626 Honda Z, Islrii S, Shimizu T (2002) Platelet-activating factor receptor. J Biochem 131 773-779 Hou ST, MacManus JP (2002) Molecular mechanisms of cerebral ischemia-induced neuronal death. Int Rev Cytol 221 93—148... [Pg.61]

Pig. 33 Pathways associated with ROS- and RNS-mediated ceU death in cerebral ischemia. Phosphohpase A2 (PLA2) nitric oxide synthase (NOS) cyclooxygenase-2 (COX-2) arachidonic add (ARA) lyso-phosphophatidylcholine (lyso-PtdCho) platelet-activating factor (RAF) reactive oxygen species (ROS) reactive nitrogen species (RNS) superoxide (O2) peroxynitrite (ONOO ) transcription factor-a (TNF-a) interleukin-ip (IL-ip) and interleukin-6 (IL-6)... [Pg.71]

FrancescangeU, E, Domanska-Janik, K and Goracci, G (1996) Relative contribution of the de novo and remodelling pathways to the synthesis of platelet-activating factor in brain areas and during ischemia. J Lipid Medial Cell Signal, 14, 89-98. [Pg.128]

Fig. 3 Pathogenesis of acute vascular rejection. Activation of endothelium by xenoreactive antibodies (Ab), complement (C), platelets, and perhaps by inflammatory cells (natural killer (NK) cells and macrophages (M0) leads to the expression of new pathophysiologic properties. These new properties, such as the synthesis of tissue factor (TF) and plasminogen activator inhibitortype 1 (PAI-1), promote coagulation the synthesis of E-selectin and cytokines such as I LI a promote inflammation. These changes in turn cause thrombosis, ischemia, and endothelial injury, the hallmarks of acute vascular rejection. (Adapted from Nature 1998 392(Suppl.) 11-17, with permission.) (See Color Plate p. xxiii). Fig. 3 Pathogenesis of acute vascular rejection. Activation of endothelium by xenoreactive antibodies (Ab), complement (C), platelets, and perhaps by inflammatory cells (natural killer (NK) cells and macrophages (M0) leads to the expression of new pathophysiologic properties. These new properties, such as the synthesis of tissue factor (TF) and plasminogen activator inhibitortype 1 (PAI-1), promote coagulation the synthesis of E-selectin and cytokines such as I LI a promote inflammation. These changes in turn cause thrombosis, ischemia, and endothelial injury, the hallmarks of acute vascular rejection. (Adapted from Nature 1998 392(Suppl.) 11-17, with permission.) (See Color Plate p. xxiii).
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See also in sourсe #XX -- [ Pg.579 ]



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