Factor Activation Of Platelets
Mostrando 1-12 de 85 artigos, teses e dissertações.
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1. Inovações metodológicas em hematologia clínica: uso da citometria de fluxo no estudo da ativação plaquetária na pré-eclâmpsia
Preeclampsia (PE) is a serious complication of pregnancy associated to maternal-fetal morbidity and mortality, whose etiology has not been established. In pure form, is characterized by the appearance, in normal pregnant women after the 20th week of gestation, hypertension and proteinuria. Hemostatic and inflammatory changes associated with normal pregnancy
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 28/02/2012
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2. Sinalização intracelular e expressão de receptores mediados por LDL modificada e peptídeos da apolipoproteínaB-100 em monócitos/macrófagos humanos. / Intracellular signaling and receptor expression mediated by modified LDL and apolipoproteinB-100 peptides in human monocytes/macrophages.
The Low Density Lipoprotein (LDL) may undergo oxidative or enzymatic modifications, producing lipid or proteic compounds that interact with macrophages, contributing to inflammatory response in the atherosclerosis. Into the arterial intima, the macrophages interact with minimally modified LDL (LoxLDL) and with highly oxidized LDL (HoxLDL). Moreover, in the a
Publicado em: 2009
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3. Contribuição ao estudo da ação in vitro do veneno da aranha marrom, Loxosceles gaucho, sobre plaquetas humanas e de coelho. Participação das plaquetas na dermonecrose induzida experimentalmente pelo veneno loxoscélico em coelhos / Contribution to the study of the in vitro action induced by the venom of the brown spider, Loxosceles gaucho, on human and rabbit platelets. Platelet participation in the dermonecrotic lesion experimentally induced in rabbits by the loxoscelic venom
Venoms from Loxosceles spiders exhibit a wide range of activities on different cells, tissues and systems, being specially evident their ability to cause a dermonecrotic lesion. In a previous paper, we showed that Loxosceles gaucho spider venom induces intense thrombocytopenia in rabbits. Thus, in the present study, we firstly aimed to evaluate the in vitro
Publicado em: 2007
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4. Expressão genica global e estudo do gene JUNB em policitemia vera / Global gene expression and study of the JUNB gene in polycythemia
Polycythemia vera (PV) is a chronic myeloproliferative disorder that arises through clonal proliferation of multipotent hematopoietic progenitors. PV patients present bone marrow trilineage expansion, leading to increased production of mature red cells, granulocytes and platelets. Important PV features are elevated red cell mass, despite normal or subnormal
Publicado em: 2007
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5. Platelet receptor-mediated factor X activation by factor IXa. High-affinity factor IXa receptors induced by factor VIII are deficient on platelets in Scott syndrome.
We have studied factor IXa binding and factor X activation with normal platelets and with platelets obtained from a patient with a bleeding disorder and an isolated deficiency of platelet procoagulant activity termed Scott syndrome. In the absence of factor VIIIa and factor X, normal, thrombin-treated platelets exposed 560 +/- 35 sites for factor IXa with a
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6. Regulation of factor XIa activity by platelets and alpha 1-protease inhibitor.
We have studied the complex interrelationships between platelets, Factor XIa, alpha 1-protease inhibitor and Factor IX activation. Platelets were shown to secrete an inhibitor of Factor XIa, and to protect Factor XIa from inactivation in the presence of alpha 1-protease inhibitor and the secreted platelet inhibitor. This protection of Factor XIa did not aris
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7. Activation of Coagulation Factor V by a Platelet Protease
Factor V must be converted to Factor Va in order to bind to a high affinity platelet surface site and participate in prothrombin activation. Osterud et al. (10) presented data that suggested that human platelets contain an activated form of Factor V and a Factor V activator. We find that the Factor V released when platelets are disrupted by freezing and thaw
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8. A platelet alpha granule membrane protein that is associated with the plasma membrane after activation. Characterization and subcellular localization of platelet activation-dependent granule-external membrane protein.
We have identified and purified a platelet integral membrane protein (140,000 mol wt), using the KC4 monoclonal antibody specific for activated platelets, that is internal in resting platelets but exposed on activated platelets (Hsu-Lin S.-C., C.L. Berman, B.C. Furie, D. August, and B. Furie, 1984, J. Biol. Chem. 259: 9121-9126.). The expression of the prote
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9. Inhibition of the activation of Hageman factor (factor XII) by peripheral blood cells.
Suspensions of peripheral blood mononuclear cells (PBMC), monocytes, T or B lymphocytes, platelets or granulocytes, and cell-depleted supernatant fluids of these suspensions inhibited activation of Hageman factor (HF, Factor XII) by ellagic acid, a property not shared by erythrocytes. PBMC also inhibited HF activation by glass or sulfatides. Contaminating pl
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10. Platelet adhesion to damaged coronary arteries: Comparison in normal and von Willebrand disease swine.
The early response to coronary artery injury was investigated in normal swine and in swine with von Willebrand disease (vWD). Thirty minutes after coronary endothelial denudation, a monolayer of platelets was adherent to areas of simple injury in both bleeder and normal swine. The number of adherent platelets was not significantly different in the two phenot
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11. An endothelial cell-dependent pathway of coagulation.
Although the endothelial cell is considered antithrombogenic, endothelium has recently been shown to participate in procoagulant reactions. In this report cultured bovine aortic endothelial cells are shown to propagate a procoagulant pathway starting with factor XIa, leading to activation of factors IX, VIII, X, and prothrombin, culminating in fibrinopeptide
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12. Role of human factor VIII in factor X activation.
The cofactor function of human Factor VIII in Factor X activation was investigated by an initial-rate assay of 3H-Factor X activation in the presence of human factor IXa, Ca2+, and either phospholipid or fresh washed human platelets. Purified Factor VIII that has not been activated by thrombin or Factor Xa supports Factor X activation after a lag of several