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thrombosis/prolina
L'enllaç es desa al porta-retalls
Pàgina 1 des de 55 resultats
The effect of prolil-glycil-proline (PGP) peptide and PGP-rich substances on haemostatic parameters of rat blood.
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The effect of intravenous and intranasal administration of proline-containing peptide, especially prolil-glycil-proline (PGP), on the haemostatic system of rats was investigated. Tripeptide PGP after single intravenous (0.2, 1.0 and 1.5 mg/kg) or intranasal (0.5 mg/ kg) administration increased (P <
Antithrombin III Utah: proline-407 to leucine mutation in a highly conserved region near the inhibitor reactive site.
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A dysfunctional antithrombin III (ATIII) gene encoding a qualitatively and quantitatively abnormal anticoagulant molecule is responsible for hereditary thrombosis in a Utah kindred [Bock et al. (1985) Am. J. Hum. Genet. 37, 32-41]. Nucleotide sequencing of the entire protein-encoding portion of the
Influence of a novel inhibitor (UM8190) of prolylcarboxypeptidase (PRCP) on appetite and thrombosis.
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Preclinical pharmacological characterization of a novel inhibitor (UM8190) of prolylcarboxypeptidase (PRCP) was investigated. We synthesized and evaluated a library of proline-based analogs as prospective recombinant PRCP (rPRCP) inhibitors and inhibitors of PRCP-dependent prekallikrein (PK)
Risky communication in atherosclerosis and thrombus formation.
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Atherosclerosis, a progressive disease of medium- and large-sized arteries, constitutes the major cause of death in developed countries, and is becoming increasingly prevalent in developing countries as well. The main consequences of atherosclerosis are myocardial infarction, cerebral infarction and
The PlA1/A2 polymorphism of platelet glycoprotein IIIa is not associated with deep venous thrombosis.
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BACKGROUND
Platelet glycoprotein (GP) IIb/IIIa, a fibrinogen and von Willebrand factor binding membrane receptor, has an important role in platelet aggregation. A common leucine33-proline polymorphism (PlA1/A2) of the gene encoding the GP IIIa subunit is associated with platelet reactivity and has
Local thrombin synthesis and fibrin formation in an in vitro thrombosis model result in platelet recruitment and thrombus stabilization on collagen in heparinized blood.
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The role of the local synthesis of thrombin in platelet recruitment and thrombus stabilization in heparinized blood was examined in vitro. Mural thrombosis was visualized and measured in a thin, rectangular, collagen-coated capillary under controlled rheological conditions by using fluorescence
Structural characterization and optimization of antibody-selected phage library mimotopes of an antigen associated with autoimmune recurrent thrombosis.
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The presence of high titers of anti-cardiolipin antibodies (ACA's) of autoimmune origin, which are known to bind to plasma beta2-glycoprotein I (aka apolipoprotein H), correlates clinically with autoimmune recurrent thrombosis. Soluble beta2-glycoprotein I binds to solid-phase ACA (immobilized on a
Platelet membrane collagen receptor glycoprotein VI polymorphism is associated with coronary thrombosis and fatal myocardial infarction in middle-aged men.
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Glycoprotein VI is a platelet collagen receptor binding to subendothelial collagen after a rupture of an atherosclerotic plaque. The GPVI gene is polymorphic with several SNPs and the T13254C polymorphism predicting amino acid substitution (serine to proline) has been associated with the risk of MI
[Heterozygous protein C deficiency: apropos of 2 cases with cerebral venous thrombosis in the neonatal period].
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Thrombotic accidents in the newborn, particularly cerebrovascular accidents, are reported in case of abnormalities in the coagulation system and rarely in heterozygous protein C deficiency; a low protein C level could be either physiological or acquired.
METHODS
Two cases of heterozygous protein C
The 536C-->T transition in the human tissue factor pathway inhibitor (TFPI) gene is statistically associated with a higher risk for venous thrombosis.
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Tissue factor pathway inhibitor (TFPI) is an important regulator in the extrinsic blood coagulation pathway. Although the regulatory biochemical role of TFPI is evident, the clinical significance of this proteinase inhibitor remains to be elucidated. The definition of a clinical TFPI deficiency
Factor XII: what does it contribute to our understanding of the physiology and pathophysiology of hemostasis & thrombosis.
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Factor XII (FXII) is a coagulation protein that is essential for surface-activated blood coagulation tests but whose deficiency is not associated with bleeding. For over forty years, investigators in hemostasis have not considered FXII important because its deficiency is not associated with
N-Acetyl-Seryl-Aspartyl-Lysyl-Proline Augments Thrombolysis of tPA (Tissue-Type Plasminogen Activator) in Aged Rats After Stroke.
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Background and Purpose- Stroke is a leading cause of disability worldwide, mainly affecting the elderly. However, preclinical studies in aged ischemic animals are limited. N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) is a naturally occurring tetrapeptide with vascular-protective properties. The
Low-Fouling and Biodegradable Protein-Based Particles for Thrombus Imaging.
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Nanomedicine holds great promise for vascular disease diagnosis and specific therapy, yet rapid sequestration by the mononuclear phagocytic system limits the efficacy of particle-based agents. The use of low-fouling polymers, such as poly(ethylene glycol), efficiently reduces this immune
Thymidine phosphorylase participates in platelet signaling and promotes thrombosis.
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BACKGROUND
Platelets contain abundant thymidine phosphorylase (TYMP), which is highly expressed in diseases with high risk of thrombosis, such as atherosclerosis and type II diabetes mellitus.
OBJECTIVE
To test the hypothesis that TYMP participates in platelet signaling and promotes
Focal Adhesion Kinases in Platelet Function and Thrombosis.
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The focal adhesion kinase family includes 2 homolog members, FAK and Pyk2 (proline-rich tyrosine kinase 2), primarily known for their roles in nucleated cells as regulators of cytoskeletal dynamics and cell adhesion. FAK and Pyk2 are also expressed in megakaryocytes and platelets and are activated
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