INT71933
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Augmented local thrombin production in myocardial infarction patients with glucose >7.0 mmol/l was accompanied by increased platelet activation, reflected by elevated sCD40L levels in venous plasma and bleeding time blood. | |||||||||||||||
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We used the following definitions: cardiac failure was defined as requiring use of inotropic agents; respiratory failure was defined as the need for assisted ventilatiory support; ARDS was defined as clinical deterioration with severe arterial hypoxaemia and diffuse bilateral infiltrates on chest radiograph; disseminated intravenous coagulation (DIC) was defined as elevated prothrombin time (PT) with elevated activated partial thromboplastin time (APTT), and decreased fibrinogen (FIB) level with thrombocytopenia; liver function impairment was defined as aminotransferase (ALT or AST) levels ? | |||||||||||||||
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The following data were collected from the Institutional Database or direct analysis of the perfusion files: demographics: age (months), weight (kg), gender; type of surgical operation with Aristotle complexity score [16]; preoperative laboratory data: hematocrit (percentage), platelet count (cells/microliter), prothrombin time (seconds), activated partial thromboplastin time (seconds), antithrombin (percentage), serum creatinine value (milligrams per deciliter); CPB data: CPB duration (minutes), lowest temperature on CPB (degrees Centigrade), use of blood prime, ScVO2 values (percentage), and lactate values (mmol/L). | |||||||||||||||
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We used the following definitions: cardiac failure was defined as requiring use of inotropic agents; respiratory failure was defined as the need for assisted ventilatiory support; ARDS was defined as clinical deterioration with severe arterial hypoxaemia and diffuse bilateral infiltrates on chest radiograph; disseminated intravenous coagulation (DIC) was defined as elevated prothrombin time (PT) with elevated activated partial thromboplastin time (APTT), and decreased fibrinogen (FIB) level with thrombocytopenia; liver function impairment was defined as aminotransferase (ALT or AST) levels ? | |||||||||||||||
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This condition develops as the result of the formation of antibodies to the heparin-platelet factor 4 complex, which causes secondary activation of platelets, coagulation, and ultimately increased thrombin production.33 | |||||||||||||||
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Hypercoagulability develops in septic patients, resulting in enhanced thrombin generation, thrombin activation, and fibrin formation. | |||||||||||||||
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Our results show that unfractionated and low molecular weight heparins potently inhibit monocytic tissue factor induced thrombin generation. | |||||||||||||||
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Acute hyperglycemia activates platelet aggregation, enhances thrombin generation, and activates coagulation factor VII (9). | |||||||||||||||
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In summary, our findings demonstrate that acute hyperglycemia in acute myocardial infarction patients without a previous history of diabetes is associated with increased thrombin generation and platelet activation at the site of vascular injury as well as greater resistance to fibrinolysis. | |||||||||||||||
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Hypercoagulability develops in septic patients, resulting in enhanced thrombin generation, thrombin activation, and fibrin formation. | |||||||||||||||
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The prothrombin mutation is associated with elevated plasma prothrombin levels (factor II activity >130 percent) and is present in about 25 percent of healthy individuals. | |||||||||||||||
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Prostacyclin production in tryptase and thrombin stimulated human bladder endothelial cells: effect of pretreatment with phospholipase A2 and cyclooxygenase inhibitors. | |||||||||||||||
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Real time RT-PCR analysis of thrombin treated collagen embedded hUtSMC mRNA | |||||||||||||||
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Frequent risk factors include trauma, steroid therapy or hypercortisonism [2-4], alcohol abuse and different coagulopathies, for example, activated protein C (APC) resistance, protein S deficiency, prothrombin mutations and hyperhomocysteinaemia [5,6]. | |||||||||||||||
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This increased lipid accumulation was accompanied by enhanced expression of tissue factor and plasminogen activator inhibitor-1, as well as enhanced thrombin formation, transforming macrophages into a prothrombotic phenotype. | |||||||||||||||
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Therefore protein C activation will be correspondingly low, and the negative feedback that controls TNF-induced thrombin formation correspondingly weak (Figure 1a), further enhancing concentrations of the above adhesion molecules. | |||||||||||||||
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Tissue factor is a membrane-bound glycoprotein that functions in the extrinsic pathway of blood coagulation by acting as a cofactor for factor VII, and the resulting complex leads to thrombin production in vivo. | |||||||||||||||
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Four factors were considered to increase the angiogenic potential of the PRP, including the concentrations of thrombin and calcium for platelet activation, the subsequent release of vascular endothelial growth factor (VEGF), production of platelet microparticles (PMPs), and inclusion of only peripheral blood mononuclear cells (PBMNCs) among white blood cells (WBCs). | |||||||||||||||
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To date, two studies have found an increase in thrombin generation following exercise, and only one of these showed an increase in fibrin breakdown in patients with IC who were not on statin therapy. | |||||||||||||||
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In one study, colonic biopsies from IBS patients were found to produce elevated levels of serine protease [89]. | |||||||||||||||
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