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phosphatidic acid/krvarenje
Veza se sprema u međuspremnik
Stranica 1 iz 18 rezultatima
Phosphatidic acid signaling mediates lung cytokine expression and lung inflammatory injury after hemorrhage in mice.
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Because phosphatidic acid (PA) pathway signaling may mediate many basic reactions involving cytokine-dependent responses, we investigated the effects of CT1501R, a functional inhibitor of the enzyme lysophosphatidic acid acyltransferase (LPAAT) which converts lysophosphatidic acid (Lyso-PA) to PA.
A haemorrhagic platelet disorder associated with altered stimulus-response coupling and abnormal membrane phospholipid composition.
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Haemorrhagic diatheses due to platelet function defects are a heterogenous and poorly understood group of conditions. We report the investigation of a female with a lifelong history of epistaxes, haemarthroses, menorrhagia and persistent iron-deficiency anaemia. Although platelet numbers and
Protease-activated receptors differentially regulate human platelet activation through a phosphatidic acid-dependent pathway.
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Pathological conditions such as coronary artery disease are clinically controlled via therapeutic regulation of platelet activity. Thrombin, through protease-activated receptor (PAR) 1 and PAR4, plays a central role in regulation of human platelet function in that it is known to be the most potent
2-carba cyclic phosphatidic acid suppresses inflammation via regulation of microglial polarisation in the stab-wounded mouse cerebral cortex.
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Traumatic brain injury (TBI) is caused by physical damage to the brain and it induces blood-brain barrier (BBB) breakdown and inflammation. To diminish the sequelae of TBI, it is important to decrease haemorrhage and alleviate inflammation. In this study, we aimed to determine the effects of
Hemorrhagic thrombocytopathy with platelet thromboxane A2 receptor abnormality: defective signal transduction with normal binding activity.
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Subnormal platelet responses to thromboxane A2 (TXA2) were found in a patient with polycythemia vera, and the mechanism of this dysfunction was analyzed. The patient's platelets showed defective aggregation and release reaction to arachidonic acid, enzymatically generated TXA2 and synthetic TXA2
Pathogenesis of a bleeding disorder characterized by platelet unresponsiveness to thromboxane A2.
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A platelet disorder characterized by the absence of thromboxane A2 (TXA2)-induced platelet aggregation is a new clinical entity of platelet dysfunction. The platelets of three patients had the ability to bind exogenous TXA2, but synthetic TXA2 mimetic-induced postreceptor biochemical events, such as
Impairment of phosphatidylinositol metabolism in a patient with a bleeding disorder associated with defects of initial platelet responses.
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Phosphoinositide/polyphosphoinositide (PI/PPI) metabolism, measured by the increase of 3H-phosphatidic acid (PA) and the decrease of 3H-phosphatidylinositol (PI) in 3H-arachidonate-labeled platelet suspensions, was assessed in five patients whose platelet functional defects included impaired initial
Monoclonal immunoglobulin M lambda coagulation inhibitor with phospholipid specificity. Mechanism of a lupus anticoagulant.
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Prolongation of all phospholipid-dependent coagulation tests was found in a patient with macroglobulinemia, despite absence of bleeding manifestations. The purified monoclonal IgM lambda protein and its Fabmu tryptic fragment induced similar changes in normal plasma. Patient IgM and Fabmu completely
The importance of blood platelet lipid signaling in thrombosis and in sepsis.
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Blood platelets are the first line of defense against hemorrhages and are also strongly involved in the processes of arterial thrombosis, a leading cause of death worldwide. Besides their well-established roles in hemostasis, vascular wall repair and thrombosis, platelets are now recognized as
Pathogenetic analysis of five cases with a platelet disorder characterized by the absence of thromboxane A2 (TXA2)-induced platelet aggregation in spite of normal TXA2 binding activity.
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Five patients with mild bleeding tendencies characterized by defective thromboxane A2 (TXA2)-induced platelet aggregation are reported. The platelets of all the patients had the ability to bind exogenous TXA2. Bleeding time was markedly prolonged in one patient. In three of the five patients,
Synthesis of phospholipids in mitochondria and other membrane fractions of rabbit reticulocytes.
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1. Reticulocytosis of 40-50% was obtained in rabbits by daily bleeding. Reticulocytes (plus erythrocytes) were subfractionated into plasma membrane fraction, mitochondria and the post-mitochondrial fraction. 2. In all fractions, fatty acids were incorporated into phospholipids. This process was ATP
Diacylglycerol kinase ζ is a negative regulator of GPVI-mediated platelet activation.
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Diacylglycerol kinases (DGKs) are a family of enzymes that convert diacylglycerol (DAG) into phosphatidic acid (PA). The ζ isoform of DGK (DGKζ) has been reported to inhibit T-cell responsiveness by downregulating intracellular levels of DAG. However, its role in platelet function remains undefined.
Detection of antiphospholipid antibodies in children and adolescents.
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The prevalence of antiphospholipid antibodies (APAs) has not yet been studied in children and adolescents with various diseases. We assayed plasma samples of 203 children and adolescents, aged 0.1 to 21 years (median 6 years), by enzyme-linked immunosorbent assay detecting immunoglobulin G (IgG) and
A novel role for phospholipase D as an endogenous negative regulator of platelet sensitivity.
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Platelet aggregation, secretion and thrombus formation play a critical role in primary hemostasis to prevent excessive blood loss. On the other hand, uncontrolled platelet activation leads to pathological thrombus formation resulting in myocardial infarction or stroke. Stimulation of heterotrimeric
Shock: ischemia, reperfusion, and inflammation.
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The pathophysiology of shock after trauma and hemorrhage has traditionally been viewed as a result of ischemic cellular damage. However, it is now clear that ischemia alone does not result in all cellular damage after shock. Rather, much of the cellular injury follows reperfusion and subsequent
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