Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0220723 (PCA)
 4,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A successful case undergoing the ECA-PCA bypass operation with the use of an interposition saphenous venous graft for vertebrobasilar progressing stroke was reported and details of the operative techniques were described. A 40-year-old man was admitted because of confused mental state following sudden onset of headache, vomiting, vertigo, and ataxic gait. Neurological examinations revealed he was confused and restless, and left-sided Weber's syndrome, bulbar palsy and dysphasia were noticed. CT scan showed multiple small low density areas with no enhancement scattering in both occipital lobes and cerebellar hemispheres. Angiographical studies showed that the left vertebral artery was occluded at the vertebrobasilar junction and the right vertebral artery stenosed up to 90% or more at the branching site of the PICA. There was no visualization of the vertebrobasilar system through the right posterior communicating artery. The left posterior communicating artery was not examined. The patient was treated with Urokinase amounting to 740,000 units for ten days. Thirteen days later, however, he became progressively drowsy and he became unable to speak and swallow. Quadriparesis also appeared. Progressive deterioration of these brain stem ischemic symptoms was assumed to originate from critically lowered perfusion of the vertebrobasilar circulation. Therefore, the ECA-PCA anastomosis by means of a venous graft was carried out on the right side in expectation of the rapid restoration of the blood flow in the affected brain stem. A venous graft was chosen because it would carry larger amount of blood immediately after completing the bypass surgery than small calibered arterial graft such as a superficial temporal artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[ECA-PCA anastomosis with the use of an interposition saphenous vein graft for vertebrobasilar progressing stroke]. 404 16

AML patients may suffer from a disseminated coagulopathy, which can aggravate a pre-existing bleeding tendency due to thrombocytopenia and platelet dysfunction. The cellular and molecular mechanisms underlying this coagulopathy, however, are not completely understood. Indeed, the broad and increasing therapeutic use of cytotoxic drugs and growth factors is likely to contribute to the complexity of hemostatic abnormalities encountered in this hematologic malignancy. The nature of coagulation activation in AML was therefore investigated in vitro using the human leukemic cell line, HL60. Tissue factor (TF) was almost entirely located on the cell surface and bound factor VIIa, but only 15-25% of this TF was primarily functionally active. Treatment with increasing concentrations of daunorubicin or cytosine-beta-D-arabinofuranoside, two cytotoxic drugs commonly used in AML therapy, induced apoptosis and secondary necrosis of HL60 cells and resulted in marked decryption of TF PCA independent of de novo protein synthesis. This PCA-modulating effect was concomitant with and functionally dependent on the exposure of phosphatidylserine on the outer membrane leaflet. Similar observations were made in analogous ex vivo studies on patient-derived myeloblasts. Incubation of HL60 cells with GM-CSF, a cytokine expressed in the bone marrow microenvironment and used as an adjunct to AML treatment, evoked a cellular response, which included both enhanced TF production and release of VEGF-A and uPA into the culture medium. We conclude that both decryption of pre-formed TF PCA by chemotherapeutic drugs and de novo induction of TF by cytokines such as GM-CSF can regulate the pro-coagulant phenotype of HL60 cells in vitro.
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PMID:An in vitro study on the mechanisms of coagulation activation in acute myelogenous leukemia (AML): role of tissue factor regulation by cytotoxic drugs and GM-CSF. 1554 44

Activated platelets contribute to the arrest of bleeding by forming aggregates at sites of vascular injury and by providing a surface for assembling enzyme complexes involved in fibrin formation (platelet procoagulant activity; PCA). Impairment in the latter property of platelets has been observed in some disorders of hemostasis. In Scott syndrome, there is a defect in membrane vesiculation and in the surface expression of phosphatidylserine (PS), the phospholipid that is necessary for assembling the factor VIIIa/IXa (tenase) and factor Va/Xa (prothrombinase) complexes involved in thrombin formation. A family with an isolated defect in vesiculation, but normal prothrombinase activity, has also been reported. In the Quebec platelet disorder, overexpression of the fibrinolytic enzyme urokinase-type plasminogen activator results in the degradation of alpha-granule proteins, including factor V, and a specific abnormality in platelet factor V is the basis for the prothrombinase defect in platelet factor V-New York. The impaired prothrombinase activity in patients with delta-storage pool deficiency may be due to a failure to provide sufficient amounts of secreted adenine nucleotides which, when bound to P2 purinergic receptors, are necessary to maintain the intracellular Ca (2+) levels that are required for the surface expression of PS. Platelet prothrombinase activity and thrombin potential in patients with Glanzmann thrombasthenia (GPIIb-IIIa deficiency) may be decreased, normal, or increased, depending on the experimental conditions, for reasons that are not currently clear. The most consistent platelet PCA abnormality in the Bernard-Soulier syndrome (GPIb-complex deficiency) is an abnormally short serum prothrombin time, associated with a defect in the process by which an interaction between fibrin, von Willebrand factor, and GPIb promotes PCA.
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PMID:Impaired platelet procoagulant mechanisms in patients with bleeding disorders. 1940 96