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thrombocytopenia/protease
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Pagina 1 a partire dal 331 risultati
Response of severe HIV-associated thrombocytopenia to highly active antiretroviral therapy including protease inhibitors.
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OBJECTIVE
To investigate the response of HIV-associated severe thrombocytopenia (STP) to highly active antiretroviral therapy (HAART) including protease-inhibitors.
METHODS
In this retrospective study, 15 patients with HIV-associated STP (platelet count < 50 x 10(9)/l mostly antiretroviral
Evidence implicating calpain (Ca(2+)-dependent neutral protease) in the destructive thrombocytopenia of the Wiskott-Aldrich syndrome.
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The Wiskott-Aldrich syndrome (WAS) is an inherited platelet/T-lymphocyte disease characterized by small platelets, thrombocytopenia and immunodeficiency. Because degradative events have a significant role, we directly examined calpain (Ca(2+)-dependent neutral protease), a prominent protease in the
Congenital microangiopathic hemolytic anemia and thrombocytopenia with unusually large von Willebrand factor multimers and von Willebrand factor-cleaving protease.
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Infantile or congenital cases of thrombotic microangiopathy have been reported that were familial and characterized by ongoing microangiopathic hemolysis and thrombocytopenia in the absence of regular fresh-frozen plasma transfusions. The authors describe a child with congenital microangiopathic
The cholesterol, fatty acid and triglyceride synthesis pathways regulated by site 1 protease (S1P) are required for efficient replication of severe fever with thrombocytopenia syndrome virus.
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Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by the SFTS virus (SFTSV), which has a high mortality rate. Currently, no licensed vaccines or therapeutic agents have been approved for use against SFTSV infection. Here, we report that the cholesterol,
Cleavage of anti-PF4/heparin IgG by a bacterial protease and potential benefit in heparin-induced thrombocytopenia.
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Heparin-induced thrombocytopenia (HIT) is due to immunoglobulin G (IgG) antibodies, which bind platelet factor 4 (PF4) modified by polyanions, such as heparin (H). IgG/PF4/polyanion complexes directly activate platelets via Fc gamma type 2 receptor A (FcγRIIA) receptors. A bacterial protease,
Acute thrombocytopenia secondary to the administration of the peptidomimetic HIV protease inhibitor MK-639(L735524)
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Efficacy of protease inhibitor-based anti-retroviral therapy in severe HIV-associated thrombocytopenia unresponsive to AZT.
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Reevaluation of platelet function in chronic immune thrombocytopenia: impacts of platelet size, platelet-associated anti-αIIbβ3 antibodies and thrombopoietin receptor agonists.
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Platelet function of immune thrombocytopenia (ITP) has been controversial because of methodological problems associated with low platelet counts. In this study, we evaluated platelet function in 21 patients with chronic ITP (cITP) using the recently developed flow cytometry (FCM)-based platelet
Characterization of an antibody to the integrin beta 3 subunit (GP IIIa) from a patient with neonatal thrombocytopenia and an inherited deficiency of GP IIb-IIIa complexes in platelets (Glanzmann's thrombasthenia).
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Patient A.F. is a 28-year-old polytransfused woman with an inherited bleeding disorder, Glanzmann's thrombasthenia. An abnormal platelet function is linked to severe decreases in the platelet content of the integrins GP IIb and GP IIIa. In 1987 the patient gave birth to a child with severe anemia
Pathogenesis and management of heparin-induced thrombocytopenia and thrombosis.
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Heparin-induced thrombocytopenia and thrombosis is a severe immune-mediated adverse drug effect caused by the IgG antibodies to platelet factor4/heparin complexes. Activated platelets, vascular endothelium, and monocytes generate the life-threatening thrombocytopenia and thrombosis. In this review,
[HIV-related thrombocytopenias].
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Thrombocytopenia is a relatively frequent hematological complication in patients infected with the human immunodeficiency virus type 1. Occurring in all risk groups (homosexuals, intravenous drug addicts, hemophiliacs, heterosexuals) this complication has an overall prevalence varying between 5 and
Thrombocytopenia and severe hyperbilirubinemia in the neonatal period secondary to congenital thrombotic thrombocytopenic purpura and ADAMTS13 deficiency.
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Congenital thrombotic thrombocytopenic purpura (TTP) is an inherited form of TTP due to the deficiency of von Willebrand factor (vWF) cleaving protease ADAMTS13. The authors describe two children with congenital TTP who presented with thrombocytopenia, hemolytic anemia, elevated LDH levels, and
Decreased von Willebrand factor protease activity associated with thrombocytopenic disorders.
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Recent studies investigating thrombotic thrombocytopenic purpura (TTP) have implicated abnormal plasma von Willebrand factor (vWF)-cleaving metalloprotease activity in this disorder. It has been proposed that a metalloprotease cleaves unusually large (UL) multimers of vWF, which enter the
Role of Malt1 protease activity in pathogenesis of inflammatory disorders mediated by FcγR signaling.
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MALT lymphoma-translocation protein 1 (Malt1) protease activity is triggered by stimulation of various immune receptors. Activation of Malt1 protease induces cleavage of negative regulators for immune responses, resulting in lymphocytes activation. Although Malt1 protease mediates the signaling
Treatment of post-transfusion graft-versus-host disease with nafmostat mesilate, a serine protease inhibitor.
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BACKGROUND
Cytotoxic T lymphocytes from donors are thought to injure the target organs in post-transfusion graft-versus-host disease (PT-GVHD) through perforin-granzyme- and Fas-dependent cell killings. The protease involved is a serine protease, and nafmostat mesilate (NM), a serine protease
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