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Sivu 1 alkaen 572 tuloksia
Thromboelastographic assessment of the contribution of platelets and clotting proteases to the hypercoagulable state of dogs with immune-mediated hemolytic anemia.
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BACKGROUND
Hypercoagulability is a well-known feature of canine immune-mediated hemolytic anemia (IMHA) and is believed to increase the risk of thrombosis. This study was undertaken to differentiate the relative contribution of platelets and clotting proteases to this hypercoagulability using
Ferritin and sideroblastic anaemias: inhibition of protein synthesis by protease contaminants in commercial preparations of ferritin.
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Commercial preparations of ferritin inhibited reticulocyte-lysate cell-free protein synthesis and disaggregated polyribosomes to monoribosomes and ribosomal subunits. These effects were prevented by addition of reduced glutathione (GSH) to the incubation medium, but ferritin did not lower GSH
Increased plasma glycosidase and protease activity in uraemia: possible role in the aetiology of the anaemia of chronic renal failure.
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We have measured plasma N-acetyl-beta-D-glucosaminidase (EC 3.2.1.30) and neuraminidase (EC 3.2.1.18) activities as markers of glycosidase activity and immunoreactive trypsin (EC 3.4.21.4) levels as a marker of proteolytic potential in the plasma of normal and uraemic subjects. The levels of all of
A mutation in the TMPRSS6 gene, encoding a transmembrane serine protease that suppresses hepcidin production, in familial iron deficiency anemia refractory to oral iron.
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BACKGROUND
Hepcidin plays a key role in body iron metabolism by preventing the release of iron from macrophages and intestinal cells. Defective hepcidin synthesis causes iron loading, while overproduction results in defective reticuloendothelial iron release and iron absorption.
METHODS
We studied a
Role of ITPA and SLC28A2 genes in the prediction of anaemia associated with protease inhibitor plus ribavirin and peginterferon in hepatitis C treatment.
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BACKGROUND
Anaemia is a common side-effect of ribavirin (RBV) use that overwhelms management of hepatitis C when protease inhibitors are added.
OBJECTIVE
To assess the pharmacogenomic impact of candidate genes SLC28A2, SLC28A3 and ITPA on anaemia in patients receiving triple
Expression of the protease gene of equine infectious anemia virus in Escherichia coli: formation of the mature processed enzyme and specific cleavage of the gag precursor.
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A 620-bp Bg/II restriction fragment containing the putative protease coding sequence from equine infectious anemia virus (EIAV) proviral DNA was cloned and expressed in E. coli as a Pol precursor protein. In contrast to the 25-kDa fusion protein predicted from the expressed pol sequence, a protein
delta-Aminolevulinic acid synthetase in erythroblasts of patients with pyridoxine-responsive anemia. Hypercatabolism caused by the increased susceptibility to the controlling protease.
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Properties of delta-aminolevulinic acid synthetase in erythroblasts of patients with pyridoxine-responsive anemia were investigated with special reference to the protease in mitochondria of erythroblasts. delta-Aminolevulinic acid synthetase activity in erythroblasts of patients with this disease
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
Matriptase-2 mutations in iron-refractory iron deficiency anemia patients provide new insights into protease activation mechanisms.
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Mutations leading to abrogation of matriptase-2 proteolytic activity in humans are associated with an iron-refractory iron deficiency anemia (IRIDA) due to elevated hepcidin levels. Here we describe two novel heterozygous mutations within the matriptase-2 (TMPRSS6) gene of monozygotic twin girls
[Accessory use of protease-inhibiting agents for disease remission in a patient with autoimmune hemolytic anemia associated with B-CLL].
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Protease inhibiting agents, which have inhibitory effects on complement system, were used to treat a patient with autoimmune hemolytic anemia (AIHA) associated with B cell chronic lymphocytic leukemia (B-CLL). Although this patient had failed to respond thoroughly to prednisolone, the additional use
Demonstration of kallikrein-like protease activity in nonactivated plasma of patients with Cooley's anemia.
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Routine evaluation of 12 children with Cooley's anemia revealed that each one had a prolonged partial thromboplastin time. However, prothrombin time and thrombin time were within the normal range. Specific assays demonstrated low levels of the four contact factors: factors XI, XII, prekallikrein,
Microangiopathic haemolytic anaemia in metastasizing malignant tumours is not associated with a severe deficiency of the von Willebrand factor-cleaving protease.
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Complete deficiency of von Willebrand factor-cleaving protease (VWF-cp) has recently been identified as a pathogenetically important factor for thrombotic thrombocytopenic purpura (TTP). Microangiopathic haemolytic anaemia (MAHA) with thrombocytopenia in patients with metastasizing neoplasms is
Protease inhibitors-based therapy induces acquired spherocytic-like anaemia and ineffective erythropoiesis in chronic hepatitis C virus patients.
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OBJECTIVE
The addition of protease inhibitors, boceprevir (BOC) or telaprevir (TRV), to peg-interferon and ribavirin (PR) increases the incidence of anaemia in patients with chronic hepatitis C virus (HCV) infection. Although genetic variants in inosine triphosphatase (ITPA) gene have been linked to
Expression of functional protease and subviral particles by vaccinia virus containing equine infectious anaemia virus gag and 5' pol genes.
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Cells infected with vaccinia viruses expressing the equine infectious anaemia virus (EIAV) gag gene (VGag) or gag plus the 5' pol encoding protease (VGag/PR) were evaluated with monoclonal antibody to a p26 capsid protein linear epitope (QEISKFLTD). Both recombinant viruses expressed Gag precursor
Predictors of early treatment discontinuation and severe anemia in a Brazilian cohort of hepatitis C patients treated with first-generation protease inhibitors.
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The aim of this study was to determine risk factors for adverse events (AE)-related treatment discontinuation and severe anemia among patients with chronic hepatitis C virus (HCV) genotype 1 infection, treated with first-generation protease inhibitor (PI)-based therapy. We included all patients who
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