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Страница 1 од 225 резултати
Disruption of Structural Disulfides of Coagulation FXIII-B Subunit; Functional Implications for a Rare Bleeding Disorder.
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Congenital FXIII deficiency is a rare bleeding disorder in which mutations are detected in F13A1 and F13B genes that express the two subunits of coagulation FXIII, the catalytic FXIII-A, and protective FXIII-B. Mutations in FXIII-B subunit are considerably rarer compared to FXIII-A.
A retrospective controlled study of thiol disulfide homeostasis as a novel marker in Crimean Congo hemorrhagic fever.
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OBJECTIVE
Crimean Congo hemorrhagic fever (CCHF) is the second most common hemorrhagic fever worldwide. This study aimed to evaluate the oxidant-antioxidant balance of patients with CCHF by detecting dynamic thiol disulfide homeostasis (TDH), which is a novel oxidative stress marker, and other
Murine tissue factor disulfide mutation causes a bleeding phenotype with sex specific organ pathology and lethality.
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Tissue factor is highly expressed in sub-endothelial tissue. The extracellular allosteric disulfide bond Cys186-Cys209 of human tissue factor shows high evolutionary conservation and in vitro evidence suggests that it significantly contributes to tissue factor procoagulant activity. To investigate
Crystal structures of acutolysin A, a three-disulfide hemorrhagic zinc metalloproteinase from the snake venom of Agkistrodon acutus.
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Acutolysin A alias AaHI, a 22 kDa hemorrhagic toxin isolated from the snake venom of Agkistrodon acutus, is a member of the adamalysin subfamily of the metzincin family and is a snake venom zinc metalloproteinase possessing only one catalytic domain. Acutolysin A was found to have a high-activity
Characterization of intramolecular disulfide bonds and secondary modifications of the glycoprotein from viral hemorrhagic septicemia virus, a fish rhabdovirus.
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Viral hemorrhagic septicemia virus (VHSV) infections cause high losses in cultured rainbow trout in Europe. Attempts to produce a recombinant vaccine based on the transmembrane glycoprotein (G protein) have indicated that proper folding is important for the antigenicity and immunogenicity of the
Diallyl Disulfide Prevents Cyclophosphamide-Induced Hemorrhagic Cystitis in Rats through the Inhibition of Oxidative Damage, MAPKs, and NF-κB Pathways.
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This study investigated the possible effects and molecular mechanisms of diallyl disulfide (DADS) against cyclophosphamide (CP)-induced hemorrhagic cystitis (HC) in rats. Inflammation response was assessed by histopathology and serum cytokines levels. We determined the protein expressions of nuclear
Analysis of Neutrophil/Lymphocyte ratio and Thiol/Disulfide homeostasis parameters in patients admitted to the emergency department with ischemic stroke.
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Protein disulfide-isomerase - a trigger of tissue factor-dependent thrombosis.
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The plasmatic coagulation system is tightly controlled by natural anticoagulant mechanisms, preventing thrombosis to ensure the supply of tissues with oxygen and nutrients without provoking susceptibility to bleeding diatheses. The membrane receptor tissue factor (TF) is the principal initiator of
Mode of inactivation of arenaviruses by disulfide-based compounds.
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Several disulfide-based compounds, including intermolecular aromatic disulfides of the type Ph-S-S-Ph and dithianes with the sulfur atoms tethered in a ring structure, have shown effective inhibitory activity against the arenaviruses Junin (JUNV), agent of Argentine hemorrhagic fever, and Tacaribe
Hypodysfibrinogenemia: A novel abnormal fibrinogen associated with bleeding and thrombotic complications.
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BACKGROUND
Congenital disorders of fibrinogen are rare diseases resulting in the complete absence (afibrinogenemia), reduced concentration (hypofibrinogenemia) or altered function of circulating fibrinogen (dysfibrinogenemia). A combination of two different fibrinogen abnormalities with a
The multimeric nonstructural NS2 proteins of bluetongue virus, African horsesickness virus, and epizootic hemorrhagic disease virus differ in their single-stranded RNA-binding ability.
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The structure and single-stranded (ss) RNA-binding by the nonstructural protein NS2 of three different orbiviruses were studied and compared. African horsesickness virus (AHSV), bluetongue virus (BTV), and epizootic hemorrhagic disease virus (EHDV) were analyzed in recombinant baculovirus-infected
A novel fibrinogen gamma-chain mutation, p.Cys165Arg, causes disruption of the γ165Cys-Bβ227Cys disulfide bond and ultimately leads to hypofibrinogenemia.
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BACKGROUND
Congenital hypofibrinogenemia is a type of hereditary disease characterized by impaired fibrinogen synthesis and/or secretion induced by mutations in the fibrinogen gene.
OBJECTIVE
We investigated the phenotypes, genotypes, and pathogenesis of congenital hypofibrinogenemia in an affected
Novel gain-of-function mutations of platelet glycoprotein IBalpha by valine mutagenesis in the Cys209-Cys248 disulfide loop. Functional analysis under statis and dynamic conditions.
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Platelet-type von Willebrand disease is a bleeding disorder resulting from gain-of-function mutations of glycoprotein (GP) Ibalpha that increase its affinity for von Willebrand factor (vWf). The two known naturally occurring mutations, G233V and M239V, both enrich the valine content of an already
Evaluation of dynamic thiol-disulfide homeostasis in very low-birth-weighted preterms.
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BACKGROUND
Thiols are organic compounds containing sulfhydryl groups which exert antioxidant effects via dynamic thiol-disulfide homeostasis. The shift towards disulfides indicates the presence of oxidative environment. Thiol-disulfide homeostasis has not been evaluated in neonates. We aimed to
Carbon disulfide effects on the visual system. I. Visual thresholds and ophthalmoscopy.
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The visual effects of carbon disulfide exposure were studied in macaque monkeys with measurements of visual thresholds, fluorescein angiography and fundus photography. Five monkeys were exposed by inhalation for 6 hr a day, 5 days a week to 256 ppm carbon disulfide (CS2). The motor dysfunction
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