ristocetin oor Frans

ristocetin

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en
(medicine) A toxic antibiotic, obtained from Amycolatopsis lurida , previously used to treat staphylococcal infections

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ristocétine

Method for determining von willebrand factor activity in the absence of ristocetin and for determining the adamts-13 protease
Procédé pour déterminer l'activité du facteur von willebrand en l'absence de ristocétine et celle de la protéase adamts-13
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The present invention relates to a method for detecting von-Willebrand factor (vWF) activity comprising assaying a sample in the presence of a soluble form or portion of glycoprotein Ib($g(a)) (GPIb($g(a)) and ristocetin, or a functionally equivalent substance.
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An antithrombotic agent containing as the active ingredient a monoclonal antibody that is reactive with human Von Willebrand factor, inhibits human RIPA (ristocetin-induced platelet aggregation), BIPA (bottrocetin-induced platelet aggregation), and SIPA (stress-induced platelet aggregation), and does not cause bleeding even when it is administered in a quantity efficacious in exhibiting the antithrombotic effect.
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2¿ show no loss of platelet function as determined by ADP, collagen, or ristocetin-induced aggregation.
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Method for determining von willebrand factor activity in the absence of ristocetin and for determining the adamts-13 protease
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Methods and kits for measuring levels of von Willebrand factor function in a sample without using a platelet aggregation agonist, such as ristocetin, comprising recombinant glycoprotein Ibα having at least two of a G233V, D235Y and M239V mutations and an agent to detect a complex between the recombinant glycoprotein Ibα and von Willebrand factor.
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The method includes the use of a mutant gain-of-function variant of the GPIbα protein, thus making it possible to dispense with the use of ristocetin, botrocetin or another ristocetin- or botrocetin-equivalent substance.
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Additionally, the invention relates to the use of the aforementioned soluble form or portion of glycoprotein Ib($g(a)), of ristocetin or a functional equivalent substance, of specifically reacting anti-GPIB($g(a)) antibody(ies) and/or of specific binding partners, like specifically reacting anti-vWF antibody(ies) for carrying out the method of the invention.
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The hypothesis that the calcium modulating property of cyclandelate is responsible for the inhibition of blood platelet functions is strengthened by the inability of the drug to inhibit the calcium-independent platelet aggregation induced by ristocetin.
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Ristocetin is an antibiotic, obtained from Amycolatopsis lurida, previously used to treat staphylococcal infections.
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In some types of vWD (types 2B and platelet-type), even very small amounts of ristocetin cause platelet aggregation when the patient's platelet-rich plasma is used.
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Under these conditions, ristocetin activates VWF and gives rise to a platelet agglutination reaction.
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It is observed in the presence of different agonists such as collagen, ristocetin and mechanical stress.
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A study of the pharmacokinetics of von Willebrand factor was performed in 8 patients with type 3 von Willebrand disease by the dosing of the ristocetin cofactor (FV: RCO).
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There is a decrease in adhesion, aggregation and platelet factor III production.Multiple studies have shown a decrease in aggregability in the presence of ADP (adenosine diphosphoric acid), collagen and ristocetin, while von Willebrand factor receptors have been found intact.
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When von Willebrand disease is suspected, several specific assays can be performed, including the VWF antigen (VWF:Ag) assay, determination of Factor VIII procoagulant activity, and the VWF ristocetin cofactor (VWF:RCo) activity assay.
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Currently the standard test for evaluating bleeding pattern is VWF:RCo (ristocetin cofactor assay) which has shown problems in relation to sensitivity and ristocetin binding.
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• Corresponding reduction in VWF antigen (VWF:Ag) and in ristocetin cofactor activity (VWF:RCo)
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Follow-up treatment is based on the results of clotting tests, in particular assay of clotting activity of factor VIII and of VWF ristocetin cofactor activity. Top Contents:
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Follow-up treatment is based on the results of clotting tests, in particular assay of clotting activity of factor VIII and of VWF ristocetin cofactor activity. Contents:
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Patients who have normal initial test results, along with symptoms or signs of bleeding and a positive family history, should be tested for VWD by measuring plasma von Willebrand factor (VWF) antigen, ristocetin cofactor activity (an indirect test for large VWF multimers), VWF multimer pattern, and factor VIII levels. If thrombocytopenia is present, the peripheral blood smear often suggests the cause (see Table: Peripheral Blood Findings in Thrombocytopenic Disorders).
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