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VWFVon Willebrand Factor
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References in periodicals archive ?
To determine whether biomarkers of vascular injury are modulated in our pre-diabetes rat model, we measured the blood levels of adiponectin, soluble ICAM-1 and VCAM-1, ET-1, vWF, and PAI-1 in the animal groups.
The quantity of vWF that circulates in plasma is not only determined by the vWF gene situated on chromosome 12p12 but also determined majorly by other gene loci, of which the most important is the ABO blood group locus situated on chromosome 9q34.
VWF:Ag determinations were also performed on an ACL TOP-500 analyzer with a latex particle-enhanced immunoturbidimetric assay using HemosIL von Willebrand factor antigen kit (Instrumentation Laboratory, Bedford, MA, USA).
The standard diagnostic tests include measurement of total vWF protein (vWF antigen), a vWF activity (such as ristocetin-cofactor activity) and ristocetin-induced platelet aggregation (RIPA), which determine the ability of vWF to bind platelets.
Because estrogen increases vWF, treatment for von Willebrand syndrome should be progestin only, either oral pills, medroxyprogesterone acetate (MPA, or Depo-Provera injections), or an etonogestrel implant.
In addition, human VWF labeled with an IgG : FITC is used for visualizing suspended moving platelet-decorated VWF aggregates.
In intact vessels, at low-shear conditions, VWF circulates in a globular shape, as a "folded spring".
On the other hand, levels of miR-122 in the SHRSR positively correlated with CD31 and p-eNOS levels, whereas they negatively correlated with the levels of NF-kB, caspase 3, and vWF (Figure 5).
Factor VIII (FVIII) activity using a chromogenic assay, von Willebrand factor (VWF) antigen level, [[alpha].sub.2] plasmin inhibitor ([[alpha].sub.2]-PI) activity, plasminogen activity and D-dimer levels were measured on a BCS coagulometer by standard methods (Siemens Healthcare Diagnostic Products, Marburg, Germany).
When administered intravenously, this can cause a rapid increase of up to eightfold in circulating levels of factor VIII and VWF through release of endogenous VWF from endothelial Weibel-Palade bodies [4].
Further workup with coagulation studies showed decreased factor VIII, vWF antigen, and vWF: ristocetin cofactor assay, and negative Bethesda assay, indicating acquired von Willebrand disease.