A Method for Assaying von Willebrand’s Factor – Erratum

Macfarlane, Donald E.

doi:10.1055/s-0038-1648035

Cited by 18 publications

(18 citation statements)

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“…Serum levels of ACE and plasma levels of von Willebrand factor (vWF) were measured as markers of endothelial function/damage 16,17 with previously reported methods. 18,19 Interassay and intra-assay variation was Ͻ8% for these measurements.…”

Section: Methodsmentioning

confidence: 99%

Arterial Hemodynamics in Patients After Kawasaki Disease

et al. 2005

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Background-Histopathological findings in the acute stage of Kawasaki disease (KD) indicate widespread vascular inflammation that involves not only coronary arteries but also systemic arteries. This may cause changes in systemic arterial wall properties after KD, which could have adverse effects on arterial hemodynamics (an important predictor of cardiovascular morbidity and mortality). Methods and Results-Systemic arterial hemodynamics were investigated by measuring aortic input impedance during cardiac catheterization in 42 KD patients who had developed coronary artery lesions (CALs) in the acute stage of KD. The KD patients were subdivided into 2 groups according to the angiographic findings (group 1A, 26 patients with persistent CALs; group 1B, 16 patients with regressed CALs), and results were compared with those of 36 referents (group 2). Compared with referents, characteristic impedance was significantly higher for KD patients (137.0Ϯ5.1, 125.7Ϯ8.2, and 97.9Ϯ4.1 dyne · s · cm Ϫ5 · m 2 for group 1A, group 1B, and group 2, respectively), and total peripheral arterial compliance indexed to age-specific values was significantly lower for KD patients (group 1A 72.9Ϯ4.2% of normal; group 1B 70.6Ϯ5.9% of normal; group 2 97.7Ϯ4.0% of normal; for both variables, PϽ0.05 for each KD group versus group 2; PϭNS between KD groups), which suggests that both central and peripheral arterial wall stiffness increase after KD regardless of persistence of CALs. Also, indices of arterial wave reflection (reflection coefficient, reflection factor, and augmentation index) were all significantly higher in KD patients than in referents (PϽ0.05), with the result that the aortic pressure waveforms of the present KD patients resembled those generally observed in the elderly. In addition, levels of circulating markers of endothelial dysfunction (ACE and von Willebrand factor) were associated with increased vascular stiffening in KD patients but not in referents. Conclusions-These results indicating abnormal arterial hemodynamics after KD highlight the importance of regular monitoring of the systemic arterial bed and potentially relevant cardiovascular events in long-term follow-up of KD.

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Section: Methodsmentioning

confidence: 99%

Arterial Hemodynamics in Patients After Kawasaki Disease

et al. 2005

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“…Factor VIII-related antigen (VIIIR:Ag) was quantitated by electroimmunoassay (Laurell 1966; Takahashi 1981a) using specific antiserum against human factor VIII (Behringwerke AG, West Germany). Ristocetin cofactor (VIIIR: RCo) was measured quantitatively with a macroscopic tilt-tube method (Allain et al 1975) or an aggregometric assay (Macfarlane et al 1975; Takahashi 1981b) using formalin-fixed platelets (Macfarlane et al 1975) and ristocetin (H. Lundbeck & Co., Denmark). Serum fibrin/fibrinogen degradation products (FDP) were determined by the latex agglutination immunoassay (Teikoku Hormone Manufacturing Co., Japan).…”

Section: Assay Methodsmentioning

confidence: 99%

Profile of blood coagulation and fibrinolysis in chronic myeloproliferative disorders.

Takahashi

Hattori

Shibata

1982

Tohoku J. Exp. Med.

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“…When the effect of anti-vWf mAbs on platelet aggregation was evaluated, the mAb was preincubated with PRP for 30 min at room temperature before the addition of the inducer. The vWf RiCoF activity was measured according to MacFarlane et al (27) using fresh washed platelets.…”

Section: Platelet Aggregation Assaysmentioning

confidence: 99%

A monoclonal antibody recognizes a von Willebrand factor domain within the amino-terminal portion of the subunit that modulates the function of the glycoprotein IB- and IIB/IIIA-binding domains.

Tornai

Arnout²,

Deckmyn³

et al. 1993

J. Clin. Invest.

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We developed a monoclonal antibody, 1C1E7, against vWf that increases ristocetin-induced platelet aggregation in a dose-dependent manner and lowers the threshold concentration of ristocetin needed to obtain a full aggregatory response. The platelet aggregatory effect of asialo vWf (ASvWf) also is enhanced by 1CIE7, in the presence or absence of glycoprotein (GP) Ilb/IlIa receptor antagonism. In the presence of ristocetin, both intact 1ClE7 and its Fab fragments enhance specific binding of '25I-vWf to platelets. With 1ClE7, the intermediate and higher molecular weight multimers of vWf are preferentially bound to both GP lb and GP IIb/IIIa. Thrombin-induced 125I-vWf binding to GP IIb/Illa also is increased by 1ClE7. Maximal binding of 1C1E7 to vWf corresponds to 0.97 mol/mol vWf monomer with a Kd of 4.7 x 10-10 M. 1ClE7 reacts with a 34 /36-kD tryptic fragment (III-T4) and a 34-kD plasmic fragment (P34), which localizes the epitope between amino acid residues 1 and 272; this was confirmed by NH2-terminal amino acid sequencing. Finally, platelet aggregation by ASvWf was associated with a sharp rise in intracellular Ca2+ only in the presence of 1C1E7. An antibody-mediated conformational change of vWf may result in an improved presentation of the GP Ib-and GP IIb/ IIIa-binding domains of mainly the larger multimers; the increased density of vWf on the platelet surface leads to platelet activation. The antibody may thus recognize a domain of relevance for vWf physiology. (J. Clin. Invest. 1993. 91:273-282.)

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A Method for Assaying von Willebrand’s Factor – Erratum

Cited by 18 publications

References 0 publications

Arterial Hemodynamics in Patients After Kawasaki Disease

Arterial Hemodynamics in Patients After Kawasaki Disease

Profile of blood coagulation and fibrinolysis in chronic myeloproliferative disorders.

A monoclonal antibody recognizes a von Willebrand factor domain within the amino-terminal portion of the subunit that modulates the function of the glycoprotein IB- and IIB/IIIA-binding domains.

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