Summary. The relationships of three measurements of the factor VIII/von Willebrand factor (VWF) complex (factor VIII activity, FVIIIc (one-stage assay); VWF antigen, VWF Ag (ELISA); and VWF activity, VWF act, measured by a recentlydeveloped ELISA) to major ischaemic heart disease (IHD) events were studied in 1997 men aged 49-65 years, in the second phase of the Caerphilly Heart Study. These variables were related using logistic regression analysis to myocardial infarction or IHD death, which occurred in 129 men during an average follow-up period of 61 months. All three measurements were highly correlated (r ¼ 0·63-0·77), and each was significantly associated with incident major IHD on univariate analyses (relative odds in highest fifth compared to lowest fifth, 1·68-1·90; P ¼ 0·028-0·006) and on multivariate analyses adjusting for major IHD risk factors and for baseline IHD. Neither FVIIIc nor VWF act was significantly related to incident IHD following adjustment for VWF Ag. We therefore suggest that the associations between these three measurements of the factor VIII/VWF complex and incident IHD might have at least three explanations: VWFAg is a marker of arterial endothelial disturbance; VWF act promotes platelet adhesion/aggregation and hence the platelet component of arterial thrombosis; and FVIIIc promotes fibrin formation and hence the fibrin component of arterial thrombosis.

Summary.The clinical manifestations of the antiphospholipid syndrome (APLS) include arterial and venous thrombosis, thrombocytopenia and fetal loss, but the pathogenic mechanisms remain unclear. It has been hypothesized that platelet activation by autoantibody may be a pathogenic mechanism. We studied IgG binding, microparticle (mp) formation and P-selectin expression by flow cytometry in normal platelets after incubation in serum from 11 patients with antiphospholipid antibodies and that from 10 normal healthy subjects. Levels of platelet-associated IgG were significantly higher after incubation in patient sera (mean 17·2, range 2·0-75·0%) compared with normal sera (mean 2·0, range 1·2-3·7%, P < 0·05). Incubation of normal platelets in serum led to increased microparticle formation (P < 0·01) and P-selectin expression (P < 0·05), compared with unstimulated platelets. There was no significant difference, however, between microparticle formation nor P-Selectin expression induced by patient serum (mp 3·0 (1·6-5·0)%; P-selectin 8·0 (4·0-16·6)%) versus normal serum (mp 3·2 (2·1-4·5)%; P-selectin 10·1 (4·0-15·6); median (range)). Pre-activation of platelets with subthreshold ADP concentrations or thrombin receptor activator peptide resulted in a small increase in microparticle formation, but there was still no significant difference between the effects of patient and control sera. Despite the presence of platelet membrane binding IgG in serum from 5/11 patients with antiphospholipid antibodies, there was no evidence for associated enhanced platelet-activating ability. This study supports antiplatelet reactivity in antiphospholipid syndrome, but not a direct platelet-activating role for platelet-directed autoantibodies.

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Black and Hispanic students are consistently underrepresented in gifted and talented education and related academic programs. Attitudes, philosophy, tests and other instruments, and policies and procedures are often the fundamental barriers. In this article, recommendations and resources are shared to guide school personnel in evaluating their gifted programs in terms of equity and cultural responsiveness. Included is a federal formula for calculating underrepresentation and setting equity goals, and an equity-based culturally responsive bill of rights that targets several areas for schools to evaluate gifted and talented education in their recruiting and retaining gifted students of color.