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P Winocour

Publications and source records attributed to P Winocour.

12 recordsLinked to original sources
PubMed1997

Body mass index, waist circumference, waist-hip ratio, and glucose intolerance in Chinese and Europid adults in Newcastle, UK.

OBJECTIVE: To compare the prevalence of glucose intolerance (impaired glucose tolerance and diabetes), and its relationship to body mass index (BMI) and waist-hip ratio in Chinese and Europid adults. DESIGN: This was a cross sectional study. SETTING: Newcastle upon Tyne. SUBJECTS: These comprised Chinese and Europid men and women, aged 25-64 years, and resident in Newcastle upon Tyne, UK. MAIN OUTCOME MEASURES: Two hour post load plasma glucose concentration, BMI, waist circumference, and waist-hip ratio. METHODS: Population based samples of Chinese and European adults were recruited. Each subject had a standard WHO oral glucose tolerance test. RESULTS: Complete data were available for 375 Chinese and 610 Europid subjects. The age adjusted prevalences of glucose intolerance in Chinese and Europid men were 13.0% (p = 0.04). Mean BMIs were lower in Chinese men (23.8 v 26.1) and women (23.5 v 26.1) than in the Europids (p values < 0.001), as were waist circumferences (men, 83.3 cm v 90.8, p < 0.001; women, 77.3 cm v 79.2, p < 0.05). Mean waist-hip ratios were lower in Chinese men (0.90 v 0.91, p = 0.02) but higher in Chinese women (0.84 v 0.78, p < 0.001) compared with Europids. In both Chinese and Europid adults, higher BMI, waist circumference, and waist-hip ratio were associated with glucose intolerance. CONCLUSIONS: The prevalence of glucose intolerance in Chinese men and women, despite lower BMIs, is similar to or higher than that in local Europid men and women and intermediate between levels found in China and those in Mauritius. It is suggested that an increase in mean BMI to the levels in the Europid population will be associated with a substantial increase in glucose intolerance in Chinese people.

Adult↗
PubMed1984

Human platelets aggregate during antigen-antibody reactions at different antigen-antibody ratios.

The effects of immune complex formation on human platelets were tested in vitro using tetanus-toxoid and rabbit anti-tetanus toxoid for immune complex formation and washed human platelets. The antigen-antibody reactions took place at 37 degrees C in a stirred cuvette, constantly monitored. To this cuvette we added initially a platelet suspension and a dilution of antibody, and after this mixture reached equilibrium, antigen was added. Platelets aggregated as a consequence of immune reactions taking place at antigen-antibody ratios ranging from four times antigen excess to twenty times antibody excess (relative to equivalence). Platelets also aggregated as a result of reactions in which heat-inactivated antiserum was used, although in a more narrow range of Ag:Ab concentrations, suggesting that complement is not essential for their stimulation but may help in stabilizing the Ag:Ab reaction. Our observations provide indirect evidence in support of the involvement of human platelets in the pathogenesis of immune complex-mediated hypersensitivity reactions.

Animals↗
PubMed1983

Release of PAF by human polymorphonuclear leucocytes stimulated by immune complexes bound to Sepharose particles and human erythrocytes.

Human polymorphonuclear leucocytes (PMN) incubated with surface-bound immune complexes (IC) release a substance that induces platelet aggregation and serotonin-release. This substance was identified as platelet-activating factor (PAF) on the basis of its sensitivity to phospholipase A2 and of its purification by thin-layer chromatography in identical conditions to those used to purify zymosan-induced PAF. We used two types of substrates to absorb our IC:Sepharose particles to which we coupled human serum albumin, and which were later incubated with specific rabbit antiserum to form surface-bound immune complexes, and human erythrocytes, to which soluble IC can be passively adsorbed. Both types of surface-bound IC were found to stimulate the release of PAF by human PMN in the absence of complement. These results suggest that PMN may play a central role in the early stages of IC-induced inflammation: they recognize IC adsorbed to red cells or to any other cell able to adsorb IC, and they induce the activation of platelets and release of vasoactive amines, which leads to the increase of vascular permeability believed to be essential for extravascular IC deposition.

Animals↗