糖尿病、氧化应激与AS.pptVIP

* * In the GISSI-Prevenzione trial, 11323 patients with recent (?3 months, median 16 days) myocardial infarction were enrolled for an evaluation of polyunsaturated fatty acids and vitamin E during a mean follow-up of 3.5 years. This study made it possible to study the long-term survival according to the presence or absence of metabolic syndrome at inclusion. The definition of the metabolic syndrome used was the NCEP/ATP III but BMI (with a threshold ? 26 kg/m2) replaced waist girth which was not available at inclusion. Patients with metabolic syndrome without diabetes had a worse prognosis, both for total and cardiovascular mortality, than those without metabolic syndrome or diabetes. However, the prognosis of patients with diabetes was itself worse than that of patients with the metabolic syndrome. * * * 体内自由基的产生和清除应是平衡的，人体才能保持健康。正常情况下，自由基反应对于机体防御机制是必要的，自由基的产生与清除保持平衡。但在某些病理情况下，如果自由基产生过多或清除自由基的抗氧化防御系统能力下降，体内就会有多余的自由基（特别是氧自由基），会损伤细胞成分，导致疾病和衰老的发生。 氧化应激是指机体在遭受各种有害刺激时．机体或细胞内自由基的产生和抗氧化防御之间严重失衡，或外源性氧化物质的过量摄入，导致活性氧在机体或细胞内蓄积而引起的细胞毒性，从而导致组织损伤过程。 * * * * angina * Matrix metabolism and integrity of the plaques fibrous cap This slide depicts the current understanding of the dynamics of the plaques stability and thrombogenicity. The inflammatory cells can send molecular messages to the smooth muscle cells (interferon-g) that inhibit the ability of this cell type to synthesize new collagen to strengthen the plaques fibrous cap. In addition, the inflammatory cells can release proteolytic enzymes capable of degrading collagen and other structurally important constituents of the plaques fibrous cap. Thus, when there is inflammation in the intima, the collagen responsible for the integrity of the plaques fibrous cap is under double attack, subject to both decreased synthesis and increased degradation. This sets the stage for plaque disruption. The inflammatory cells also are responsible for signaling and producing increased quantities of tissue factor, a potent procoagulant dee