INTIMAL THICKENING & ANTITOXIDANTS IN HISPANICS & ANGLOS

描述：(改编自《调查人员摘要》)心血管疾病 仍然是美国残疾和早逝的主要原因，并有所改善 治疗和预防将源于对该病病因的了解。 动脉粥样硬化(Ath)。洛杉矶动脉粥样硬化研究(LAAS)是 以饮食和饮食为主的Ath病因的纵向调查 随机选择的573名公用事业工人的氧化机制 拉美裔美国人的过度抽样。初步结果包括保护性关系 血浆含氧类胡萝卜素与血管内膜中层1.3年变化之间的关系 颈总动脉厚度(IMT)，因果解释 叶黄素抑制低密度脂蛋白吸引单核细胞的研究结果支持 在动脉壁模型中被氧化，补充叶黄素的量减少 载脂蛋白E基因缺失小鼠的动脉粥样硬化程度增加了86%。此外，更高的摄入量 从补充剂中摄取的维生素C与 颈动脉IMT进展情况。相比之下，从食物中摄取更多的维生素C 与颈动脉IMT进展减慢有关，但这一保护作用 相关关系不显著。高密度脂蛋白胆固醇与颈动脉内膜厚度的保护关系为 通过更高的血浆、β-隐黄素和升高的血浆水平增强 一种破坏氧化脂质的酶(对氧磷酶，PON)。 这一应用程序建议继续观察LAAS队列与 增加了动脉功能障碍的两种超声测量方法和 实验室检查提示的新致病因素的探讨 合作者。更多的观测也将增加对 检测与IMT的关系。新的风险因素集中在 促进或抑制动脉壁中的低密度脂蛋白损伤和炎症反应。 动脉功能和功能障碍的新指标是：(1)内皮细胞 臂动脉的功能(管腔直径增加对 充血)；(2)颈总动脉扩张或僵硬。 这些额外措施，连同原始议定书中的措施，将 允许研究Ath的纵向变化与饮食之间的关系 抗氧化剂、抗氧化酶和遗传多态。

DESCRIPTION: (Adapted from Investigator's Abstract) Cardiovascular diseases remain the major causes of disability and early death in the U.S., and improved treatment and prevention will stem from knowledge of the etiology of atherosclerosis (Ath). The Los Angeles Atherosclerosis Study (LAAS) is a longitudinal investigation of the etiology of Ath focusing on diet and oxidative mechanisms in a randomly selected cohort of 573 utility workers, with oversampling of Hispanics. Preliminary results include a protective relation between plasma oxygenated carotenoids and 1.3 year change in the intima-media thickness (IMT) of the common carotid arteries, causal interpretation of which is supported by the findings that lutein inhibits monocyte attraction by LDL oxidized in a model of the artery wall, and that lutein supplementation reduced atherosclerosis extent by 86 percent in apo E null mice. Also, higher intake of vitamin C from supplements was significantly associated with increased progression of carotid IMT. In contrast, higher intake of vitamin C from food was associated with reduced progression of carotid IMT, but this protective relation was not significant. The protective relation of HDL-C with IMT was enhanced by higher plasma, beta-cryptoxanthin and by increased plasma level of an enzyme (paraoxonase, PON) that destroys oxidized lipids. This application proposes continued observation of the LAAS cohort with the addition of two ultrasound measures of arterial dysfunction and the investigation of new etiologic factors for Ath suggested by laboratory findings of collaborators. Additional observations will also increase power for detecting relations with IMT. The new risk factors focus on pathways that promote or inhibit LDL damage and inflammatory responses in the artery wall. The new measures of arterial function and dysfunction are (1) endothelial function of the brachial artery (lumen diameter increase in response to hyperemia); and (2) distensibility or stiffness of the common carotid artery. These additional measures, together with those in the original protocol, will allow investigation of relations between longitudinal change in Ath and dietary antioxidants, antioxidant enzymes, and genetic polymorphisms.