CONFERENCE ON LIPID MEDIATORS

花生四烯酸代谢产物是 哮喘(白三烯)和哮喘的炎症过程 类风湿性关节炎(前列腺素)以及一系列不同的 其他病理生理状态和生理功能。引言 防止生物合成或受体介导的新疗法的出现 半胱氨基白三烯的作用及其选择性治疗 诱导的前列腺素内酯合成酶-2(PGHS-2) 发现与疾病相关的多态性，提供额外的疾病预防 肠道恶性肿瘤等靶点，疗效降低 毒性。与此同时，基因破坏技术在中国的应用 小鼠帮助定义了特定的花生四烯酸的功能 酸代谢途径。计划中的会议将定义当前的 由特定干预措施提供的争议和见解 人类和小鼠基因的破坏，而集中在 在各种中心发展问题上的细胞和分子水平。 这些包括：澄清在不同细胞中的功能 10种或更多磷脂酶A2(PLA2)起源于不同的基因 以及将特定的PLA2划分为其链接的功能 与特定的核周膜相关酶结合； 二十烷类化合物生成过程中关键酶的转录调控 与疾病相关的基因多态研究 各州。还将重点关注出现的受体蛋白。 以两种方式与花生四烯酸代谢物相互作用-在 转录调控的细胞核和质膜上的 信号转导反应。该方案将假定合理 最先进的知识，并将重点放在进一步的影响 关于这些知识和悬而未决的问题，使用分子， 细胞、转基因和临床方法。

The products of arachidonic acid metabolism are central to the inflammatory processes in bronchial asthma (leukotrienes) and in rheumatoid arthritis (prostaglandins) along with a diverse array of other pathobiologic states and physiologic functions. The introduction of novel therapies to prevent the biosynthesis or receptor-mediated action of the cysteinyl leukotrienes and of novel therapy selective for the induced prostaglandin endoperoxide synthetase type 2 (PGHS-2) has uncovered disease-related polymorphisms, additional disease prevention targets such as intestinal malignancy, and efficacy with reduced toxicity. At the same time, the use of gene disruption technology in the mouse has helped to define the functions of particular arachidonic acid metabolic pathways. The meeting planned will define the current controversies and insights provided by specific interventions in the human and gene disruption in the mouse, while concentrating at the cellular and molecular level on a variety of central evolving issues. These include: a clarification of the function in various cells of the ten or more phospholipase A2 (PLA2) species derived from separate genes and the compartmentalization of a particular PLA2 to its linked function with a particular perinuclear membrane associated enzyme; the transcriptional regulation of key enzymes in the eicosanoid generating pathways; and studies of gene polymorphism in association with disease states. There will also be a focus on the receptor proteins that appear to interact with arachidonic acid metabolites in two ways - within the nucleus for transcriptional regulation and at the plasma membrane for signal transduction responses. The program will assume reasonable state-of-the-art knowledge and will focus on the further implications of that knowledge and on the unresolved issues, using molecular, cellular, transgenic, and clinical approaches.