Conference:Inflammatory Paradigms and the Vasculature II

描述（由申请人提供）：血管系统在以下方面发挥核心作用： 炎症和应激反应，作为触发的焦点， 和解决急性过程，并参与长期的过程， 慢性疾病尽管人们一直关注急性机制， 炎症相关的血管功能障碍，很少有研究 研究导致慢性血管病变的机制。机制 潜在的血管细胞信号传导，特别是与剪切和 代谢应激、缺氧、白细胞运输和巨噬细胞活化， 将在专门讨论趋化因子，转录因子， （NF-kB和Egr-1），炎症级联反应，白细胞粘附分子和 清道夫相关受体。慢性炎症网络与 动脉粥样硬化和缺氧激活的细胞机制， 将强调脂蛋白更新和剪切应力的失调。在 除了与血管病理学机制相关的更多基础研究之外， 与糖尿病血管病变和再狭窄管理相关的课程将 解决目前的治疗方法。

DESCRIPTION (provided by the applicant): The vasculature has a central role in the inflammatory and stress responses, serving as a focal point for triggering and resolving acute processes, and participating in the protracted course of chronic disorders. Whereas much attention has been focused on acute mechanisms of inflammation-associated vascular dysfunction, many fewer studies have examined mechanisms contributing to chronic vascular pathologies. Mechanisms underlying vascular cell signaling, especially as relates to shear and metabolic stress, hypoxia, leukocyte trafficking and macrophage activation, will be highlighted in sessions devoted to chemokines, transcription factors (NF-kB and Egr-1), inflammatory cascades, leukocyte adhesion molecules and scavenger-related receptors. Parallels between chronic inflammatory networks in atherosclerosis and cellular mechanisms activated by oxygen deprivation, dysregulation of lipoprotein turnover and shear stress will be emphasized. In addition to more basic studies related to mechanisms of vascular pathology, sessions related to management of diabetic vasculopathy and restenosis will address current therapeutic approaches.