TRAUMA PRIMES CELLS

我们的创伤中心拨款延续了我们第一笔资金的假设 循环：“创伤启动细胞。”这一更新设想了 五个项目。临床核心项目将继续作为创伤/MOF 注册表。然而，帕特·奥夫纳指出，输血，这是 我们最初被用作震惊的替代标记，独立预测 国防部。他提出，输血中的脂质在血液循环中处于初始状态 中性粒细胞。吉恩·摩尔的项目令人信服地展示了我们的 创伤后内脏低血症可能是第一个资金周期 不会转移人体内的细菌/内毒素。他目前假定 损伤后的肠道缺血启动了循环中的中性粒细胞和 远端血管内皮细胞。Shin Meng的项目承认 巨噬细胞在多器官功能衰竭中的中心作用 微囊化HSP-72转导巨噬细胞可控制其细胞毒作用 肿瘤坏死因子的产生。奥尔登·哈肯假设内源性肿瘤坏死因子的产生是通过 心脏直接损害心脏功能，延迟术后早期 创伤性器官修复并加重晚期多器官功能衰竭。Ani Banerjee的项目 假设描述后-的细胞信号语言 应激/损伤引发可以被识别并进行治疗操作。 除了创伤研究中心，我们把自己想象成一个创伤 研究培训中心。

Our center trauma grant continues the hypothesis of our first funding cycle: "Trauma primes cells." This renewal envisions the interweaving of five projects. The clinical core project will continues as a trauma/MOF registry. Pat Offner has noted, however, that a blood transfusion, which we initially used as a surrogate marker of shock, independently predicts MOF. He proposes that lipids in transfused blood prime circulating neutrophils. Gene Moore's project convincingly demonstrated during our first funding cycle that post -traumatic splanchnic hypofusion probably does not translocate bacteria/endotoxin in man. He currently postulates that post-injury gut ischemia primes both circulating neutrophils and distant vascular endothelial cells. Shin Meng's project recognizes the central role of the macrophage in MOF and proposes that liposome encapsulated HSP-72 transfer into macrophages can control their cytotoxic TNF production. Alden Harken postulates that endogenous TNF production by heart directly compromises cardiac function which delays early post- traumatic organ repair and exacerbates late MOF. Ani Banerjee's project postulates that the cell signaling language delineating post- stress/injury priming can be identified and therapeutically manipulated. In addition to a trauma research center, we envision ourselves a trauma research training center.