MECHANISMS OF REPAIR OF ISCHEMIC INJURED INTESTINE

这个实验室的目标是确定肠道修复的机制。 以利于损伤肠管的恢复。肠缺血 再灌流损伤尤其令人感兴趣，因为它在心脏损伤中的作用。 马绞痛综合征，马的主要杀手。一种模型 将在猪体内形成缺血/再灌注损伤。这是有可能的 猪将为人和马提供更好的模型， 因为黄嘌呤氧化酶的水平也很低。相对的 缺血和再灌注对肠道损伤的贡献将是 下定决心。在大型动物中，缺血性损伤似乎更重要 物种多于再灌流损伤，而不是啮齿动物模型 再灌流损伤明显。因为阻断再灌流失败 马的损伤，以及啮齿动物模型与 对人体再灌注损伤，修复过程会有一定的刻画。 谷氨酰胺(Gln)和生长因子促进细胞增殖的能力 以及谷氨酰胺促进修复的机制 他仔细检查了一下。具体地说，Jun核蛋白的激活和 丝裂原激活的激酶，对诱导“早期-- 这些研究应该会为我们提供基本的 上皮细胞增殖机制及替代方案的研究进展 缺血性损伤的治疗方法。

The goal of this laboratory is to identify mechanisms of intestinal repair in order to facilitate recovery of injured intestine. Intestinal ischemial reperfusion injury is of particular interest because of its role in the equine colic syndrome, the principal killer of horses. A model of ischemia/ reperfusion injury will be developed in the pig. It is possible that the pig will provide a better model for the human and the horse, because of similar low levels of xanthine oxidase. The relative contribution of ischemia and reperfusion to intestinal injury will be determined. Ischemic injury appears to he more important in large animal species than reperfusion injury, as opposed to rodent models in which reperfusion injury is prominent. Because of a failure to block reperfusion injury in the horse, and the questionable relevance of rodent models of reperfusion injury to the human, the repair process will be characterized. The ability of glutamine (GLN) and growth factors to enhance proliferation will be investigated, and the mechanism by which GLN facilitates repair will he examined. Specifically, activation of Jun-nuclear kinase and Mitogen-activated kinase, enzymes critical for the induction of "early- immediate" genes, will be assessed. These studies should provide basic information on mechanisms of epithelial proliferation and alternative therapeutic approaches to ischemic injury.