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Currently, the replacement of a beta-cell function in type I diabetes has hailed to provide satisfactory long-term results. The reasons for eventual failure of islet cell transplants include the cellular response to injury and in long term beta-cell population dynamics. Present work focuses on the first of these: on stress signaling within the islet and their response to cytokine stimuli encountered during isolation/purification and engraftment. This is part of a multi-organ system approach to resolving the mechanisms of ischemia-induced injury during transplantation. The development of strategies to minimize organ damage at the molecular level in pancreas/islets, kidney and liver is the larger context within which specific research projects are developed