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Atkinson, Carl
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Heart transplantation is an accept treatment modality for patients with end-stage heart disease. These patients have reached the end of conventional pharmacological therapy or surgical interventions and the only therapeutic option left is heart transplantation. Current first year survival rates post transplantation varies between 80-95%, and patients surviving beyond the first can expect an average half-life of 11 years. While these results are acceptable patients eventually succumb to chronic rejection which manifests as an obliterative vascular lesion which restricts the hearts blood supply and eventually leads to heart failure. The precise mechanisms that contribute to the development of chronic rejection are unknown, but recent data implicates the early ischemic damage these hearts receive due to the transplant process and brain death.
Results from kidney transplantation have shown that the quality of the donor organ is important for post transplant survival. Organs donated from living donors perform better than those harvested from cadaveric donors. It is believed that the processes stimulated during brain death in these cadaveric donors, activates the donor heart rendering it more susceptible to ischemic damage, upon implantation, and ultimately acute and chronic rejection. The mechanisms responsible for these inflammatory changes to the donor organ are poorly characterized. Our research focuses on the elucidation of these mechanisms and the application of novel therapies that can be applied to the donor prior to transplantation to limit donor organ damage. During brain death all of the organs in the body are exposed to ischemia and chaotic changes in blood supply and pressure. Our studies have implicated the complement system in the activation of the donor heart. The complement system is composed of a series of serum proteins that work in a concerted fashion to induce cell death, promote inflammation and pro-inflammatory cytokines. We have been working with complement inhibitory proteins with the aim to reduce complement mediated brain death induced inflammation and ultimately to reduce the incidence and severity of both acute and chronic rejection.
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Atkinson, Carl