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div>Recent organ donor audits from Australian tertiary hospitals (Dr. Helen Opdam, DonateLife, personal communication), and the Massachusetts General Hospital (27), confirm the potential category III DDCD pool to be of approximately equal size to the DDND pool. We postulate that the successful implementation of a category III DDCD donation process at the majority of large hospitals would therefore further increase the overall number of LTx performed. Considering that kidney and lung transplants are numerically the organs most Vemurafenib mouse usually recovered from Australian DDCD donors (21), and DDCD does not currently involve heart procurement for transplantation, it is therefore important to note that over the same period there U-0126 has been no decrement in heart transplantation and actually a steady increase in DDND donor numbers (21) (Figure 1A). The broad outcomes of this series of Australian DDCD LTx are excellent, with surprisingly superior patient survival when compared to DDND transplants performed over the same period. By definition the DDCD donors have different underlying disease etiologies and pathophysiology, although the overall use of extended organs, recipient choices, operative variables and postoperative management are the same as for DDND. The available data here suggest a low PGD rate and intriguingly a low BOS rate in DDCD LTx recipients that might explain this apparent survival advantage. BOS is well recognized as the single biggest cause of allograft loss post-LTx (26). Interestingly, early and intermediate term data from other small single center series also suggests a possible pooled survival advantage (2,5,8�C14). Further, there were no clinically important airway complications, or other unexpected outcomes found in this series, in up to 5-year follow-up. Although clearly more data are required to confirm the above, it is Ruxolitinib cost now apparent that category III DDCD LTx is not inferior to DDND LTx. Any differences between the outcomes of DDCD and DDND LTx have the potential to aid our understanding of the pathophysiology of acute and chronic allograft dysfunction. In theory, the absence of the ��brain storm�� inflammatory injury associated with DDND donors (4,28) could contribute to the apparent low rate of PGD and BOS seen here. Kang and coworkers provide some evidence in humans to support this theory (29). Looking to the future, differences in cytokines, gene transcription or surfactant properties might suggest therapeutic targets to address in the donor or recipient aimed at optimizing early and late allograft function (28,29). The standardization of definitions and detailed collection of data provides data to inform debate about the optimization and limits of DDCD warm ischemia. We have previously discussed the importance of recording times of withdrawal, donor blood pressure <50 mmHg, asystole, onset of ventilation and initiation of pulmonary arterial preservation solution flush (20).</div>