Hans Winkler

TL;DR: It is found that the endothelial cells in hamster hearts that accommodate themselves in rats express genes that in vitro protect ECs from apoptosis and prevent upregulation in those cells of proinflammatory genes such as cytokines, procoagulant and adhesion molecules.

TL;DR: Evidence was consistent with the hypothesis that the same membrane carriers were involved in active transport by control cells and facilitated diffusion by poisoned cells, and the most striking finding was that the addition of metabolic inhibitors reduced the KT of exit about two orders of magnitude, whereas the Kt of entrance remained constant.

TL;DR: It is likely that until the basis of DXR is more clearly understood there can be no further significant progress toward clinical xenotransplantation, but still further genetic engineering of donor pigs, involving the introduction of additional or multiple genes to regulate macrophage and NK cell responses, local coagulation, and endothelial cell activation, may once again prove to be an attractive, practical, powerful therapeutic option.

TL;DR: In porcine aortic endothelial cells, either IL‐1 alpha, TNF alpha or LPS upregulates an inhibitor of NF kappa B which is referred to as ECI‐6 which could represent a novel feedback mechanism by which NFKappa B downregulates its own activity after transient activation of target genes has been achieved.

TL;DR: The current resurgence of interest in xenotransplantation will result in better definition of the mechanisms responsible for xenograft rejection and should facilitate appropriate therapeutic strategies to provide for long-term graft survival.