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Accelerated coronary disease in the cardiac allograft (TxCAD) is a major complication affecting long-term survival of heart transplant patients. Since the transplanted heart remains denervated, the first sign of TxCAD may be silent myocardial infarction or sudden death. The prevalence of this disease has been unaltered since the advent of cyclosporine immunosuppression.

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The Heterophile Transplantation Antigen (HT-A) is a clinically important antigen which is found in some human kidneys and on the erythrocytes and in the serum of rats and some other mammals. Recent reports suggest the possibility that the anti-HT-A antibodies responsible for graft rejection may cross react with one or more HL-A specificities. The ideal way to investigate this possibility would be to perform careful serological and biochemical comparisons of purified HT-A and HL-A.

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A series of HL-A defined, nonrelated blood transfusions given in small aliquots from the same donor to prospective cadaveric and living-related donor recipients has been presented. The results to date show 100% kidney survival in this small series over a relatively short period of time. The rejections noted have been very mild, and easily reversed.

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A new hypothesis is presented to explain the mechanism of non-rejection of a natural allograft: the mammalian fetus during early development. Using the rabbit as a model, it is proposed here that uteroglobin (UG., MW.

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An unsuccessful human fallopian tube transplant is reported. A microsurgical technique is described which initially secured a viable transplant. However, the allograft subsequently died, probably as a result of rejection.

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