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Summary The red cells of a normal male blood donor, K.S., were first grouped as B but he was found to lack anti‐A in his serum. Closer investigation revealed that his red cells had very weak A activity, demonstrable only by absorption and elution of anti‐A. He is a non‐secretor of ABH and a secretor of Lea. Blood group A‐, B and H‐gene specified glycosyltransferases were detected in his serum. In contrast to the finding of a B antigen of normal strength on his red cells, the B transferase in his serum was only about 30% of the normal level and, despite the very weak A activity of K.S.'s red cells, the A transferase level was about 50% of that found in the serum of group A individuals with normal strength of A antigen. Moreover, the A transferase on the basis of its pH optimum, Km values for donor and acceptor substrates, activation by divalent cations, isoelectric focusing profile and capacity to convert O to A‐active cells, was characterized as the product of an A1 gene. A family study showed that K.S.'s wife is group A2 and that they have two sons, one group A2 and the other group B. The group B son is assumed to have inherited a B gene from the propositus but the level of B transferase in the son's serum is three times as high as that in his father's serum. The wife of the propositus and his group A2 son have normal A2 transferases in keeping with their A2 red cell status. The A2 son therefore appears to have inherited an A2 gene from his mother but neither the A1 nor the B gene shown to be carried by his father. The distribution of transferase activities in K.S.'s red cells differs from that in his serum. A level of B transferase within the normal range was found in his red cell membranes but a very low level of A transferase was detected. The discrepancies between the serum transferases and ABO‐red cell group, together with the pattern of inheritance within the family, led to a suspicion of chimaerism. This was confirmed by the finding of fibroblasts with the female 46XX karyotype in cultures of the propositus' skin. These results suggest that K.S. is a dispermic chimaera with two different cell lines of the genotypes BO and A1O or A1A1. The group A2 son is assumed to have inherited an O gene from his father. It seems probable that K.S.'s bone marrow and reproductive organs are comprised predominantly of the XY cell line which carries the blood group BO genotype whereas his skin and other tissues which contribute the A1 transferase to his plasma, are partly made up of the XX cell line which carries the blood group A1O or A1A1 genotype.

The classical assessment of nephrotoxicity by the measurement of serum urea nitrogen and creatine is insensitive and nonspecific. Selection from a battery of clinical pathology tests allows the sensitive and specific measurement of renal dysfunction and injury. This requires the collection of urine specimens of good technical quality, with appropriate preservation. Interaction of the test article with urinary enzymes should be evaluated prior to their measurement for the assessment of tubular injury. This enables the localization and quantification of the injury within the regions of the nephron. High resolution proton nuclear magnetic resonance spectroscopy, a technique for measurement of low molecular weight metabolites, shows great promise for the evaluation of renal tubular injury in toxicologic studies.

Thirteen of 18 owl monkeys inoculated with intact Herpesvirus saimiri (HVS) developed lymphomas with a protracted clinical course. Lymphadenopathy and splenomegaly were apparent 40-177 days postinoculation in affected monkeys which survived 56-203 days. Lymphocytic leukemia was present in 10 of the 13 affected animals, and actively motile lymphocytes were, present in peripheral blood of all affected monkeys. Lymphomas were also induced in 2 of 2 owl monkeys inoculated with repeated injections of heat-inactivated HVS, and in 2 of 3 monkeys inoculated with HVS-induced lymphoma cells.