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P Toy

Publications and source records attributed to P Toy.

20 records · Page 2Linked to original sources

Does anti-Jra cause hemolytic disease of the newborn?

A Jr(a-) Japanese female developed anti-Jra during her first pregnancy. Both father and infant red cells were Jr(+), and anti-Jra was eluted from the infant's red cells. The antibody was determined to be IgG1. Hemolysis could not be definitively established from the clinical data. The pitfall of using the presence of jaundice as the sole evidence for hemolysis is emphasized. We conclude that the present case, and other previously reported cases, do not unequivocally establish that anti-Jra significant hemolytic disease of the newborn (HDN). Amniocentesis probably should not be performed during the pregnancy of mothers sensitized to Jra antigen. Jra HDN is probably a mild disease, like ABO HDN.

Adult↗

The effects of different levels of selenium administered to rats in drinking water on distribution and glutathione peroxidase.

Studies were conducted in an attempt to define a biochemical index of selenium toxicity rather than weight loss, liver disease and death. Rats, maintained on selenium deficient diets, received in drinking water various levels of selenium as Na2SeO3(0.1, 1.0, 1.5, 2.0 ppm). Changes in selenium dependent glutathione peroxidase (GSH-Px) activities and specific activities (nCi75Se/ug Se) were determined in liver, kidney and plasma at baseline and two and ten weeks after repletion. In intial selenium deficient rats, GSH-Px activities were markedly depressed and specific activities elevated as compared to 0.1 ppm controls. After two weeks, liver and plasma GSH-Px activiities increased, and plasma, liver and kidney specific activities decreased in a concentration dependent manner. In kidney, there were no differences in enzyme activity at either two or ten weeks. At ten weeks, liver GSH-Px activities continued to increase in the 1.0 ppm group, but were depressed at both the 1.5 and 2.0 ppm levels. Specific activities were also depressed in liver and excretion was not increased at these levels. This suggests a biochemical toxicity in liver at levels above 1.0 ppm after ten weeks, prior to the onset of gross pathological changes.

Animals↗