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Biomedical subjects

J N Thompson

Publications and source records attributed to J N Thompson.

At least 199 records · Page 11Linked to original sources
PubMed1975

A test of the influence of isoallelic variation upon a quantitative character.

In order to test the assumption that isoalleles can contribute to polygenic variation, several isoalleles of cubitus interruptus were examined for their influence upon the quantitative expression of a related venation mutant, veinlet. In spite of the fact that veinlet and cubitus interruptus affect closely related developmental processes, the ci isoalleles had no effect upon the expression of veinlet. This test does not, of course, disprove the hypothesis that isoalleles play a part in polygenic variation. It is clear, however, that not all seemingly relevant isoalleles are necessarily effective elements in a given polygenic system.

Alleles↗
PubMed1975

Selenium content of food consumed by Canadians.

Four composite diets from three cities, each representing the daily per capita consumption of foods in Canada, contained on analysis 191, 220, 113, and 150 mug selenium. Cereals provided the most selenium (62-112 mug) followed by meat, poultry, and fish (25-90 mug) and dairy products (5-25 mug). The average daily intake of selenium in Canada was also calculated from published analytical data and the per capita disappearance of unprepared foods. The total intake was 197 mug/day, and the major sources were wheat flour (98 mug), pork (21 mug), poultry products (24 mug), and fish (17 mug). Because the average diet is rich in selenium, the possibility of a deficiency in the adult is considered to be remote. Milk is relatively low in selenium, and thus the greatest deprivation in humans would occur during infancy.

Adult↗
PubMed1973

N-acetyl-beta-hexosaminidase: role in the degradation of glycosaminoglycans.

Extracts of cultured normal human skin fibroblasts released radioactivity from a (14)C-labeled heptasaccharide prepared by addition of [(14)C]N-acetylgalactosamine to the nonreducing terminus of a hexasaccharide derived from chondroitin 4-sulfate whereas fibroblast extracts from patients with Tay-Sachs and Sandhoff-Jatzkewitz diseases did not. The results suggest that N-acetyl-beta-hexosaminidase A is responsible for degradation of the oligosaccharide substrate.

Carbohydrate Metabolism, Inborn Errors↗