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S A Abrams

Publications and source records attributed to S A Abrams.

93 records · Page 6Linked to original sources
PubMed1988

Bone mineral content reflects total body calcium in neonatal miniature piglets.

We measured bone mineral content (BMC) in 18 neonatal miniature piglets by single photon absorptiometry, total body calcium (TBC) by total body neutron activation analysis, growth, and serum indices of mineral status (calcium, phosphorus, alkaline phosphatase activity). Measurements were begun on day 6, when the piglets were weaned, and were continued to day 19. After weaning, the piglets were assigned randomly to receive one of three diets which differed only in their concentrations of calcium and phosphorus: 100% of the recommended level (diet A), 60% (diet B), and 20% (diet C). No differences were observed among groups during the 19-day study, either in weight gain (48 +/- 2 g/day) or increment in crown-rump length (2.4 +/- 0.2 cm/wk). BMC correlated significantly (p less than 0.001) with TBC at 6 (r = 0.83), 13 (r = 0.77), and 19 (r = 0.93) days. BMC correlated significantly (p less than 0.001) with the ash weight (r = 0.87) and calcium content (r = 0.90) of the corresponding tibial bone segment. Anthropometric parameters and serum indices of mineral status did not predict TBC as accurately as did BMC measurements. We observed a range in BMC measurements in this study that was similar to the range reported for infants in the 1st yr of life. The high correlation between BMC and TBC suggested that BMC is useful in the assessment of mineral status in infants.

Animals↗
PubMed1987

Mutations that create new promoters suppress the sigma 54 dependence of glnA transcription in Escherichia coli.

Escherichia coli rpoN mutants lack sigma 54 and are therefore unable to initiate the transcription of glnA at glnAp2, which is required for the production of a high intracellular concentration of glutamine synthetase. We have found that the dependence on sigma 54 can be overcome by mutations that have apparently created a new sigma 70-dependent promoter. The position -35 RNA polymerase contact site of this new promoter overlaps glnAp2. The initiation of transcription at the new promoter is inhibited by sigma 54-RNA polymerase even in the absence of nitrogen regulator I-phosphate, the activator required for the initiation of transcription at glnAp2. The results suggest that in cells growing with an excess of nitrogen and therefore lacking nitrogen regulator I-phosphate, sigma 54-RNA polymerase is bound at glnAp2.

Base Sequence↗