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Biomedical subjects

R Shankar

Publications and source records attributed to R Shankar.

At least 109 records · Page 6Linked to original sources
PubMed1985

Phosphocitrate inhibition of 45Ca2+ uptake in rat aortic smooth muscle cells in primary culture.

Phosphocitrate inhibits 45Ca2+ uptake by rat aortic smooth muscle cells in primary culture. Unlike the Ca2+ channel blocking effect of diltiazem, the phosphocitrate effect is neither time dependent nor reliant on a depolarized membrane. Phosphocitrate and diltiazem together in maximum inhibitory concentration show an additive effect. The data suggest that different Ca2+ uptake mechanisms are involved. The potential exists for phosphocitrate to have a therapeutic role in atherogenesis through modulating Ca2+ movements in arterial smooth muscle.

Animals↗
PubMed1984

Lipid peroxidation in developing rat brain during undernutrition.

The effect of undernutrition has been studied in relation to lipid peroxidation, both in vitro and in vivo, in the brain of developing rats. Lipid peroxidation in brain homogenates as well as in the mitochondrial fraction of brain was significantly higher in undernourished groups than in controls. This difference was maximal at the 12th postnatal day. Following rehabilitation for two weeks, this increased lipid peroxidation in brains of undernourished rats could no longer be observed. Determination of malonaldehyde levels in vivo did not show an appreciable difference between control and undernourished animals.

Age Factors↗
PubMed1984

Effectiveness of phosphocitrate and N-sulpho-2-amino tricarballylate, a new analogue of phosphocitrate, in blocking hydroxyapatite induced crystal growth and calcium accumulation by matrix vesicles.

Phosphocitrate and its analogue N-sulpho-2-amino tricarballylate were compared with ethane-1-hydroxy-1,1-diphosphonate for inhibition of calcium phosphate crystallization in hydroxyapatite induced crystal growth and 45Ca uptake by matrix vesicles. Phosphocitrate (1 microM) was the most potent inhibitor followed by ethane-1-hydroxy-1,1-diphosphonate and N-sulpho-2-amino tricarballylate, the latter requiring a high concentration (100 microM) to be equally effective as an inhibitor.

Animals↗
PubMed1984

Total gangliosides, ganglioside species and the activity of neuraminidase in different brain regions and spinal cord of normal and undernourished rats.

Total gangliosides, their concentrations and the distribution of individual ganglioside species were determined in the spinal cord, pons-medulla, midbrain, cerebellum, hypothalamus, cerebral cortex, olfactory lobes and the rest of the forebrain, of 18- and 33-day-old normal and food-restricted and rehabilitated rats. The activity of neuraminidase in the different regions of the brain and spinal cord was determined. Differences in total gangliosides as well as individual species in different regions of the brain were observed. Among brain regions, while total ganglioside content was significantly reduced in the case of the cerebellum, the hypothalamus was the most affected in the distribution of ganglioside species and the activity of neuraminidase was decreased. The significance of the distribution of ganglioside species in different brain regions in relation to the activity of neuraminidase is discussed.

Animals↗
PubMed1984

Phosphocitrate and its analogue N-sulpho-2-amino tricarballylate inhibit aortic calcification.

This study reports the ability of phosphocitrate and its enzyme-resistant analogue N-sulpho-2-amino tricarballylate to inhibit aortic calcification. Dystrophic calcification of aorta was induced by transplanting fresh aortic segments in Millipore chambers to the peritoneal walls of recipient rats. Daily intraperitoneal injection of the new inhibitors remarkably reduced calcium accumulation by the aortae and prevented the appearance of hydroxyapatite-like crystalline structures. Phosphocitrate was the most effective of the anti-calcifying agents tested, preventing aortic calcification at 1 mumole/day/rat. N-sulpho-2-amino tricarballylate was less effective, reducing aortic calcification by 60% at 10 mumoles/day/rat. The new inhibitors might prove therapeutically useful in man to arrest soft tissue calcification.

Animals↗
PubMed1981

Erythrocytic enzymes and amino acids related to glutamic acid metabolism in childhood hypoproteinemic states.

The erythrocyte enzymes of glutamic acid metabolism (glutaminase I, glutaminase II, glutamic acid decarboxylase, glutamine synthetase, and transaminases) and related amino acids (glutamine, glutamic acid, aspartic acid, alanine, and gamma-aminobutyric acid) were estimated in 69 children with protein-energy malnutrition, 13 with nephrosis, and 10 with Indian childhood cirrhosis. Twenty-one apparently healthy children served as controls. There was a significant increase in the activities of erythrocytic glutaminase I, glutaminase II, glutamic acid decarboxylase, and glutamine synthetase in all the three hypoproteinemic states, while the activities of the transaminases showed a decrease in all the conditions. The concentrations of all the amino acids were significantly increased in both the varieties of protein-energy malnutrition (edematous and nonedematous). In nephrosis and Indian childhood cirrhosis, aspartic acid, alanine, and gamma-aminobutyric acid showed a significant rise. The concentration of glutamic acid was also significantly increased in nephrosis. The observations of the present study suggest an increase in intracellular production of glutamic acid in hypoproteinemia.

Alanine Transaminase↗