Biomedical subjects

R P Feldman

Publications and source records attributed to R P Feldman.

3 recordsLinked to original sources

PubMed1991

Isolation of mitotic p34cdc2 apoenzyme from human cells.

A simple procedure was devised for isolating from homogenates of mitotic cells the human homolog to the fission yeast cdc2 gene product. The identity of the purified protein was established with anti-p34cdc2 antibodies and p13suc 1, both specific ligands for p34cdc2. Active-site labeling with oxidized [alpha 32P]ATP showed the purified molecule to be an ATP-binding protein. Its ability to phosphorylate casein but not histone, and its phosphorylation on tyrosine, detected by anti-phosphotyrosine antibodies, indicates the form of p34cdc2 purified is the inactive or apoenzyme form. Purified quantities of human p34cdc2 should be of considerable value in establishing the mechanism of its activation at mitosis by phosphatases.

Apoenzymes↗

PubMed1977

L-ascorbate 2-sulfate and mobilization of cholesterol from plaque deposited in rabbit aortas.

Rabbits were randomly assigned to two groups. Age and body weight distribution were equal in both groups. All animals were placed on a high cholesterol diet for 9 wk, then returned to a normal diet for 1 wk. At the end of this dietary regimen, one group of animals received subcutaneous injections of psysiological saline 3 times/day, 5 days/wk for 10 wk, and the other group recieved L-ascorbate 2-sulfate (0.37 mmole) according to the same timetable. On alternate weeks, the serum levels of total and free cholesterol were determined. After 10 wk of treatment the animals were killed; the plaques were excised from the aortas and examined for total mass and cholesterol content. We observed that, under these dietary conditions, L-ascorbate 2-sulfate does not mobilize cholesterol or its esters from preformed aortic plaque. However, we did observe that animals showing high cholesterol levels in their sera died prematurely when injected with L-ascorbate 2-sulfate. Gross and histopathological investigations of organs and tissues did not reveal any significant differences among the animals that died prematurely and those that survived to the termination of the experiment.

Animals↗

PubMed1976

L-ascorbic acid, L-ascorbate 2-sulfate, and atherogenesis.

Rabbits on a high cholesterol diet were divided into three groups: one group received subcutaneous injections of physiological saline 3 times/day, 5 days/wk for 10 wk; another group received subcutaneous injections of L-ascorbic acid (0.37 mmole) according to the same timetable; and the third group was administered an equivalent amount of L-ascorbate 2-sulfate as outlined above. Each week the serum levels of total and free cholesterol and triglycerides were measured. At the end of 10 wk the animals were killed and the cholesterol content of the livers, spleens, and adrenal glands was measured. The aortas were examined for plaque deposition; the deposits were excised and pooled according to groups; and the total mass and cholesterol contents of the pooled plaques were determined. Administration of ascorbic acid or ascorbate 2-sulfate did not prevent hypercholesterolemia or elevated levels of serum triglycerides. No significant differences among the groups were found either in tissue cholesterol levels or in the extent or type of lesions found. Although plaque deposition appeared to be similar in the aortas of these animals, a marked difference was found in total mass and cholesterol content of the plaques: The plaques of the saline-treated group had a total mass and cholesterol content approximately 2.5 times that found in the group injected with ascorbic acid and about 1.5 times that found in the animals treated with ascorbate 2-sulfate. These results indicate that ascorbic acid, in particular, minimizes the total quantity of plaque deposition even though it is ineffective in preventing hypercholesterolemia, elevated serum triglycerides, and accumulation of cholesterol by several tissues.

Adrenal Glands↗