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Biomedical subjects

S Segal

Publications and source records attributed to S Segal.

At least 613 records · Page 34Linked to original sources
PubMed1975

Specific mitogenic activity of 8-Br-guanosine 3',5'-monophosphate (Br-cyclic GMP) on B lymphocytes.

8-Br-cyclic GMP has been found to be a specific B cell mitogen; it triggers athymic nude mice spleen cells and "B mice" spleen cells, nylon adherent, anti-theta and complement-treated cells to proliferate. It does not stimulate thymocytes or purified T cells. The kinetics of the response to Br-cyclic GMP and LPS are almost identical. The mitogenic effect of LPS and Br-cyclic GMP is additive when the two mitogens are given together to cells. Spleen cells (C3H/HeJ strain) that did not respond to LPS were triggered by Br-cyclic GMP to make DNA. In order to achieve maximal stimulation by Br-cyclic GMP, the drug had to be in contact with the cells for more than 24 hr. Br-cyclic GMP was found to be mitogenic for spleen cells from five different mouse strains, but not for human leukocytes. DB-cyclic AMP was found to inhibit the DNA synthesis of T lymphocytes after they interacted with Con A; DB-cyclic AMP had no effect on the ability of the B lymphocytes to be transformed by LPS. The differential effects of cyclic nucleotides on B vs. T lymphocytes are discussed.

Animals↗
PubMed1974

Regulation of amino acid transport in kidney cortex of newborn rats.

After incubation at 37 degrees C the subsequent uptake of alpha-aminoisobutyric acid, cycloleucine, glycine, and L-proline by newborn (as compared to adult) rat kidney cortex slices is enhanced. The effect is abolished by the presence of cycloheximide, actinomycin D, and high concentrations of the above-mentioned amino acids in the medium during the 37 degrees C incubation prior to measurement of uptake. The data suggest that there is an adaptive control mechanism which is expressed on incubation at 37 degrees C and which can regulate amino acid transport in newborn rat kidney cortex.

Amino Acids↗
PubMed1974

Uptake and utilization of exogenous cystine by cystinotic and normal fibroblasts.

The uptake of l-[(35)S]cystine was studied in six cystinotic and six normal fibroblast lines grown for five days either on cover slips or in 32-oz plastic flasks. Cystinotics showed greater uptake than normals. The apparent K(t) for cystine entry in both types of cells was 0.043 mM but cystinotic cells showed a higher maximum velocity of entry. A comparison of the fate of l-[(35)S]cystine incubated for 20 min with monolayers of cells showed 30% and 15% of the intracellular (35)S to be l-cystine in cystinotic and normal cells, respectively. The (35)S effluxed more slowly from cystinotic than from normal cells after a 20-min preloading with l-[(35)S]cystine. Identification of (35)S compounds in efflux media after 3 min showed 75% of the total (35)S was l-cystine with the remainder in cysteine and acidic sulfur metabolites of cystine with no essential difference between cystinotics and normals. In paired experiments, the specific activity of the effluxed l-[(35)S]cystine after both efflux periods was the same as that entering the cell, thus indicating that the free l-[(35)S]cystine had not exchanged with the pre-existing pool in the cystinotic cells. During 3 min efflux, the l-cystine pool in normal cells was depleted mainly by loss of free cystine. In cystinotic cells, a new steady state was attained after 21 min of efflux and the intracellular l-[(35)S]cystine had the same percentage of total radioactivity seen after the initial 20-min uptake. After the rapid efflux of l-[(35)S]cystine from normals, [(35)S]cysteine and other labeled cystine metabolites appeared in the efflux media. By the end of a 3-min efflux, cystinotic cells had incorporated more label into reduced glutathione than had normal cells. However, when the new steady state was attained in cystinotics, the amounts of (35)S in glutathione were not markedly different in the two types of cells. Approximately 95% of the total label could be accounted for in free sulfur compounds. The data show an increased uptake and decreased efflux of cystine from cystinotic cells. However, it is not possible to conclude if these differences are due to primary changes in membrane function or to the reflection of metabolic defects without further investigation.

Adolescent↗