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Biomedical subjects

D L Nelson

Publications and source records attributed to D L Nelson.

At least 523 records · Page 29Linked to original sources
PubMed1975

The cytotoxic effector potential of some common non-lymphoid tumors and cultured cell lines with phytohemagglutinin and heterologous anti-erythrocyte antisera.

We have found that a) phytohemagglutinin can induce red blood cell cytolysis by non-lymphoid tumors and cell lines, b) rabbit anti-chicken red blood cell antibody but not turkey anti-chicken red blood cell antibody can mediate an antibody-directed cellular cytotoxicity type of cytotoxicity utilizing P815Y mastocytoma cells or rat embryo fibroblasts as effectors, and c) none of these cell line effectors was capable of killing metabolically active cultured cell line targets in the presence of phytohemagglutinin.

Animals↗
PubMed1972

Transport of magnesium by a repressible and a nonrepressible system in Escherichia coli.

Wild-type cells of E. coli take up Mg rapidly when grown in media with high (10 mM) or with low (50 muM) concentrations of Mg. Previous work has provided evidence that a transport system for Mg in E. coli also functions for the uptake of Co. Mutants resistant to Co have now been found to possess a system for Mg uptake that is repressed by high concentrations of Mg in the growth medium, and does not function effectively for the uptake of Co. The rate of Mg uptake by such mutants increases at least 50-fold within one generation after a transfer from growth medium with high Mg to one with low Mg concentrations. We conclude that there are at least two systems for the uptake of Mg in E. coli. System I is nonrepressible and can catalyze the uptake of Co as well as Mg; it is present in wild type but not in Co-resistant mutants. System II is repressible and has little affinity for Co; it is present in both wild-type and mutant strains.

Biological Transport↗
PubMed1972

Effects of colicins E1 and K on permeability to magnesium and cobaltous ions.

The energy-dependent exchange of intracellular Mg(2+) with extracellular Mg(2+) or Co(2+) is inhibited by colicin E1 and, less strongly, by colicin K. Treatment with either colicin causes a net loss of intracellular Mg(2+). This loss begins immediately in cells treated with colicin E1, but in colicin K-treated cells the onset of Mg(2+) loss is delayed 1 to 10 min, depending upon the temperature and the multiplicity of colicin K. Both colicins differ from chemical inhibitors of energy-yielding metabolism; energy poisons block transport of Mg(2+) and Co(2+), but both colicins increase passive permeability to Mg(2+) and Co(2+). Inhibitors of energy-yielding metabolism (and of Mg(2+) exchange) block the initiation of Mg(2+) loss by either colicin, but do not stop colicin-promoted efflux once it has begun. Colicin E1 added before colicin K prevents the more rapid Mg(2+) efflux characteristic of colicin K-treated cells. Quantitative comparisons of the effects of colicins E1 and K upon permeability to Mg(2+) and Co(2+) lead us to conclude that the two colicins are not identical in their mode of action.

Biological Transport, Active↗