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Biomedical subjects

L Frank

Publications and source records attributed to L Frank.

At least 163 records · Page 9Linked to original sources
PubMed1977

Oxygen therapy and hyaline membrane disease: the effect of hyperoxia on pulmonary superoxide dismutase activity and the mediating role of plasma or serum.

In vitro and in vivo hyperoxic exposure of the lungs of normal immature animals resulted in a rapid increase of pulmonary superoxide dismutase activity. The increase of pulmonary SOD activity with in vitro hyperoxic exposure requires the presence of plasma or serum in the incubation medium. Twenty-three out of 26 plasma samples from premature infants without hyaline membrane disease were found to support the hyperoxic increaase of pulmonary SOD activity, whereas only five of 15 plasma samples from infants with HMD were effective. A defective plasma-lung interaction in infants with HMD may result in an inability to increase pulmonary levels of this presumed protective enzyme during hyperoxic therapy.

Animals↗
PubMed1976

Developmental characteristics of pulmonary superoxide dismutase: relationship to idiopathic respiratory distress syndrome.

Pulmonary superoxide dismutase (SOD) acitivity was determined for various groups of human fetuses, infants, and adults. Enzyme activity was found to increase with age from a low of 17 +/- 1 units/mg DNA in fetal lung to 49 +/- 6 units/mg DNA in infant lung and finally to 110.2 +/- 14.8 units/mg DNA in adult lung (P less than 0.05). No difference in lung SOD activity was demonstrated between normal infants and those with idiopathic respiratory distress/hyaline membrane disease (IRDS/HMD). No significant differences in SOD activity were found among all the samples of infant blood. Adult blood samples, however, contained significantly greater SOD activity both in terms of heme concentration and volume of whole blood (P less than 0.05). SOD activity in lung tissue from both rats and rabbits were also found to increase with age from a low value in fetal animals to a maximum activity in adults (P less than 0.05). Exposure of New Zealand White rabbits, prematurely delivered by caesarian section, to 80% oxygen for 24 hr resulted in a 42% increase in lung SOD activity. Similarly, 7-day-old Sprague-Dawley rats exposed to 85% oxygen for 24 hr showed a 43% increase in pulmonary SOD activity. No increase in pulmonary SOD was observed when adult rats were exposed to 85% oxygen for 24 hr. The effect of hyperoxia on SOD activity in excised lung was investigated. Rat lung, incubated in either heparinized whole blood or in plasma and exposed to 100% oxygen, showed a 30% increase in SOD activity after 2 hr. This capacity of lung tissue to respond to hyperoxia in vitro with increased SOD activity was age dependent. The maximum increase in SOD activity was seen with lungs from 10-12-day-old rats. The oxygen-stimulated increase in lung SOD activity disappeared at about 19-20 days of age.

Adult↗
PubMed1974

Sodium-stimulated glutamate transport in osmotically shocked cells and membrane vesicles of Escherichia coli.

Three phenotypically distinct strains of Escherichia coli B were studied: one in which the transport of glutamate was strongly stimulated by sodium, one in which the transport was relatively independent of sodium, and one which did not transport glutamate. Membrane vesicle preparations from the three strains followed the behavior of whole cells with respect to sodium-stimulated transport. Although glutamate-binding material could be released from cells by osmotic shock, its affinity for glutamate was not significantly influenced by sodium. Furthermore, the shocked cells retained sodium-stimulated transport. The accumulated results suggest that the sodium-activated glutamate transport system resides in the cytoplasmic membrane and that releasable binding protein(s) is not intimately involved in its function.

Biological Transport, Active↗
PubMed1969

Sodium-stimulated transport of glutamate in Escherichia coli.

Wild-type Escherichia coli B grew poorly on glutamate as the sole carbon source, except at very high concentrations of the amino acid. The addition of sodium ion markedly stimulated the growth. It had the same effect in a mutant of E. coli B selected for the ability to grow at low glutamate concentrations. Sodium ion also potentiated growth inhibition by analogues of glutamate. The uptake of glutamate by nongrowing cells of the mutant was markedly stimulated by sodium ion in the presence of an energy source, chloramphenicol, and arsenite, which retarded glutamate degradation.

Ammonia↗