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Biomedical subjects

D Clark

Publications and source records attributed to D Clark.

At least 361 records · Page 20Linked to original sources

Development of a radioimmunoassay for alpha-melanocyte-stimulating hormone in the rat.

A sensitive and specific radioimmunoassay for alpha-melanocyte-stimulating hormone (alpha-MSH) was developed. Extracts of the neurointermediate lobe of the rat produced displacement curves which were parallel to those obtained with synthetic alpha-MSH. The mean immunoreactive alpha-MSH concentration in neurointermediate lobes from normal adult rats was 2768 +/- 200 (S.E.M.) ng/lobe. This accounted for approximately 78% of the MSH activity of the neurointermediate lobe as measured by bioassay. Much lower levels of immunoreactive alpha-MSH were found in the anterior lobe of the rat. Extracts of rat serum and plasma also contained immunoreactive alpha-MSH and the mean level was found to be 237 +/- 20 pg/ml. This was slightly lower than the level measured in rat plasma by bioassay. Increased levels of alpha-MSH were found in plasma of rats 1 and 3 h after a single injection of trifluoperazine and after 1-5 min of ether anaesthesia. These changes were reflected by decreases in the alpha-MSH content of the neurointermediate lobe.

Adrenocorticotropic Hormone↗

Manganese-resistant mutants of Escherichia coli: physiological and genetic studies.

Manganese is growth inhibitory for Escherichia coli. The manganese concentration required for inhibition is dependent upon the magnesium concentration of the medium. Mutants have been isolated which are partially resistant to manganese inhibition in both liquid and solid media. From conjugation experiments, the genetic locus for manganese-resistance, mng, appears to be between 34 and 37 min on the E. coli genetic map. Experiments with radioactive (28)Mg lead to the tentative conclusion that the mng mutants are altered in the inhibition constant for manganese as a competitive inhibitor for the mangnesium accumulation system. Once high manganese enters the cells, it displaces internal magnesium and leads to a net cellular loss and hence growth inhibition. The mng mutants are somewhat less subject to manganese-induced magnesium loss under comparable conditions than are manganese-sensitive wild-type cells.

Biological Transport↗

Experimental emphysema. Histologic changes and alterations in pulmonary circulation.

Detailed study of the pathogenesis of bullous emphysema has been hampered by lack of a suitable animal model of this disease. Prolonged exposure of rats and dogs to elevated partial pressures of oxygen produced a chronic obstructive disease in the lungs of these animals which anatomically resembles bullous emphysema in man. The disease was characterized by extensive bullae formation, alveolar septal destruction, airway obstruction and pronounced circulatory changes. It is suggested that this condition in laboratory animals may serve as a model for the study of pulmonary obstructive disease.

Animals↗