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Biomedical subjects

P E Carson

Publications and source records attributed to P E Carson.

71 records · Page 4Linked to original sources
PubMed1968

Gametocytocidal and sporontocidal effects of primaquine and of sulfadiazine with pyrimethamine in a chloroquine-resistant strain of Plasmodium falciparum.

Studies with 3 volunteers were conducted to determine the effects of a combination of sulfadiazine and pyrimethamine and the effects of primaquine upon mature gametocytes of a strain of chloroquine-resistant Plasmodium falciparum-the Malayan (Camp.) strain. One volunteer was treated with sulfadiazine and pyrimethamine; two other volunteers each received a single dose of 45 mg of primaquine base. The combination of sulfadiazine and pyrimethamine, although active against blood schizonts, did not exert a marked sporontocidal effect against the Malayan (Camp.) strain. In sharp contrast, primaquine, although not effective as a blood schizontocide, exerted a marked gametocytocidal and sporontocidal effect against this strain.The findings emphasize the need for further studies of the sporontocidal and gametocytocidal effects of drugs, particularly primaquine, against chloroquine-resistant strains of P. falciparum and suggest that primaquine may come to play an important role in preventing the transmission of such strains.

Adult↗
PubMed1967

Characterization of enterobacteria by starch-gel electrophoresis of glucose-6-phosphate dehydrogenase and phosphogluconate dehydrogenase.

Specific activities and electrophoretic mobilities of glucose-6-phosphate dehydrogenase and phosphogluconate dehydrogenase were determined in 38 isolates of the family Enterobacteriaceae and in 10 isolates of the related Pasteurella. The deficiency of glucose-6-phosphate dehydrogenase in P. pestis was verified. Enzymes obtained from different strains of the same species exhibited an unexpected degree of heterogeneity. For example, 8 and 11 apparent variants of glucose-6-phosphate dehydrogenase and phosphogluconate dehydrogenase, respectively, were found in 14 strains of Escherichia coli. Although similar frequencies of heterogeneity were noted in 7 strains of P. pseudotuberculosis, 5 species of Shigella, and 8 species of Salmonella, differences in mobility were generally small in comparison with those observed between strains of E. coli. Values obtained for the pasteurellae, shigellae, and salmonellae, thus fell within narrow ranges that may prove typical for the genera. However, most of these ranges, as well as many values observed for single species of other genera, were overlapped by the wide range recorded for E. coli. The significance of this observation was discussed with respect to the relative age and taxonomic position of the organisms in question. The method could be used to distinguish between most wild-type strains of the same species and should thus facilitate investigations of genetic transfer and epidemiology.

Electrophoresis↗
PubMed1966

The haemolytic effects of diaphenylsulfone (DDS) in normal subjects and in those with glucose-6-phosphate-dehydrogenase deficiency.

The need to investigate further the phenomenon of sulfone-induced haemolysis is becoming greater as the use of sulfones may increase, particularly for malaria therapy in areas where Plasmodium falciparum is found to be resistant to chloroquine. The authors report on studies of the haemolytic effects of diaphenylsulfone (DDS) administered orally, in doses ranging from 25 mg to 300 mg daily for 21 days, to normal healthy men and to healthy Negro men with deficiency of glucose-6-phosphate dehydrogenase (G-6-PD). The latter proved more susceptible to diaphenylsulfone-induced haemolysis than did normal men. There was a direct relationship between the dose of diaphenylsulfone and the extent of haemolysis in both groups of men studied. Comparison of the haemolytic effects of diaphenylsulfone with those of the antimalarial drug primaquine revealed that, on a dose for weight basis, diaphenylsulfone is more haemolytic than primaquine in normal persons and less so in G-6-PD-deficient persons. A marked decrease in the content of reduced glutathione (GSH) in red cells, comparable to the changes in levels of erythrocytic GSH known to occur during primaquine-induced haemolysis, occurred just before and early during the acute haemolytic episode that resulted from administration of diaphenylsulfone to G-6-PD-deficient subjects; in contrast, levels of erythrocytic GSH increased early during the course of diaphenylsulfone-induced haemolysis in normal men.

Adult↗
PubMed1966

The effects of diaphenylsulfone (DDS) against chloroquine-resistant Plasmodium falciparum.

In view of the problems caused by the chloroquine-resistance of some strains of Plasmodium falciparum, the authors have investigated the effectiveness of diaphenylsulfone against two such resistant strains, from Malaya and Viet-Nam. They found that diaphenylsulfone given during acute attacks of malaria had a blood schizontocidal activity against the Malayan resistant strain but was not rapidly effective in terminating acute attacks in non-immune persons, and that, when the drug was given prophylactically in relatively small doses, it was substantially effective in preventing patency of mosquito-induced infection with the same strain. The protective effect of diaphenylsulfone is that of a clinical prophylactic or suppressive drug; it does not appear to be a true causal prophylactic. It was also found that the protective effect is vitiated by the concurrent administration of paraaminobenzoic acid.These studies indicate a need for further assessment of the antimalarial value of sulfones and sulfonamides, both alone and in combination with other drugs, for prevention and cure.

Adult↗
PubMedDate not supplied

Beta blocker treatment in heart failure.

The sympathetic nervous system occupies a prominent role in heart failure both as a marker of severity of disease and also as an important factor in its progression. Beta blocker therapy, once thought heretical in heart failure, has consistently improved cardiac function and slowed progression of disease. Large clinical trials of mild to moderate heart failure show improved survival as well as reduction in hospitalization. Beta blockers now have stronger data in heart failure than converting enzyme inhibitors, and should be considered standard therapy in mild-moderate heart failure. Ongoing trials are addressing beta blocker therapy in advanced heart failure and comparisons between agents.

Adrenergic beta-Antagonists↗