Biomedical subjects
Publications and source records attributed to D Chun.
Almost all strains of Vibrio parahaemolyticus produced Kanagawa-type hemolysis on media of high salt content in the presence of fermentable carbohydrates.
In a study of the Kanagawa phenomenon of Vibrio parahaemolyticus, both Kanagawa-positive and -negative strains were found to produce hemolytic factors that could not be differentiated on Wagatsuma blood agar. The presence of fermentable carbohydrates in media containing high concentrations of NaCl promoted the growth of V. parahaemolyticus and resulted in a marked decrease in medium pH and increased hemolysin production. The Kanagawa hemolysis of test strains differed according to the carbohydrates added. Clearly defined Kanagawa hemolysis was observed in blood agars of high salt content, but the distinction was lost in media containing 3% NaCl. From the results of this study, the Kanagawa hemolysis was interpreted as an expression of quantitative difference in hemolysin production, a conclusion that is clearly demonstrated on special blood agar of high salt content.
A medium which contained 3% NaCl and 0.2% Teepol in 1/15 M phosphate buffer was prepared and was evaluated to be a useful enrichment medium for the isolation of Vibrio parahaemolyticus in marine specimens. Glucose salt Teepol broth produced a poorer result than direct culture.
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In a study of the effect of glycerin in transport media on Vibrio parahaemolyticus and Salmonella, it was found that a concentration of 30% glycerin was highly inhibitory for V. parahaemolyticus and to a lesser degree for Salmonella. The incorporation of peptone or human feces in media did not reduce the inhibitory effect of glycerin. In media with 15% glycerin, viable counts of V. parahaemolyticus and Salmonella increased after 24 hr of incubation both in the presence and absence of feces. Due to the concurrent increase in the total bacterial count in the media containing feces, no enrichment effect was noted.
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In the study of the relationship between bacteriophage and strains of staphylococci showing inhibition, slight differences were observed in the ability to adsorb phage between staphylococci of full phage sensitivity and those showing inhibition by phage. Only a few plaques were produced by inhibitory phages adsorbed on strains showing inhibition, whereas almost all of the phages adsorbed on corresponding phage-propagating strains produced plaques. Some strains showing inhibition were converted to full sensitivity to certain phages by heat shock or trypaflavine treatment. Treated strains adsorbed inhibitory phages to almost the same degree as nontreated strains, but most of the phages adsorbed on treated strains produced plaques. Killing was not always observed in cells adsorbing inhibitory phages. These results suggest that inhibition is not due to low adsorption rates, but rather to plaque formation by a small number of the sensitive fraction of the population and overgrowth by nonlysed cells.
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Strains of coagulase-positive staphylococci which were nontypable with the routine typing set of phages could be typed by lysogeny with phage-propagating strains as indicators and with ultraviolet induction. About 10% of the strains could be typed without induction. About 36% of them could be typed by this method when ultraviolet irradiation was used as an inducing agent. The phage groups from which the majority of the nontypable staphylococci originated were easily identified by this method of typing.
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Previous studies have established that (1) a 1-min episode of theta pulse stimulation (TPS) is sufficient to reverse potentiation during the early phases of LTP in area CA1 without causing depression when administered to nonpotentiated pathways; (2) the magnitude of depotentiation is inversely related to the delay between LTP induction and reversal attempts; and (3) pharmacological facilitation of AMPA receptor-mediated currents significantly enhances the strength of the reversal mechanism. The present experiments confirm and extend these results by showing that the depotentiating action of TPS on prior LTP is antagonized by inhibitors of protein phosphatases and adenosine A1 receptors but is not affected by NMDA receptor blockade, and, moreover, that TPS interferes with subsequent LTP induction by triggering an inhibitory mechanism that is active for a few minutes and is blocked by phosphatase inhibition. The possible implications of these results are discussed.