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Biomedical subjects

M Kono

Publications and source records attributed to M Kono.

At least 361 records · Page 20Linked to original sources
PubMed1978

New plasmid (pTU512), mediating resistance to penicillin, erythromycin, and kanamycin, from clinical isolates of Staphylococcus aureus.

Multiply drug-resistant strains of Staphylococcus aureus were isolated from pediatric patients with severe staphylococcal infections in 1974 through 1976. Resistance to benzylpenicillin, erythromycin, and kanamycin was jointly eliminated without exception from these multiply drug-resistant strains by treatment with ethidium bromide. It was also found that the triple drug resistance in a representative strain, TK512-200, was always transduced to a susceptible strain simultaneously. Moreover, a single class of plasmid deoxyribonucleic acid was isolated from a transductant and found to be 14.4 +/- 0.6 mum in length, with a molecular weight corresponding to 29.8 x 10(6). From these results, it is concluded that the plasmid (pTU512) is a new one, mediating resistance to penicillin, erythromycin, and kanamycin.

DNA, Circular↗
PubMed1978

Microbial degradation of cephalothin by cephalothin-susceptible Escherichia coli.

Cephalothin (CET)-susceptible Escherichia coli, which can degrade CET after prolonged incubation in broth containing a concentration of the drug greater than the minimum inhibitory concentration, was found in a clinical specimen. The substrate specificity of the partially purified enzyme to cephalosporin analogs strongly indicated the occurrence of CET-specific degradation. Nuclear magnetic resonance analysis of the degradation reaction demonstrated the appearance of two new signals attributed to deacetyl CET. This suggests the possibility of the presence of acylesterase.

Cephalothin↗
PubMed1978

Testosterone-induced focal myocarditis in rats. I. Morphological and biochemical studies with special reference to pathogenetical mechanism and species differences.

Focal myocarditis characterized by interstitial edema, round cell infiltration and fibrosis occurred in rats given a subcutaneous administration of testosterone propionate in a dose of 50 mg/kg for 30 consecutive days or longer. Biochemical analysis showed a two to five time increase of deoxycorticosterone and a moderate decrease of corticosterone in blood plasma of these rats as well as in those treated with 50 mg/kg of testosterone propionate for 15 days. It was also shown that myocarditis did not occur in adrenalectomized rats after administration of testosterone propionate 50 mg/kg for 30 days, while subcutaneous injections of deoxycorticosterone acetate in a dose of 15 mg/kg for 30 days invariably produced cardiac lesions in both adrenalectomized rats and sham-operated rats. Regarding species difference, administration of testosterone did not produced either a high blood level of deoxycorticosterone or focal myocarditis in guinea pigs or rabbits. From these results, it is concluded that focal myocarditis in rats after administration of large amounts of testosterone propionate is related to the elevation of deoxycorticosterone in blood plasma but not to the direct effects of testosterone propionate on the myocardium.

Adrenalectomy↗
PubMed1977

Serotyping of Pseudomonas aeruginosa isolated from clinical specimens.

Serotyping of 168 clinical isolates by the slide agglutination test using TIBS (Toshiba Institute of Biological Science) serotyping sera, which were prepared from Homma's serotype strains at the request of Pseudomonas aeruginosa Serotype Committee in Japan, was performed and the results were compared with serotyping using IMSUT (Institute of Medical Science, University of Tokyo) serotyping sera by the tube agglutination test. When heat-killed antigen from clinical isolates were used, both sets of serotyping sera showed similar results and the slide agglutination test using TIBS serotyping sera could be substituted for the tube agglutination test using IMSUT sera. It was also discovered that serotyping by the slide agglutination test with TIBS serotyping sera could be carried out using live bacteria. However, in serotyping with live bacteria, there is some difficulty in observing the agglutination time. To solve this problem, we propose that positive agglutination should be determined within 60 sec. The authors also performed serotyping of the clinical isolates using Difco serotyping sera prepared by the Difco Company based on Liu's serotyping system, and the results were compared with those obtained with serotyping sera prepared with Homma's serotype strains. The results indicated that in serotyping of clinical isolates using Difco serotyping sera more cross reaction occurred than in serotyping with sera obtained from Homma's serotype strains.

Agglutination Tests↗
PubMed1976

Association of a penicillin resistance gene with a tetracycline resistance plasmid (PTP-2) in Staphylococcus aureus.

On transduction with a lysogenic strain of Straphylococcus aureus isolated from a clinical specimen and having tetracycline (TC)-penicillin (PC)-chloramphenicol (CP)-resistant plasmids, the three-drug-resistant strain was frequently obtained. By repeatedly transducing from this strain, a strain (TP-2) having stable resistance to TC and PC could be obtained. In transformation with the deoxyribonucleic acid (DNA) of TP-2 as donor, all of the transformants obtained by selecting with either TC or PC were both TC and PC resistant. According to electron microscopy study of the covalently closed circular DNA of TP-2, the plasmid DNA size was 1.37 +/- 0.03 mum (2.84 x 10(6) daltons). The plasmid (P(TP-2)) is presumed to be a new plasmid in which the PC resistance gene was integrated into the TC-resistant plasmid.

Culture Media↗
PubMed1976

Mechanisms of streptomycin(SM)-resistance of highly SM-resistant Pseudomonas aeruginosa strains.

Three clinical isolates, K-Ps 94, K-Ps 97 and K-Ps 102, of Pseudomonas aeruginosa having R factor and showing MIC of more than 51,200 mcg/ml to streptomycin (SM), were examined for mechanisms of SM-resistance. Among the strains, K-Ps 94 and K-Ps 102 had R factor conferring SM-resistance. In K-Ps 94, the mechanism of SM-resistance was mainly owing to SM-phosphorylating enzyme and also owing to decreased permeability by an R factor, kR94. In K-Ps 97, it was considered to be due to SM-adenylylating enzyme by the chromosomal gene but not R factor, kR97. In K-Ps 102, the reduced permeability of the cell membrane to SM by an R factor, kR102, and the reduced affinity of the ribosome to the drug by the chromosomal gene contributed to the mechanisms of SM-resistance.

Adenosine Triphosphate↗
PubMed1976

Mechanism of chloramphenicol-resistance mediated by kR102 factor in Pseudomonas aeruginosa.

The chloramphenicol (CP)-resistance mechanism of five-drug-resistant R factor (kR102) of Pseudomonas aeruginosa K-Ps 102 derived from a clinical specimen was investigated. Neither inactivation by acetyltransferases of CP nor induced resistance by CP was recognized. Reduced affinity of the ribosome to the drug was not seen in the result of incorporation experiment of 14C-valine by phage f2 RNA and risosome of K-Ps 102. However, on spheroplasts by glycine treatment, remarkable increase of CP susceptibility was observed. From the above evidence, it was considered that the CP-resistance barrier controlled by kR102 factor would be in the cell wall and the surface layer of cytoplasma and that the mechanism of CP-resistance was possibly by decreased membrane permeability of CP. However, the susceptibility to CP of the susceptible strain still increased by the formation of spheroplasts. Consequently, it was considered that R factor might be controlling the function of membrane permeability of the cells.

Acetyltransferases↗