Search

Your search keyword '"Muratani T"' showing total 5 results
Start Over Author "Muratani T" Journal antimicrobial agents and chemotherapy
5 results on '"Muratani T"'

3. Protective effect of piperacillin against the nephrotoxicity of cisplatin in rats

Author

Hayashi, T, Watanabe, Y, Kumano, K, Kitayama, R, Muratani, T, Yasuda, T, Saikawa, I, Katahira, J, Kumada, T, and Shimizu, K

Abstract

The protective effect of piperacillin against the nephrotoxicity of cisplatin was compared with that of fosfomycin in Fischer 344 rats. Blood urea nitrogen, serum creatinine, and morphological changes were evaluated as the renal toxicological parameters. Rats receiving 2 mg of cisplatin per kg of body weight for 5 days showed significant (P less than 0.01 by multiple-comparison test) elevation of blood urea nitrogen and serum creatinine concentrations compared with rats receiving saline alone and also exhibited development of cell lesions in the pars recta of the tubules in the outer stripe of the outer medulla. However, piperacillin (250 and 1,000 mg/kg) significantly (P less than 0.01 by multiple-comparison test) reduced these toxicological parameters in comparison with results for cisplatin alone. The protective effect of piperacillin was superior to that of fosfomycin, although platinum levels in the kidney were higher with the combination of cisplatin and piperacillin than with cisplatin plus fosfomycin. Although the nephrotoxicity of cisplatin was also reduced when cisplatin was administered concomitantly with sodium chloride in mole-equivalents to 250 and 1,000 mg of piperacillin per kg, its protective effect was less than that of the corresponding piperacillin dose. These results suggest that piperacillin may have a role as a protective agent against the nephrotoxicity of cisplatin.

Published
1989
Full Text
View/download PDF

4. Mechanisms of resistance to imipenem and ampicillin in Enterococcus faecalis.

Author

Ono S, Muratani T, and Matsumoto T

Subjects
Amino Acid Substitution, Bacterial Proteins genetics, Bacterial Proteins metabolism, Enterococcus faecalis genetics, Enterococcus faecalis metabolism, Humans, Microbial Sensitivity Tests, Molecular Sequence Data, Sequence Analysis, DNA, Ampicillin pharmacology, Anti-Bacterial Agents pharmacology, Drug Resistance, Bacterial genetics, Enterococcus faecalis drug effects, Imipenem pharmacology, Penicillin-Binding Proteins genetics
Abstract

We found ampicillin- and imipenem-resistant isolates of vanA-possessing Enterococcus faecalis with MICs of 8 to 16 microg/ml and 4 to 32 microg/ml, respectively. There have been few reports about penicillin- and imipenem-resistant E. faecalis. Two mechanisms of beta-lactam resistance in E. faecalis, the production of beta-lactamase and the overproduction of penicillin-binding proteins (PBPs), have been reported. The resistant isolates in the current study did not produce any beta-lactamases and analysis of the PBPs showed no overproduction. However, the affinities of PBP4 for beta-lactams in the resistant strains were lower than those of susceptible strains but the affinities of other PBPs for beta-lactams did not change. Accordingly, whole pbp4 fragments from these resistant isolates were sequenced. Two amino acid substitutions at positions 520 and 605 were observed in the highly resistant strains compared to the susceptible ones, Pro520Ser and Tyr605His, and a single Tyr605His amino acid substitution was found in the low-resistance strains. These two point mutations exist in the region between the active-site-defining motifs SDN and KTG of the penicillin-binding domain, the main target of beta-lactams. A strong correlation was seen between these substitutions and decreasing affinities of PBP4 to beta-lactams. In E. faecalis, resistance due to mutations in PBPs has not been reported, though it has in Enterococcus faecium. Our results suggest that development of high-level resistance to penicillins and imipenem depends on point mutations of PBP4 at positions 520 and 605.

Published
2005
Full Text
View/download PDF

5. Outbreak of cefozopran (penicillin, oral cephems, and aztreonam)-resistant Neisseria gonorrhoeae in Japan.

Author

Muratani T, Akasaka S, Kobayashi T, Yamada Y, Inatomi H, Takahashi K, and Matsumoto T

Subjects
Adult, Aztreonam pharmacology, Aztreonam therapeutic use, Cephalosporins pharmacology, DNA, Bacterial genetics, Disease Outbreaks, Drug Resistance, Microbial, Drug Resistance, Multiple, Female, Gonorrhea epidemiology, Gonorrhea microbiology, Humans, Japan epidemiology, Male, Microbial Sensitivity Tests, Monobactams therapeutic use, Neisseria gonorrhoeae genetics, Penicillins pharmacology, Penicillins therapeutic use, Polymorphism, Restriction Fragment Length, Cefozopran, Anti-Bacterial Agents therapeutic use, Cephalosporins therapeutic use, Gonorrhea drug therapy, Neisseria gonorrhoeae drug effects
Abstract

We have previously reported that the Neisseria gonorrhoeae isolates from clinical failure cases treated with cefdinir and aztreonam, beta-lactams exhibited high MICs. These resistant isolates were clearly separated from the isolates exhibiting a low level of resistance to beta-lactams as shown by the MIC distribution of cefozopran. Restriction fragment length polymorphism DNA typing revealed that the outbreak of cefozopran-resistant isolates in Kitakyushu, Japan, occurred as a result of clonal spread.

Published
2001
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results