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Biomedical subjects

T Nishimura

Publications and source records attributed to T Nishimura.

At least 1,621 records · Page 90Linked to original sources

Electrogenic absorption of sugars and amino acids in the small intestine of the human fetus.

Some characteristics and the degree of intestinal absorption in the developing human fetus were examined by measuring solute evoked potentials and 14C-D-glucose uptake into the everted jejunal segments. In all segments, the Michaelis-Menten relationship was observed between D-glucose concentrations and the evoked potentials or D-glucose uptake. Increase of Na-ion concentrations enhanced both D-glucose evoked potentials and uptake. Both D-glucose and L-alpha-alanine evoked potentials increased in a significant correlation to the fetal age; however, the apparent Michaelis constants did not show any signficant change. The structural specificity of sugar for generating evoked potentials was the same as that reported for adult mammals. Among amino acids, only the L-form of neutral and acidic amino acids generated markedly high evoked potentials, but the basic ones hardly at all. Oligopeptides such as glycyl-glycine and glycyl-glycyl-glycine also generated high evoked potentials. Our results have indicated that the active transport system of sugars and amino acids in the human fetus have already developed by as early as the sixth month of gestation.

Aging↗

Mechanism of adriamycin resistance in a subline of mouse lymphoblastoma L5178Y cells.

The biochemical mechanism of anthracycline resistance was studied with an adriamycin-resistant subline of mouse lymphoblastoma L5178Y cells. Both uridine and thymidine uptakes in the resistant cells were observed more resistant to adriamycin and daunorubicin than those in the parental cells. Aclacinomycin A exhibited the same degree of inhibition of nucleic acid syntheses in the sensitive cells and in the resistant cells. The resistance pattern observed by the inhibition of RNA and DNA syntheses seemed to parallel that by growth inhibition. No significant difference was demonstrated between the parental and resistant cells in the inhibition of RNA and DNA polymerase reactions with isolated nuclei. The uptake and retention of [3H]adriamycin was observed significantly less in the resistant cells than in the sensitive cells. The results suggested that the adriamycin resistance may be due to alteration of the cytoplasmic membrane and/or cytoplasm, resulting in decreased uptake and retention of the antibiotic in the resistant cells.

Animals↗

The biochemical effect of auromomycin on bacterial cells.

The mechanism of action of auromomycin was studied with intact cells of Bacillus subtilis. The antibiotic exhibited a preferential inhibition of DNA synthesis over RNA and protein syntheses. The strand scission of cellular DNA was induced by the drug, and DNA was degraded into acid-soluble fragments. The results suggested that DNA is the chemoreceptor of auromomycin.

Anti-Bacterial Agents↗

[Laboratory and clinical studies on cefamandole (author's transl)].

The authors have carried out the laboratory and clinical studies of cefamandole (CMD). The results are as follows: The sensitivity was measured by plate dilution method on 26 strains of Staphylococcus aureus, Escherichia coli, Klebsiella pneumoniae and 14 strains of Salmonella typhimurium isolated from patients. The distribution of sensitivity of S. aureus was 0.39 approximately 3.13 micrograms/ml and the peak of distribution was 1.56 micrograms/ml. The distribution of sensitivity of E. coli was 0.78 approximately greater than 100 micrograms/ml, and K. pneumoniae, 1.56 approximately greater than 100 micrograms/ml. The distribution of sensitivity of Salmonella typhimurium was 6.25 approximately greater than 100 micrograms/ml and its peak was 6.25 micrograms/ml. CMD were given intravenously for 30 and 60 minutes at a single dose of 25 mg/kg body weight to 6 children. The serum mean levels of CMD were 105.3 micrograms/ml at 30 minutes, 15.1 micrograms/ml at 1.5 hours, 1.6 micrograms/ml at 2.5 hours after drip infusion for 30 minutes, respectively, and 34.7, 5.2, 0.6 micrograms/ml at 1, 2, 3 hours after drip infusion for 60 minutes, respectively. And the serum level at 4 hours after administration was not detected. The mean urinary excretion rates were 73.3% in the drip infusion for 30 minutes and 60.7% in its for 60 minutes, up to 8 hours after administration. Half life was 26 minutes. CMD was effective in 18 of 21 cases of bacterial infections. No side effects were observed except for 2 cases with elevation of serum transaminase.

Bacterial Infections↗

[Laboratory and clinical studies on cefuroxime (author's transl)].

The authors have carried out the laboratory and clinical studies of cefuroxime (CXM). The results were as follows: The sensitivity was measured by plate dilution method on 26 strains of S. aureus, 22 strains of E. coli and 24 strains of K. pneumoniae isolated from patients. The distribution of sensitivity of S. aureus was 0.78 approximately 3.13 micrograms/ml and the peak of distribution was 1.56 micrograms/ml. The distribution of sensitivity of E. coli was 1.56 approximately 50 micrograms/ml and the peak was 6.25 micrograms/ml. The growth of 79.2% K. pneumoniae was inhibited in concentration of less than 3.13 micrograms/ml. CXM was given intravenously for 30 minutes at a single dose of 20 mg/kg to 3 children. The serum mean levels of CXM were 99.0 +/- 10.6 micrograms/ml at 30 minutes, 18.0 +/- 10.7 micrograms/ml at 1 hour, 7.0 +/- 2.0, 2.2 +/- 0.6, 0.79 +/- 0.2 microgram/ml at 2, 4 and 6 hours after drip infusion for 30 minutes, respectively. Mean half life was 48 minutes. The mean urinary recovery rate was 96.2% up to 8 hours after administration. CXM was effective in 9 of 10 cases of bacterial infections. No side effect was observed except for 1 case with elevation of serum transaminase.

Adolescent↗

[Pharmacokinetics and clinical studies on CS-1170 (author's transl)].

The authors have carried out the pharmacokinetics and clinical studies of CS-1170. The results were as follows; CS-1170 was given by drip infusion for 1 hour dose of 20 mg per kg body weight to 3 children. The maximum blood level was reached at one hour after drip infusion. This blood levels were 38 micrograms/ml, 68 micrograms/ml and 86 micrograms/ml, respectively, (mean 64 micrograms/ml), and level at 2 hours, 11.5 micrograms/ml, 9.4 micrograms/ml, 16 micrograms/ml respectively, (mean 12.3 micrograms/ml), the blood level at 6 hours was not determined. The urinary excretion rates were 94.8 approximately 96.8% up to 6 hours after drip infusion dose of 20 mg per kg body weight. CS-1170 was effective in 7 of 8 cases with pediatric bacterial infections. An ineffective case was a pneumonia due to Serratia marcescens. No side effect was observed except for 2 cases with diarrhea and one case with elevation of GOT and GPT.

Adolescent↗

DNA strand scission in vivo and in vitro by auromomycin.

The mechanism of action of auromomycin, a new tumor-inhibitory antibiotic, was studied in a growing culture of mouse lymphoblastoma L5178Y cells and with isolated viral DNA. Auromomycin prevented growth of L5178Y cells completely and irreversibly at antibiotic concentrations higher than 0.03 microgram/ml. DNA synthesis was preferentially inhibited by the antibiotic, whereas RNA and protein syntheses were not significantly affected. In synchronous cultures of L5178Y cells, results indicated that limited auromomycin-induced inhibition of DNA synthesis may occur independently of a much stronger inhibition of mitosis. In a short incubation period, a marked strand scission in cellular DNA of auromomycin-treated L5178Y cells was observed by an analysis of alkaline sucrose gradient centrifugation. In vitro, the antibiotic also induced strand breaks in linear duplex T-7 phage DNA and in the supercoiled circular duplex of SV40 DNA. 2-Mercaptoethanol neither enhanced nor was required for strand scission of isolated DNA by auromomycin. These data indicate that the mechanism of the antitumor activity of auromomycin is different from that of bleomycin, neocarzinostatin, or macromomycin.

Animals↗