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T Nishimura

Publications and source records attributed to T Nishimura.

At least 1,549 records · Page 86Linked to original sources
PubMed1981

[Laboratory and clinical studies of cefoxitin in pediatric field (author's transl)].

The authors have carried out the laboratory and clinical studies of cefoxitin. The results were as follows: The sensitivity was estimated by plate dilution method on 26 strains of S. aureus, 25 strains of E. coli, 24 strains of K. pneumoniae, 27 strains of Serratia and 17 strains of Salmonella isolated from patients. The distribution of sensitivity of S. aureus was 1.56-3.13 microgram/ml and the peak of distribution was 3.13 microgram/ml. The strains of 76.0% of E. coli was inhibited at concentration of less than 3.13 microgram/ml. The strains of 91.7% of K. pneumoniae was inhibited at concentration of less than 3.13 microgram/ml. The distribution of sensitivity of Serratia was 6.25-more than 100 microgram/ml and the peak of distribution was 100 microgram/ml. The all strains of Salmonella were inhibited at concentration of less than 3.13 microgram/ml. Cefoxitin was given by intravenous administration for 5 minutes at a single dose of 25 mg/kg of cefoxitin to 2 children, and by drip infusion for 60 minutes at a single dose of 25 mg/kg of cefoxitin to 4 children. After intravenous administration of cefoxitin, the mean peak of serum level was 67.3 +/- 6.3 microgram/ml at 15 minutes, and at 4 and 6 hours after administration was not detected. Half-life time was 22 minutes. And after drip infusion of cefoxitin for 60 minutes, the mean peak of serum level was 35.7 +/- 5.3 microgram/ml at 1 hour, and at 4 and 6 hours after administration was not detected. Half-life time was 20 minutes. The mean urinary recovery rate was 82.4 +/- 3.0% and 90.2 +/- 6.8% up to 6 hours after intravenous administration and drip infusion respectively. Cefoxitin was effective in all of 15 cases with bacterial infections. No side effects was observed.

Adolescent↗
PubMed1981

[Effect of bromhexine on the tracheal secretory cells with enhanced mucus synthesis by pilocarpine treatment (author's transl)].

The effects of bromhexine on secretory activities of canine tracheal secretory cells with stimulated synthesis of acid glycoprotein (AGP) by pilocarpine 10(-6)M treatment an on behaviour of glycoprotein in these secretory cells were investigated histologically and histochemically. Following bromhexine treatment, the number of total glycoprotein-containing goblet cells (GC) remained unchanged. The numbers of AGP-containing and sulphated glycoprotein (SGP)-containing GC significantly decreased, while neutral glycoprotein (NGP)-containing GC significantly increased. The acinar inner diameter of the submucosal gland and the acinar inner diameter of this gland to wall ratio slightly increased. Thickness of the acinus and Reid index slightly decreased, concentration-dependently. AGP and SGP content in glandular cells decreased, while NGP content in these cells markedly increased. Bromhexine 10(-5) and 10(-4)M treatment resulted in increased total saccharide and protein concentrations in the incubation fluid, whereas the agent significantly decreased N-acetylhexosamine, in a concentration-dependent manner. These findings suggest that while bromhexine does not stimulate secretory activities of GC, it does slightly stimulate the activities of the submucosal glands. Bromhexine markedly dissolves AGP in the granules of these secretory cells.

Animals↗
PubMed1981

Dissociation of the 5 alpha-reductase activity from the specific dihydrotestosterone binding activity in cultured human fibroblasts.

Four fibroblast lines (F1-4) were established from abdominal (F1 and F2) and vulvar (F3 and F4) skin samples obtained from women who underwent delivery. The concentration of dihydrotestosterone (DHT) binding sites was measured along with the maximum velocity for the formation of DHT from testosterone in fibroblasts from each cell line. The concentration of DHT binding sites (fmoles/mg protein) was 12.8 +/- 1.1 for F1, 12.3 +/- 1.0 for F2, 14.7 +/- 1.3 for F3 and 13.4 +/- 1.1 for F4 (mean +/- S.D. of two determinations). The respective values for the maximum velocity for the formation of DHT from testosterone (pmoles DHT formed/mg protein/h) were 8.40 +/- 0.64, 21.5 +/- 1.69, 11.8 +/- 0.85, and 31.0 +/- 2.26 (mean +/- S.D. of two determinations). These results, which demonstrate a wide diversity among values for the maximum velocity for the formation of DHT from testosterone while values for the concentration of DHT binding sites in these fibroblasts are uniform, suggest a lack of correlation between these two activities of fibroblasts.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1981

[Variation of lipids in rats fed a cholesterol diet (author's transl)].

Experimental hyperlipemia induced by a high cholesterol diet (HCD) in male Sprague-Dawley rats was investigated by measuring lipid levels in serum, liver and aorta. For old rats were fed a laboratory chow diet containing 0.5, 1.0 and 2.0% of cholesterol, for 6 weeks. Serum total lipid (TL) and total cholesterol (TC) in 1.0% HCD were markedly increased and reached peaks by feeding HCD for 18 to 21 days. Although the degree of increase in serum TL and TC was similar in both 0.5 and 2.0% HCD groups, these levels decreased more rapidly in the former and more slowly in the latter, after the levels had been reached a peak. The serum free cholesterol level reached a peak in those fed 0.5% HCD for 12 days and those fed 1.0% HCD for 21 days, but the subsequent reduction was smaller in extent as compared with serum TL and TC. Serum phospholipid (PL) level reached a peak in those fed both 0.5 and 1.0% HCD groups for 12 days and this level was maintained until 42 days in the 1.0% HCD group. Serum triglyceride (TG) levels increased during the first half of the experimental period, but decreased in the second half, with no significant difference between the 0.5 and 1.0% HCD groups. Cholesterol in high density lipoprotein (HCD-C) decreased in rats on the HCD and there was a tendency toward reversion to normal levels from the 4th week in the group on the 2.0% diet, however, a continual decrease occurred in the 0.5 and 1.0% groups. The change in phospholipid in HDL (HDL-PL) was similar to that of HDL-C in both the 0.5 and 1.0% HCD groups. In liver lipids, TL and TC were markedly increased by HCD, but TG increased at first and then decreased as did serum TG. Liver PL decreased by 0.5 and 1.0% HCD groups. In aorta lipids, TL and TC decreased. As a remarkable increase in serum lipids and decrease in HDL-C and HDL-PL were continuous in the 1.0% HCD in comparison with 0.5 or 2.0% HCD, 1.0% HCD appears to be the most suitable experimental model of hyperlipemia in rats. In addition, it is considered that 0.5% HCD is suitable for investigation of the effect of a drug for a relatively short period of treatment.

Animals↗
PubMed1981

[Laboratory and clinical studies of cefroxadine (author's transl)].

The authors have carried out the laboratory and clinical studies of cefroxadine (CXD), and obtained the following results. The antibacterial activities of CXD were measured by plate dilution method on 26 clinical isolates of S. aureus, E. coli and K. pneumoniae. CXD inhibited the growth of all strains of S. aureus at concentrations less than 6.25 microgram/ml, the peak of activity distribution was obtained at 3.13 microgram/ml with an inoculum size of 10(6) cells/ml. And the p eak sensitivity distribution of E. coli was obtained at 6.25 microgram/ml. The growth of all strains of K. pneumoniae was inhibited at concentrations of less than 25 microgram/ml. Phagocytosis was determined by QUIE'S method. In the presence of CXD, phagocytosis of human PMNs was not enhanced to E. coli and K. pneumoniae. For pharmacokinetic study, CXD was given orally at a single dose of 10 mg/kg to 3 children before and after meals. The serum levels of CXD on fasting were 14.2 microgram/ml, 11.0 microgram/ml, 4.0 microgram/ml and 0.57 microgram/ml at 0.5, 1, 2. 4 hours after administration respectively, and the level at 6 hours was not detectable. Half-life was 0.65 hours. The serum levels of CXD after meals were 3.9 microgram/ml, 5.3 microgram/ml, 5.3 microgram/ml, 2.4 microgram/ml and 0.42 microgram/ml at 0.5, 1, 2, 4, 6 hours after administration respectively, but at 8 hours it was not detectable. Half-life was 0.95 hours. The 8-hour urinary excretion rates on fasting and non fasting were 89.4%, 89.0% respectively. CXD was given to 31 cases with tonsillitis, 4 with bronchitis, 1 with impetigo, 3 with cervical lymphadenitis, 7 with U.T.I, totalling 46. A daily dose of CXD 400 approximately 1,500 mg was given for 4 approximately 14 days. Clinical results obtained were good and excellent responses in 43/46 (93.5%) cases. No side effects were observed except for 1 case with elevation of GOT, 2 cases with elevation of GOT and GPT and 1 case with eosinophilia.

Adolescent↗