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O Katoh

Publications and source records attributed to O Katoh.

143 records · Page 8Linked to original sources

[Study on administration method of dibekacin].

The serum concentration of dibekacin (DKB) were determined in 4 healthy adult volunteers after intramuscular injection, intravenous injection and 1-hour or 2-hour intravenous drip infusion of 100 mg of DKB, and 1-hour drip infusion of 50 mg. The mean peak concentration after the 2-hour drip infusion of 100 mg of DKB was a rather low level. While the 1-hour drip infusion of 50 mg of DKB produced a peak concentration of 7.9 micrograms/ml, which is comparable to that after intramuscular injection of 100 mg. In the cases of the 1-hour drip infusion of 100 mg, the peak serum level reached 13.3 micrograms/ml, which is a relatively higher level than that after intramuscular injection of the same dose. Based on the above findings, it is suggested that the 1-hour intravenous drip infusion of DKB in doses of 50 mg to 100 mg be practically applied for therapeutic use.

Adult↗

The present status of active tuberculosis in a general hospital; a study of 186 cases.

To study the present status of TB in a general hospital, we reviewed the records of 186 patients with TB at the Saga Medical School Hospital. Ninety-two patients (49.5%) had extrapulmonary tuberculosis and 59 patients (31.7%) had complicated severe diseases. The variety of TB lesions and underlying diseases often caused diagnostic delay and misdiagnosis. In fact, 16 cases were not identified to be TB until after death. The TB prevalence was significantly high in malignant disease, diabetes mellitus, collagen disease and chronic renal failure among the total number of patients discharged. Twenty-one patients developed TB while on an intensive therapy for underlying diseases. Unfortunately, 22 patients with TB died in our hospital. These findings suggest that special care must be taken to prevent TB in a general hospital. We emphasize that early diagnosis of TB depends on the suspicion of this infection on the part of the physician.

Adult↗

The early phase of colon tumorigenesis induced by dimethylhydrazine in ICR mice.

In order to study the influence of fiber supplements on dimethylhydrazine induction of colon tumorigenesis six-week-old CD1 (ICR): Crj mice were injected i.m. at a dimethylhydrazine (DMH) dose 10 mg/kg body weight once weekly for 10 weeks with or without dietary supplementation with 3% polydextrose, lactosucrose or cellulose, or 3% polydextrose and 3% cellulose in combination. There were no significant differences in colon tumor induction among the groups. However, microadenomas were observed 10 weeks after the first treatment of DMH so that this protocol may be useful for studies of the early phase of colon carcinogenesis in mice.

Adenocarcinoma↗

Effects of azoxymethane on X-ray induced intestinal metaplasia in Donryu rats.

The present study was undertaken to determine the effect of azoxymethane (AOM) administration on intestinal metaplasia induced by X-irradiation in male Donryu rats. Five-week-old animals were X-irradiated with two doses of 10 Gy each at a 3-day interval or three X-ray doses of 10 Gy at a 2-day interval and then received AOM injections i.m. at a dose of 15 mg/kg body weight once weekly for 3 weeks, 6 months after irradiation. Alkaline phosphatase positive foci were decreased after AOM treatments, but aberrant crypt like-foci appeared within areas of intestinal metaplasia. In contrast no induction was observed in normal-appearing gastric mucosa.

Alkaline Phosphatase↗

Tumorigenesis in F1 offspring mice following paternal 12.5 cGy 252Cf fission neutron irradiation.

Experiments were conducted to determine whether following genetic damage at germ cell stages induced by paternal exposure to 252Cf fission neutron could lead to tumorigenesis in the offspring. Seven-week-old C3H/HeNCrj male mice were irradiated with 252Cf fission neutrons, at doses of 0 and 12.5 cGy and were mated with nine-week-old C57BL/6NCrj females two weeks after the exposure. Three weeks later, it was found that the proportion of abnormal sperm in the 12.5 cGy-irradiated males was higher than that of 0 cGy-irradiated group. Embryo lethality among the F1 offspring was also found to be higher in the 12.5 cGy group than in the 0 cGy group, while the incidence of liver tumors among the F1 offspring increased in males only. These results suggest that the paternal 12. 5 cGy radiation exposure may have caused genetic transmission of liver tumor-associated traits, which is in line with findings that show steep increase in incidence of tumorigenesis in B6C3F1.

Animals↗

No susceptibility of colon tissue implanted into the glandular stomach of rats to N-nitroso-N-methylurea carcinogenesis.

The present study was undertaken to determine the response of colonic mucosa implanted into the stomach fundus in 6-week-old male F344 rats to oral administration of N-nitroso-N-methylurea (MNU). In graft + MNU, 15% animals had tumors in the implanted colon tissue whereas a 26% incidence of gastric tumors was observed for the pyloric mucosa. In MNU alone, 30% of rats demonstrated gastric tumors. In graft alone 10% of tumors were observed in the grafted site but none in the pylorus. Thus while graft tissue may intrinsically have an elevated risk of tumor development, no susceptibility to MNU was observed in the present study.

Animals↗

Induction of ovarian tumors by heavy ion irradiation in B6C3F1 mice.

Six-week-old B6C3F1 mice were exposed to 0.439 Gy heavy ion irradiation as a 290 MeV/u carbon-ion beam (LET 10 keV/micron) at 2 cm from the upper proximal point of a spread Bragg beam and autopsied 13.5 months after the irradiation. In males total tumor incidences, mainly liver tumors, were 37.0% in irradiated group and 25.0% in control (P>0.05). In females the total tumor incidences were 32.3%, mainly ovarian tumors, in the irradiated group and 0% in the controls. These results indicate that heavy ion irradiation induces ovarian tumors in females but does not target any organ in males.

Adrenal Glands↗

Influence of concomitant miso or NaCl treatment on induction of gastric tumors by N-methyl-N'-nitro-N-nitrosoguanidine in rats.

Six-week old male Sprague-Dawley (CD) rats were treated with 100 ppm N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) for 16 weeks in their drinking water with control, miso or sodium chloride (NaCl) supplemented diets. All animals were autopsied 12 months after the beginning of the MNNG treatment. Despite higher intake of MNNG in the high dose miso and NaCl groups, the total tumor incidences were decreased compared to middle and lowest values. The glandular stomach adenocarcinoma incidences in the 10% and 5% miso groups were significantly decreased as compared to those in the 2.2% or 1.1% NaCl groups, with the same concentration of NaCl.

Animals↗

Prevention of the development of preneoplastic lesions, aberrant crypt foci, by a water-soluble extract from cultured medium of Ganoderma lucidum (Rei-shi) mycelia in male F344 rats.

The modifying effects of a dietary water-soluble extract from cultured medium of Ganoderma lucidum (Rei-shi or Mannentake) mycelia (MAK) on the development of azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF) were investigated in male F344 rats. Rats were given subcutaneous injections of AOM (20 mg/kg body weight) once a week for three weeks to induce ACF and fed on diets containing 0, 1.25, 2.5 and 5.0% MAK for five weeks, starting one week before the first dose of carcinogen. MAK significantly and dose-dependently prevented the development of ACF, decreasing the total number of AC and inhibiting cyst formation. MAK (2.5 and 5.0%) also significantly reduced the longitudinal-cross section areas of colon epithelium. MAK in all doses significantly reduced the PCNA positive index, area of the germinal region and number of cells per half crypt. In an additional in vitro experiment, MAK inhibited anchorage-independent growth of several colon carcinoma cell lines. The present results thus indicate that dietary MAK could act as a preventive agent for colon carcinogenesis.

Animals↗

Expression of lung-resistance protein gene is not associated with platinum drug exposure in lung cancer.

BACKGROUND: Platinum drug resistance is an important problem in lung cancer chemotherapy. In this study, we examined lung-resistance protein (LRP) gene expression in vivo and in vitro in relation to platinum drug exposure. MATERIALS AND METHODS: The expression levels of the LRP gene were assessed by the reverse transcription polymerase chain reaction, in 80 autopsy samples (40 lung tumors and 40 corresponding normal lung tissues), two lung cancer cell lines and in peripheral mononuclear cells collected from 8 lung cancer patients before and after platinum drug administration. RESULTS: The LRP gene expression levels of autopsy specimens exposed antemortem to platinum drugs were not significantly different to those of specimens without platinum drug exposure, for both lung tumors and normal lung tissues. Our results also demonstrate that LRP gene expression was not induced by platinum drugs either in vitro or in vivo. CONCLUSIONS: The present results indicate that LRP gene expression is not associated with platinum drug exposure in lung cancer.

Adenocarcinoma↗