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Biomedical subjects

N Endo

Publications and source records attributed to N Endo.

At least 163 records · Page 9Linked to original sources
PubMed1984

Outbreak of nosocomial urinary tract infections caused by Serratia marcescens.

A prolonged outbreak (December 1980 to July 1982) of nosocomial urinary tract infections appeared to be due to strains of Serratia marcescens that were resistant to currently available antibiotics. The serotyping and antibiotic susceptibility patterns suggested a few endemic strains of serotypes O13, O2/3, O12/14, and nontypable strains. These strains were isolated from the urine samples of inpatients with urinary tract infections in the urology ward and in other wards. The strains of O12/14 (gentamicin susceptible) were replaced with those of O2/3 (gentamicin resistant) between June and September 1981, whereas the other serotypes were isolated continuously. They were resistant to sulbenicillin, cefmetazole, gentamicin, and amikacin, and susceptible to micronomicin and of loxacin, a new quinolone antibiotic. Most of them were also resistant to the disinfectant chlorhexidine, which had been used widely for hand washing in the hospital.

Anti-Bacterial Agents↗
PubMed1984

[Study on follow-up procedure for postmolar patients].

Since 1974, in Chiba prefecture patients with trophoblastic disease have been registered with the Department of Obstetrics and Gynecology, Chiba University School of Medicine as the registration and management center. An original follow-up system for postmolar patients has been used and following results obtained. From 1974 to 1981 (8 years), 1544 hydatidiform mole patients were registered. The number of deliveries was 582,641. The incidence of hydatidiform mole in deliveries was 1:377. Postmolar patients whose hCG titers were greater than 10,000 IU/l, 1,000 IU/l and 100 IU/l at the fifth, eighth and twelfth week respectively, were treated as trophoblastic sequelae. In these check points, 155 cases (10.0%) were treated as sequelae, namely, 9 cases (0.6%) of choriocarcinoma, 54 cases (3.5%) of invasive mole and 94 cases undetermined (6.1%). At the fifth week after molar evacuation, there were 96 cases whose hCG titers were from 1,000 to 10,000 IU/l, and at the eight week, 86 cases were from 100 to 1,000 IU/l. Among the former there were 30 cases (31.2%) and among the latter, 36 cases (41.9%) of spontaneous remission. By using this follow-up system, 66 cases (36.3%) were able to avoid over treatment.

Chorionic Gonadotropin↗
PubMed1983

Stimulation of complement production in mice by N alpha-(N-acetylmuramyl-L-alanyl-D-isoglutamine)-N epsilon-stearoyl-L-lysine.

N alpha-(N-acetylmuramyl-L-alanyl-D-isoglutamine)-N epsilon-stearoyl-L-lysine, a synthetic muramyl dipeptide analog, stimulated the production of the third component of complement (C3) in mice. The serum concentration of C3 was elevated significantly by subcutaneous treatment with a single dose (10 to 100 micrograms per mouse) of the adjuvant 24 h before assay of the serum. Thereafter, the concentration decreased gradually with time and returned to the normal level on day 4 to 5. Immunoelectrophoretic analysis of the serum revealed that the decrease in serum C3 could not be accounted for by the cleavage to C3a and C3b. By intermittent treatment with the adjuvant on every fifth day, a significant increase in serum C3 was repeated. However, no continuous retention of the serum level of C3 was established even during continuous treatment with the adjuvant once a day for 10 consecutive days. Instead, in this case, the level of C3 increased repeatedly at almost 5-day intervals.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1983

[Effect of suloctidil in the protection of the cerebral function].

It has been demonstrated that suloctidil [erythro-1-(4-isopropylthiophenyl)-2-n-octylaminopropanol] has a protective effect against cerebral hypoxia to elongate the survival time of mice subjected to normobaric hypoxia (96% N2 + 4% O2 gas mixture). In this study, further experiments were done to elucidate the mechanism of protection against cerebral hypoxia with a variety of experimental models. Pretreatment (30 min) with suloctidil (12.5-50 mg/kg, i.p.) increased the number of gasping in the decapitated head of mouse as a complete ischemic model. Pyrithioxine (25, 50 mg/kg, i.p.) or cinnarizine (50, 100 mg/kg, i.p.) did not increase the gasping number. In the histotoxic anoxia with KCN (4 mg/kg, i.v.) in mice, suloctidil showed 30.8% and 46.2% survival rates at the doses of 25 and 50 mg/kg, i.p., respectively. Concerning this result, it has been revealed that suloctidil did not have any methemoglobin formation liability in rats (unpublished). Pyrithioxine did not show such protection following the injection of 12.5-50 mg/kg, i.p.. Suloctidil (3.0-50 mg/kg, i.p.) and pyrithioxine (3.0, 10 mg/kg, i.p.) significantly prolonged the survival time of mice subjected to hypobaric hypoxia (210 mmHg). In this cerebral hypoxia model, suloctidil kept glucose at a significantly higher level and lactate at a lower level in the brain of mice that were administered this drug than the control group. ATP was kept at higher level after suloctidil than the control under hypobaric hypoxia. Taking these evidences together, it can be concluded that suloctidil exerts its cerebral anti-hypoxic effect through cerebral glucose metabolism coupled with oxidative phosphorylation to yield the high energy substance ATP in a variety of models tested in this study. The fact obtained in this study, together with increase in cerebral blood flow by suloctidil, may also elucidate the protective effect of suloctidil against cerebral hypoxia.

Animals↗
PubMed1982

[Effects of prophylactic treatment of central nervous system leukemia in children. Analysis of CNS prophylactic treatment with cyclic high dose multichemotherapy, craniospinal irradiation, and high dose infusion of MTX].

Thirty-five children with previously untreated ALL or AUL who received CNS prophylactic therapy with 8 treatment regiments were analyzed. After eutering complete remission, patients received CNS-prophylaxis with one of the following regimens: Group A- cyclic high dose multichemotherapy plus intermittent intrathecal methotrexate (MTX); Group B-craniospinal irradiation plus intermittent intrathecal MTX; Group C-intermittent high dose intravenous MTX. Incidence of CNS-leukemia and bone marrow relapse was less frequent in Group B. EEG abnormalities were seen in 38.5% of Group A, 40% of Group B, and 28.6% of Group C respectively, but the abnormalities were transient. IQs of three groups were above 100, but IQs of CNS-leukemia patients, especially VIQs had a tendency to be low.

Adolescent↗