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Biomedical subjects

T Hara

Publications and source records attributed to T Hara.

At least 1,063 records · Page 59Linked to original sources
PubMed1983

Lithium therapy for cyclic neutropenia in children.

2 children with cyclic neutropenia were treated with lithium carbonate. In one patient, fever and stomatitis were ameliorated, but the duration of neutropenia was increased and parotitis occurred. In another patient, aphthous stomatitis disappeared but fever persisted. The duration of neutropenia was prolonged and submaxillaritis and sinusitis occurred. Thus, lithium administration may lead to complications when the duration of neutropenia is prolonged. We recommend discontinuation of the drug, even in the presence of amelioration of symptoms.

Agranulocytosis↗
PubMed1983

Effects of riboflavin and selenium deficiencies on glutathione and its relating enzyme activities with respect to lipid peroxide content of rat livers.

Weanling male rats were fed a riboflavin- or selenium-deficient diet for 5 weeks, and the glutathione content and its relating enzyme activities in the livers were examined. The glutathione content and glutathione reductase activity were decreased by deficiency of riboflavin, but not by that of selenium. Glutathione peroxidase activity was increased by addition of selenium to the diet, but without its addition, the activity was higher in the riboflavin-deficient rats than in the riboflavin-sufficient rats, in spite of the increase of lipid peroxides in the former rats. Glucose 6-phosphate dehydrogenase activity was decreased significantly by riboflavin deficiency. In another experiment, riboflavin was intraperitoneally injected into rats fed the diet to which neither riboflavin nor selenium had been added. The glutathione content and activities of glutathione reductase and glucose 6-phosphate dehydrogenase returned to the control level of riboflavin-sufficient rats in 24 h, the lipid peroxide level in 48 h, and the glutathione peroxidase activity, being higher than that in the control rats, in 72 h after the injection, respectively. These findings indicate that the increase of lipid peroxides in the livers of riboflavin-deficient rats is caused by the decrease in the glutathione content as well as glutathione reductase activity rather than by that in the selenium-dependent glutathione peroxidase activity.

Animals↗
PubMed1983

Oral toxicity of Kintoki bean (Phaseolus vulgaris) lectin.

There are several antinutritive factors in the Kintoki bean such as lectin, trypsin inhibitor, lack of methionine etc. The present experiment has revealed that lectin is mainly responsible for the growth impairment of experimental animals orally fed raw Kintoki bean. Mice fed raw Kintoki bean as the only protein source lost their body weight and died in 8 days, while mice fed the heated bean grew normally. When mice on a 10% albumin diet ingested 20 mg or 40 mg or 60 mg Kintoki bean lectin by daily stomach-feeding, their body weights were reduced to 84%, 74%, 71% of the control group after 5 days respectively and some of them could not live to complete the experiment. The apparent rates of the intestinal absorption of carbohydrate, lipid, and protein were considerably reduced, when rats were fed a diet containing 0.4% lectin. Especially, the rate of protein absorption was decreased to 26.3% from 55.5% of the control rate. The main tissues of mice that had ingested Kintoki bean lectin by stomach-feeding were subjected to microscopic observation. No changes were observed in the liver, kidney, spleen and pancreas. But in the small intestine, the epithelial cells lining the villi were considerably disordered and conspicuously disrupted. These results indicate that the Kintoki bean lectin is one of the most promoting factors for growth impairment in experimental animals and that the first target organ in the case of oral feeding is the small intestine.

Administration, Oral↗
PubMed1983

Toxic effects of Kintoki bean (Phaseolus vulgaris) lectin on cultured animal cells.

Effects of a toxic lectin from Kintoki beans (Phaseolus vulgaris, cultivar, Kintoki) on four types of animal cells were investigated. The cells used in this study were mouse L 929, human HeLa S3, and tendon and liver cells from chick embryo. The Kintoki bean lectin agglutinated these cells not only in suspension but also in monolayer, resulting in the marked growth inhibition of these cells. The incorporations of 3H-thymidine and 3H-leucine into trichloroacetic acid insoluble fraction of the cells were considerably inhibited by this lectin. There was, however, some lag period before the revelation of the inhibition. Kintoki bean lectin bound to these cells within 1 hr. The type of the lectin receptor seemed uniform for each cell type and the number of the binding sites per cell was different from cell type to cell type. When Kintoki bean lectin was removed from the culture medium, these cells slowly recovered back to normal growth.

Animals↗
PubMed1983

[Preparation and anti-tumor activity of monoclonal antibody against ascitic mammary tumor MM46 cells].

In an approach to antitumor agents with improved tumor specificity, the ricin toxic subunit A chain was covalently coupled with a monoclonal IgG2b antibody directed against MM antigen, a tumor-specific antigen on syngeneic mouse mammary tumor MM46 cells (anti-MM46 IgG), using N-succinimidyl-3-(2-pyridyldithio) propionate as a cross-linking agent. The conjugate thus prepared (anti-MM46 conjugate) showed potent dose-dependent cytotoxicity against MM antigen-positive MM46 cells in vitro and inhibited the cell growth at concentrations above 1 microgram/ml. The immunological specificity was verified by the observation that anti-MM46 conjugate did not show cytotoxicity against MM antigen-negative MM48 cells. In Winn-type tumor-neutralizing assay in which C3H/He mice were inoculated i.p. or s.c. with MM46 cells preincubated with a test material, anti-MM46 conjugate showed greater activity compared that of anti-MM46 IgG. When a group of five C3H/He mice inoculated i.p. with 5 X 10(4) MM46 cells were treated with an i.p. injection of 1 microgram of anti-MM46 conjugate on days 1, 3, and 5, all mice survived tumor free, although those treated with 1 microgram of anti-MM46 IgG died before day 20 with a life span similar to those of mice treated with nonimmune conjugate or phosphate-buffered saline (control). Anti-MM46 conjugate also showed antitumor effects when injected i.v. to C3H/He mice bearing s.c. inoculated MM46 (inoculum, 2 X 10(6] on Day 1 at a dose of 5 to 50 micrograms. Thus, the in vivo efficacy of anti-MM46 conjugate over anti-MM46 IgG alone was demonstrated by therapeutic experiments as well as by tumor-neutralizing assays.

Animals↗
PubMed1983

[Clinical use of ticarcillin in the field of obstetrics and gynecology. Efficacy of ticarcillin in single administration and in combination therapy with S-sulfonated human immunoglobulin].

Single use of ticarcillin (TIPC, Monapen) was administered in 57 cases and combination therapy of TIPC and S-sulfonated human immunoglobulin (Venilon) was carried out in 23 patients who were either with severe infection, very old or in poor general conditions. The results obtained were as follows. Effective rate of single use of TIPC was 100% (3/3) in cases with infection, 50% (3/6) in cases with infection in which prior antibiotics therapy was poorly effective and 100% (48/48) in post operative cases. Effective rate of combination therapy of TIPC with S-sulfonated human immunoglobulin was 85.7% (6/7) in cases with infection, 71.4% (5/7) in cases with infection in which prior antibiotics therapy was poorly effective and 100% (9/9) in post operative cases. In laboratory findings, mild elevations of transaminase were recognized in 6 cases but restored to normal values without specific therapy. Side effect such as diarrhea, exanthema, fever, nausea and vomiting was not found in our cases.

Adult↗
PubMed1983

[Safety evaluation of micronomicin IV. Acute toxicity in rats, rabbits and dogs after drip intravenous infusion].

Micronomicin (MCR) is a new aminoglycoside antibiotic produced by Micromonospora sagamiensis var. nonreducans which was isolated from soil collected at Sagamihara City by Nara et al. This antibiotic shows a close similarity to gentamicin C components in physical and chemical properties. The antibacterial activity of MCR is broad-spectrum and almost equal to that of gentamicin C complex. MCR exhibits particularly high activity against Pseudomonas, Proteus, Klebsiella pneumoniae, Serratia, etc, as well as against some Pseudomonas aeruginosa strains resistant to gentamicin C1a. Toxicological studies of MCR were carried out for safety evaluation as follows: Studies were carried out to assess acute toxicity, when administered in 1 hour by drip intravenous infusion to Wistar rats, Japanese White rabbits and Beagle dogs. The results of the studies are summarised as follows: There was no difference on acute toxicity between drip intravenous infusion (d.i.v.) and intramuscular injection (i.m.) in rats. However, acute toxicity of d.i.v. was less than that of bolus intravenous administration (i.v.) in rats. Acute toxicity of d.i.v. was stronger than that of i.m. in dogs when administered in rats. Acute toxicity varied with species, and it was ranked in rabbits not equal to dogs greater than rats. There was no difference on symptoms between d.i.v. and i.m.

Aminoglycosides↗
PubMed1983

[Safety evaluation of micronomicin V. Subacute toxicity in rats after intravenous injection].

Micronomicin (MCR) is a new aminoglycoside antibiotic produced by Micromonospora sagamiensis var. nonreducans which was isolated from soil collected at Sagamihara City by Nara et al. This antibiotic shows a close similarity to gentamicin C components in physical and chemical properties. The antibacterial activity of MCR is broad-spectrum and almost equal to that of gentamicin C complex. MCR exhibits particularly high activity against Pseudomonas, Proteus, Klebsiella pneumoniae, Serratia, etc. as well as against some Pseudomonas aeruginosa strains resistant to gentamicin C1a. Toxicological studies of MCR in rats were carried out by intravenous injection for safety evaluation. Study on subacute toxicity: Wistar rats were injected intravenously with MCR at the dose levels of 4, 10, 25, 63 mg/kg and 100 mg/kg for 30 days. The results of the studies are as follows: In the subacute toxicity study, animals died at the dose level of 100 mg/kg (10 out of 30 animals). Main changes observed were renal disorders and ataxia which showed a close similarity to those seen in intramuscular toxicity studies in rats. The renal histological disorders occurred mainly at the dose levels of 25 mg/kg and over, but they were slight at the dose levels of 25 mg/kg. Ataxia was observed at the dose levels of 63 mg/kg and over, but its grade was slight at the dose level of 63 mg/kg. The maximum safety dose was equal to in the intramuscular subacute toxicity in rats, 10 mg/kg.

Aminoglycosides↗
PubMed1983

[Safety evaluation of micronomicin VI. Subacute toxicity in rabbits after drip intravenous infusion].

Micronomicin (MCR) is a new aminoglycoside antibiotic produced by Micromonospora sagamiensis var. nonreducans which was isolated from soil collected at Sagamihara City by Nara et al. This antibiotic shows a close similarity to gentamicin C components in physical and chemical properties. The antibacterial activity of MCR is broad-spectrum and almost equal to that of gentamicin C complex. MCR exhibits particularly high activity against Pseudomonas, Proteus, Klebsiella pneumoniae, Serratia, etc. as well as against some Pseudomonas aeruginosa strains resistant to gentamicin C1a. Subacute toxicity studies of MCR in rabbits were carried out by drip intravenous infusion (d.i.v.) comparing with intramuscular injection (i.m.) for 30 days (doses; d.i.v. = 4, 25, 63 mg/kg, i.m. = 63 mg/kg). The results of the studies are as follows: Animals did not die at any dose. Renal disorders occurred mainly at the dose level of 63 mg/kg; they were almost similar to those observed when administered by i.m., and the grade of disorders in d.i.v. was the same as in i.m. The maximum safety dose was 4 mg/kg.

Aminoglycosides↗
PubMed1983

[Safety evaluation of micronomicin VII. Fertility study by intravenous injection in rats].

Micronomicin (MCR) is a new aminoglycoside antibiotic produced by Micromonospora sagamiensis var. nonreducans which was isolated from soil collected at Sagamihara City by Nara et al. This antibiotic shows a close similarity to gentamicin C components in physical and chemical properties. The antibacterial activity of MCR is broad-spectrum and almost equal to that of gentamicin C complex. MCR exhibits particularly high activity against Pseudomonas, Proteus, Klebsiella pneumoniae, Serratia, etc. as well as against some Pseudomonas aeruginosa strains resistant to gentamicin C1a. Fertility studies of MCR in rats were carried out by intravenous injection for safety evaluation (Dose: 25, 50 mg/kg and 75 mg/kg). The results of studies are as follows. There was no adverse effect on fertility ability at any dose. Suppression of adult body weight gain was observed slightly at all dose level in male and at the dose level of 75 mg/kg in female.

Abnormalities, Drug-Induced↗