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Biomedical subjects

M Nishida

Publications and source records attributed to M Nishida.

At least 469 records · Page 26Linked to original sources

Protective effect of 4,6-O-ethylidene glucose against the cytotoxicity of streptozotocin in pancreatic beta cells in vivo: indirect evidence for the presence of a glucose transporter in beta cells.

Ethylidene glucose (4,6-O-ethylidene glucose; EG) is known to bind the outer surface of the glucose transporter in the membranes of human erythrocytes and other mammalian cells. If a glucose transport system is present on pancreatic beta cells and recognizes the glucose moiety of streptozotocin (STZ), EG should protect beta cells from the cytotoxicity of STZ when it is administered with STZ. This possibility was examined in in-vivo experiments in rats. When EG and STZ were injected into rats together the animals did not become diabetic, as judged by their blood glucose levels, response in a glucose-tolerance test, and insulin secretion in response to feeding. These results suggest that there is a glucose transporter present in beta cells and also the transport of streptozotocin into beta cells through this system.

Animals↗

[Experimental studies on the antitumor effect of oral antitumor agents on gynecological malignant tumors].

In order to evaluate the antitumor effect of oral antitumor agents on gynecological malignant tumors, experimental studies were carried out using nude mice which had received implants of human endometrial carcinoma. The agents used for the study were tegafur (T) and UFT, and their effects on inhibiting tumor growth, and on preventing tumors from implanting or recurring were investigated in mice in continuous long-term administrations. The results were as follows: As to the inhibitory effect on the tumor growth, while both T and UFT had no inhibitory effect on large to medium tumors, both were mildly effective on small tumors having a diameter of 2-3 mm (Inhibition Rate (IR): T-60.0%, UFT-71.0%), however, the no effect great enough to reduce the tumor size was recognized with either agent. The implantation rates of tumor under the administration of T and UFT were 80.0% and 70.0% respectively, indicating no significant differences from the control (90.0%) and either agent, however, UFT was judged to have the effect of preventing tumors from implanting to a certain extent. The recurrence rates for tumor under the administration of T and UFT were 30.0% (6/20) in both cases, which was significantly lower than the control (70.0%) (p less than 0.05). Both agents were evaluated as useful for preventing tumors from recurring. These findings, indicated that while the maintenance therapy of an oral antitumor agent has no effect on macroscopic tumors, a fairly good effect is expected on microscopic tumors, especially on the prevention of tumor recurrence.

Adenocarcinoma↗

Human urinary kallikrein (HUK): large-scale purification and direct solid-phase radioimmunoassay (RIA).

HUK was purified from 1,000 liters of fresh urine by the following procedures: silica gel adsorption, gel filtration on Sephadex G-75, DEAE-Sephadex chromatography, bentonite treatment, affinity chromatography on aprotinin-Sepharose 4B, and rapid gel filtration on a TSK Gel G-3000 SWG column. Seventeen mg of HUK being found to be pure by means of various analyses was obtained. The pI values of the heterogeneous components of HUK were 3.5, 3.8, and 4.1, while the corresponding molecular weights of these components were 5.4 X 10(4), 4.9 X 10(4), and 4.4 X 10(4), respectively. The antigens (125I- and non-labeled HUK) were incubated for 4 hrs at 37 degrees C in polystyrene test tubes to which anti-HUK rabbit IgG had been immobilized. The quantitative range of the standard curve was 1-128 ng. This Ria principally recognized active form of HUK. Therefore, total and inactive HUK also could be determined by the combination of the RIA with trypsin treatment of the urine sample. The RIA correlated closely with both S-2266 amidolytic assay and kininogenase assay.

Antibodies↗

Conjugal transfer of beta-lactamase-producing plasmids of Neisseria gonorrhoeae to Neisseria meningitidis.

Twenty clinical isolates of beta-lactamase-producing Neisseria gonorrhoeae from Japanese sources were studied to define their ability to serve as donors for their plasmids in conjugation with Neisseria meningitidis. These twenty strains of N. gonorrhoeae harbored the 4.5-megadalton (Mdal) beta-lactamase-producing plasmids and the 24.5-Mdal conjugative plasmids. We found that only three of twenty N. gonorrhoeae strains showed a detectable conjugation frequency (greater than 10(-5)) with N. meningitidis as the recipient although all strains were capable of mobilizing beta-lactamase-producing plasmids to N. gonorrhoeae and to Escherichia coli. The 4.5-Mdal beta-lactamase-producing plasmid was maintained in N. meningitidis, but the large 24.5-Mdal conjugative plasmid has not been found in N. meningitidis transconjugants.

Bacterial Proteins↗

Subacute toxicity of methylmercuric chloride and mercuric chloride on mouse thyroid.

Intoxication effect on mouse thyroid by prolonged administration of either CH3HgCl or HgCl2 was studied. It was found by giving CH3 203HgCl and 203HgCl2 through stomach intubation at either a single or a 30 d treatment that thyroid is a moderately susceptible organ to both mercurials. Animals were given 50, 100 and 150 micrograms/d of either mercurial in drinking water for a month. At the lowest amount of HgCl2, body weight was increased, whereas at the highest dose, there was a transient delay in growth. With lower amounts of CH3HgCl, no change in growth was observed. However, at the highest amount, a severe growth inhibition occurred. The thyroid weight was unaffected by lower amounts, but was significantly reduced by 150 micrograms/d of either mercurial. The 24 h radioiodide uptake in the thyroid, expressed by cpm/mg organ weight, was reduced by lower levels of mercurials. CH3HgCl and HgCl2 suppressed the rate of radioiodide incorporation into the iodothyronine fraction, but not into the iodotyrosine fractions, indicating that mercurials do not interfere with organification of iodide but do inhibit the coupling process. Serum thyroxine (T4) level was affected by mercurials, but serum triiodothyronine (T3) was not. This result suggested that even thyroidal secretion of T4 was inhibited by mercurials, but the peripheral conversion of T4 to T3 may not be affected in the maintenance of an active hormone level.

Animals↗

Establishment of passive hemagglutination assay (PHA) system for anti-HBc in plasma.

A sensitive and specific assay system for anti-HBc, the passive hemagglutination (PHA) method, has been established. The reactivity of PHA cells prepared by conjugating purified recombinant HBcAg-particles with fixed sheep blood cells (SRBC) was highly specific to monoclonal- and polyclonal anti-HBc IgGs. The sensitivity of PHA method was higher than that of radioimmunoassay (RIA). However, uncertainty for the positivity of anti-HBc still remained in plasma with the PHA titers lower than 2(5). A relatively high ratio (19%, 37 of 196) of anti-HBc-positive plasma, which had been confirmed to be HBsAg negative, was demonstrated in blood donors whose bloods have been considered suitable for transfusion. The hazards of anti-HBc-positive bloods and the importance of anti-HBc detection in plasma are discussed in this paper.

Antibodies, Monoclonal↗

New diabetogenic streptozocin analogue, 3-O-methyl-2-([(methylnitrosoamino) carbonyl]amino)-D-glucopyranose. Evidence for a glucose recognition site on pancreatic B-cells.

The nonmetabolizable glucose analogue 3-O-methyl-glucose is known to protect pancreatic B-cells against streptozocin (STZ) when injected with or just before STZ. If 3-O-methyl-glucose and the sugar moiety of STZ compete for a glucose recognition site on B-cells, it seemed likely that 3-O-methyl-2-deoxy-2-( [(methylnitrosoamino)carbonyl]amino)-D-glucopyranose, an analogue of STZ with a 3-O-methyl-glucosyl residue, would cause experimental diabetes. This possibility was tested by synthesis of this analogue (alpha-anomer) and comparison of its diabetogenic activity in Wistar rats with that of STZ. Results showed that the compound was diabetogenic and as potent as STZ. This new analogue is the first of the various STZ derivatives reported to show diabetogenic activity. Its activity supports the idea that 3-O-methyl-glucose and STZ bind competitively with a glucose recognition site on pancreatic B-cells.

3-O-Methylglucose↗