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Biomedical subjects

J Sato

Publications and source records attributed to J Sato.

At least 469 records · Page 26Linked to original sources
PubMed1981

Xylitol mediated amelioration of acetylphenylhydrazine-induced hemolysis in rabbits.

Xylitol was investigated for its ability to ameliorate hemolytic anemia induced by acetylphenylhydrazine in rabbits. Animal experiments were performed using two different concentrations of xylitol, a 5% and a 10% solution with a total dose of 2 g/kg body weight and infusion rates of 10 mg and 20 mg xylitol per kg body weight per minute respectively. Two doses of acetylphenylhydrazine (APH), 5 and 10 mg per kg, were injected intraperitoneally as hemolytic inducers in different groups of rabbits. All the rabbits infused with xylitol showed significantly less acute APH-induced hemolysis. The isotonic 5% xylitol solution was found to maintain and restore the hematological parameters (packed cell volume, hemoglobin concentration, reduced glutathione (GSH) content, and reticulocyte counts) better than the 10% xylitol solution. Increased 51CR-red cell survival confirmed the beneficial effect of xylitol. The survival of erythrocytes as represented by chromium-labeling in rabbits infused with 5% xylitol after treatment with 10 mg/kg APH increased from about 33% (the survival of red cells in rabbits injected with APH alone) to 67% of normal rabbits' red cell survival. Erythrocytes in APH-treated animals took up xylitol more readily than erythrocytes from control animals. Our results in rabbits suggest that (1) non-toxic dosage of xylitol is effective in ameliorating the hemolytic episode induced by APH, (2) there is a dose relationship between the hemolytic effect induced by APH and the preventive effect offered by xylitol, (3) drug-challenged cells effectively acquired two to three fold more xylitol to compensate for the cellular needs than that of the normal cells, and (4) sufficient xylitol (55 mg/dl) to act as substrate for xylitol dehydrogenase was recovered intracellularly in drug-challenged rabbit erythrocyte in vivo, in spite of a low plasma (less than 30 mg/dl) concentration of the substrate. This antihemolytic affect of xylitol is likely accomplished through NADPH generation, which maintains the level of GSH and protects the hemoglobin and other structural and functional proteins against peroxidative damage.

Animals↗
PubMed1981

Gas-containing brain abscess due to Fusobacterium nucleatum.

Gas-containing brain abscesses are rarely seen. Recently, in a 28-year-old man, such an abscess ruptured into the lateral ventricle but was treated successfully. Fusobacterium nucleatum, an anaerobic bacillus, was cultured from the pus obtained.

Adult↗
PubMed1981

Chromosome 14q+ in adult T-cell leukemia.

Cytogenetic studies were performed on leukemic cells from two patients with adult T-cell leukemia. A 14q+ marker chromosome was found in the peripheral blood leukocytes from patient No. 1 and in a leukemic T-cell line (MT-1) derived from the peripheral blood of patient No. 2. The 14q+ resulted from a t(12;14) in patient No. 1 and from a t(Y;14) in patient No. 2 with a break point at 14q32 in each case. In addition, the leukemic cells from patient No. 1 showed a t(1;7) and a 9q-, while the MT-1 line had numerous structural abnormalities. Thus, it is clear that a 14q+ translocation is not restricted to B-cell neoplasms but occurs in T-cell neoplasms as well.

Adult↗
PubMed1981

Effect of acetazolamide on the anticonvulsant potency of phenobarbital in mice.

Effect of acetazolamide (AZA) on the anticonvulsant potency of phenobarbital (PHB) was investigated in mice by maximal electroshock seizure (MES) test. By coadministration with AZA, a remarkable increase an prolongation of the anticonvulsant activity of PHB was brought about. The type of the synergism of PHB with AZA was not additive but of potentiation. The potentiation of the anticonvulsant activity of PHB with AZA was rather related to inhibition of carbonic anhydrase (CA) in brain than in blood. The anticonvulsant activity of PHB was also increased by coadministration with methazolamide which had a great ability to inhibit brain CA. Furosemide, which had no inhibitory effect on brain CA, on the other hand, failed to show any potentiation on the anticonvulsant activity of PHB. Thus it was inferred that the inhibition of brain CA may play a significant role for the potentiation of the anticonvulsant activity of PHB. Although reserpinization completely abolished the protective effect of AZA on MES, the potentiation of the anticonvulsant activity of PHB was still observed by AZA. These results suggest that pharmacodynamic and/or pharmacokinetic effect of AZA independent of its anticonvulsant action may contribute to the potentiation of the PHB action.

Acetazolamide↗
PubMed1981

Abnormalities of chromosome no. 1 related to blood dyscrasias: study of 10 cases.

Partial excess of chromosome 1 (q25-q32) was noted in malignant cells from all of 10 patients who had disorders such as non-African Burkitt's lymphoma, adult T-cell leukemia, myelofibrosis, malignant lymphoma, chronic lymphocytic leukemia or chronic myelocytic leukemia in blast crisis. The break points on chromosome 1 were at centromere, q12, q21, q23, q25 and q32. Variations in the specific region of the long arm of chromosome 1, q25-q32, were thought to be important in the evolution of malignant cell proliferation.

Adult↗
PubMed1981

A 14q+ chromosome in adult T-cell leukemia.

Chromosome studies were conducted on two patients with adult T-cell leukemia. In both patients, a marker chromosome 14q+ and a structural change involving chromosome 1 with trisomy of the q arm were found in peripheral blood leukocytes. The 14q+ marker chromosome had resulted from translocation from #5p in one patient and #5q in the other patient. The present and previous studies suggest that the donor chromosomes involved in the 14q+ translocation are variable. This indicates that the 14q+ marker chromosome rather than the donor chromosome is intimately related with adult T-cell leukemia.

Adult↗
PubMed1981

Metabolism of xylitol and glucose in rats bearing hepatocellular.

The variation in metabolism of glucose and xylitol by diverse rat hepatocellular carcinomas and partially hepatectomized rat livers was studied. The AS-30D and FB56 tumors demonstrated a significantly different degree of utilization of glucose and xylitol in vitro. This correlated partially with the low activity of polyol dehydrogenase when xylitol was used as a substrate. The activity ofa nicotinamide adenine dinucleotide-dependent polyol dehydrogenase in various hepatomas ranged from nondetectable to 30 nmol/min/mg protein, with the lower activities in FB56 and AS-30D tumors at 0 and 0.22 nmol/min/mg, respectively; while nicotinamide adenine dinucleotide phosphate-dependent xylitol dehydrogenase activities ranged from 0 to FB56 to 3.31 nmol/min/mg protein in liver regenerated for 1 week. The activities of nicotinamide adenine dinucleotide phosphate-dependent enzyme for normal liver and AS-30D tumors measured 2.2 and 0.14 nmol/min/mg protein, respectively. Although only the 311C tumor had an activity equivalent to that of normal liver, the range of the nicotinamide adenine dinucleotide phosphate-dependent polyol dehydrogenase activities among the cell lines studies is narrow. The ratios of metabolites of [14C]glucose or [14C]xylitol were determined in rats bearing AS-30D tumors. Animals were given i.v. injections of a 10% solution of [14C]glucose or [14C]xylitol, 2 g/kg body weight. Assays of neutral sugar metabolites from each substrate in the acid-soluble fraction of liver or AS-30D tumor showed that xylitol in the liver was converted primarily into glucose while in the tumor 80 to 90% of the xylitol remained unchanged. This hepatocellular carcinoma is also markedly deficient in the ability to synthesize acid-insoluble glycogen and glycoprotein from xylitol as compared to the liver.

Aldehyde Reductase↗