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Biomedical subjects

T Usui

Publications and source records attributed to T Usui.

At least 577 records · Page 32Linked to original sources

[Effects of cefoxitin on infections secondary to hematopoietic malignancies].

Cefoxitin (CFX) was administered to 12 patients for evaluation of clinical effects of CFX against secondary infections complicated with hematopoietic malignancies, and the following results were obtained. 1. The clinical effects were excellent in 1 and good in 8 out or 11 cases with efficacy rate of 81.8%. Out of 12 cases treated with CFX, 1 case was excluded from clinical evaluation because of prophylactic use. It is noted that all cases with pyelitis showed good response to CFX. 2. The serum levels of CFX were determined in 1 patient with renal failure. After intravenous drip infusion of 2 g in 200 ml of glucose solution, the serum concentrations were 67.2 micrograms/ml and 7.53 micrograms/ml at 14 hours and 24 hours (after hemodialysis), respectively. 3. No side effects attributed to CFX were observed. These results indicate that CFX is an effective and safe antibiotic for the treatment of severe infections accompanying hematopoietic malignancies.

Adult↗

Induction of human autorosette forming cells by phorbol myristate acetate.

Human peripheral blood lymphocytes were examined for rosette formation with autologous erythrocytes. When normal human lymphocytes were stimulated with phorbol myristate acetate (PMA) in the presence of autologous serum, the levels of autorosette forming cells (ARFC) were strongly enhanced. Pre-culture was necessary for the generation of ARFC by PMA and the maximal level of ARFC was observed at 72 hr of culture. ARFC appear to belong to a T cell subset and the induction of ARFC by PMA was noted in monocyte depleted lymphocyte fractions, indicating monocyte independency.

Humans↗

Biochemical activities of lysosomal acid hydrolases in leukemic cells.

The biochemical activities of 8 lysosomal acid hydrolases in leukemic cells from 48 patients were examined. Characteristic alterations were found in alpha-mannosidase, beta-galactosidase and N-acetyl-beta-glucosaminidase activities of leukemic cells. The level of alpha-mannosidase activity was much higher in myelo(mono)genous leukemias (AML, AMoL, AMMoL, CML and CMMoL) than in lymphogenous ones (ALL, T-cell leukemia, hairy cell leukemia and CLL) without exception. The beta-galactosidase activity also differed as a result of alpha-mannosidase, except in T-cell leukemia. In T-cell leukemia it was within the range of normal lymphocytes, but in the other lymphogenous leukemias it was significantly below normal. N-acetyl-beta-glucosaminidase activity in myelo(mono)genous leukemic cells was above the range of normal granulocytes. The changes in these enzyme levels were consistent. The lymphocytic or myelocytic nature of three cases of acute undifferentiated leukemia could be determined by enzyme studies. In two cases it was lymphocytic and in one it was myelocytic. The enzymatic abnormalities were also found in morphologically mature neutrophils from patients but not only chronic types (CML, CMMoL) but also acute types (AMoL, AMMoL) of leukemias, and were similar to those of their respective leukemic cells. Analysis of lysosomal enzymes (at least three of those mentioned above), can elucidate one of the biochemical properties of leukemic cells and may be valuable in the differentiation of leukemias.

Humans↗

The chemical structure of neutral and acidic sugar chains obtained from bovine colostrum kappa-casein.

One neutral oligosaccharide alditol (tetrasacchariditol, 10%) and three acidic oligosaccharide alditols (a tri (28%), tetra (17%) and a pentasacchariditol (44%) were isolated from, colostrum kappa-casein taken 6 h after parturition. The neutral tetrasacchariditol and the acidic pentasacchariditol only contained a characteristic N-acetylglucosamine, and the latter was the main carbohydrate portion. The chemical structures were analyzed by methylation analysis with gas-liquid chromatography-mass spectrometry and by anomer analysis with 13C nuclear magnetic resonance, and were identified to be galactosyl-beta-1-3-[galactosyl-beta-1-4-N-acetylglucosaminyl-beta-1-6-]-N-acetylgalactosaminitol, N-acetylneuraminyl-alpha-2-3-galactosyl-beta-1-3-[galactosyl-beta-1-4-N-acetylglucosaminyl-beta-1-6-]-N-acetylgalactosaminitol, N-acetylneuraminyl-alpha-2-6-N-acetylgalactosaminitol. The former two were the novel carbohydrate chains of colostrum kappa-casein, but the latter two were identical with those which have been found in normal kappa-casein.

Animals↗

[A study on testosterone-estradiol binding globulin (TeBG). I. Purification and some immunological properties of bovine serum TeBG (author's transl)].

Bovine serum TeBG was purified by 17 alpha -carboxyethynyl-17-hydroxy-4-androsten-3-one sepharose 4B affinity chromatography (T-sepharose) and hydroxylapatite column chromatography. The chemical and immunological properties of the purified TeBG were surveyed and the following results were obtained. 1) The procedures yielded 400 microgram of protein from 1 L of bovine serum with an overall purification of about 7,560 fold. 2) The purified TeBG was homogenous and was about 80,000 in molecular weight based on sucrose density gradient ultracentrifugation and polyacrylamide gel electrophoresis. 3) The antibody prepared against the purified bovine TeBG did not cross-react with dog and human sera, suggesting the species specificity of TeBG. 4) 125I-bovine TeBG, labelled by the lactoperoxidase method, had a high binding capacity to the anti-bovine TeGB antibody. These results indicate the applicability of purified TeBG and the antiserum for TeBG RIA.

Animals↗

Glycosaminoglycan synthesis by cultured skin fibroblasts from a patient with Lowe's syndrome.

Glycosaminoglycan metabolism in cultured skin fibroblasts from a patient with Lowe's syndrome (oculocerebrorenal syndrome) was compared with that in normal fibroblasts. Cells were incubated with [3H]glucosamine and 35SO42-, and then the labeled glycosaminoglycans in the medium, trypsinate, and cell membrane fractions were analyzed by means of enzymatic and chemical degradations and by electrophoresis. Glycosaminoglycans, mostly chondroitin sulfates and dermatan sulfate, were markedly undersulfated in Lowe's syndrome. Undersulfation was most pronounced in the cell membrane fraction of cells which had been incubated at 0.03 mM sulfate concentration. Even at 0.52 mM or a higher sulfate concentration, undersulfation of chondroitin sulfates in the cell membrane fractions was significant. The undersulfation was the result of depressed sulfation rather than that of increased desulfation, as demonstrated by pulse-chase experiments using 35SO42-. Hyaluronate synthesis was not significantly impaired in the Lowe's syndrome fibroblasts. It was inferred, based on the results of the present study and those previously reported that the undersulfation of glycosaminoglycans is a consequence of a lower level of active sulfate (adenosine 3'-phosphate 5'-phosphosulfate) in the Lowe's syndrome fibroblasts, caused by an elevation of nucleotide pyrophosphatase activity degrading adenosine 3'-phosphate 5'-phosphosulfate.

Cell Division↗

A new approach to detection of heterozygotes for adenosine deaminase deficiency: a hypothetical method.

In a second and third families with ADA deficiency found in Japan, we tried a new approach to evaluate heterozygote detection. This is based on the hypothesis that ADA activity of red blood cell is the quantitative sum of the activities of ADA proteins expressed by two allelic genes at the ADA autosomal locus, and that these activities are not changed by the gene transmission from parents to children. We have detected red blood cell-ADA activities expressed by the one normal allelic gene in heterozygotes (including parents and paternal or maternal grandfather or grandmother) and from these values have determined combinations for the pair of ADA activities expressed by the two allelic genes of other family members. These combinations were consistently made in all relatives examined in the two families, and we conclude that several members of each family who were judged to have nil activity in the combinations were heterozygotes for ADA deficiency.

Adenosine Deaminase↗