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Biomedical subjects

T Sakano

Publications and source records attributed to T Sakano.

At least 127 records · Page 7Linked to original sources
PubMed1982

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↗
PubMed1981

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↗
PubMed1980

High plasma, erythrocyte, lymphocyte and granulocyte zinc concentrations in a patient with the Chediak-Higashi syndrome.

Zinc determinations were made in a 5 month-old female with the Chediak-Higashi syndrome. Zinc concentrations in plasma, erythrocytes, lymphocytes and granulocytes from the patient were significantly higher than those in healthy children of a similar age, and were higher than--or equal to--those of healthy adults. Lymphocyte zinc levels in the parents were significantly lower than those of healthy adults. Although the cause of the high zinc concentrations in these samples cannot be fully explained , abnormally high zinc levels may be partially responsible for impairment of some leukocyte functions in patients with CHS since zinc plays a central role in cellular metabolism.

Chediak-Higashi Syndrome↗
PubMed1980

Visceral larva migrans caused by Trichuris vulpis.

Two brothers with visceral larva migrans caused by Trichuris vulpis were diagnosed after they had been investigated for an eosinophilia. Both patients were almost asymptomatic. The diagnosis of visceral larva migrans was based on the results of immunoelectrophoretic studies and no liver biopsy was performed. After administration of thiabendazole, the number of eosinophils and serum total IgE levels gradually decreased, and the patients have remained well.

Animals↗
PubMed1980

Enhancement of T-cell response to PWM by neuraminidase-treated non-T cells.

The effect of neuraminidase (from Cl. perfringens, CPN) on the human lymphocyte response to pokeweed mitogen (PWM) was studied. CPN treatment greatly increased [3H]-thymidine incorporation by human lymphocytes at lower concentrations of PWM. This enzyme acted specifically on T-cell proliferation and had no direct effect on non-T-cell proliferation. When CPN-treated non-T cells were added to autologous T cells, [3H]-thymidine incorporation was markedly enhanced at lower concentrations of PWM. However, the addition of T cells pre-treated with mitomycin C (MMC) to CPN-treated non-T cells failed to increase [3H]-thymidine incorporation in contrast to the controls. MMC-blocked, CPN-treated non-T cells significantly enhanced T-cell proliferation, whereas the effect of MMC-blocked, CPN-treated adherent cells was equal to that of the controls. These data indicate that cell-surface properties of non-T cells other than monocytes affect T-cell proliferation in some situations.

Cell Division↗