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Y Fukata

Publications and source records attributed to Y Fukata.

42 records · Page 3Linked to original sources
PubMed1993

The decreased immune responses in macular mouse, a model of Menkes' kinky hair disease.

The macular mutant mouse is a murine model of the Menkes' kinky hair disease, characterized by a copper deficiency in serum. The immune response of its hemizygote (ml/y) was examined, herein. Ml/y mice which were not treated with Cu were atrophy of lymphoid tissues on day 14. However, kidney, brain, heart and lung weights were higher in ml/y mice without Cu treatment than in normal (+/y) mice. When compared to cells from +/y mice, spleen cells from ml/y mice exhibited similar proliferation-curves stimulated by Con A or LPS. Lymph node cells from ml/y mice showed a significantly decreased mixed lymphocyte reaction (MLR) response when stimulated by spleen cells from Balb/c mice. Spleen cells from ml/y mice demonstrated similar stimulation against lymph node cells from Balb/c mice. Antibody production against sheep red blood cells (SRBC) in vivo, a T cell dependent response, was suppressed in ml/y mice. By contrast, the antibody production against dinitrophenyl-ficoll, a T cell independent response was similar in +/y and ml/y. The antibody production against SRBC in vitro was also suppressed in ml/y mice. However, when the T cell-enriched fraction of ml/y mouse spleen cells was replaced by the T cell-enriched fraction of +/y mouse spleen cells, the antibody production against SRBC was recovered. The percentage of Ly-5-positive cells (B cell) from ml/y mice was greater than those from +/y mice. The percentage of Thy-1.2-positive cells (T cell) was decreased, and the decrease was most prominent with the L3/T4-positive T cell (helper T cell) subset.

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PubMed1993

Recovery of decreased antibody production by ceruloplasmin in the macular mutant mouse.

The macular mutant mouse is a murine model of Menkes' kinky hair disease, characterized by a serum copper and ceruloplasmin deficiency. The hemizygote (ml/y) had a decreased antibody response to sheep red blood cells (SRBC). 1) In vivo; the administration of ceruloplasmin recovered antibody production in ml/y mice, but, had no effect on that of normal mice (+/y). The administration of heat treated ceruloplasmin did not increase antibody production in ml/y mice, whereas the administration of various concentrations of copper suppressed the anti-SRBC plaque-forming response in both ml/y and +/y mice. 2) in vitro; ceruloplasmin had no effect upon antibody production against SRBC in both ml/y and +/y mouse spleen cells. In contrast to ceruloplasmin, 1 microgram/ml of copper inhibited the antibody production in spleen cells from both +/y and ml/y mice as well as in vivo. These findings suggested that the decreased antibody production in ml/y mice was considered to be due the decreased ceruloplasmin.

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PubMed1992

Comparison of KRN2391 with nicorandil and nifedipine on canine coronary blood flow: antagonism by glibenclamide.

The mode of action of KRN2391 [N-cyano-N'-(2-nitroxyethyl)-3- pyridinecarboximidamide monomethanesulfonate] in coronary circulation was examined in anesthetized dogs in comparison with those of nicorandil and nifedipine. Administration of KRN2391 (10 micrograms/kg i.v.), nicorandil (300 micrograms/kg i.v.), and nifedipine (3 micrograms/kg i.v.) caused an increase in coronary blood flow (CBF) and decreases in mean blood pressure (MBP) and in coronary vascular resistance (CVR). Heart rate (HR) was slightly and simultaneously increased by the drugs. Glibenclamide (5 mg/kg i.v.) blocked the changes of these parameters caused by KRN2391 and nicorandil, but not those caused by nifedipine. The present study suggests that the mechanism of action through ATP-sensitive K channels which are blocked by glibenclamide may contribute, at least in part, to the effects of KRN2391 and nicorandil on CBF and blood pressure (BP).

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