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Biomedical subjects

M Minoda

Publications and source records attributed to M Minoda.

At least 37 records · Page 2Linked to original sources

Mixed lymphocyte reaction in interferon-gamma treated (NZB x NZW)F1 mice.

Mouse interferon-gamma was administered to (NZB x NZW)F1 mice, which develop a disease like human systemic lupus erythematosus. Class II antigens on adherent spleen cells and their activity to stimulate allogeneic T lymphocyte in mixed lymphocyte reaction were observed as well as the changes of the clinical findings of the mice. In interferon-gamma treated mice, as compared to control mice, the positive rate for class II antigen on adherent spleen cells was increased, and the mixed lymphocyte reaction using the cells of interferon-gamma treated mice as stimulator cells was enhanced. These findings suggest that the enhancement of antigen presenting activity of adherent spleen cells to T lymphocytes might be associated in the exacerbation of the disease in interferon-gamma treated (NZB x NZW)F1 mice.

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Examination of the inhibitory effects of interferon-gamma on interleukin-4-induced stimulation of resting B cells from NZB/NZW F1 mice.

Percoll fractionation of NZB/NZW F1 mouse B cells revealed an increased ratio of low-density fraction ('activated' B cell fraction) and a decreased ratio of high-density fraction ('resting' B cell fraction), in comparison to normal mouse B cells. Resting B cells of B/W F1 mice were hyperresponsive to interleukin-4 (IL-4), with increased proliferation and IgG anti-DNA antibody production, in comparison to normal mice. The hyper-responses of resting B cells from NZB/NZW F1 mice to IL-4 were affected with dose dependency by interferon-gamma (INF-gamma); specifically, cell proliferation and anti-nuclear antibody production were suppressed in the presence of IFN-gamma. This suppressor action of IFN-gamma was most noticeable when it was added to the culture system simultaneously with IL-4. These findings suggested that the abnormally activated state of NZB/NZW F1 mice B cells can be attenuated by the action of IFN-gamma on resting B cells.

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Effect of interferon-gamma on the abnormality of T cell activation in NZB mice.

It is known that New Zealand black (NZB) mice have a defect in the autoantigen recognition mechanism by T cells. The present study was carried out to examine whether the defect could be improved by normalizing the self Ia molecule expression on thymic reticuloepithelial cells (TRC) by using interferon-gamma (IFN-gamma). Syngeneic mixed lymphocyte reaction (SMLR) was used as an indicator of the mechanism of autoantigen recognition. In the reaction, T cells separated from the thymus were used as responders, and machrophages separated from the spleen were used as stimulators. When the responders were cultured with TRC, in which self Ia molecule expressions had been enhanced by IFN-gamma, for activation, the low level of SMLR in NZB mice was elevated close to the normal level. It was suggested, therefore, that IFN-gamma could normalize the defective autoantigen expression on TRC in NZB mice and improve the abnormal T cell activation against autoantigens.

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The relationship between the defect in the syngeneic mixed lymphocyte reaction and thymic abnormality in New Zealand mice.

Whether a defect the syngeneic mixed lymphocyte reaction (SMLR) is caused by an abnormality in the recognition of autoantigen (Ia antigen) by T cells or by an abnormality in macrophages (Mø) which provides the Ia antigen was examined using New Zealand black (NZB) mice, a model animal for human autoimmune diseases. The level of activation of T cells by Ia antigen was lower in NZB mice than in normal mice, despite the fact that the quantity of Ia antigen expressed on the surface of Mø was much the same in the NZB mice. Furthermore, less Ia antigen was expressed on thymic reticuloepithelial cells (TRC) in NZB mice than in normal mice. These findings suggest that the defect in the SMLR in NZB mice is mainly due to T cells, namely, to abnormality in the activation of the Ia antigen receptors on the T cells, which occurs as a result of the contact between T cells and TRC in the process of T cell maturation and differentiation.

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The effects of macrophages on interleukin 2 production in thymocytes of New Zealand black mice.

The New Zealand Black (NZB) mouse is a model animal for human autoimmune disease. Abnormalities in Interleukin 2 (IL-2) production were studied in these mice to investigate whether they arise from disorders in T cells or from abnormalities of macrophages (M phi). T cells were separated from thymocytes using peanut agglutinin (PNA), while M phi were separated from spleen cells using the adherence method. Cultures were prepared from T cells and M phi obtained from normal control mice and NZB mice and the activity of IL-2 in the supernatant of the culture was studied. The results indicate that abnormalities in the production of IL-2 in NZB mice are due to functional disorders in both T cells and M phi.

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Morphological study on the relationship between the muscular architecture of the ventricles and cardiac hypertrophy in the M strain of stroke-prone spontaneously hypertensive rats.

The relationships between blood pressure and hypertrophy in cardiac muscle cells and their nuclei were histometrically and microphotometrically examined in the M strain of stroke-prone spontaneously hypertensive rats (M-SHRSP). In 60-day-old M-SHRSP, hypertrophy of the cardiac muscle nuclei preceded increases in cardiac muscle cell diameters (MCD) and lengths (MCL). Increases in MCD started in the middle and deep layers of the lateral wall of the left ventricle. At 90 days of age, hypertrophy of cardiac muscle cells and nuclei occurred equally in the middle and deep layers of the left ventricle. Right ventricular hypertrophy began to appear after 90 days of age. In the middle and deep layers of the left ventricle and in the septum in 150-day-old M-SHRSP the MCL were 1.4 times those in 30-day-old M-SHRSP and the MCD were 1.8 times those in 30-day-old M-SHRSP.

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Inverted papilloma of ureter.

A rare case of inverted papilloma of the ureter in a sixty-eight-year-old man is presented, and the literature is reviewed.

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The function of thymic reticuloepithelial cells in New Zealand mice.

This study was undertaken to clarify the function of thymic reticuloepithelial cells (TRC) in the New Zealand black (NZB) mouse as a model animal of human autoimmune disease. Attention was focused on whether or not any defect in the TRC function participating in the maturation process from immature T cells to mature T cells was present. Precursor T cells isolated from bone marrow cells were cultured with TRC. Induction of Thy-1.2 antigen on the surface of precursor T cells was measured, in addition to the increased responsiveness of precursor T cells to T-cell mitogens and in mixed lymphocyte reaction (MLR). When NZB mouse precursor T cells were cultured with normal mouse TRC, the induced T-cell function proved to be similar to the function noted when normal mouse precursor T cells were cultured with normal mouse TRC. On the other hand, when normal mouse precursor T cells were cultured with NZB mouse TRC, the induced T-cell function proved to be inferior to the one noted in culture with normal mouse TRC. From these results, it was concluded that the NZB mouse had nothing remarkable in precursor T cells, but something abnormal in the TRC function.

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