Biomedical subjects
Publications and source records attributed to T Kishida.
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The authors radioimmunoassayed cyclic nucleotide concentrations in plasma and biopsied muscles of muscular dystrophy and muscles of chicken embryo. c-AMP concentrations in plasma were significantly lowered in Duchenne-type muscular dystrophy and this lowered degree was correlated with the stage of progression. Plasma c-GMP levels were also depressed in Duchenne-type dystrophy. In biopsied muscles, c-AMP concentrations per milligram of non-collagen protein were within normal limits. Therefore, the decrease of plasma c-AMP concentrations might be an expression of total metabolic changes rather than a pathologic process of the muscle itself. As for the dystrophic chicken embryo, both c-AMP and GMP concentrations were decreasing in the pectoral muscles in parallel with the advancement of hatching stages.
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Adult A/J mice inoculated with 1 x 10(6) syngeneic C1300 neuroblastoma cells had a palpable tumor after 1 week, and the tumor grew uniformly. The hypertonic KCl extract of the tumor induced blastogenic response of syngeneic spleen cells from tumor-bearing mice, and tumor antigens were considered to be solubilized by KCl from tumor cells. Although a higher blastogenic response to insoluble tumor antigens coupled to Sepharose 4B beads could have been expected as demonstrated in this mixed lymphocyte-tumor cell reaction (MLTR) assays, the blastogenic activity, which was approximately equal to that of soluble tumor antigens, was less than one-third of that in MLTR. The initial information of blastogenic response was found to be transmitted to the responder cells with out the entrance of tumor antigens into the cells by the use of insoluble tumor antigens. Blastogenic responses to soluble tumor antigens and to irradiated tumor cells (MLTR) in spleen cells from tumor-bearing mice were serially assayed after tumor inoculation. The response to soluble tumor antigens reached a peak 2 weeks after inoculation but a progressive depression of the responses was observed after a marked tumor growth. Although the blastogenic activity of soluble tumor antigens was small, changes in consecutive response to soluble tumor antigens in tumor-bearing mice were well correlated with those in MLTR. The blastogenic responses to soluble tumor antigens and MLTR were considered to be the manifestation of tumor-specific cell-mediated immunity. Furthermore, the serial blastogenic responses to concanavalin-A and lipopolysaccharide were also coincident with those of tumor-specific immunity.
The preparations of interferon or virus-inhibiting factor produced in L cell (L-IF) and mouse brain (MB-IF) enhanced the killing of Staphylococcus aureus (S.a.) by the mouse peritoneal macrophage. The L-IF, heat-inactivated at 80 degrees or 60 degrees for 30 min., and mock L-IF could not enhance the killing of S.a. The heterologous human and rabbit interferon preparations didn't enhance the bactericidal activity of macrophage. The L-IF didn't have any effect on the release of lysozyme from the macrophages.
Human leukocyte interferon (HL-IF) enhanced the NBT reduction of human peripheral neutrophil in vitro. Dose relation between IF activity and the NBT reduction was recognized. Heat-inactivated HL-IF, HL-IF neutralized by anti-IF serum or heterologous IF could not increase the NBT reduction.
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High doses of rabbit interferon (2 X 10(6) and 2 X 10(5) units/ml, a drop of about 0.1 ml administered topically into the eye twice daily) suppressed the rejection of rabbit corneal xenograft, whereas a low dose (2 X 10(3) units/ml) enhanced it, However, neither heat-inactivated rabbit interferon nor mouse L cell interferon showed any effects on rabbit corneal grafts.
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It was found that the phagocytosis of human peripheral monocytes was enhanced by human leukocyte interferon preparations. This activity showed species-specificity and a positive correlation between interferon titer and phagocytic activity. When human monocytes were treated by interferon, the pahagocytic activity was enhanced. But when interferon was added to the latex, the enhancement was not observed. The interferon preparation did not only increase the number of phagocytic cells, but also enhanced the degree of phagocytosis in individual cells. The factor responsible for the enhancing effect was inactivated by trypsin, but was not inhibited by actinomycin D.
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