[Case of renal cancer associated with marked calcification and ossification].
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Biomedical subjects
Publications and source records attributed to M Homma.
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Sendai virus grown in L cells (L Sendai) caused little hemolysis, whereas the one grown in fertile eggs (egg Sendai) induced distinct hemolysis. Enzymatic treatment with trypsin at low concentrations markedly enhanced the hemolytic activity of L Sendai but not that of egg Sendai. Both sonic treatment and freezing and thawing greatly enhanced the hemolytic activity of egg Sendai, but they gave little enhancing effect on that of L Sendai which could, however, be greatly increased by successive treatment with trypsin. Dose response and kinetic experiments on the trypsin effect have suggested that a similarity exists in the inhibitory mechanism of infectivity for L cells and hemolytic activity of L Sendai. Treatment of L cells with trypsin at later stages of infection released a highly hemolytic L Sendai from those cells. The present study, by reference to the density centrifugation studies in a previous report (4), has shown that a variation in infectivity for L cells and in the hemolytic activity of L Sendai is a type of host-controlled modification distinguishable from the density variation.
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Sendai virus grown in fertile eggs (egg Sendai) infects L cells in which the synthesis of L Sendai (grown in L cells) occurs by the one-step mechanism. L Sendai is not infectious for L cells when tested by the tube titration method although it is infectious for chick embryos. When L cells infected with egg Sendai were dispersed by trypsin and plated on a monolayer culture of L cells, the viral agents spread to the adjacent recipient cells in which the synthesis of L Sendai occurred. The newly infected L cells became infectious for L cells again by trypsin treatment. Kinetic experiments suggested that the target of trypsin is the mature virus, of L Sendai nature, just budding from the L-cell surface. By using an immunofluorescent cell-counting technique, recovery of the infectivity of L Sendai for L cells due to a direct enzymatic action of trypsin was demonstrated. Under the optimal condition, the infectivity increased 1,000-fold for L cells and 10-fold for chick embryos, and both the titers could favorably be compared. No increasing effect of trypsin was observed on the infectivity of egg Sendai. Density centrifugation studies revealed a difference between egg Sendai and L Sendai in the density. Trypsin treatment which induced the maximal enhancement of L Sendai infectivity did not affect both the densities, showing that variations of Sendai virus in the infectivity for L cells and in the density are independent types of host-controlled modification.
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