Dysfunction of the Beall mitral prosthesis and its detection by cinefluoroscopy and echocardiography.
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Biomedical subjects
Publications and source records attributed to M L Johnson.
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The induction of interferon (IF) by lactic dehydrogenase virus (LDV) and the action of exogenous IF on LDV multiplication have been studied in vivo and in vitro. In vivo the induction of serum IF by LDV was shown to correspond with the virus challenge dose. In vitro LDV-infected macrophages did not produce detectable IF. As to the action of IF in vivo, the prophylactic or therapeutic administration of IF to mice reduced the LDV serum titers only temporarily. In vitro, (i) the sensitivity of LDV to IF in macrophage culture was 30 times less than that of vesicular stomatitis virus, and 5 times less than that of Sendai virus, and (ii) prolonged exposure of LDV-infected macrophages to high IF concentrations did not cure the chronic infection, but only decreased the virus titer. The probable role of IF in the establishment of the early phase of a persistent but reduced viremia in mice is discussed.
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Etiolated mung bean seedlings were examined for chorismate mutase activity. Evidence for the occurrence of two forms of the enzyme (designated CM-1 and CM-2) was obtained by ammonium sulfate fractionation, anion exchange cellulose chromatography, and isoelectric focusing. The two forms showed distinctly different properties, as CM-1 was inhibited by phenylalanine and tyrosine and activated by tryptophan, but inhibition by phenylalanine and tyrosine was reversed by tryptophan. The other form, CM-2, was unaffected by any of the three aromatic amino acids. Isoelectric points of the two forms were CM-1, pH 4.6, and CM-2, pH 5.6. The molecular weights estimated by molecular sieving on Sephadex G-200 were CM-1, 50,000, and CM-2, 36,000.
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The immunosuppressive drug cyclophosphamide was used to study the effect of immunosuppression on the degree of chronic lactic dehydrogenase virus (LDV) viremia in mice. Weekly injections of cyclophosphamide caused an increase of LDV viremia of ca. 2.5 log(10) 50% infectious doses per ml as compared to the viremia in the nontreated mice. This increase occurred at about the same time that the formation of antibody with a neutralization index of 2 to 3 log(10) per ml could be demonstrated in the serum of control mice, whereas both neutralizing antibody and sensitized (antibody-bound but infectious) virus were absent in the immunosuppressed mice. In one experiment, antibody did not reappear 28 weeks after a 24-week course of cyclophosphamide treatment. In another experiment in which the drug was given for 12 weeks, antibody appeared again in the treated mice 14 weeks after cessation of drug administration and was accompanied by a decrease in viremia. The normal decrease of early viremia during the first 2 weeks of infection in immunosuppressed mice suggests that the immune response is not the cause of this initial decrease in LDV viremia but that interferon and perhaps other nonimmune factors may be involved here. The increased viremia in the immunosuppressed mice during the later stages of infection indicates that the immune response plays an important role in partial control of chronic viremia. The quantitative correlation between the decrease in neutralizing antibody and the increase in viremia in immunosuppressed mice suggests that antibody rather than cellular immunity may be the more important immune factor in the control of chronic viremia.
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