Potassium efflux as a function of age and external potassium in the chick embryonic heart.
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Biomedical subjects
Publications and source records attributed to M Lieberman.
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Interferon was identified in the milk of mice injected with an interferon inducer. The kinetics of interferon appearance in serum and in milk were similar, but maximum concentrations in milk were 10 to 20 percent of those in serum. Interferon administered orally to neonatal mice was detected in their serums. Significantly more newborns survived an oral challenge with vesicular stomatitis virus when interferon had been induced in the lactating mothers.
Cardiac muscle cells obtained fronm disaggregated embryonic chick hearts were cultured on difjerentially treated oriented substrata. Subsequent cell reaggregation, growth, and attachmwent produced linearly organized strands of cardiac muscle with dimensions suitable for electrophysiological analysis. Along the strand, areas that contained few muscle cells demonstrated reduced conduction velocity and were subject to propagation failure.
Equine abortion virus, a member of the herpesvirus group, produces a lethal infection in hamsters. With this system, the protective effect of certain inhibitors of deoxyribonucleic acid viruses, inducers of interferon and exogenous interferon, was evaluated. Of the various agents studied, 9-beta-d-arabinofuranosyladenine markedly suppressed mortality, and 5-iodo-2'-deoxyuridine, distamycin A, and N-ethylisatin beta-thiosemicarbazone were inactive. Of the inducers tested, statolon, ultraviolet-irradiated Newcastle disease virus, and polyriboinosinic:polyribocytidylic acid (poly I:C) were protective, and endotoxin, polyacrylic acid, and polymethacrylic acid did not protect. Administration of exogenous interferon did not afford protection. Statolon and ultraviolet-irradiated Newcastle disease virus induced circulating interferon in hamsters, whereas poly I:C, endotoxin, and polyacrylic acid did not produce interferon. Because of the severity of the disease produced in hamsters by equine abortion virus, lack of protective activity by an agent in this system should not preclude possible efficacy against other members of the herpesvirus group.
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Stimulation of ethylene production by cauliflower (Brassica oleracea var. botrytis L.) tissue in buffer solution containing 4-S-methyl-2-keto-butyric acid is not due to activation of the natural in vivo system. Increased ethylene production derives from an extra-cellular ethylene-forming system, catalyzed by peroxidase and other factors, which leak from the cauliflower tissue and cause the degradation of 4-S-methyl-2-keto-butyric acid. This exogenous ethylene-forming system is similar to the ethylene-forming horseradish peroxidase system which utilizes methional or 4-S-methyl-2-keto-butyric acid as substrate. We conclude that 4-S-methyl-2-keto-butyric acid is probably not an intermediate in the biosynthetic pathway between methionine and ethylene.
Rhizobitoxine, an inhibitor of methionine biosynthesis in Salmonella typhimurium, inhibited ethylene production about 75% in light-grown sorghum seedlings and in senescent apple tissue. Ethylene production stimulated by indoleacetic acid and kinetin in sorghum was similarly inhibited. With both apple and sorghum, the inhibition could only be partially relieved by additions of methionine. A methionine analogue, alpha-keto-gamma-methylthiobutyric acid, which has been suggested as an intermediate between methionine and ethylene, had no effect on the inhibition.Incorporation of (14)C from added methionine-(14)C into ethylene was curtailed by rhizobitoxine to about the same extent as was ethylene production. These results suggest that rhizobitoxine interferes with ethylene biosynthesis by blocking the conversion of methionine to ethylene and not indirectly by inhibiting the biosynthesis of methionine. Ethylene production by Penicillium digitatum, a fungus which produces ethylene via pathways not utilizing methionine as a precursor, was not affected by rhizobitoxine.
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The transformation of cells in culture by a murine sarcoma-leukemia virus complex leads to the formation of identifiable foci. Titration patterns of focus counts vs. virus dilutions have been explained as being due to the interactions of three virions: leukemia, defective sarcoma, and competent hybrid. This interaction is analyzed quantitatively and equations are derived which permit determination of the composition of a sarcoma virus pseudotype as well as use of the technique for the assay of exogeneous leukemia virus. The analysis is based on the statistical distribution of virions in the culture cells and assumes that all virions have equal probability of infecting a cell and that transformation of any one cell will lead to focus formation. Limitations of the assumptions and expected measurement accuracy are discussed.
A quantitative study has been made of the interactions between radiation leukemia virus (RadLV), its murine sarcoma virus pseudotype, and their C57BL host cells. The elimination of interference phenomena by delayed infection of cells with RadLV made possible the quantitative determination of the pseudotype in terms of defective sarcoma and endogenous RadLV particles. This in turn permitted the quantitative assessment of RadLV helper activity and of the various factors which influence the accuracy and sensitivity of the helper assay.
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