THE FAILURE OF SULPHHYDRYL COMPOUNDS, AET, MEA, AND GLUTATHIONE TO PROTECT AGAINST X-RAY INDUCED CHROMOSOME ABERRATIONS IN MALE DROSOPHILA.
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Hybrid, bivalent antibody molecules bearing specific combining sites for both ovalbumin and bovine gamma globulin were produced by reoxidation of a mixture of the 3.5S fragments of the two specifically purified antibodies. The dual specificity and the properties of the hybrid antibody were demonstrated by mixed agglutination and two stage agglutination experiments, and by test systems utilizing inhibition of agglutination or dispersal of agglutinates followed by antiglobulin reactions.
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Tyndall, R. L. (The Pennsylvania State University, University Park) and E. H. Ludwig. l-Cystine requirement for production of Coxsackie B3 virus in cultured monkey heart cells. J. Bacteriol. 85:1339-1345. 1963.-The requirement for l-cystine in both the production of Coxsackie B3 virus in cultured monkey heart cells and in prolonging the survival of the cultured monkey heart cells is demonstrated. d-Cystine, dl-homocystine, dl-allo-cystathionine, dl-homocysteine thiolactone, 2-mercaptoethlyamine, allylglycine, 3,3'-dithiopropionic acid, and dl-ethionine could not replace l-cystine in either supporting Coxsackie B3 virus production or prolonging monkey heart cell culture survival time. By their ineffectiveness, these compounds suggest the specificity of the l-cystine requirement. Allylglycine, 3,3'-dithiopropionic acid, and dl-ethionine were likewise incapable of inhibiting the l-cystine effect in supporting both virus production and cell survival. Prolonged starvation of cell cultures prior to virus inoculation failed to reveal any additional marked nutritional requirements, but rather tended to accentuate the l-cystine requirement for virus production. Increased cell starvation did, however, lead to the establishment of a latent Coxsackie B3 virus infection of cultured monkey heart cells, the activation of which is l-cystine-dependent.
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