Serum triglyceride levels of untreated diabetics in relation to vascular lesions and obesity.
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Biomedical subjects
Publications and source records attributed to H Kudo.
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Cycloheximide, at a concentration of 10 mug/ml, rapidly blocked protein synthesis in L cells infected with reovirus. When the drug was added before 5 hr postinfection, synthesis of both single- and double-stranded varieties of virus-specific ribonucleic acid (RNA), which normally commences between 6 and 7 hr after infection, was blocked. When the cycloheximide was added at 9 hr after infection, uptake of uridine-H(3) into RNA, for the succeeding 6 hr at least, was similar to that of an infected culture without the drug. This latter uptake of uridine-H(3) in the presence of cycloheximide was largely into single-stranded RNA, since double-stranded RNA synthesis was rapidly and markedly inhibited by the cycloheximide. Single-stranded RNA formed in the presence of cycloheximide was found not to be a precursor of viral progeny, double-stranded RNA. Synthesis of double-stranded RNA in the infected cell probably requires prior synthesis of a new protein, which has a rapid rate of turnover. The possibility that formation of single-stranded RNA is preceded by synthesis of a second new protein is discussed.
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Kudo, Hajime (The Wistar Institute of Anatomy and Biology, Philadelphia, Pa.), and A. F. Graham. Synthesis of reovirus ribonucleic acid in L cells. J. Bacteriol. 90:936-945. 1965.-There is no inhibition of protein or deoxyribonucleic acid (DNA) synthesis in L cells infected with reovirus until the time that new virus starts to form about 8 hr after infection. At this time, both protein synthesis and DNA synthesis commence to be inhibited. Neither the synthesis of ribosomal ribonucleic acid (RNA) nor that of the rapidly labeled RNA of the cell nucleus is inhibited before 10 hr after infection. Actinomycin at a concentration of 0.5 mug/ml does not inhibit the formation of reovirus, although higher concentrations of the antibiotic do so. Pulse-labeling experiments with uridine-C(14) carried out in the presence of 0.5 mug/ml of actinomycin show that, at 6 to 8 hr after infection, two species of virus-specific RNA begin to form and increase in quantity as time goes on. One species is sensitive to ribonuclease action and the other is very resistant. The latter RNA is probably double-stranded viral progeny RNA, and it constitutes approximately 40% of the RNA formed up to 16 hr after infection. The function of the ribonuclease-sensitive RNA is not yet known. Synthesis of both species of RNA is inhibited by 5 mug/ml of actinomycin added at early times after infection. Added 6 to 8 hr after infection, when virus-specific RNA has already commenced to form, 5 mug/ml of actinomycin no longer inhibit the formation of either species of RNA.