Personal space as a measure of a dying child's sense of isolation.
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Biomedical subjects
Publications and source records attributed to M Karon.
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The cell cycle specificity of chromatid breakage induced by inhibitors of DNA synthesis depends on the mechanism of drug action. 5-Hydroxy-2-formylpyridine thiosemicarbazone, hydroxyurea, and guanazole, compounds that inhibit ribonucleotide reductase, do not cause chromatid breakage during G(2) phase. In contrast, two active antitumor agents, arabinosylcytosine and 5-azacytidine, which are either incorporated into polynucleotides or affect DNA polymerase, produce chromatid breakage during G(2) phase. All of these agents except guanazole also induce breakage in S phase.
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Exposure to ultraviolet light can reduce the frequency of chromatid breaks induced by cytosine arabinoside in the DNA synthetic and post-DNA synthetic phases of the cell cycle. This effect can be correlated temporally with a decrease in the uptake of tritiated thymidine after ultraviolet treatment, implying that the genesis of such breakage is intimately related to DNA synthesis and that such synthesis is not confined to the DNA synthetic phase.
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