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Biomedical subjects

T Kurimura

Publications and source records attributed to T Kurimura.

At least 109 records · Page 6Linked to original sources

Inhibition of multinucleation of cells treated with cytochalasin-B by cyclic dibutyryl-AMP.

Multinucleation of SV40-transformed mouse cells was induced by Cytochalasin-B as a result of inhibition of cytokinesis. Multinucleated cells with nuclei, whose number is other than that that can be obtained by raising the power of 2, were frequently observed. By simultaneous addition of Cytochalasin-B and cylic dibutyryl-AMP to SV40-transformad mouse cellls, multinucleation was fairly inhibited and the predominance of the cells with 2 or 4 nuclei was characteristic. In case of normal mouse cells (BALB/3T3), addition of both Cytochalasin-B and cyclic dibutyryl-AMP lessened the number of nucleic in a cell compared with treatment of the cells with Cytochalasin-B alone. These results suggested that cyclic dibutyryl-AMP inhibited multinucleation of cells treated with Cytochalasin-B and that the chemical regulated the division of nuclei in a cell to divide simultaneously.

Animals

Identification of the simian virus 40 which replicates when simian virus 40-transformed human cells are fused with simian virus 40-transformed mouse cells or superinfected with simian virus 40 deoxyribonucleic acid.

Simian virus 40 (SV40) was rescued from heterokaryons of transformed mouse and transformed human cells. To determine whether the rescued SV40 was progeny of the SV40 genome resident in the transformed mouse cells, the transformed human cells, or both, rescue experiments were performed with mouse lines transformed by plaque morphology mutants of SV40. The transformed mouse lines that were used yielded fuzzy, small-clear, or large-clear plaques after fusion with CV-1 (African green monkey kidney) cells. The transformed human lines that were used did not release SV40 spontaneously or after fusion with CV-1 cells. From each mouse-human fusion mixture, only the SV40 resident in the transformed mouse cells was recovered. Fusion mixtures of CV-1 and transformed mouse cells yielded much more SV40 than those from transformed human and transformed mouse cells. The rate of SV40 formation was also greater from monkey-mouse than from human-mouse heterokaryons. Deoxyribonucleic acid (DNA) from SV40 strains which form fuzzy, largeclear, or small-clear plaques on CV-1 cells was also used to infect monkey (CV-1 and Vero), normal human, and transformed human cell lines. The rate of virion formation and the final SV40 yields were much higher from monkey than from normal or transformed human cells. Only virus with the plaque type of the infecting DNA was found in extracts from the infected cells. Two uncloned sublines of transformed human cells [W18 Va2(P363) and WI38 Va13A] released SV40 spontaneously. Virus yields were not appreciably enhanced by fusion with CV-1 cells. However, clonal lines of W18 Va2(P363) did not release SV40 spontaneously or after fusion with CV-1 cells. In contrast, several clonal lines of WI38 Va13A cells did continue to shed SV40 spontaneously.

Animals