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We found that RITA induced a marked increase in the percentage of replication forks in p53+/+ cells but not in p53−/− cells.
Curve fitting (dashed lines) showed that the percentage of replication failures was approximately inversely proportional to the number of licensed origins that is, doubling the number of licensed origins approximately halves the probability of replication failure.
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In contrast, the intron-modified TMV cDNA generated by Marillonet et al [ 14] must have resulted in a higher percentage of replication-competent TMV RNAs being exported into the cytoplasm.
This approach enabled us to obtain the percentage of replications of ICER below €30,000 per QALY gained, and therefore could be considered as a cost-effective intervention.
Furthermore, a larger percentage of the replication population had T1DM and the patients with T2DM were significantly younger.
Moreover, the cell percentage of DNA replication in S phase at spermatogonia (chromosome duplication of spermatogonia) increased significantly after 2 weeks of exposure [ 17].
We showed that 24 h exposure of NALM-6 cells to 1 μℳ JQ1 led to increased replication fork stalling as indicated by shortening specifically of the second label in ongoing forks and a substantial increase in the percentage of stalled replication fork structures.
Slides double-stained for Ki67, a marker of replication, and cytokeratin, a marker of ductal structures, were examined to determine the percentage of replicating ductal cells.
The numbers at the nodes indicate the bootstrap values as percentage of 1000 replications.
Using the results of the Monte Carlo simulation, we calculated the percentage of the replications lying below a range of values for the RBAT.
Bootstrap values, expressed as percentages of 1000 replications, are given at branching points.
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