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While estimates of mutation rates exist for nearly two dozen viruses, estimates of replication modes exist for only a few (Sanjuan et al., 2010).
In order to incorporate the gene-specific factors of replication timing and expression level into the background mutation model, external estimates of replication timing were first obtained from Chen et al. (2010), who sequenced the DNA from HeLa cell lines at various stages of the synthesis phase of the cell cycle and provided timing estimates over 100 kb windows across the entire genome.
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Peaks identified from the global profiles of DNA replication timing T50 have been commonly used to estimate origins of replication [2], [4].
Commercially available quantitative HBV DNA assays with increased sensitivity and wider linear range give a more accurate estimate of viral replication and contribute decisively in the initiation and the monitoring of the response to HBV therapy.
16 To estimate the development of replication compartments (RCs) in the HCECs or HFFs, at least 100 cells were scored as described previously.
If this is the case then any method that utilizes composition skews to estimate the origin of replication, whether our ML approach or a graphical approach, would be misled.
Given that our estimates of phage genome replication depend on this normalization, we place our emphasis on the proportional advantage or disadvantage conferred by phage psbA, rather than the absolute number of genomes.
Thus, estimates of poliovirus per-replication event mutation rates can vary over 10-fold depending on the assumed replication mode (Drake, 1993; Sanjuan et al., 2010).
Mortality rates were estimated with three-fold replication for each of the 12 evolved lines.
The minimum P-value was recorded for each of 10,000 replicates and the adjusted P-values were estimated as the proportion of replication P-values less than the corresponding unadjusted P-value.
A conservative effect estimate will lead to over-estimation of necessary replication sample size.
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