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M i is either zero (if the enzymatically active metabolic replicator set within the metabolic neighbourhood of site i is incomplete), or it is greater than or equal to 1. Obviously, M i = 0 implies C i = 0 (Eq. 3) and, consequently, no chance of replication for the replicator at site i.
This in turn implies no local monomer production and therefore no chance of replication for the focal molecule f.
These results bring the number of strongly confirmed associated loci to 13. Replication in independent studies is indispensable for considering a genetic factor in this category, although the common use of multiple case control sets inside the same study or of large sample collections has increased the chances of replication [ 2].
Levinson and Gutman [ 62] have proposed that if replication slippage is an important mechanism, a longer repeat would tend to show more variation, since the chance of replication errors is higher for a longer stretch of repeated sequence.
The division rate of human cells is not slower than that of rat cells, indicating that the chance for DNA replication mistake in human cells is not any less than that of a rat's.
In this case, M has a greater chance of replication.
Similar conclusions were drawn by Gorroochurn et al. (2007), who showed that for commonly observed P-value thresholds (P = 0.02 0.01, when α = 0.05), replication probabilities are surprisingly low (around 60 70% chance of replication).
However, by selecting 47 SNPs out of half a million for replication we potentially missed the opportunity to replicate real effects that by chance fell lower down the list; replicating a greater number of the top SNP associations from this first stage in a second population would increase our chances of winnowing real associations from the thousands of possibilities.
Among the 83 genes tested for replication in female liver, by chance we would expect to see ∼2.1 genes agreeing with our prediction of which is the more variable strain at this two-sided p = 0.05 cutoff, and ∼2.1 disagreeing.
Cells containing this vector rapidly died when transfected with plasmids containing full-length viral genomic DNA, completely eliminating the chance for HIV-1 replication.
Of course, although the data presented here show significant technical correspondence between platforms, this does not obviate the need for replication at the biological level in order to assess the likelihood that these changes are simply chance occurrences.
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