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The six screened FLG null mutations were considered to be a single null allele for the purposes of this analysis; the rationale for this approach is based on biochemical and immunohistochemical evidence that each null mutation produces truncated forms of profilaggrin which result in a marked reduction or absence of processed filaggrin when present in the homozygote or compound heterozygote state.
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To enable fitting between the inferred and observed frequencies in the case of very short polymorphisms (the extreme case being a single observation), null "observations" of zero frequency were added to the start of each trajectory, with further observations, representing fixation or death as appropriate, being added to the end of the trajectory.
When this occurs, it suggests each group represents a good sample of the underlying distribution, and the two groups are combined to form a single null ensemble used to calculate final statistics.
Permutations were combined across all pairs to generate a single null distribution.
DNA templates containing a single consensus promoter for T7 RNAP (+1), or a single null mutant promoter (cross), were immobilized on a surface, with the promoter directing transcription towards the free end (+295).
Thus, for each null model, nestedness measures are calculated for each of the null matrices in a single null ensemble, enabling direct comparison of results.
Starting from a single null divertor (SND), a sequence of desirable SF configurations can be realized whereby the PF-coil currents are below the maximal design limits.
It was a single arm study, testing a null hypothesis of 50% overall survival at 9 months against an alternate hypothesis of 70%.
Note that since both of these networks are fully connected there is a single distribution that serves as the null model for each of the nodes.
In all but one case, the null model was a single-nucleotide "point substitution" model that was reversible and strand-symmetric (but otherwise fully general).
Aspa deaf14 is also likely to be a null allele, because (1) the single-nucleotide substitution causes a conversion of codon 172 to a stop codon, (2) no truncated protein was detected in p26 brain and (3) the Aspa deaf14/deaf14 mutant phenotype is similar to that of Aspa null mutant mice (Mersmann et al., 2011).
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CEO of Professional Science Editing for Scientists @ prosciediting.com