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This large duplication is predicted to result in the production of a truncated CFTR protein lacking the terminal part of NBD1 domain and beyond and thus can be considered a null allele.
At least D-cblK26 can be considered a null allele of D-cbl.
Nonetheless, fam46bb tpl18 can be considered a null mutant of fam46bb.
Interestingly this was observed also with the W447X truncating mutation, indicating that this should not be considered a null allele.
When simulating phenotype data, we considered a null scenario of no association vs. a simple alternative scenario of one X-linked causal variant.
First, to avoid confusion the multifunctionality ranking (or a node degree ranking) should not be treated as a "method" for prediction, as it is referred to by Singh-Blom et al. It should be considered a null.
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Since a null is an extreme condition, lets consider a null as a channel gain that tends to zero.
Consider a null hypersurface ((M^{n+1},g)) of a ((n+2))-dimensional Lorentzian manifold ((overline{M},overline{g})) of constant index (0
We can consider a Null Hypothesis of no correlation between the rankings S and (V^{(1)}), in which the metric (P S,V^{(1)})) has an expected value of zero.
The z test statistic was calculated that measured the difference between the observed and expected values of R, i.e. it considers a null hypothesis that the spatial distribution is random.
Additionally, a likelihood-ratio-test conducted on the Cox regression, considering a null model with the sole GSS and an extended model with all covariates, reported a consistently worse fit of the null model as compared to the extended model (Lnull = -7573.536, Lextended = -7361.47, χ2 = 424.13 on 41 degrees of freedom, p < 0.0001).
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