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The combination of legacy and tillage elucidated interactions with the different groups of fauna, for example, epigeic earthworms, wireworms, and prostigmatid mites showed changes in abundance dependent on the combined effect of forage and tillage.
Without a dominant clone, this snapshot of diversity within a single population is unlikely to follow a simple predator-prey model in which there are oscillations in strain abundance dependent upon resistance.
In the event that the gene of interest is subjected to abundance dependent bias variation, only qualitative information can be obtained.
Other studies established that amplification-induced changes are particularly sequence dependent and not abundance dependent [ 10, 15], suggesting a fairly constant bias.
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A variety of transcripts encoding immune receptors (CCR1, CCRL2, CD1D, CD14, CD19, CR2, CXCR7, IL13RA1, IL27RA, IL6R, IL7R, TLR2, TLR4, TNFRSF1, TNFRSF1B, TRAF5, TREM1) showed different mRNA abundances dependent on the affiliation to either the HS or LS group in females but not in males (Table 4).
Quantitative-matrix (Procrustes) analysis confirmed both the discordance between old-growth and disturbed-forest, and the combined effect of both abundance-dependent and -independent effects thereupon.
Because epiphyte-tree network nestedness was caused by a combination of abundance-dependent and -independent effects, we used quantitative network (Procrustes) analysis to evaluate the relative contribution of both types of effects to the changes in network structure associated to disturbance.
The mixed contribution of abundance-dependent and -independent effects to network topology was confirmed by Burns' null-model analysis [21], which indicated that the degree of epiphyte species is influenced, but not fully explained by (epiphyte and host tree) species abundances (see figure S1).
Nonlinear biases were observed between replicates, indicating the need for abundance-dependent normalization.
This abundance-dependent protein localization pattern might be particularly relevant in the case of Chr21 trisomic cells, which over-express the KCNE2 gene.
Here we construct a plasticity metric that is less abundance-dependent by design, and which we then correct for residual effects of protein abundance (see Methods).
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