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Surveys were distributed through direct email to instructors of evolution as determined by institutional faculty listings on department websites, if known, and to department heads if not.
ML and BMCMC approaches assumed best-fit models of protein evolution, as determined using ProtTest [51].
To address these questions, we analyzed the distribution of E2-60G and E2-226I mutations among known CHIKV isolates (supplemental data Table S2) and correlated this distribution with their evolution as determined using phylogenetic relationships.
Phylogenetic tree construction was performed with PAUP* version 4.0b10 [34] by using a maximum likelihood (ML) approach, under an optimum model of evolution as determined by MODELTEST v3.7 [35].
The sequence differences carry the hallmark of accelerated evolution as determined by elevated dN/dS ratios (Stukenbrock and Mcdonald 2007).
All sequence partitions were executed with a GTR + I + Γ model of evolution, as determined by the Akaike Information Criterion AICC) via MrModeltest 2.2 [ 131].
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Each data partition was allowed its own model of sequence evolution, as previously determined with MrModeltest.
The model applies multi-scale stress and local fracture mechanics analyses to distinguish between two microscopic damage mechanisms, which govern the damage evolution, as well as determining the magnitude of the damage evolution rate associated with each microscopic damage mechanism.
We analyzed four independent runs, each using the general time reversible (GTR) model plus gamma distribution plus invariant sites model of molecular evolution (GTR+G+I), as determined by Modeltest version 3.7 [ 38].
For both ML and BA, the best-fitting model of evolution was applied, as determined by Modelgenerator V.85 following the Hierarchical Likelihood Ratio Test (with four discrete gamma categories).
Evolution of nephropathy, as determined by change in measured clearance, was compared within matched pairs.
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