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When studies had several adjustment models, we extracted those that reflected the maximum extent of adjustment for potentially confounding variables.
From these models, we extracted and aligned fingerprint patterns to identify proteins with similar or divergent DNA binding capacities.
From these models, we extracted the estimated variance components and calculated repeatability as the proportion of the between-individual variance relative to the total variance (Nakagawa and Schielzeth 2010; Dingemanse and Dochtermann 2013).
For the final gene models, we extracted representative gene models remaining one of the genes, which have a longest complete form existing both start and stop codon in same locus of assembled transcripts.
From the animal models, we extracted the additive genetic variance (VA) and the heritability (the ratio of additive genetic variance to total phenotypic variance, [ 58]) of all traits (Table 1).
To assess whether apoptosis was induced by cytarabine in these dMMR models, we extracted cell lysates from MLH1-deficient and proficient cells exposed to cytarabine/ ara-c for 72 h, and quantified levels of cleaved PARP, produced as a consequence of caspase activation by immunoblotting.
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From each SNP-BN model, we extracted the SNP that was not in the set of previously identified LOAD SNPs.
With the finalized QTL model, we extracted effect sizes, explained phenotypic variance, LOD scores, and 1.8-LOD intervals for each QTL.
For each model, we extracted the variable weights of the expression probes, ranked these variable weights and selected the 5% highest and 5% lowest ranked expression probes.
From the promoter model we extracted the motif in Figure 3A, which could be used to predict promoters of genes strongly bound by MSL.
When the authors reported results from more than one multivariate model, we extracted data deriving from either the model that included the maximum number of covariates, or the model that included severity of illness and FiO2.
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