To illustrate the pattern, we focus on sample analysis of "young" families in mammals representing lineages with different taxonomic structure.
Therefore, although ideally our aim was to distinguish marker-specific replicability patterns, we focused onto associations among genes and diseases.
Second, besides detecting the genome-wide DNA methylation patterns, we focused on identifying differentially methylated regions between humans and non-human primates.
Under the assumption that regional covariance in local brain tissue properties reflects anatomical connectivity patterns we focused on investigation of corticosubcortical circuits integrating within the STN.
To examine whether transcriptional level regulation can explain the periodical expression patterns, we focused our analysis on proximal genomic features: trans-features, TF binding data from ChIP-chip experiments, and cis-features, motifs profiles in gene promoter regions.
Having analysed the TIPs with the broadest expression patterns, we focussed on the two TIPs which seem to have a more limited expression range in roots.
Since it is impossible to predict the fourth digit of an EC number because it usually reflects on many other factors rather than only the reaction patterns, we focus on the prediction of the first three digits of the EC number (EC sub-subclass) in this study.
Since it cannot be formally excluded that the other eight cases were not yet infected with Mtb (all > 140 days prior to diagnosis) and therefore did not show specific gene expression patterns, we focussed on the IL13 expressing cases to obtain more insights into the pathophysiology of TB.
Thus, to obtain qualitative ecological patterning rules, we focused on strong interactions in which ↑ and ↓ exert fitness effects large enough to be comparable to the recipient's basal fitness.
