In this review, we summarize the major findings from each of these models and their limitations as well as how discrepancies between these models may be reconciled.
This means that strong phenotypic effects of the CAT, GPX1, GSR, GCLM, EPHX1, CYBA, and IL5 genes (they showed the similarity between the models) may be considered as major gene effects.
Apple and Google pursue very different paths to innovation, but the gap between their two models may be closing a bit.
However, other differences between the two models may be equally important.
One possibility for this disparity in damage between species and models may be the degree of fiber strain during stretch.
The differences between these two models may be explained by the difference in perturbation of D3 (TGPAT has approx. 50% WT levels, whereas Dio3−/− has complete ablation) or additional involvement of other chromosome 12-imprinted genes in the TH phenotype.
In many cases the difference in discontinuation rates for the treatment of interest between the two models may be quite small, and the practical impact of this difference unclear.
The discrepancy in nonstressed plasma corticosterone levels between the two models may be related to environmental or strain differences: here, backcrossed to C57BL/6J for five generations, whereas Ridder et al. (40) examined F1 offspring of a C57BL/6J X FVB/N cross.
One explanation for the performance gap between mESC and GM12878 models may be the selection of individual TFs, which vary between cell types.
The differences in FO feeding-induced cardiac electrical remodeling between rabbit and pig models may be due to a combination of factors: differences in cellular and membrane environment of ion channels in cardiac myocytes which can impact the effects of n-3 PUFA enrichment, differences in gene regulation, and differences in the animal diets.
