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Ladiges et al. [14] recently reported that only 3 (Ames (Prop1df/df), Snell (Pit1dw/dw), growth hormone receptor knockout (GHR-KO)) out of 20 published long-lived mouse models showed consistent lifespan extension across separate studies.
Adjustment for age, sex, and level of education in the Cox proportional hazards models showed consistent patterns (Table 3, model 1).
All five models showed consistent impacts on susceptibility, with the presence of AGTR1-F showing increased susceptibility to traffic proximity on LVM.
Individual hourly lag models showed consistent negative associations of ST-segment level with increased BC for the first 12 hr before testing, but with waning effects after 12 hr.
The same trend was observed for the correlations between the predictions from BLUP and the genomic prediction models, with average correlations of 0.46, 0.52 and 0.76 for lines B1, B2 and W1, respectively.> Correlations between predictions from the same pair of models showed consistent trends across the three lines (Table 5).
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We found that overall the gridded and lumped regionalisation approaches are marginally different and the two models show consistent regionalisation results.
When GC content varies from low to high, both models show consistent predictions for expected codon compositions that are very similar to the distributions of the observed.
Most of these mouse models show consistent amyloid pathology, but often there is poor correlation between the development of morphological brain changes of deposition of amyloid plaques and disturbances in learning and memory function.
The cluster with a high concentration of childhood mortality identified by the Discrete Poisson Probability Model showed consistent results estimated by the Kaplan Meier survivorship functions and Log-rank test.
While our universal 56-gene model showed consistent prediction performance on the three independent test sets, we further investigated whether these predictions could be improved by using biomarkers that preserved highly concordant expression patterns between different cell types of leukocytes.
Notably, the prognostic index (PI) derived from the genomic model showed consistent prognostic prediction specificity in each validation cohort and produced similar mortality hazard estimation across all three cohorts.
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