In addition, in most of our models, we simulated 5,000 generations, but when simulations ran for 10,000 generations, the probability of speciation increased 1.2-fold (results not shown).
To evaluate the performance of dynamic marginal structural models, we simulated 1000 observational studies (n = 3,000) with CD4-dependent treatment initiation.
In order to validate further the meta-GRN models, we simulated mutations in the GRN and compared the resulting patterns with the reported phenotypes.
To generate the dataset for the true mean trajectory of the mRNAs in the two-gene circuit models, we simulated each deterministic model and sampled the mRNA levels at 31 equally spaced time points.
Using the effect size and variance component estimates from the longitudinal models, we simulated clinical trials to reflect the changes observed over time in the ADNI cohort for each biomarker/outcome combination with 7 years of follow up.
Under different demographic scenarios and the population epigenetic selection models, we simulated SMPs with the mean of θ m = 0.1 per site per generation, which is gamma distributed among the sites with α = 0.5.
For each of these models, we simulated sample sizes of 1, 2, 3, 5, 10, 20, and 30 diploid individuals per population (2, 4, 6, 10, 20, 40, and 60 chromosomes).
Consequently, in order to retain all valid data, maintain maximal sample size for the MLR, and make the datasets the same for each of the 10 HRQOL models, we simulated missing data for all variables using multiple imputation (MI).
In the second model, we simulate long n-alkanes.
Using a model we simulate leaf assemblage isotope patterns from canopy data binned by elevation.
