To specify the measurement model for each sample, we created parcels by calculating the mean of all of the items within a particular subscale and using these means as indicators of the higher-order EALS constructs.
For each sample, we created an adjacency matrix A such that an element aij is equal to 1 when a flight exists between cities i and j and is equal to 0 otherwise.
From this sample, we created a subset of 1,055 unrelated adults (≥ 20 years of age).
For each DNA sample, we created two sequences using both AR11 and AF05 primers.
Combining the enrichment and depletion scores for each pathway in each sample, we created pathway aberration profiles that describe all the pathway aberrations in each sample.
From the entire sample we created a derivation cohort by randomly selecting two-thirds of the patients, and the remaining third became the validation cohort.
To unravel any possible link between the genomic differentiation and geographic stratification in the sample we created a pruned subset of SNPs in approximate linkage equilibrium with each other in order to capture the structure that reflects geographic origin.
In order to validate to some extent these results, and without immediate access to a truly independent sample, we created 10 validation samples by randomly re-creating the case groups (F) from the full pool of cases (N = 270), and similarly for the control groups (C).
Since we did not know the true relative abundance of each cell type in each sample, we created relative abundance vectors for each of CD4 T-cells, CD8 T-cells, B-cells, T-cells, and neutrophils based on perfect purifications for the purified populations and average relative abundances for the mixed cell populations.
Furthermore, the following phenotype subsets (see also table 1) were selected from the total study sample: We created a subset of 67 families with one child having asthma symptoms before the age of 2 years and another child having asthma symptoms before the age of 4 years.
