First, following the same procedure as in [32, 34], we collected a phenotypic disease similarity matrix from [50], where an element of the matrix represents degree of similarity between two phenotypes.
Similarly, in the bivariate model there are also shared and child-specific environmental correlations (rC and rE), which represent overlap in environmental influences between two phenotypes, and can also vary between 0 and 1.
To represent the relationships, we connect the nodes between two phenotypes only if they are identical mycobacteria, i.e. the same mycobacterial occurrence/event between two phenotypes.
We show experimentally that these cells fluctuate between two phenotypes.
Thus, the three basic cell phenotypes represent distinct differentiation states of NB with distinct tumorigenic properties.
If the two phenotypes essentially represent stable and unstable pair-bonding predispositions (see Walum et al. [ 11]), we might expect there to be some tendency for assortative mating between the phenotypes.
We initially tested for associations between each of the 34 polymorphisms and our two primary outcomes, intermediate phenotypes representing a measure of global AD pathologic burden on autopsy and a measure of global cognitive function proximate to death (Table 2).
Complementation test, also called cis-trans test, in genetics, test for determining whether two mutations associated with a specific phenotype represent two different forms of the same gene (alleles) or are variations of two different genes.
The first ET represented the common features between SWD length and incidence while the second ET represented features that are disparate between the two phenotypes.
The lines between two numbers still represent even divisions.
