The clear implication is that a mere increase in the number of hydrogen atoms does not necessarily result in increased H3+ yield as H3+ formation pathways are defined by unique features of the molecular structure, such as the prevalence of α-hydrogen atoms.
The oxidative and reductive pathways are defined as pathway 1 and 2 which run at the specific production rates (q_{{p_{1} }}) and (q_{{p_{2} }}), respectively.
Transition pathways are defined to represent all possible conversions simulated within the model including changes associated with alternative succession, wildfire, large storms, restoration, management, and changes in the size and spatial distribution of moisture strata (Fig. 2).
These interdependent complex pathways were defined to be provided through the two biologically opposing arms of Yin (tumoricidal, apoptosis, growth arrest) and Yang (tumorigenic, wound healing or growth promote) pathways of acute inflammation or effective immunity [18, 22, 37 39, 44, 45, 62 65].
All pathways were defined as gene lists (containing genes associated with the pathway).
Using gene expression profile datasets of cell culture and mouse models from previously published studies (listed in Table 1), gene signatures of 14 different oncogenic pathways were defined.
This assumption may not hold since many pathways are defined based on observed protein-protein and protein-DNA interactions, metabolic fluxes, and subsets of particularly well-studied genes.
Pathways were defined as blocks of genes of different size.
Biological pathways were defined according to "GeneGO Pathway Maps" manually curated database.
The seven patient treatment pathways are defined as shown in Table 1.
