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This definition makes the concept of natural selection dependent on that of fitness, which is unfortunate since many philosophers find the concept of fitness deeply mysterious (see e.g., Ariew and Lewontin 2004).
9 Preferred drug classes for combination regimens include angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, calcium channel blockers, and diuretics, with selection dependent on individual patient factors, including additional CV risk factors and comorbidities.
In general, primary drug resistance mutations showed consistent positive selection, whereas accessory mutations often showed only conditional positive selection, dependent on the presence of a primary drug resistance mutation.
Preferred drug classes for combination regimens target the renin-angiotensin system (RAS), such as ARBs and angiotensin-converting enzyme (ACE) inhibitors, CCBs and diuretics, with selection dependent on individual patient factors, including additional CV risk factors and comorbidities [ 4, 7].
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In standard Darwinian terms, aneuploidy has been typified as altered selection-dependent phenotypic expression directed towards differential fitness in an adaptive landscape [67].
Figure 5 shows the selection-dependent degree of adaptation α(f) of this process at three consecutive times.
However, the universal proximal cause, most likely, is the increase or decrease of the effective population size of the corresponding organisms that affects the strength of selection and modulates the selection-dependent components of the evolution rate.
Hence, their degree of adaptation and fitness flux increase to values characteristic of unlinked sites, In addition to the selection-dependent quantities discussed so far, our theory also predicts how genome-wide characteristics of the adaptive process depend on its input parameters.
Stationary adaptation in our minimal fitness seascape is characterized by ongoing selection flips, which occur with rate γ per site and generate an excess of beneficial over deleterious substitutions, with rates V > V (see Equation 5). Figure 3A shows the selection-dependent fixation probability G in a linked genome undergoing stationary adaptive evolution.
The selection-dependent substitution rate is given by the product of the mutation rate and probability of fixation G of a mutation with selection coefficient σ, (3) V = G U. For unlinked sites, the fixation probability is given by Kimura's classical result, G0 = (1 − exp[−2σ])/(1 − exp[−2 Nσ]) (Kimura 1962).
The selection-dependent degree of adaptation, which is defined as α(f) = λb(f) − λd(f), varies between 0 for a randomly fixed genomic site and 1 for a perfectly adapted genomic site, which carries the beneficial allele with probability 1.
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