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In order to determine whether phenotypic variation in pre and post-copulatory behaviours could be attributable to additive genetic variation in males and/or females, we used a hemiclonal analysis approach (see [ 29, 30]).
Estimates of heritability from the two studies were however remarkably similar; in the UK 65% of the variance in nevus density was estimated to be attributable to additive genetic effects compared with 68% in Australia (Wachsmuth et al, 2001).
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For all simulations, background variance was modeled such that, after accounting for the QTL-effect, the environmental main effect, and the interaction, 30% of the remaining variance was attributable to additive polygenic genetic effects (A), and 70% was due to non-shared environmental effects (E).
Genetic modeling using acne scores showed that 81%95%5% confidence interval 73 87%) of the variance of the disease was attributable to additive genetic effects.
Using 110 baboons (80 females, 30 males), we 1) characterize normal variation in midshaft geometry of the femur with regard to age and sex, and 2) determine the degree to which the residual variation is attributable to additive genetic effects.
Therefore, twin studies reveal that approximately one-half of the variation in migraine is attributable to additive genes, while the remainder is caused by unshared rather than shared environmental factors between twins [4, 5].
Most of the genetic variance (σg) was attributable to additive effects (31.1%, Table 2).
More than half of the variability in intelligence tests is attributable to additive genetic effects (Deary et al. 2009a; Lee et al. 2010; Plomin & Spinath 2004).
For example, 41% (i.e.,.44 + .46) of the variance in the CBCL rating at age 7 is attributable to additive genetic effects, 36% (.60) is attributable to dominant genetic effects.
The narrow-sense heritability, h, is defined as the proportion VA of the phenotypic variance VP in a population that is attributable to additive genetic causes, i.e., h = VA/ VP (Visscher et al. 2008).
Multivariate genetic analysis of fainting and blood-injury-injection fear with and without fainting indicated that the genetic variance in blood-injury-injection fear was attributable to additive genetic factors shared with fainting (55%) (Page and Martin 1998).
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