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Another noteworthy fact is that the independent variables in the regression model (table 4) explain only a low portion of utilisation of private primary services.
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Although we observed for FT highly significant epistatic interactions, these explained only a low proportion of the genetic variance compared to the main effects and, therefore, might be disregarded in marker-assisted selection for this trait.
These observations are similar to those reported by others, and the observations of Stone and colleagues who found low bone density to explain only a modest number of fractures [ 21- 23].
Further, the relatively low correlations suggest that the association explains only a small proportion of the variance in treatment outcomes.
Several susceptibility variants for AF have been found [ 19- 21] but their combined predictive ability is low as they explain only a fraction of the heritability [ 1].
These analyses have provided valuable insights into the genetics of complex diseases; however, they typically detect only common, low-risk variants each with small effect and explain only a tiny proportion of disease heritability [ 4].
Nevertheless, the 3-year incidence of these findings is very low, and at best explains only a very small proportion of incident symptomatic cases.
If coverage scores are very low this would indicate that the causal condition explains only a limited set of the cases with an outcome.
This could also explain why only a low percentage of genes undergo circadian alternative splicing, as cotranscriptional splicing is approximately 2-fold less efficient in mouse liver.
Since Table 3 shows how observed characteristics explain only limitedly overeducation (given the low pseudo-R2), unobserved idiosyncrasy differences among individuals could therefore be relevant on our study.
The detection of relatively low tag counts for HHV8 specific ORF's can be explained by only a low percentage of cells expressing HHV8 RNA.
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