Figure 4 Experimental amorphous As2S3 solubilities at 25°C from ref. 15 (squares) compared to predicted solubilities based upon (a) thioarsenite formation constants in Table 4 and selected thermodynamic constants (see text) and (b) the 2-species model, for example, as proposed in ref. 15.
Other theoretical frameworks (for example, as proposed by Cabana et al).
Therefore, other strategies are needed to prove causality of our detected potentially causal genes, for which several integrative approaches are available, for example, as proposed by Schadt et al. [ 94].
However, it is also conceivable that the 'arm' density is due to other structural rearrangements within the Class1 TatAd complexes, for example as proposed in the recent 'charge zipper mechanism' for TatA function [44].
If data follow this distributional pattern, known sample size formulas, for example as proposed by Bernardo and Harrington [ 27], can be applied indicating that a sample size of 160 individuals is required for the detection of a statistically significant intervention effect with a power of 80%%.
The fact that the risk increases progressively with the number of affected relatives suggests the effect of a fairly large number of genetic risk groups, consistent with, for example, a polygenic model as proposed by Antoniou et al. [ 12].
After dividing large families into smaller nuclear families and applying some quality controls to the data (for example, as the proposed test cannot analyze half-sibs, we deleted half-sibs from the data), we finally identified 5456 family members from a total of 1815 nuclear families.
After dividing large families into smaller nuclear families and applying some quality controls to the data (for example, as the proposed test cannot analyze half-sibs, we deleted one of sibs from the data), we finally identified 5,942 subjects for analysis, 5,456 of which are family members from a total of 1,815 nuclear families and the remaining 486 are singletons.
This appears to be an example of "genetic assimilation" as proposed by C H Waddington in the 1940s, which proposes that exposure to a novel environment causes the expression of previously hidden genetic variation, which is then "assimilated" and expressed even in the absence of the novel environmental stimulus [ 8, 9].
It is worth mentioning that if substitution-failure is attributed to a separate mechanism, for example a 'hidden indexical' mechanism as proposed in (Crimmins 1992) or (Forbes 2000), there is no need to assign the more complex type (ip p to cicero and tully rather than the simpler i. orator cicero) and orator tully) would then be the same proposition, as a non-Fregean would expect.
Qualification as surrogate endpoints requires significant resources and will, in many cases, only be possible in a concerted effort of academia, industry and regulatory authorities, as proposed for example by the Biomarkers Consortium (http://www.biomarkersconsortium.org), a public-private partnership managed by the Foundation for the National Institutes of Health in the USA.
