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The link between HS and systemic associations may be attributed to common genetic or environmental factors or shared inflammatory pathways.
The results demonstrate that, in West African countries, under-five mortality is spatially structured with adjusted mortality risks displaying similar patterns among neighbouring regions/countries which might be attributed to common childhood disease prevalence, general healthcare practices, similar poverty level and acute malnutrition caused by food insecurity.
In household model the excess of similarity between siblings may be attributed to common early childhood environment and the variance is defined by Var(Ti) = σa2+σe2+σs2 and the covariance as Cov(Ti, Tj) = 2φi,jσs2+Isib(i,j) σs2 where Isib i,j) corresponds to 1 for full siblings and 0 for other pair of individuals on genealogy.
The result showed that 83% (standard error 37%) of the variance between crosses could be attributed to common, autosomal variants with minor allele frequencies >5%.
To estimate h L 2, the proportion of phenotypic liability variation which can be attributed to common SNPs, we first use LDAK (Speed et al., 2012) to calculate a kinship matrix based on allelic correlations across autosomes, using an additive encoding of SNPs, with values centred and scaled to have mean zero and variance one.
This method allows the total phenotypic variance to be partitioned into a proportion caused by polygenic effects and a proportion caused by random environmental effects, including the proportion of variance in a trait that can be attributed to common environmental factors/ household effects (c).
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Despite the fruitful findings of recent GWAS [4], it is still disappointing that only a small portion of phenotypic variation has been attributed to common, identified genotypic variants for the traits studied.
At least five specific mutations in these genes have been found to recur in cancer families of French Canadian descent [ 2- 5] and this has been attributed to common founders [ 1, 3, 6- 9].
The high rate of mutations leading to size homoplasy in the present study provides support for alleles of identical size being attributed to common descent and hence causing bias in population genetic estimates.
Successful outcomes of Indigenous maternal and child health programs were attributed to common contributing factors such as the presence of Indigenous and female staff, outreach, home-visiting and transport.
In other words, a combined study of MC and MK may help to define and distinguish cytogenetic patterns that can be attributed to 'common features' of the pathology versus patterns that can be attributed to 'personal or individual features' that are not common but could affect the response or resistance of some individuals to therapy and modulate prognosis.
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Justyna Jupowicz-Kozak
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