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We evaluated the association of each polymorphism with SLE, adjusting for the admixture proportion utilizing logistic regression under the multiplicative genetic model for minor alleles by combined analysis.
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The final models for minor mishaps and unsafe conditions excluded race due to non-convergence.
Odds ratios were calculated based on a dominant model for the minor allele, i.e. major allele homozygotes versus heterozygotes and minor allele homozygotes and, in the case of APOE ε4, no-ε4 versus at least one copy of ε4.
Extensions of the model for the minor anions of natural waters at the present time are difficult due to the lack of reliable activity coefficient data for Na, K, Mg and Ca salts over a wide range of temperatures.
The model loci had a dominant model for the minor allele with MAF of 0.2.
Genetic associations were assessed using both an additive per allele model (as supported by the associations with long-chain fatty acids [19], [20]) and a recessive model for the minor allele (as reported by Caspi et al [23]).
SNP 2. Additive model for the minor allele, MAF = 0.3.
For SPP1 rs28357094, a dominant model for the minor allele G was adopted.
SNP 4. Recessive model for the minor allele, high penetrance, MAF = 0.25.
SNP 5. Dominant model for the minor allele, low penetrance, MAF = 0.3.
Some parameter types are additionally tunable within a pre-defined weighting model (for example, minor allele frequency (MAF)).
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