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Weir and Cockerham explored the consequences of implementing the method to estimate LD by using the samples in which some genotypes are missing and stressed that the method should not be used to estimate the parameter from non-random samples [ 13], but neither appropriate theory nor method has been developed for inferring population disequilibrium from non-random samples.
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Population linkage disequilibrium occurs as a consequence of mutation, selection, genetic drift, and population substructure produced by admixture of genetically distinct ethnic populations.
Thus most SNP pairs in this study displayed a level of within population Linkage Disequilibrium (LD) close to that observed between unlinked SNPs.
Within each population, linkage disequilibrium was tested between loci based on random permutations of genotypes performed with the software FSTAT [39] and followed by a Bonferroni correction for multiple tests.
Replication, detailed genotyping, and functional studies subsequently determine which of the variations in a given locus are most likely to be directly associated with disease and which are inherited along with other variants in the population (linkage disequilibrium).
Phasing was done using DagPhase [ 26], accounting for both family structure and population linkage disequilibrium.
We further extend the basic HMM to incorporate population linkage disequilibrium (LD).
For each population, linkage disequilibrium was measured as r2 [ 27] for all SNP pairs within each gene region.
In a large population, linkage disequilibrium of the base population, D0, changes to Dt at generation t with a recombination rate c [ 19].
High levels of population linkage disequilibrium are expected to be generated by frequent bottlenecks in subdivided populations subject to extinction and recolonization (Ohta 1982).
Motivation: Understanding the patterns of association between polymorphisms at different loci in a population (linkage disequilibrium, LD) is of fundamental importance in various genetic studies.
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