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In addition, taken together, genetic risk markers have very limited application in individual risk prediction [ 29].
This relatively small reduction in overall imputation accuracy is primarily due to the fact that most genotypes (and markers) have very high INFO scores.
Because microsatellites have a faster mutation rate than mitochondrial genes and therefore these markers have very different temporal scales of inference, our measures of gene flow based on microsatellite loci indicate that contemporary gene flow is prevented by both barriers (the isthmus and the coastal plain).
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The mitochondrial markers had very low levels of polymorphism and did not amplify well in all samples, therefore only a few representative individuals were sequenced from each ITS group.
In each of these studies, the presence of increased levels of this marker had very significant abilities to predict overall outcome from the disease being treated.
However, within Parmeliaceae, mitochondrial markers generally have very low intraspecific variation [ 28, 31, 34, 36].
The genotype profiles of neighboring markers tend to have very high correlations and some are even identical.
In doing so, we minimise the chance of throwing away important markers that may have very low variability but huge effects on survival.
We recommend supplying an upper bound for effect size to minimise the chance of throwing away important markers that may have very low variability, but huge effects on survival.
H|H is a measure of haplotypes but it depends on an individual marker: for example, a minor variant leading to a selective sweep of the pre-existing major haplotype would result in a very low conditional entropy and thus a very high H|H score, but it would be in linkage to other major haplotype markers that would have very low H|H scores.
Thus, an allele error rate of 1.2% in imputation from the 7K to the 54K marker data may have very little influence on the reliability of genomic predictions.
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