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Significant correlations between copy number alterations on such loci and clinicopathological parameters reflecting the malignant potential of UCs may be at least partly attributable to silencing or activation of the listed genes.
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Chromosome 1p36 was one such loci.
The 42 orthologous gene neighborhoods that contain a lincRNA locus represent a significant 34% increase (two-tailed chi-squared test, P < 4.5 × 10−2) on the expected number of such loci.
Although the results presented here provide evidence for the existence of PsA-specific risk loci, the study design is not ideal for the detection of such loci.
Due to the strong signature they leave on the genome, such loci are often identified in scans for positive selection [ 20- 22].
On Chromosome 4, six markers with distorted segregation were in the region where no such loci were reported earlier.
The individual loci underlying quantitative traits (QTLs) are the hardest to study directly in natural populations, and simulations suggest that such loci will exhibit patterns very similar to neutral marker loci, in spite of strong selection on the traits they code for.
For instance, epistatic interactions among several unlinked loci on the same chromosome may result in a similar inheritance pattern, as long as there is no recombination among such loci.
One such locus is the HBS1L-MYB intergenic polymorphism, block 2 (HMIP-2) [1] on chromosome 6q23.3.
Furthermore, inferences based on one locus, such as mtDNA, is very susceptible to the effects of genetic drift on lineages.
Similarly, the role of multi-locus interactions on such regulation and the environment-dependence of these regulatory interactions are not clear.
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