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Whether this variant contributes to bipolar disorder is not known because of lack of knowledge about the involved gene [37].
How this variant contributes to increased risk of CD is not known, but studies with transfected cell lines and gene-targeted mice have demonstrated that ATG16L1 is required for autophagy, control of interleukin-1-β and autophagic clearance of intracellular microbes.
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Despite the fact that the carrier rates among the various epilepsy cohorts and controls were not statistically different, Dibbens et al 23 suggested that this functional variant contributes to idiopathic generalized epilepsy and possibly other polygenic epilepsies.
The higher iNOS activity observed was further supported by higher levels of NT staining in colonic biopsies of VEO-IBD patients with the risk genotype, suggesting that the higher NO production from this risk variant contributes to higher nitrosative stress and peroxynitrite damage in the intestines of IBD patients.
Thus, the variant contributing positively to the skin property was given a value of +1, whereas the variant not contributing positively to the skin property was given a value of −1.
It is unlike any other known gene, so it is not yet possible to say what the gene normally does or how the new variant contributes to prostate cancer.
Although APOE was identified as a susceptibility factor for AD over 15 years ago [33], it is still not clear how the ε4 variant contributes to disease risk.
It has been shown that the 1858T variant contributes to an earlier age at onset of the disease [ 12, 13].
Note that assuming independence of tests is actually a different assumption than assuming that each variant contributes independently to risk.
Therefore, it is possible that this variant may contribute to the phenotype of variant carriers.
This observation is consistent with the original study that this variant may contribute to the risk of ECD.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com