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Despite that modest genetic contribution, mitochondrial DNA with mutant genes can cause serious and sometimes fatal diseases.
Heritability estimates of longevity derived from twin registries and large population-based samples suggest a significant but modest genetic contribution to human lifespan (heritability ∼15 to 30% [21].
These results confirm the existence of a modest genetic contribution to drinking behavior around the time of pregnancy.
In general, this work underlines the importance of a homogeneous study population with a specific outcome formulation, to avoid allowing the modest genetic contribution to be overwhelmed by the clinical diversity of the subjects.
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Twin studies on concordance suggest a relatively low genetic contribution for rheumatoid arthritis, ulcerative colitis, and systemic sclerosis; a modest contribution for Crohn's disease and lupus; and a high contribution for type 1 diabetes and autoimmune thyroid disease.
Notably, consistent with Donnellan et al. (2008), we found modest but significant genetic contributions to the attachment-related avoidance dimension (27%).
We were here unable to demonstrate any haplotype dependent association to overall risk of MS. However, the genetic contribution of the described SNP is modest, since meta-analyses suggest an overall 1.14 1.19 fold increased risk of ALS or AD in subjects carrying the −2578AA genotype [17], [18] and relative risks of this magnitude are too small to be detected by our study.
Thus, the relative genetic contribution (or heritability) of spatial ability was a modest 27%.
The overall genetic contribution of MAPT variants to LOAD risk appears to be modest, in contrast to primary tauopathies, where the H1 haplotype, for example, has an estimated OR of 5.5 from the PSP GWAS [ 8].
At present we cannot explain this apparent inconsistency; it could be partly related to the ACE genotype although the genetic contribution to ACE levels has only been shown to be relatively modest [ 12], and unfortunately we did not have information on the ACE genotype in our population so we could not explore this.
Whereas Mendelian diseases are caused directly by rare mutations, in common diseases such as psoriasis, the genetic contribution is usually a complex sum of common genetic variants, with many individual alleles conferring modest risk.
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