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Whether this phylogenetic group possesses the ability to integrate the novel mecA variant needs to be further investigated.
This criterion was adopted to create the variant-sharing profile, i.e. a 'shared' variant needs to be of the same type and be present at the same position.
This variant needs to be distinguished from carcinoma arising in Schneiderian papilloma, NUT midline carcinoma, HPV-associated basaloid, or papillary sinonasal SCC, SNUC, and metastatic atypical teratoid/rhabdoid tumors of the central nervous system.
Since these data have been obtained in the Japanese population, less prone to T1D than other ethnic groups, the possible role of TYK2 promoter variant needs to be verified in different populations.
A genetic variant needs to be identified that can 'alter the level of, or mirror the biological function of, a modifiable environmental exposure' 25, 26 that is purported to be related to the outcome of interest.
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However, the pathological role of these variants needs to be determined by functional studies.
These findings require replication in large samples and the role of these variants needs to be clarified by functional studies.
Each of the underlying variants needs to be scrutinized with regard to possible annotation errors and to be confirmed by Sanger sequencing.
Each of the putative stop codon introducing variants needs to be scrutinized by manual examination of the reads, the re-annotation of the affected genes and Sanger sequencing.
However, because of the relatively small effect size of the two SNV in PPARA and POR*28, the clinical applicability of the genetic testing of these sequence variants needs to be further investigated in even larger cohorts.
Due to the extensive non-independence between SNPs and the limited haplotype diversity within regions of strong LD (LD blocks) in the human genome, only a subset of selected SNPs, instead of all variants, needs to be analyzed to capture the majority of common genetic variation within such blocks.
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