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Significantly increased levels of the endocannabinoid anandamide and related NAEs were found in carriers of the FAAH 385 A mutant alleles compared with wild-type FAAH controls.
An analysis comparing severely obese FAAH 385 A carriers versus normal weight FAAH-WT subject groups using 2-way ANOVA which controls for BMI to analyze the direct effect of FAAH 385 A mutant alleles compared to subjects with the wild-type FAAH C/C genotype also showed significant (p<0.05)) elevation of AEA and related NAEs (Table 4).
No significant changes in S- or H-lignin monomers were observed in all fpgs1 mutant alleles compared to the wild-type plants (Fig. 2b).
Digestion of the template eliminated amplification of the extraneous target and allowed the identification of four additional mutant alleles compared to untreated template.
Furthermore, there was no reduction of mtDNA content in cells overexpressing mutant alleles compared with cells overexpressing the wild‐type CHCHD10 protein (Fig 4D).
Both the cobas KRAS test and therascreen tests had short turnaround times (1 day) and were more sensitive for detecting KRAS mutations at 5% mutant alleles compared with Sanger sequencing.
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Table 2 shows that 77.1% of DCIS and 75.5% of IDC samples contain at least one mutant allele compared with only 35.3% of histologically normal samples (P<0.0001), confirming that mutant alleles are present in higher frequency in tumours.
BR levels are increased in the bas1-2 sob7-1 double-null mutant (first-exon T-DNA insertion alleles) compared with the wild type or either single null allele.
Therefore, we investigated the possibility of an unbalanced expression of the wild-type (wt) and the mutant alleles, by comparing the sequence of PRPS1 mRNA at the mutant position, amplified by RT-PCR from PBMC RNA, with that obtained from genomic DNA (Supplementary Methods).
Even without excluding protein coding sequence mutants, we found BRCA1 expression was significantly lower in TNBC tumor cores from patients harboring the BRCA1-3'UTR-variant (TT) alleles compared to patients harboring hetero and homozygous wild-type (TG and GG) alleles.
The expression of CHCHD10 S59L or CHCHD10 P34S mutant alleles also delayed cytochrome c release compared with HeLa cells expressing wild‐type CHCHD10 (Appendix Fig S10).
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