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There was a trend of better OS in patients with IDH2 mutation (hazard ratio 0.563, 95% confidence interval 0.292 1.086, P=0.087).
The increase in introns, elevated rates of amino acid substitution, and repetitive elements are consistent with the mutation hazard model of Lynch and Conery (2003).
In the adjusted analysis, the survival experience of carriers of the BRCA2 mutation was better than that of carriers of the BRCA1 mutation (hazard ratio 0.45, 95% confidence interval 0.26 to 0.81), but among patients treated with chemotherapy, the survival advantage for carriers of the BRCA2 mutation was attenuated (0.62, 0.30 to 1.31).
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The risk of eczema further increased with exposure to cats at birth among children with filaggrin gene mutations (hazard ratios 11.11 and 3.82, respectively).
Both CD56 negative tumors (Hazard ratio: 2.6 (95% CI: 1.14-6.00); p = 0.019) and K-ras mutations (Hazard ratio: 4.74 (95% CI: 1.8-12.3); p = 0.001) contribute as significant independent negative prognostic factors for the PFS (table 3).
However, the presence of DNMT3A nonsynonymous variations (hazard ratio 1.229, P = 0.724), deleterious mutations, and R882 mutations (hazard ratio 2.285, P = 0.313 in both) did not affect OS significantly as well as increasing age and BM blasts, although the trend was toward to adverse prognosis.
In univariate analysis, prognostic significance for survival ( from metastases until death) was seen for BRAF mutations (Hazard Ratio HR 8.1, 95% CI 3.4-19 3.4-19n 12-only KRAS mutations (HR 1.62, 95% codon12-only high AREG mRNA expression only in KRAS wild type CRC (HR 0.47, 95% CI 0.3-0.7) and high EREG mutationsession irrespective of KRAS mutation status (HR 0.45, 95% CI 0.28-0.7).
Despite the generality of these drift-based "mutation-hazard" (MH) models of eukaryotic and bacterial genome evolution, changes in genome size are often viewed as adaptive.
We addressed the mutation-hazard hypothesis apropos plastid-genome evolution by measuring πsilent of the Chlamydomonas reinhardtii plastid DNA (ptDNA), the most noncoding-DNA-dense plastid genome observed to date.
We conclude that changes in genome size within Ascomycota have occurred using two different routes: large-scale genome expansions are catalyzed by increasing drift as predicted by the mutation-hazard model of genome evolution and small-scale modifications in genome size are independent of drift.
According to the mutational-hazard hypothesis, introns with higher mutation rates are more likely to be eliminated.
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