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We obtained about 88 116 million paired-end sequencing reads for each (supplementary table S2, Supplementary Material online).
There was no significant interaction between baseline insulin usage and treatment response at any time point (P > 0.39 for each) (supplementary Fig. 1).
Significantly greater decreases in A1C were observed in the ACM+HT group relative to the CC group at 3 months (1.7 vs. 0.7%) and 6 months (1.7 vs. 0.8%), corresponding to differential decreases of ∼0.9% (P < 0.001 for each) (supplementary Table A3).
XEN-R0703 potently inhibited recombinant Kir3.1/3.4 (IC50 = 57 nM, nH = 0.52 ± 0.1) and had nominal effect on other cardiac channels dispotently100-fold selectinhibitedrecombinant0 5.6 μM, nH = 0.99 ± 0.2) and > 300-fold selectivity over Nav1.5, Cav1.2 and Kir3.1/3.450 » 10 μM for each) (Supplementary FIC507 and Supplementary Table S8).
Findings were similar for hypoglycemic AUC (0.2 on the day prior to SH vs. 0.1 on other days, P = 0.002) and LBGI (1.1 vs. 0.8, P = 0.003), with PPVs being low and false-positive rates being high for each (Supplementary Table 2).
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Two DNA pools were built for each species (supplementary table S6, Supplementary Material online).
Approximately 16 kb of the genome was resequenced for each individual (supplementary table S1, Supplementary Material online).
This trend is also observed in the individual box plots for each project (supplementary file S3, Supplementary Material online).
Codon optimality was defined as the odds ratio of codon usage between highly and lowly expressed groups, calculated separately for each codon (supplementary table S1, Supplementary Material online).
Plotting processed ratio as a function of chromosome coordinates allows visualizing replication dynamics for each chromosome (supplementary fig. S1, Supplementary Material online).
For example, SNORD100 (HBII-429) showed the highest RPKM values among snoRNAs for each day (supplementary tables S5 S7 and fig. S3, Supplementary Material online).
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