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Timing of firing at origins is approximated by the average replication timing of the peak loci.
We estimated the average firing timings T50 and the (maximum) firing efficiencies ηf at the predicted origins using the average replication timing T50 and replication efficiency ηr of the peak loci (Figure 5A).
Nevertheless an analysis was also conducted on all other peak loci (Table 1a) derived from whole brain analysis for parametric responses to learning (see Figure 4 for these additional results).
Using average recombination rate (Flagstaff and Pikes Peak), loci were placed into 25 recombination categories: 0.00−0.25 cM/Mb, >0.25−0.50 cm/Mb,..., >5.75−6.00 cM/Mb, and >6.00 cM/Mb.
To identify consensus peroxisome proliferator response element (PPRE) motifs for PPARβ/δ in the binding region set, the loci associated with each peak loci were expanded to yield 400 bp regions for motif searching.
In each case, we use the original probability matrices defined at the peak loci; partial pedigree information; per-individual values for phenotype; and per-individual values for pre-determined covariates (defined in Valdar et al. 2006b)—sibship, cage, sex, testing chamber (FPS only), and date of birth (CHOL only) (all provided in File S3).
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Secondly, this analysis was conducted from all other peak point loci, which showed a correlation between learning and BOLD response but were not part of our original hypothesis (given in Table 1a).
The annotations of peak locus (corresponding to each prophage) were retrieved from protein table file (ptt) of respective bacterial genomes.
The peak locus was typically in the hand region of the motor cortex, verified by isometric contraction (Fig. 4).
Teki et al. (2011) also reported heightened response to random compared with isochronous auditory stimuli in STG bilaterally but more posterior (x = 66, y = −39, z = 3) to our peak locus (x = 63, y = −15, z = 3).
In addition, the peak locus on chromosome 7 still reached genome-wide significance when association mapping was conditioned using adiposity (% fat) or insulin resistance (HOMA-IR) as covariates, indicating that the effect of the chromosome 7 locus on hepatic steatosis is independent of obesity and diabetes.
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