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Indeed we observed a correlation with the DNA binding ability of MutL for MutH activation.
Here, we would like to reiterate that although we observed a correlation with hemoglobin A1c, we did not observe a correlation with fasting glucose levels (2).
We also examined gene loci known to be highly expressed in the ZPA or AER and observed a correlation with H3K27ac peak presence.
In addition, we observed a correlation with genes whose expression is associated with epithelial-to-mesenchymal transition (EMT): Vim, Cdh2, Snai1, Snai2 and Twist1 were elevated, whereas Cdh1 and Ocln were down-regulated (Fig. 4).
Interestingly, we observed a correlation with clinical outcome, recognizing a group of patients (belonging to cluster n.2) with the shortest survival respect to all other individuals enrolled in this study.
In the Esserman dataset, we also observed a correlation with most, but not all, genes of the EMT signature: VIM, SNAI1 and TWIST1 were elevated, whereas CDH1 and OCLN were decreased (Fig. 5A,C).
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In terms of water coordination, we do not observe a correlation with the observed potentials.
While individuals of the currently tested sample set were characterized by multiple clone variants, we did not observe a correlation with geography for the genes gdh and ITS.
We did not observe a correlation with escape from inactivation and location in either of the two marsupial X evolutionary strata [ 36].
When comparing A1C change in patients who were more vs less compliant to canagliflozin (PDC ≥ 0.80 vs < 0.80) we did observe a correlation, with a greater mean change occurring in the more adherent group (0.84 % vs 0.77 %, respectively).
We observed a correlation of IL-6 with endotoxin concentration, but no statistically significant correlation with endotoxin remained when sample 16 was eliminated from the set.
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