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Significantly, we found that regulatory regions identified, using the same promoter constructs, differed depending upon whether we performed the assays with the cell lines versus the retinal explants, with the explants giving stronger evidence of cell-type specificity.
In each case, a vast majority of genes were found to be activated by p110 CUX1, whether we performed siRNA-mediated knockdown or overexpression of p110 CUX1.
Failing to remember whether we performed, or merely imagined performing, an everyday action can occasionally be inconvenient, but in some circumstances it can have potentially dangerous consequences.
The second most significant algorithmic choice was whether we performed a combined or a supertree analysis, with CA-MP more accurate than MRP-MP and wMRP-MP, and similarly CA-ML more accurate than MRP-ML and wMRP-ML.
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To investigate proteins whether could potentially phosphorylate, we performed a time-course assay of the inhibitory effect of pinocembrin on the expressions of non-Smad (FAK/MAPK) and Smad signaling pathways by TGF-β1-induced to clarify the underlying mechanisms.
To examine whether risk influenced decisions, we performed a one-sample t-test to assess whether overall PropRisk (PropRiskall i.e., collapsed across gains and losses) was significantly different from 0.5.
To examine whether valence influenced decisions, we performed a one-sample t-test to assess whether ImpValence was significantly different from 0. Second, we used regression analyses to determine whether these influences on decision-making are independent and whether they show different developmental patterns during adolescence.
To examine whether AA activated PKB/Akt, we performed Western blotting of lysates from untreated or AA-treated NRK-49f cells using antibodies against phospho-PKB/Akt.
To test whether PMA/Io activates NFAT, we performed EMSAs with nuclear extracts obtained from HT29 cells treated for 60 min with PMA/Io using a commercial oligonucleotide with consensus binding sites for NFAT as the probe.
To test whether such clusters exist we performed a clustering analysis of the putative PCSK target genes.
To assess whether this introduced bias, we performed a sensitivity analysis with imputed values for missing SF-6D data and re-ran the regression analysis using data from all 178 patients.
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