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The basis for each interaction was a decrease in phenotype in HG2P compared to HGC and no difference between B62P and B6C.
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The effect of the "thickness-contact angle" interaction is a decrease of 0.1778 in the estimated ITS value when one of the two factors is at the lowest level; the other is at the high level, and the factor at the highest level goes to the lower level.
The basis of these interactions was a decrease in HG2M female and an increase in HG2M male adiposity, with no differences in fat accumulation across B62M sexes.
The effect of Rate:Sel interaction was a 10.3% speedup decrease.
Notably, this interaction was strongly decreased with a synthetic peptide containing Ser6 in a phosphorylated state (pNEP-NT; Fig. 3A).
Nonetheless, the net effect of calnexin interactions with the channel is a decrease of Cav3.2 surface expression, consistent with a reduction of the whole cell Ca2+ conductance.
However, upon H2O2 treatment, the TGF-β1-induced Smad3 and Smad4 interaction was markedly decreased in a dose-dependent manner in BRCA1-mutated HCC1937 cells.
This decreased MDM2 p53 interaction was concomitant with decrease in p53 ubiquitination, suggesting that CK2-I increases p53 levels by preventing ubiquitin-mediated p53 degradation.
Of note, in BRCA1-mutated HCC1937 cells, the TGF-β1-induced Smad3 and Smad4 interaction was decreased in a dose-dependent manner upon H2O2 treatment, while reconstitution of wild type BRCA1 in HCC1937 cells restored the TGF-β1-induced TGF-β1-induced TGF-β1-induced
For the Training Group × Time interaction, there was a significant decrease in self-report fear for PIT from post-extinction retest to post-reinstatement; no such effect was observed for PVT.
Interestingly, this interaction was strongly decreased with the NEP-NT phosphorylated at Ser6 (Fig. 4D).
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