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This suggests that dATP alteration may also be an early event, and in this case not further altered with disease severity.
Syncytiotrophoblast differentiation was also restored (increased 84%) in PPARγ−/− TS cells by reintroducing PPARγ using adenovirus, and was not further altered by rosiglitazone (Figure 10).
The ratios were not further altered when cells were cotransfected with 300 nM oligonucleotide, and could not be accounted for by alterations in mRNA levels (data not shown).
In contrast, animals with aortic banding (BAND NORM) showed elevated expression of HIF-1α under normoxia, and the elevated HIF-1α expression was not further altered by hypoxia (BAND HYPOX).
In the first 6 h of the release, microporous structure of AMS was not further altered.
Animal evidence suggests that preformed DAPs are not further altered in the body (Timchalk et al. 2007).
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Overexpression of p63 at day 7 did not further alter gene expression.
The addition of the p38 MAPK inhibitor SB202190 did not further alter the wound closure rates of fibroblasts cultured on native collagen (66% ±4.0% suggesting that p38 MAPK dependent activation of AKT controls migration along native collagen.
The additional presence of PPARγ increased percentage of syncytiotrophoblast well above and beyond this DMSO effect; however, rosiglitazone did not further alter differentiation of PPARγ-virus-infected null TS cells as assessed either by morphology or by qRT-PCR (Figure 10C, and data not shown).
Additional adjustment for CRP and IL-6 did not further alter this lack of association.
However, it did not further alter the frequency of S-phase HCT116 or HCT116 p53−/− cells containing pSer10 histone H3.
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