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Mechanistically, this could be mediated by direct binding of NF-κB to the promoter of cell-cycle mediators, as it has been shown to transcriptionally regulate cyclin d1[ 38].
This could be mediated by changes in affect regulation, cognitive functioning or an increased impulsivity in association with maladaptive coping mechanisms.
This could be mediated by always performing gapped local alignment similar to that implemented within BFAST.
This could be mediated by specific lipids that participate in the regulation of neuroinflammation, including cannabinoids and omega lipids [16], [19].
This could be mediated by the sst2 receptor type since sst2 receptor mRNA [20] [22] and binding sites [23] [28] are predominant in the developing rat and human brain.
This could be mediated by the increased expression and/or activity of related proteins, such as PHD, the VHL ubiquitin ligase, a protein that activates PHD or VHL, or a protein that deactivates an inhibitor of VHL or PHD.
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Importantly, this inhibition could be mediated through suppression of integrin-mediated mechanisms [ 24].
A possible explanation for this association is that this relationship could be mediated through mental disorders such as major depression: we observe a positive association between heavy drinking and depression in this paper, and previous analyses of our dataset have shown that the prevalence of mental disorders including depression is higher among those with chronic pain [ 27].
We postulated that this effect could be mediated by increased availability of NO, due to apocynin-mediated decrease in superoxide production.
It has been pointed out that this association could be mediated by obesity but in our study this relationship persisted after adjusting for BMI.
This tropism could be mediated by several receptor-ligand combinations, which is correlated with reduced tumor burden[95].
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