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We found that β-naphthoflavone represses ER-driven vitellogenin promoter activity and that this action is mediated by the AHR.
Collectively, we have shown that peripheral neurosteroids potentiate P2X-induced mechanical allodynia and that this action is mediated by sigma-1, but not by GABAA nor NMDA, receptors.
This action is mediated by the specific phosphorylation of p53 in Thr18 by VRK1 [19], [44], [45], [45].
We speculate that this action is mediated by changes in the Ca2+-triggered process that leads from primed SNARE complexes to membrane fusion.
Finally, we have demonstrated that HIMF is chemotactic for undifferentiated murine bone marrow-derived (BMD) cells and this action is mediated through Bruton's tyrosine kinase (BTK) [5].
Since the two receptors, A1R and A2AR, have opposing biological effects, and A1R domination precedes the elevation of A2AR, we sought to examine whether A1R activation would be one of the factors that trigger the anti-inflammatory phase, and whether this action is mediated by upregulation of the A2AR.
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This action was mediated in part through an up-regulation of gene expression of the anabolic growth factor IGF-1 even in the presence of the inflammatory cytokine IL-1.
In addition, it has also been reported that gp96 isolated from mouse liver induced the production of NO in both murine (Raw264.7) and human (THP-1) macellhage celinesnes and that this action was mediated by the binding of gp96 to CD36 [ 62, 63].
In this paper we describe experiments designed to test the idea that exposing isolated hemocytes to lipopolysaccharide (LPS) evokes formation of hemocyte microaggregates and this cellular action is mediated by PGs.
It has been argued that this detrimental action is mediated by reducing cell defences to oxidative stress which, in turn is harmful for neuronal survival.
It is unclear, however, whether any of this protective action is mediated by vagal efferent fibres of the 'cholinergic anti-inflammatory pathway'.
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