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TNC may loosen the strong adhesion of cardiomyocytes from the matrix and upregulate the expression and activity of matrix metalloproteinases [28,29], promoting degradation of the extracellular matrix and slippage of myocytes and facilitate inflammatory cell infiltration within the ventricular wall, resulting in an increased risk of ventricular thinning and dilatation.
Here, we have demonstrated that integrin α3β1 co-operates with TLR2/1 to facilitate inflammatory responses to bacterial lipopeptides by macrophages.
Recent studies have revealed that NLRP3 is the major receptor for endogenous danger insults to facilitate inflammatory responses.
In contrast, IgG molecules might easily reach either peritumour sites or intratumour sites, which in turn facilitate inflammatory reactions at the tumour cites.
RAGE interacts with leukocyte Mac-1 integrin, monocyte chemoattractant protein-1, and CD11c/CD18 to facilitate inflammatory cell recruitment [ 33, 34].
The results suggest that (1) spinal IL-17 is produced by astrocytes and enhances p-NR1 to facilitate inflammatory pain, and 2) EA inhibits hyperalgesia by suppressing IL-17.
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In addition to tubular atrophy and EMT, proteoglycan expression in the tubular BM could be involved in binding of L-selectin, thereby facilitating inflammatory responses in tubules [30], [64].
Thus, angiogenesis may exacerbate inflammation in OA, by facilitating inflammatory cell infiltration [ 111].
Ovarian steroid hormones, particularly estrogen, can activate NF- κB signaling, which induces the gene expression of inflammatory mediators such as IL-1, TNF α, and metalloproteinases (MMPs), thereby facilitating inflammatory processes [ 108, 112, 113].
Furthermore, RAGE interacts with the leukocyte Mac-1 integrin (CD11b/CD18) and p150,95 (CD11c/CD18) to facilitate leukocyte inflammatory cell recruitment [13].
The short-lived IL-17A response probably reflects the tight regulation on this immune effector arm, which can facilitate severe inflammatory responses and autoimmune manifestations [26].
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