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Inhibition of the activin A signalling pathway with follistatin enhances CD40L-mediated production of numerous inflammatory mediators by activated monocyte-derived DC (IL-6, IL-8, IL-12p70, CCL2 (MCP-1), CCL5 (RANTES), CXCL10), consistent with an anti-inflammatory action of activin A [ 53].
Therefore, numerous inflammatory mediators are acting simultaneously on cancer cells.
Numerous inflammatory mediators have been implicated in silica-induced pathology.
The activated STAT1 pathway can modulate the expression of numerous inflammatory mediators, including chemokines [ 14].
Multiple studies demonstrate that high-dose salicylates inhibit activity of NF-κB (34– 36), which regulates transcription of numerous inflammatory mediators.
In addition to constitutive expression of ICAM-1 and ICAM-2 on endothelial cells, ICAM-1 expression may be augmented by numerous inflammatory mediators [ 46, 47, 48].
Similar(48)
EGR1 is induced by a variety of cellular stresses, including hypoxia, and may function as a master switch that triggers the expression of numerous key inflammatory mediators.
Numerous cytokines and inflammatory mediators have been found to rise in patients exposed to CPB including IL-1β, IL-6, IL-8, TNF-α [ 4- 6].
Numerous cytokines and inflammatory mediators, including IL-1, IL-6, IL-12 and TNF-α, are documented to be released in the early phase of sepsis, while HMGB1 is released at the late phase [ 7]. High serum concentrations of TNF-α are correlated with sepsis-induced mortality [ 31].
After peripheral nerve injury, glial cells are initially activated and subsequently generate numerous pro-inflammatory mediators, contributing to the development of neuropathic pain [10, 11].
This induces the release of cytokines, growth factors and numerous pro-inflammatory mediators, leading to platelet aggregation and the activation of intrinsic and extrinsic pathways of coagulation and fibrin clot formation [ 1].
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