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Eosinophil-derived mediators can stimulate a secretory response from epithelial cells in vitro; this may represent an important pathway in the development of diarrhea.
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Mediator can stimulate or repress transcription and its subunits exhibit gene-specific effects.
The Mediator can stimulate basal transcription and as an interface between RNA polymerase II (RNAPII) apparatus and hundreds of transcription factors can also function as a coactivator or corepressor.
Hepatocellular injury usually leads to inflammation and activation of the innate immune system, leading to release of growth factors, cytokines and small molecular mediators that can stimulate extracellular matrix (ECM) synthesis by activation of quiescent hepatic stellate cells and fibroblasts/myofibroblasts (collectively named HSCs) [1], [2].
An acute insult to the central nervous system (CNS) triggers microglial activation, leading to a series of changes in microglia, notably in shape, increased proliferation, and production of inflammatory mediators that can stimulate the recruitment of peripheral leukocytes to the CNS.
Mediator itself can stimulate CTD phosphorylation (Plaschka et al., 2015, Søgaard and Svejstrup, 2007).
These mediators in turn can stimulate the sympathetic nervous system (SNS) to release catecholamines, which ultimately regulate inflammation-associated impairment in tissue perfusion, myocardial impairment and vasodilatation.
Once activated, plasmin can stimulate lipid mediator release, increase the biosynthesis of leucotrienes, promote cytokine release and induce the expression of some inflammatory genes.
In addition, they can produce specific angiogenic mediators including histamine and heparin, which can stimulate endothelial cell proliferation and may contribute to the hyperpermeable nature of newly formed microvessels during pathological angiogenesis (Ribatti et al, 2001), and a variety of proteases, particularly MMP9, which are involved in angiogenesis.
These matrix fragments can stimulate production of multiple mediators of matrix destruction, including various cytokines and metalloproteinases.
Interestingly, NGF expression is induced in an inflammatory context and mediators such as IL-1β and PGE2 can stimulate NGF synthesis [ 13, 20].
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