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Parenteral MTA administration reduces the production of inflammatory mediators triggered by bacterial lipopolysaccharide or pro-inflammatory peptides in mice [16] [18], and protects from liver injury in rats treated with CCl4 or with the carcinogen diethylnitrosamine [19], [20].
Anaphylaxis results from the release of inflammatory cell mediators triggered by binding and cross-linking of cell-bound allergen-specific IgE by the relevant allergen.
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The response to H. pylori infection and the subsequent pattern of gastritis depends on the genotype of the patients and in particular a polymorphism in interleukin 1 beta, an inflammatory mediator triggered by H. pylori infection, is known to be of importance as will be discussed (El-Omar et al. 2000).
The production of inflammatory mediators is triggered by the activation of Toll like receptors (TLRs) and lymphocyte antigen receptors which; through intracellular signaling pathways such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κβ) and signal transducers and activators of transcription (STATs) leads to mediator release.
Caspases are critical protease mediators of apoptosis triggered by different stimuli.
The death receptors TRAIL-R1 (DR4), TRAIL-R2 (DR5) and CD95 (Fas) are specialised members of the TNF receptor superfamily and are key mediators of apoptosis triggered by ligands expressed by cells of the immune system, namely TRAIL (TNF-related apoptosis-inducing ligand), which activates TRAIL-R1 and TRAIL-R2, and CD95L (FasL), which activates CD95.
The process by which proinflammatory mediators trigger inflammatory pain is well established as mentioned above.
Current theories for the pathogenesis of sepsis implicate the dominant role of cells of the innate immune system i.e. monocytes and neutrophils for the biosynthesis of pro-inflammatory mediators after triggering by bacterial pathogens [ 2]; these mediators elicit further clinical signs of the septic host.
Also the expression of active caspase 9, a mediator of apoptosis triggered by TNF- α, was reduced in SOCS3 and SOCS1 compared with activated MOCK or SOCS2 clones.
RBL-2H3 cells were passively sensitized with murine sera, and after removal of unbound antibodies mediator release was triggered by the addition of Bet v 1.
It has been demonstrated that COX activity is reduced, the COX2 subunit is degraded and the levels of cytochromes a + a 3 are decreased when cells are exposed to acetic acid, which is accompanied by an increase in ROS production, a known mediator of apoptosis triggered by acetic acid in S. cerevisiae cells [ 8].
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