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This review investigates: A) the presence of vasodilator fibers in masseter muscle ; B) the possible neural pathway leading to vasodilatation mediated by activation of these fibers when the somatic pathway of the trigeminal afferent nerve is electrically stimulated ; and C) the physiological role of neurally-mediated vasodilatation in jaw muscle hemodynamics.
We considered how once fear is aroused by activation of these amygdala circuits, biological processes in the brain and body perpetuate fear and lead to the generalization of fear to stimuli or situations that might not have been feared previously.
The increased expression of inflammatory genes can be explained both by increased numbers of infiltrating cells, mainly T-cells and dendritic cells, and by activation of these cells.
UPR is mediated by three types of ER transmembrane proteins: inositol-requiring protein-1 (IRNA-dependentendent protein kinase like ER eukaryotic translation initiation factor 2α kinase (PERK), and activating transcription factor 6 (and6) [1], and expression of both BiP and CHOP mRNAs are upregulated by activation of these pathways.
To confirm that apoptosis was mediated by activation of these caspases, we cultured the three cell lines in the presence of the broad caspase inhibitor ZVAD-fmk.
Notwithstanding the lack of [Ca2+]i elevations in response to sensory and CT stimulation, transient inward currents were elicited in NG2+ cells by activation of these two afferents (Fig. 7A) (2-ms stimuli of 200 400 μA at 50 Hz).
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This receptor expression was enhanced by activation of the lymphocytes, and when these receptor-positive cells were cultured with EBAG9/RCAS1 peptides, their growth was strongly suppressed, and they were eventually led to cell death by apoptosis (Nakashima et al, 1999).
In contrast, none of the melanoma cell lines expressed sufficient amounts of receptors for IL-10-type cytokines (IL-19, -20, and -24) and do therefore not react to these cytokines by activation of the Jak/STAT pathway.
Additionally, an indirect detoxification process could be triggered in these cells, by activation of the pentose phosphate shunt, in which NADP produced from NADPH in the aldose reductase pathway is effectively utilised.
We demonstrate that P450 induction, liver growth and hepatic triacylglycerol (triglyceride) homoeostasis are intimately linked and provide evidence that the observed phenotypes result from hepatic accumulation of unsaturated fatty acids, which mediate these phenotypes by activation of the nuclear receptor CAR (constitutive androstane receptor) and, to a lesser degree, PXR (pregnane X receptor).
It also has analgesic properties which may be mediated by activation of the central opioid system.
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