Exact(5)
Upon IL-8 or PMA stimulation, the release of TIMP-2 from neutrophils increased by a similar extent in patients and controls.
In response to CD30 and LPS stimulation, the release of IL-8 was decreased in hypoxia and after reoxygenation compared to normoxia (Fig. 5).
Upon PMA stimulation, the release of MPO increased significantly in the control group, whereas there was no statistically significant increase in the patient group.
After lipopolysaccharide stimulation, the release of TNFα was significantly higher in Fs than in FOCs.
While release of aggrecanase-generated ARGSVI-G2 fragments were elevated at all time-points in the study-period in response to catabolic stimulation, the release of G1/G2 could not be detected at late stages in the supernatant.
Similar(55)
Studies using nonselective stimulation (high potassium, electric shocks) and unphysiological detection (e.g., radioimmunoassay) suggested that neuropeptide release required more stimulation than the release of smaller transmitters (Dutton and Dyball, 1979, Haass et al., 1989, Lundberg et al., 1986, Verhage et al., 1991).
On the other hand, it is also known that pro-inflammatory agents activate and/or sensitize nociceptors by means of TRPA1 [44] and their stimulation causes the release of neuropeptides.
IL-1β stimulation increased the release of all three MMPs.
We ignored the fact that antibody opsonization induces stimulation of the release of various cytokines from neutrophils and macrophages [ 76].
Their stimulation reduces the release of norepinephrine and suppresses the production of aqueous humor.
Breast stimulation facilitates the release of oxytocin from posterior pituitary gland leading to cervical ripening.
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