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This scenario is physiologically relevant insofar as it is conceivable that an excess of extracellular glutamate concentration is regulated after a delay, triggering a decrease of neural activity after the initial increase.
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Therefore, it is conceivable that ZnO NP-induced ROS triggers a decrease of mitochondria membrane potential that leads to apoptosis in astrocytes.
Stimulation thus triggers a decrease of the 535 nm/470 nm ratio, i.e., of the FRET signal (Fig. 2A lower panel).
Then diffuse replacement of normal marrow with tumor cells triggers a decrease of marrow T1 signal intensity.
Indeed, in both isolates, the two metal treatments triggered a decrease of the transcription levels for genes assigned to this particular COG class.
PGF2α induces the expression of the nuclear orphan receptor and transcription factor Nur77 in the CL, which in turn leads to the stimulation of 20α-HSD, triggering a decrease in serum progesterone, which is essential for parturition [ 18].
Furthermore, silencing of MGMT gene expression triggered a decrease in the levels of both MGMT and ER-α proteins.
Concomitant CtIP and LIG3 inhibition triggered a decrease in the number of fusions (to approximately 49.5%) comparable to that caused by LIG3 inactivation alone (approximately 40.1%).
In contrast there are reports showing that oxidative stress triggers a decrease in the expression of Nav1.5 [ 37] which is likely to be seen in the left ventricle with atherosclerosis (an inflammatory disease associated with oxidative stress).
All of the nanoparticles triggered a decrease in membrane resistance, indicating nanoparticle-induced disruption of the tBLM.
Likewise, a single infusion of infliximab also triggered a decrease in OPN serum levels in our cohort of AS patients [ 107].
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