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Thus, we hypothesized that modulation of animal performance by diet could be explained by modulation of the population of ruminal microorganisms.
In view of findings from human experimental data, migraine-like attacks after PACAP38 infusion could be explained by modulation of dural or extracranial trigeminal nociceptors outside of the BBB [68].
These findings could probably best be explained by modulation of classic angiogenesis signaling pathways (e.g. VEGF/VEGFR-2) by the PDGF/PDGFRβ axis.
Most, if not all, of the structural changes observed on flown cells can be explained by modulation of RhoGTPases, which are mechanosensitive switches responsible for cytoskeletal dynamics control.
In addition to the PDE IV activity, this might be explained by modulation of expression of the VIP receptors (VPAC1 and VPAC2) on these cells.
These effects could be explained by modulation of target genes, such as MET, mammalian target of rapamycin (mTOR), and hypoxia-inducible factors (HIF -1 α [ 63, 88, 89].
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Interestingly, xenobiotic effects along this axis could be explained by modulations in iNOS that lead to altered hormonal action of NO.
The abnormal activity of the central drive could be explained by direct modulation of motor neurons through the cortico-bulbar system, or indirectly through modulation of the multisynaptic reflexes mediated by the lateral reticular formation.
The link between adverse lipid profile and tendinopathy could be explained by adipokine modulation of certain enzymes' production which are important for tenocyte functioning.
Some previous studies indicate that the protective effect of GGA may be explained by its modulation of nitric oxide [32], [33].
Overall, the observed electroresistance in nanoscaffold film can be explained by the modulation of the interfacial electronic barrier due to the migration of V o ¨.
More suggestions(15)
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