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Using in vivo and in vitro models, we examined the effect of metformin on maternal and fetal inflammation.
Using in vitro models, we subsequently demonstrated that hypoxia and PGE2 synergise to induce expression of PTGER4 leading to increased cellular proliferation.
Using both in vivo and in vitro models we tested the ability of this mutant to form biofilms on the oral mucosa and dissected the specific contribution of Bcr1-regulated genes in this phenotype.
Unfortunately, despite using a variety of in vitro models, we were unable to obtain quantifiable levels of LTB4.
Using primary human astrocytes as in vitro models, we show increased mitochondrial depolarization and apoptosis accompanied by concomitant induction of cPLA2/CYP2E1 and enhanced AA release.
Through in vitro models, we have demonstrated that miR-363 decreases migration of SCCHN cells by targeting myosin 1B, a motility protein.
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In summary, using an in vitro model, we have found that treatment with pravastatin results in a reduction of MMP-3 and MMP-9 mRNA expression and MMP enzyme activity.
In an in vitro model, we evaluated the capacity of naturally processed Epstein-Barr virus-transformed B-lymphoblastoid-cell line (LCL -derived peptides to activate virus-specific CD8+ T ceL -derivedopeptides healtoy individuactivate
In our in vitro model, we observed that moDCs and MDMs treated with M-hMPV were induced to produce cytokines and chemokines associated with their maturation and activation.
The in vitro model we have established can recapitulate the developmental processes in vivo and provides new insights into the mechanism of PGC specification.
For quantification of TJ impairment in the brain endothelial monolayer area of the NVU in vitro model, we used Metamorph imaging software similar as documented before [26].
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CEO of Professional Science Editing for Scientists @ prosciediting.com