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Using an in vitro model we studied mast cells and C. albicans interactions using different approaches to qualitatively and quantitatively access this interplay.
Specifically, as in vitro model we used SH-SY5Y human neuroblastoma cells differentiated with retinoic acid to a neuron-like state; as ex vivo model we used striatal slices from adult rats.
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 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 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.
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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.
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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