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Studies using an in vitro model show high glucose-induced NADPH oxidase level and activity elevation, NOX4 upregulation, SOD production, caspase-3 activation, and apoptosis induction in podocyte [ 13– 17, 28].
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Conclusions: Our in vitro model shows that the combination of cytokine removal and controlled PMB release by the same adsorbent results in a strong suppression of inflammatory effects in blood.
Although, this in vitro model shows some role played from HA on tendon derived cells, the study have some limitations.
The in vitro model shows that both these variants, G1145S and, more strongly, F941V, impair CR3-mediated phagocytosis of iC3b-coated targets.
The LAMA-84 in vitro model shows downregulation of the antiapoptotic proteins XIAP and survivin during differentiation into the megakaryocytic lineage in agreement with other reports.
Summary: Use of this in vitro model showed that sodium valproate (VPA) can reverse the muscle phenotype from a McArdle-like to a normal histological and biochemical profile.
For example, a prior in vitro model showed that moderate compressive stress enhanced cancer cell motility, whereas excessive compressive stress induced cancer cell death [ 39].
This in vitro model shows clear parallels with the reported in vivo production of cytokines during IL-2 therapy, and may prove useful in designing new therapeutic strategies.
45 Polio and Groszmann 46 using an in vitro model showed that rupture of varices was related to the tension on the variceal wall.
However, another in vitro model showed that resistance to trastuzumab, but not lapatinib, was associated with PTEN loss and PI3CKA mutation [ 57].
We provide for the first time an in vitro model showing that the direct contact of clinically relevant concentrations of ZA with epithelial or fibroblast cells induces apoptosis and prevents cell proliferation, with the potential result being ONJ.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com