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In an animal model they demonstrated that exercise is beneficial to reduce atherosclerosis only when combined with dietary intervention [ 36].
Using this same injury model, they demonstrated that a fibrinolytic agent, tissue plasminogen activator, decreased pulmonary edema, airway obstruction and airway pressures and improved gas exchange [ 68].
By using conditional knockout mice for Dicer crossed with a K-Ras driven lung cancer model they demonstrated that a global reduction of miRNA biogenesis leads to reduced survival in affected mice.
In a mouse model, they demonstrated that ABCA1, a membrane transporter regulating the transbilayer distribution of PS at the outer leaflet of the plasma membrane, contributes to the pathogenesis of cerebral malaria by affecting MP shedding.
39 These data have been confirmed by Daydé et al who reported that in mice rituximab concentrations were inversely correlated with tumor burden, and using a pharmacokinetic pharmacodynamic model, they demonstrated that tumor burden significantly influenced rituximab efficacy.
In a mammary cancer model they demonstrated that although estradiol and the antiandrogen tamoxifen increased mRNA and intracellular VEGF protein, the secreted VEGF to the extracellular phase, and thereby angiogenesis, was decreased by the latter substance.
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Using a zebrafish model, they demonstrate that coenzyme-A-activated polyunsaturated fatty acids (PUFACoAs) can inhibit cholesterol synthesis.
First, as a general model, they demonstrate that DNA-intercalating drugs can block cell growth by selectively reducing the efficiency of different transcription factors.
Using these cells transplanted in the mammary fat pad model, they demonstrate that there exist subsets of long-lived label-retaining epithelial cells (LRECs) that can divide asymmetrically and retain their labelled strand.
Using a three dimensional (3D) organotypic tissue model, they demonstrate that the SHG-B intensity comprises a quadratic dependence upon excitation power, it decays exponentially with depth, and it is spectrally dependent [ 21].
While no significant increase of REST RNA levels was found in HD cellular and mouse models, they demonstrated that loss of Htt function leads to nuclear translocation of REST in various HD cellular models, thereby causing a REST-mediated repression of several neuronal genes and contributing to neuronal dysfunction.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com