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Therefore, we characterized the MTT assay in our system and examined its practicability to measure cell toxicity in OHCs.
This can be used to assess DNA damage and somatic mutations under physiological and pathological conditions and can serve as a strategy to measure cell toxicity as a guide for devising innovative cancer preventions and treatments.
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We therefore measured cell toxicity on CHO cells after 48 hours of peptide incubation.
While toxicity due to interference with RNAi pathway functions is difficult to measure in vitro using standard cell toxicity assays, competition studies comparing the effects of shRNA vs miRNA based hairpins can be used to detect inhibitory effects on the post-transcriptional RNAi machinery [33].
We measured cell toxicities of cartilage-targeted low-generation dendrimer-linked nitroxide MR contrast agents and gadopentetate dimeglumine (Gd-DTPA) on cultured chondrocytes.
The ACE inhibitory activities of the synthetic peptides were measured, and the cell toxicity was evaluated by cell viability testing on the hepatocyte cell line HepG2.
As expected, PlyC cytotoxicity on PMN varied across incubation time with greater cell toxicity measured at 2 h of incubation as compared with 0.5 h and is primarily attributed to the short life of PMN ex vivo.
After treatment, gene expression was measured by quantitative PCR (qPCR), protein expression was assessed by immunocytochemistry and transepithelial resistance and cell toxicity were measured.
The activity of Stx, which was measured on the basis of cell toxicity of Stx to HEp-2 cells, was significantly inhibited, as compared with no treatment (0 min), by 30 min of nitrogen gas plasma treatment using BLP-TES (*p < 0.05, **p < 0.01).
Cell toxicity was measured by the MTT assay 24 hours post-exposure to surfactants.
Cell toxicity was measured with the 3- 4,5-dimethylthiazol-2-yl -2,5-diphenyltetrazolium bromide (MTT) assay.
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