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In addition, a good correlation between the gene expression data and protein data was confirmed, indicating the usefulness of this method for the comprehensive monitoring of DME activity in rat livers treated with xenobiotics.
A possible explanation for our findings is that MYC appears to be only capable of inducing the activation of Cyclin B1-Cyclin-dependent kinase 1 (Cdk1) in embryonic/neonatal hepatocytes or in adult livers treated with hepatotoxins.
AREG was dramatically increased in livers treated with CCl4.
Low et al. characterized the proteome of rat livers treated with thioacetamide (TAA).
The genomic DNA from each of 4 mouse livers treated with 2 ml/kg CCl4 for 2 weeks were pooled.
The genomic DNA from 3 mouse livers treated with olive oil for 2 weeks was pooled and used as control.
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Expression of c-Myc was still significantly higher 6 h after treatment of VPA/Li2CO3/LY2157299. Expression levels of all these genes were reduced 12 h after PHx in liver treated with either drug cocktail or saline (Fig. 4C).
SOD can obviously increase in rats liver treated with COPTIS CHINENSIS aqueous extract, which acts as an anti-oxidant agent against CCL4-induced chronic oxidative stress [ 22].
For DNA-damage related genes, we founDNA-damage relatedA expression in rat liver treated with furan at 2 mgenesbwe
JNKs were initially identified as the stress-activated protein kinases (SAPKs) in the mouse liver treated with cycloheximide to induce inflammation and apoptosis [ 19].
The mRNA expression profiles of genes related to cell cycle, apoptosis, and DNA damage in rat liver treated with furan concentrations of 0.1 and 2 mg/kg bw were measured by quantitative polymerase chain reaction (PCR) arrays.
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