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Consistent with this observation, a larger proportion of genes encoding nucleic acid binding proteins have been found by microarray analysis in HCV-infected cirrhotic livers [ 41].
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No single genetic variation could be found by microarray to explain the increased virulence observed for the serotype 19A isolate.
The tcaR gene was found by microarray analysis to be up-regulated (>3-fold) in MRSA252 under the linoleic challenge conditions (Table 1).
Primers were designed for twelve genes that were found by microarray to be differentially expressed between the two conditions at 72 hours; seven genes were upregulated and five were downregulated in the forskolin condition.
Numerous developmental stage or tissue-specific microRNAs including, miR-17, miR-18a, miR-29c, miR-106a, miR-135a and b, miR-221 and miR-222 were found by microarray analysis.
Results were normalised to bpa-miR-100c, which was found by microarray to be present at similar levels throughout the developmental stages examined.
PRIM1 was found by microarray analysis to be down-regulated during cirrhosis, dysplasia and very early HCC, followed by increasing up-regulation in the successive stages of HCC.
For all four genes, the regulation by prednisolone in WT and GRdim mice was qualitatively similar to what was found by microarray analysis.
An additional four retinol-related genes [ RBP7, nucleolar protein 7 (NOL7), transthyretin (TTR) and retinol dehydrogenase 1 (RDH1)] were found by microarray analysis (Additional file 3).
For example, approximately 80% of genes were found by microarray to be expressed in at least half of the samples, compared with approximately 90% by RNA-Seq, with the difference mostly in genes with low expression.
Similar to what was found by microarray data, MMP-1 mRNA expression was 90 fold higher in Scp-2 cells than in Scp-21 cells and 17 fold higher than in MDA-MB-231 cells.
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