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Based on our microarray assays, we identified 63 genes that were differentially regulated between 3937 and WPP96.
Combining computational predictions with microarray assays, we identified 46 B. mori miRNAs, 13 of which were miRNA*s.
In conclusion, combining computational predictions with microarray assays, we identified 46 B. mori miRNAs, 13 of which were miRNA*s.
Additionally, to confirm the expression pattern revealed by our microarray assays, we analysed six differentially expressed genes (Mgp, Tfpi, Hif1α, Mospd3, Canx, Sat1) by qRT-PCR (Table 1 and Table 2, in bold).
Hence, as for the microarray assays, we analyzed data from a total of 18 replicates at least (3 biological replicates × 3 within plate technical replicates × 2 technical replicates i.e. repeated measurements) obtained from each real time PCR experiment.
To understand how Tag-Seq compares with microarray assays, we compared expression data generated from the same human sample assayed by both Tag-Seq and by an Affymetrix Human Genome U133 Plus 2.0 microarray (supplementary fig. 1, Supplementary Material online).
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For microarray assay, we sacrificed one mice of different stage of development: one day after birth mouse (neonate) and fifty days after birth mouse (adult).
To confirm that absence of lhx1 affects expression of the kidney genes found in the microarray assay, we injected 300 pg of lhx1-AS into 8-cell embryos (1xV2) and fixed them at stage 32 for in situ hybridization.
Using a tissue microarray assay, we found that Btk is overexpressed in prostate cancer tissues.
In the microarray assay, we employed the GCRMA normalization method [ 49] and a Bayesian z-score measure as detailed in [ 55].
For the microarray assay, we observed a significantly lower diagnostic sensitivity (62% vs. 96%, p < 0.0001, Table 2) whereas the specificity was equal (99% vs. 99%, p = 1.0) compared with a previous study [ 20].
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