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In contrast to any conventionally performed end-point analysis based on counting numbers of dead/immobile specimens we performed a fully automated time-resolved video data analysis to dynamically assess the effect of a reference toxicant on selected behavioral parameters.
To assess the ability of the STAMP assay to discriminate similar specimens, we performed replicate analyses using DNA isolated from M091 cells that were either untreated or treated with the hypomethylating agent, 5-aza-2'-deoxycytidine (decitabine).
Finally, to prove that this interaction occurred also in clinical tumor specimens we performed ChIP to assess binding of ERG to the EZH2 promoter in ERGhigh and NoETS samples (Fig. 3G).
For subsequent specimens we performed FISH on 2+ and 3+ IHC subgroups.
By combining signal from normal and tumor specimens, we performed a sensitivity analysis, evaluating how normal contamination affected tumor classifiers.
To detect FCoV in clinical specimens, we performed RT-PCR using a random primer plus a single PCR targeted nsp14 constructed in the present study.
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When more than one pathogen is detected simultaneously in respiratory and stool specimens, we perform a semiquantitative analysis of individual viral nucleic acids based on the cycle threshold (Ct) value.
After we removed the resected specimen, we performed a stapler or a handwork anastomosis.
To identify these specimens further, we performed molecular characterization by sequencing the ribosomal second internal transcribed spacer (ITS2) and the mitochondrial CO1 loci.
To compare gene expression profiles generated from each FNA-FNA and FNA-surgical specimen pair, we performed an unsupervised hierarchical cluster analysis [ 10].
To ascertain the glioma origin of the CD133+ cell fraction in our low-grade and high-grade glioma specimens, we subsequently performed CD133 expression analysis in combination with CD45 and CD31 staining.
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