Comparisons of the amount of inflammatory markers were performed with Kruskal Wallis one-way analysis of variance.
Laboratory tests, including erythrocyte sedimentation rate, C-reactive protein, hemocromocytometric, and liver and kidney function markers, were performed at follow-up until 6 months after surgery and whenever SSI was suspected.
To characterize these cell lines, several assays including an assessment of intensive alkaline phosphatase activity, karyotyping, embryoid body formation, expression analysis of the pluripotency-associated markers, and the three germ layerassociated markers were performed.
Coexpression experiments on fresh colorectal cancer specimens using specific cell population markers were performed.
Statistical analyses comparing the pAUC of the most highly ranked markers and combinations of markers were performed using a permutation test [36].
After single marker analyses were completed, haplotype analyses with multiple markers were performed to determine risk haplotype and estimate the size of the associated region.
Polymerase chain reaction (PCR) amplifications of the Mit markers were performed according to the PCR protocol described in our previous paper [17].
To further define the intracellular localization of COMMD1, double-labeling experiments of COMMD1 and organelle markers were performed in our wt-CFTR expression model (Figure 3).
Tests for deviations from Hardy-Weinberg proportions within and across the microsatellite markers, and linkage disequilibria between markers, were performed with the methods implemented in GENEPOP v.4.0.10 [33].
