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RA-induced differentiation of NT2 cells proceeds through distinct phases of neural commitment, precursor expansion and terminal differentiation to neurons and astroglia [32] and analysis of neural gene markers shows a characteristic temporal and spatial pattern of gene expression similar to neuroepithelial precursors during in vivo neurogenesis [33], [34].
Comparison of primary melanoma and metastasis using all markers shows a slight increase in metastasis (melanoma score: 70%; metastasis score: 71.4%).
Strong clustering of markers on the genetic map but with a clear physical distance between these markers shows a suppression of recombination in these areas.
For comparison, we also summarized the relative contribution of the support for the total autosomal markers (A1-A6) and X chromosomal makers (X1-X4), the concatenated dataset from the six autosomal markers shows a larger contribution (258) to the whole tree than that from the four X chromosomal markers (175) (Table 4).
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Raw data was filtered to select 2066 markers with a minimum of genotype call of 75%% individuals and to eliminate monomorphic markers showing a MAF lower than 5%%.
Nevertheless, there are patient populations in which those markers showed a good predictive accuracy in prediction of outcome [[18],[21],[22]], but still we lack data about ICU patients.
Molecular markers showed a high level of heterogeneity within populations and a low, but significant, degree of differentiation among populations defined a priori.
However, a subset of these markers showed a significantly higher level of polymorphism when applied to progenitor and related genera (Erianthus sp. and Sorghum sp).
Seven markers showed a significant linear trend predicting epithelial damage (up with CD4, IL-1β, CXCL8, CCL2, CCL21, EMP1 and down with BPI).
Concerning the geographical origin of the samples, the three HBV markers showed a statistically significant difference.
Importantly, the pentaplex markers showed a higher sensitivity for diagnosing MSH6-deficient CRCs.
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