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In a few markers, we increased the sequencing effort (rbcL, rpoC1, and psbA-trnH).
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For the purpose of marker evaluation, we increased stringency to reduce the number of candidates.
Using cytokeratin 8 (K8) as luminal, and smooth muscle actin (SMA) as basal/myoepithelial marker, we found increased proliferation in both compartments, suggesting that miR-34 loss increased overall proliferation, perhaps by affecting early progenitor cells (Fig. 3f).
Addition of a second set of DArT markers ('bPt' markers) increased coverage to 99.7%.
Overall power can be defined as a function of the thresholds t1… t m. (3) By optimizing the threshold at each marker, we can increase the overall power of a standard association study.
Investigating osteoblast markers, we found that HNE increased osteocalcin and type I collagen synthesis but inhibited alkaline phosphatase activity.
As with the proliferation markers we found that with increasing age fewer of the additional markers showed unambiguous immunoreactivity.
Since all the stem cell markers we investigated showed an increase in 1322T tumours, we assessed whether the increase in stem-like cells was consistent with the faster growth of adenomas seen in 1322T mice.
Taking into account a former QTL detection experiment [ 16] and other results [ 4, 9, 10, 15] that all showed the presence of a major QTL for seedlessness on LG 18, we replaced dominant markers and increased marker density with available and newly developed co-dominant markers.
Among the markers investigated, we detected increased levels of plated in 33%, homocysteine in 26.7%, d-dimero 25.3%, c3 in 15.4%, apcr in 5.6%.
Next, we looked for molecular markers of increased epithelial proliferation present in the IKMV glands.
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