Using a genomic, FACS and IF staining analyses with luminal, basal and mesenchymal markers, we observed that both immortalized and primary HMECs in the pre-stasis stage [ 52] resemble a phenotype similar to the MaSC/BiPs-enriched subpopulation as defined by Lim et al. [ 9].
Interestingly, when evaluating the lymphocyte expression of several potential markers, we observed a significant correlation between fatigue and expression levels of TGFB-1 and a trend for KLRC1 and BTP.
Moreover, when combining these two markers, we observed a 47% improvement in risk classification.
Concomitant to loss of GABAergic markers, we observed ectopic upregulation of glutamatergic neuron markers Pax6 and Slc17a6 (Fig. 6E,F).
When combining urine markers, we observed that the more markers are positive in different combinations, the higher is the risk for recurrence and progression.
However, in (modular, ranked) and (closed, ranked) societies (blue and red lines with diamond markers) we observe faster consensus building.
Using molecular and embryological markers, we observe an unexpected intermingling between myogenic cells and neural crest cells at various stages of development.
For macroH2A, another heterochromatin marker, we observed a similar staining pattern as for H3K9me3 (Figs. 3d and 7).
Applying slice physiology techniques to projection neurons and interneurons identified through a transgenic live fluorescence marker [26], we observed both direct and indirect NPS effects in the LA that culminated in a modulation of rhythmic cellular activities in the theta frequency range.
In terms of overall marker distribution, we observed numerous tight clusters across multiple LGs.
