Contrary to the expression of chondrogenic markers, we found that transcript levels of the de-differentiation marker COL1A1 were decreased in all investigated uni- (Fig. 3d) and biaxial loading conditions involving shear (Fig. 3e).
From the results of an immunofluorescence study using fluorescein-DBA and pancreatic specific cell markers, we found that DBA detects specifically epithelial, but neither differentiating endocrine cells nor acinar cells.
Using molecular markers, we found GCs to be predominantly hypoxic.
For all genotyped markers, we found moderate deviation from HWE in gout cases.
As with the proliferation markers we found that with increasing age fewer of the additional markers showed unambiguous immunoreactivity.
Amplifying the transcripts of the different markers we found that the mRNA levels were in accordance with the protein levels observed using immunostaining (Figure 4).
Between different molecular markers we found high tumor Ang-4 and Ang-1 expression to be moderately correlated (r = 0.18, P = 0.001).
Using simple sequence length polymorphism (SSLP) markers, we found that the pgr7 mutation is located between NGA162 and GAPAB on chromosome 3 (Figure 6A).
In contrast to cardiomyocyte markers, we found that dorsomorphin treatment from day 0 to 1 decreased the expression of the hematopoietic progenitor marker Gata1 (Figure 5C) and the smooth muscle-specific myosin heavy chain gene Myh11 (Figure 5D).
Using amacrine subtype specific markers, we found a 30% reduction in the number of GABAergic (Bhlhb5+) amacrine cells (Figure 4), but no difference in the number of cholinergic (ChAT+) or dopaminergic (TH+) amacrine cells (Figures 5 & 6A).
Using SSR (simple sequence repeat) and AFLP (amplified fragment length polymorphism) markers, we found that interspecific genetic differentiation is significant and higher than the differentiation among populations within taxa.
