Sentence examples for markers we find from inspiring English sources

(As a side note: Where the hell are all the goddam dry-erase markers?) We find ourselves at a crossroads.

Using an inducible genetic labeling approach to identify small non-myocyte cells expressing cardiac markers, we find that activated endogenous cardioblasts are rarely evident in the normal adult mouse heart.

Using real-time PCR (qRT-PCR) to quantitatively examine these markers, we find that mylpfa and myhz1.3 expression are strongly upregulated in pbx2/4-MO; prdm1a−/− embryos relative to both control and pbx2/4-MO embryos, although not quite to the levels seen in prdm1a−/− embryos (Fig. 2B,D).

The data suggest that TRIB3 is induced by hypoxia in an ATF4 dependent manner and supports hypoxia sensitivity, but from the measurements of other hypoxia markers we find that TRIB3 mRNA abundance from tumor biopsies is not merely a reflection of tumor hypoxia.

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.

Seeking blood markers, we found that lymphocytes and heart exhibited the same cholinergic abnormalities.

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).