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Figure 5 shows the emitted radiation profiles calculated by both, MC and LSSE methods.
HCT116 and HCT116 p53KO cells were seeded in six-well plates and treated with LSSE for 24 h.
extract (LSSE) for 48 h and cell viability was determined using Cell Counting Kit-8.
To elucidate the mechanism underlying the cell death induced by LSSE, we measured apoptotic cell numbers using an Annexin V-FITC assay.
As was expected in HCT116 WT cells, LSSE dose-dependently increased p53 levels and increased the levels of the p53 targeted genes p21 (Figure 4(a)) as well as NOXA, PUMA, and Bax (Figure 4(b)).
On the other hand, p53 deficiency was confirmed in HCT116 p53KO cells regardless of LSSE (Figure 4(a)).
(LSSE) on wide-type p53 (WT) and p53 knockout (KO) HCT116 cells.
Growth curves were conducted in the presence and absence of linezolid for the above 8 LRSE isolates, 1 clinical LSSE isolate (A1521, linezolid MIC 2 [micro]g/mL), and the ATCC 29213 S.
The 3 low-level LRSE isolates and the LSSE control showed moderately slower growth (p>0.05 at 24 h and 36 h) and the S.
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