After treatment, cell viability was assessed, cell growth graphed and IC50 values were calculated using Reed and Muench's method [15].
To tease apart the mechanisms responsible for the cytotoxicity of QD-PEG-NH2 to J774A.1 macrophages, we individually assessed cell proliferation and apoptosis.
In the present study, we assessed cell growth, cell metastasis and cell apoptosis in SGC7901 cells transfected with miR-24 mimics or inhibitors.
We found a strong correlation between resistance changes (ΔR) and the development of cell adhesion strength by comparing the sensor readings with independently assessed cell adhesion.
In addition, we carried out qRT PCR analysis to determine extracellular/adhesion gene marker expression and assessed cell proliferation and mineralization in response to FGF8 treatment.
Furthermore, we assessed cell toxicity and possible targets for the peptides, thereby strengthening the notion that HR2 is an attractive site for therapeutic intervention.
Attempting to explain these findings, we again assessed cell division and survival in Treg cultures using both stimuli (Figure 5C).
To explain these differences, we assessed cell division and survival in Treg cultures for both stimuli (Figure 4C).
To test this hypothesis further, we briefly incubated tendons in trypsin, embedded the tendons in fibrin gels, and assessed cell migration after 5 days.
To seek evidence of malignant transformation in our p53-knockdown BAR-T cells, therefore, we assessed cell to cell contact inhibition.
We assessed cell proliferation during wound healing by BrdU labeling, which detected cells in the S phase of the cell cycle.
