Enriched cells were then plated onto tissue culture treated 6-well plates and cultured at 37 °C, 5% CO2, monitoring for viability and morphology and passaging as appropriate until further analysis.
Cells were monitored for viability and cell growth with parallel growth curves conducted in triplicate, this data demonstrated the previously described [ 41, 42] decrease in cellular proliferation (data not shown) observed in the presence of Selenium.
The GAFQ-SupC containing diploid cells heterozygous for Sup35 were induced for sporulation and resulting sup35∆ haploids were specifically monitored for viability by selecting on media supplemented with G418 and lacking histidine (−His), indicators for the Sup35 deletion and plasmids carrying GAFQ-SupC fusions, respectively.
Multiple cancer cell lines were cultured on each scaffold material and monitored for cell viability, proliferation, adhesion, infiltration, and morphology.
To determine whether miR-29b transferred from the exosomes released in the CM of astrocytes stimulated with Tat- and morphine-controlled neuronal survival by regulating the survival factor PDGF-B, both rat primary neurons as well as SH-SY5Y cells (undifferentiated and differentiated) were treated with the respective CM (untreated and treated with Tat and morphine) and monitored for cell viability.
Animals were also monitored daily for viability.
For the initial set of experiments, relatively high concentrations were applied (10 40 μM for DOX and 16 128 μM for cisplatin) and crystal violet staining was used to monitor cell viability following treatment for 20 h and 1(b)).
Cell viability was monitored for 7 10 days.
Animal viability was monitored for at least 14 days.
Logarithmically growing atg1Δ cells were transferred to a synthetic medium without nitrogen sources (SD-N, referred to as non-buffered starvation medium), and their viability was monitored for five days using phloxine B, a reagent that stains dead cells.
