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The optimal cell death was only achieved when both p53 and NF- κB were switched on.
This exposure was too short for an optimal cell death detection, especially death induced by nutlin3a.
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Instead, an intermediate and optimal rate of virus-induced cell death optimizes treatment success [17], [18].
From this, it was found that 45 min of hyperthermia was optimal to induce further cell death (an additional ∼20% based on MTS), and further increases in the exposure time did not lead to a corresponding increase in cell death.
However, the optimal time point of cell death induction varied from 6 h with TRAIL to 24 h with ETO, Cisplatin, and FASL treatments, and to 72 h with irradiation.
The concentrations of PMA and ionomycin used for in vitro stimulation in this study were optimised to ensure optimal cytokine production and minimal cell death.
Therefore, the zebrafish is an optimal model with which to investigate cell death and differentiation for sex reversal.
We have chosen EL-4 cells and monoclonal antibody 14G2a as an optimal model to study mechanisms of cell death induced by anti-GD2 mAb.
The assay was carried out at 7 days post-infection, which appeared optimal to detect the MV-induced cell death in our experimental setting.
We assume that the pre-selection of RTMs by our inducible cell-death system accelerates the design of optimal RTMs capable to induce tumor specific cell death in skin cancer cells.
The optimal compound, compound a12, dramatically attenuated the cell death of glutamate-induced HT22 cells by preventing the generation of ROS and increasing the level of GSH.
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