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In this assay, lymphocytes were irradiated in vitro to challenge cells to repair the radiation-induction DNA strand breaks.
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In several model organisms, the interactions between gene products has been probed by analysis of coordinated changes to the transcriptome in response to challenges to the cell.
Moreover, O2− can challenge mast cells to release the proinflammatory mediators, including histamine, thereby exaggerating the inflammatory response [ 67, 68].
It should be noted that we did not challenge these cells to hypoxic stress or additional PHD inhibition.
Although this study gives reason to assume that oxidative stress is the greatest challenge for cells to cope with, the role of radiation should not be disregarded.
Using X-rays or ultraviolet (UV) light, we irradiated blood lymphocytes from 80 nonsmoking donors to challenge the cells to repair the induced DNA damage, and we analyzed expression of chromosome aberrations (CA) specific to the inducing agents.
Early studies targeting the yolk sac as a site of injection truly challenged cancer cells to enter the blood stream.
Another study by Dahlan et al. [ 19] suggested that tocotrienol rich fraction directly influenced the expression dynamics of peroxiredoxin-2 in H2O2 challenged lymphocyte cells to improve the cells ability to resist oxidative damage.
Again, our experimental design was based on the xCELLigence platform with the CIM-plates except this time, we challenged the cells to invade a matrigel layer while migrating towards the same chemotactic gradient as described above.
The schemes used for laser irradiation in the different experiments are reported in Fig. 2. In order to challenge cells with an oxidative stress, 10 μl H2O2 (final concentration 300 μM) was added to each well immediately before laser treatment.
The CORM-3 added (100 μ M) was sufficient to challenge cells without significantly reducing viability within the timeframe of the experiment (Fig. 1D, E).
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