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In addition to characterizing the toxicant-specific changes by cell line and cell type, we used toxicant-specific gene lists to make predictions on a third toxicant (ETOP) that is believed to have a similar mechanism of action as one of the training toxicants (DOX).
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This information is important to verify that the observed proteome changes represent a specific drug response rather than changes induced by cell death.
Hartisle too changes, cell by cell.
DAPI nuclear staining was performed to check the apoptotic changes shown by cell morphology.
Additional control treatments were used to account for transcriptional changes induced by cell preparation treatments.
After radiotherapy, transient changes caused by cell death are likely to occur during the oxygenation of surviving cells.
Clonal expansion is traditionally thought to be driven by genetic and epigenetic changes inherited by cell division [ 30].
Within each rectangle, the tissue is subjected to cell-autonomous anisotropic and isotropic stresses ζ and ζ ¯, and to topological changes driven by cell polarity-dependent processes λ.
In order to get insight into spectral changes induced by cell deformation, in particular those which are inaccessible by direct visual inspection, we used multivariate analysis [ 27].
The metabolic variability within each of the 4 groups was minor relative to the changes induced by cell type and oxygen conditions in the culture.
BOP exposure resulted in bilateral capillary damage, brain edema and neural morphological changes characterized by cell body shrinkage and nuclear pyknosis.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com