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Although this inhibition of cell division could be due to SA accumulation, AtIPS1 may be involved in cell cycle regulation.
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Thus the expansion of reactivated memory T cells in vivo could be due to continued division after stimulation ex vivo, or due to re-encounter with Ag in vivo.
The activation of the right STS in "unusual" conditions could be due to a division of labor between the two hemispheres according to the type of visual stimuli that is analyzed.
The loss of neurons could be due to abnormal cell division [33] or enhanced apoptosis [34], [35].
Alternatively, it could be due to an artifactual division in clusters due to methodological limitations.
This dramatic decrease could be due to the rapid division of ES cells (doubling time of 12 – 15 hours) or QD diffusion out of dividing cells over time thus causing a dilution of QD signal.
The slower growth of the mutant could be due to either slower cell division or slower cell growth or both, but in any case, it is obvious that BRs are important to this process.
An increase in JOE OPC divisions and a decrease in golli-KO cell proliferation could be due to a change in cell-cycle kinetics.
The smaller size of the pcm wing imaginal discs could be due to an increase in apoptosis, a decrease in cell division, or a combination of both.
The larger number of pre-neoplastic cells in the vicinity of a wound could be due to increased initiation of new clones or increased cell division within clones, or contributions from both of these.
We have recently shown an inverse association of telomere shortening and oxidative DNA damage [ 18] in circulating mononuclear cells in T2DM that could be due to increased oxidative DNA damage to monocyte precursors during cell division [ 18].
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