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The shoulders of the survival curves differ, but this may be explained by differences in cell kinetics.
Various strains representing different species of the two genera are characterized by differences in cell wall ultrastructure, particularly the level of preservation, rupture or gelatinization of the parental wall surrounding the daughter cells.
The enhanced response in arrays can be explained by differences in cell culture designs, diffusional effects and differences in the ratio of "scaffold mass to culture medium".
The differences in CD34+ cell recovery cannot be explained by differences in cell apoptosis/necrosis, since only a small fraction (below 10%) of the cells are affected by those (Fig. 6A).
The growth rate of transformants was not significantly modified in comparison to the wild type strain indicating that the differences in calculated transformation frequencies were not affected by differences in cell growth or survival (results not shown).
This difference in gene expression is partially explained by differences in cell populations, with significantly elevated macrophage and lineage-negative DCs and reduced T cell and B cell populations.
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To distinguish between true differential gene expression and apparent differential gene expression caused by difference in cell numbers, the cell compositions of the inguinal lymph nodes from the DA and E3 rats were investigated by flow cytometry.
Therefore, the higher apoptosis induced by Aza-dC treatment in control than in DNMT3B knockdown cells, which was observed only in NTERA2 but not other cell lines, could be explained by the formation of covalent adduct between Aza-dC-DNMT3B at genomic level rather than by difference in cell cycle profile especially in S phase.
A diverse signature was observed across these modules using pathway analysis, marked by differences in B cell and NK cell activity, as well as cellular markers of viral infection.
The biological responses to PPAR agonists are well known to differ between species [ 56], but our data support the notion that the potency of PPARγ agonists on joint cells might be influenced by differences in both cell type and species.
This disparity is caused by differences in immune cell activation, infiltration, and cytokine production during and after injury.
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