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Importantly, when polyphenols and topoisomerase II inhibitors were combined, it was possible to induce a synergistic decrease in cell proliferation (measured as ATP levels), cell-cycle arrest and induction of apoptosis in leukaemia cell lines.
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In the two lymphoid cell lines, it was shown that all studied polyphenols when used in combination with each topoisomerase II inhibitor caused a synergistic or additive decrease in cell proliferation, G2M or S phase cell-cycle arrest and apoptosis.
In myeloid cell lines there was a more differential effect: when quercetin and apigenin were used in combination with each topoisomerase II inhibitor, there was a synergistic/additive decrease in cell proliferation, cell accumulation in G2M and S phase of the cell cycle and an increase in apoptosis.
This was associated with an increase in cell packing and a decrease in cell proliferation.
Furthermore, resveratrol exerted antiapoptotic effects that were not associated with a decrease in cell proliferation.
Nevertheless, the same trend regarding a decrease in cell proliferation could be observed.
Qualitative analysis of cell proliferation illustrated a decrease in cell proliferation with increasing concentrations of vorinostat.
It may cause a decrease in cell proliferation.
This disorder is manifested by a decrease in cell proliferation.
These defects result from significant decreases in cell proliferation and aberrant cell death in both the pharyngeal endoderm and splanchnic mesoderm.
Reduced cellular proliferation was also observed in the double knockdown when Akt2 was one of the isoforms involved (i.e., Akt1/2 and/or Akt2/3); however, the double knockdown did not show synergistic effects in cell proliferation.
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