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A cell cycle arrest was observed with a significant decrease of cells in S-phase and increasing of apoptotic cell, if compared with untreated control.
We observed a decrease of cells viability and generation of reactive oxygen/ nitrogen species in the cells after incubation, estimated by oxidation of H2DCF-DA and DAF-FM-DA.
As shown in Table 1, surfactin induced a G1 arrest in both cell lines with the concomitant decrease of cells that were synthesizing DNA (cells at S phase).
Fig. 2 (a) Total number of cells of zero activity, i.e., N0 (t), and (b) the yearly decrease of cells of zero activity from 1965 to 2008.
A decrease of cells in G2 phase could indicate impaired progression through the cycle and, therefore, explain the observed cell viability reduction.
Finally, MEOX2 expression also led to an accumulation of cells in the G1 phase of the cell cycle, and a concomitant decrease of cells in S phase, consistent with cells undergoing senescence (Fig. 5).
With respect to the cycling cells, Fe-SP at 1.6 µM caused a full arrest of SKOV-3 in S-phase along with decrease of cells in G0/G1 and a total loss of cells in G2/M.
Therefore the self-renewal decrease of cells knocked-down for HP1γ results probably from a slowing-down of the cell cycle as a consequence of the deregulation of direct or indirect HP1γ target genes.
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These results showed that treatment of colon cancer cells with DPD resulted in increased G0/G1 phase with concomitant decrease of cells in S phase.
Consistent with an increased sub-G1 AGS cell population, there was a notable decrease of cells in G1, S and G2/M phases.
With respect to cycling cells, Fe-SP caused a dose-dependent decrease of cells in S-phase and an increase in G0/G1 phase.
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