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Since the initial cell viability assays showed a significant decrease in the primary cells, we also determined long‐term recovery of cells following treatment, using colony‐forming assays.
Transwell migration assays showed a significant decrease in the number of migratory JHU028 cells overexpressing miR-363 compared to control cells at 1, 3, and 5 h (Fig. 2).
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After fractionation by native PAGE, in situ activity assays showed a significant decrease of ICDH activity, as seen previously for α-KGDH [ 16]).
MTT-based cell viability assay showed a significant decrease in cell survivorship after ZnO NP exposure, and phase contrast images revealed that ZnO NP treated cells had lower density and a rounded morphology.
Additionally, a proteasomal activity assay showed a significant decrease in trypsin-, chymotrypsin- and caspase-like activities in cells treated with epoxomicin in a time-dependent manner.
In contrast, the MTT assay results showed a significant decrease in the cell viability of cells that were exposed to NaOCl at all time periods examined.
A direct correlation between Srx1 and the rest of the peroxiredoxin branch was not established across the cell lines assayed, but the Trx1 knockdown cells showed a significant decrease in Srx1 (35%, p < 0.05).
The PtdCho-specific PLC assayity assay performed on cell lysates showed a significant decrease in PLC activity with 17-AAG treatment to 66% ± 10% of control (n = 3, P = 0.02).
The findings from ELISA assay for serum PGE2 level showed a significant decrease in mice that received the combination treatment (Supplementary Figure S7B).
Both clonogenic assays and high-content microscopy counting showed a significant decrease in proliferation of FBW7 −/− cells after BUBR1 knockdown when compared with similarly infected FBW7 +/+ cells.
Wound healing assays of A549 or PE089 cells incubated with E2 showed a significant decrease in wound area.
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