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The mechanism of compound 4b was preliminarily investigated by acridine orange/ethidium bromide staining, Hoechst 33258 staining, TUNEL assay and flow cytometry, which revealed that the compound can induce cell apoptosis in MGC-803 cells.
The action mechanism of representative compound 7c was preliminarily investigated by acridine orange/ethidium bromide staining, Hoechst 33258 staining, JC-1 mitochondrial membrane potential staining and flow cytometry, which indicated that the compound can induce cell apoptosis in NCI-H460 cells.
The mechanism of compound 5f was preliminarily investigated by acridine orange/ethidium bromide staining, Hoechst 33258 staining, JC-1 mitochondrial membrane potential staining, TUNEL assay, DNA ladder assay and flow cytometry, which indicated that the compound can induce cell apoptosis in A549 cells.
Firstly, this compound can induce increased expression of the CCAAT/enhancer binding protein homologous protein and DR 5 [8].
The mechanism of cell death induced by compound 5f was further investigated by acridine orange/ethidium bromide staining, Hoechst 33,258 staining, TUNEL assay, and flow cytometry cytometry, which revealed that the compound can induce cell apoptosis in MGC-803 cells.
However, it does not prove that a compound can induce transporter-mediated efflux.
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The new compounds can induce irregular monoastral spindles, the characteristic phenotype for KSP inhibiting agents.
On the contrary, it is well known that estrogenic compounds can induce fish feminization.
What's more, the further studies indicated that the target compounds can induce apoptosis of A549 cells and arrest efficiently the cell cycle progression in G2/M phase of A549 cells.
Furthermore, additional simulations involving demixing of an organic water mixture near a surfactant-covered mineral surface demonstrate that even low concentrations of adsorbed polar compounds can induce major changes in mineral surface wettability, allowing sorption of apolar molecules.
Furthermore, androgenic compounds can induce a remission after failure of antiestrogenic therapy (reviewed in [ 19]).
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