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Although all mutant cells showed staining of the vacuolar membrane after one hour, there were still several bright spots observed in the cytoplasm and close to the cell membrane of many mutant cells (Fig. 3B).
An increase in the proportion of cells found under the 2C peak also would be consistent with cells delaying in G2 phase; however, the continuous increase of cells beyond the 2C content bracket indicates that many mutant cells are not simply spending proportionally longer in G2 phase, but are accumulating abnormally large amounts of DNA.
Because the shapes of many mutant cells are not regular, we therefore named the cells by their interfaces (int).
Many mutant cells showed elevated γH2AX and p-p53S18 but lacked DNA condensation and fragmentation, supporting that γH2AX and p53 activation in Nde1 mutants occurred prior to the programmed cell death.
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By contrast, many mutant Purkinje cells exhibited two main dendritic processes, the degree of branching was irregular and less complex, and dendrites were not in parallel alignment.
However, for many of the ΔrovA mutant cells, many small particle-like structures with high electron density were found to surround the membranes (Figure 7B, C, D), and aggregated large clumps that were possibly formed from the small particle-like structures were frequently found near the disrupted cells (Figure 7D).
ABT-263 (navitoclax), a chemical inhibitor that blocks the ability of BCL-XL to bind and inhibit pro-apoptotic proteins, in combination with a MEK inhibitor led to dramatic apoptosis in many KRAS mutant cell lines from different tissue types.
Many of our mutant cells displayed aberrant cell shapes and internal structures.
This results in many non-functional mutant cells, but a few whose genetic changes enhance their fitness.
Note the increased nuclear Yki signal in many α-spec rg41 mutant cells.
However, we also observed many baz and baz mutant cells where Crb immunostaining appeared normal (Fig. 7C C″″, arrowheads).
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