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Evans blue staining showed that death did not occur in untreated leaf tissue (Fig. 2a, b) while Fol + Th + MeJA treated plants showed minimum cell death (Fig. 2g, h).
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Some pyknotic nuclei were observed at 1 dpa, but not at 4 and 7 dpa, suggesting a minimum of cell death during the latter time frame.
Unravelling the regulation of hypometabolic states such as hibernation are of great significance for the understanding of cellular and molecular aspects of neurodegenerative disorders where hypometabolic states of a "vita minima" precede cell death.
The untreated cells (negative control) of HepG2 and HeLa cells show a normal morphology (Spindle shape/elongated cells) that adhered to the culture plate with no or minimum number of cell death In contrast to the HepG2 and HeLa cells, the CC1 cells does not show any significant morphological changes even at a concentration of 500 µg/mL (Fig. 4).
To achieve 30 40% apoptosis with a minimum of necrotic cell death, the irradiation doses were titrated (UVA, 2 100 J cm−2 and UVB, 20 1000 mJ cm−2).
We then examined the effects of a combination of DCA and bortezomib, which is a proteasome inhibitor at 4 nℳ but shows a minimum cytotoxic effect (∼20% cell death) at that concentration (Hideshima et al, 2001).
On the other hand, while both ixabepilone and paclitaxel were inactive in the CT-26 colon carcinoma model, enhanced efficacy was observed in combination with anti-mCTLA-4 mAb, suggesting that perhaps minimum induction of tumor cell death was necessary in this model to prime an immune response and potentiate the effect of CTLA-4 blockade.
We previously determined that the minimum exposure time to induce cell death for β-lap was ~2 h with LD50 values of ~3 μM in most cells, where NQO1+ cells are eliminated regardless of cell cycle position or p53 status.
These data indicate that translation inhibitors should at minimum have tumor-static effects even if cell death cannot be induced in a particular cancer.
Interestingly, the minimum β-lap treatment time required to induce cell death was decreased to 1 h with FK866 and β-lap combination treatment.
At a minimum concentration of 5 μM NAC, initiation of luminal cell death was delayed to day 22, and this was extended with increasing concentrations of NAC.
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