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We found that deletion of 52 genes caused viability to decrease by 25 fold or more upon treatment of at least one reagent, suggesting those genes play important roles in DDR (Table 1 and Additional file 1: Figure S1).
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Both MWCNTs induced low viability reduction (by WST1 assay) in A549 cells and only MWCNTs-COOH caused high viability reduction in BEAS-2B cells reaching 28.5% viability at 40 μg/mL.
Concentration of 10 μg/mL was chosen because it caused minimal viability loss to all cell lines after 24-h incubation based on the viability data (see below).
However, cell viability was decreased when the acoustic pressure was increased to the highest energy density of 12,000 J/cm, which caused cell viability to decrease by 19% (p = 0.0013).
OS extracts at pH 4 caused significant viability reduction after 7, 14, 21, 28, and 84 days.
The enhanced segregation at 33°C depends upon Spo11, since deleting SPO11 in the msh4 strains caused spore viability to mimic those observed in a spo11 strain (Table 5).
TIMP overexpression caused reduced viability during the first phase (embryonic-larval development) and complete lethality during the second phase (pupal to adult development).
In the 24 h time frame, DAC alone as well as SAHA caused slight viability decrease in CML-T1 cell line.
As shown in Figure 6(b), MSC-ad CM-induced doxorubicin resistance caused cell viability to 0.82 ± 0.04 that of control.
As shown in Figure 1A, treatment with various concentrations of rsTRAIL for 24 h caused various viability reductions in five head and neck cell lines.
Since previous in vitro experiments suggested dissociation of the tumorspheres caused decreased viability of the cells (data not shown), non-dissociated tumorspheres were injected into the mammary fat pad.
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