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Synthetic lethality occurs when two lesions that are individually non-lethal become lethal when combined.
In the case of lethal strains, the developmental stage at which lethality occurs was determined by genotyping of embryos at E14.5 and E18.5 and newborns.
Synthetic lethality occurs when co-occurrence of two genetic events is unfavorable for the survival of the cell or organism.
The analysis of the dead embryos revealed that the lethality occurs at the end of embryogenesis.
We conclude that lethality occurs at an earlier stage, in concordance with the findings of Piruat et al [11].
All samples analyzed were early second instar larvae, as this is the stage directly before dTip60E431Q induced lethality occurs.
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Interestingly, the lethal effect increased proportionally with the salinity, and 100% complete lethality occurred at 5× and higher concentrated ERM solutions (Table 1).
We then analysed when the lethality occurred and found that Atf2Δneuron embryos were born at the expected frequency.
In this genotype, careful observation revealed that lethality occurred at the pharate stage when ectopic bristles, particularly those on the dorsal side, trapped the individual within the pupal case and prevented them from eclosing.
Detailed timed pregnancy analysis of embryos showed that the lethality occurred between embryonic day 3.5 pc and 5.5 pc, a period of implantation and early development of implanted embryos.
In contrast to lipopolysaccharide-induced endotoxic shock, excessive inflammatory cytokine and nitric oxide release do not appear to contribute to the circulatory shock and lethality occurring with anthrax toxins in rodent models [10], [11], [17], [18].
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