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To test whether the increased GluRIIA and GluRIIC immunoreactivity observed in neurexin mutants might correlate with increased receptor function, we pressure ejected glutamate onto NMJs and recorded glutamate-gated currents after loss and knockdown of neurexin in embryos (Fig. 12).
To test whether the increased resistance observed in glp-4 and glp-1 mutants was due to a lack of matricide, we compared the survival of N2 wild-type, glp-4 mutant, and glp-1 mutant nematodes to that of fer-1 and fer-15 mutant nematodes.
Next, we did three random experiments to test whether the increased overlap might be introduced by some factors irrelevant to the disease status.
To test whether the increased susceptibility to oxidative stress upon COX inhibition was due to enhanced apoptosis, we examined cell death in the presence of caspase inhibitors.
To test whether the increased risk of death for those with length of stay of ≤10 days compared with length of stay of ≥11 days was time dependent, we evaluated Schoenfeld's residuals using estat phtest command (Stata software).
To test whether the increased TRAIL-R2 levels could prime the cells for increased TRAIL responsiveness, we generated stable TRAIL-R2 and as controls TRAIL-R1 knockdown clones in HCT116 cells, labeled HCT.shDR5 and HCT.shDR4, respectively.
Similar(32)
Finally, we tested whether the increased resistance of ECTV-infected MEF.BakxBax−/− and MEF.Casp3x7−/− cells to apoptosis induced by gzmB+ Tc cells yielded a higher ECTV replication rate in those cells.
Second, we tested whether the increased reproducibility might be due to the network topology.
Next, we tested whether the increased uncoupling in Sirt4KD cells was mediated by ANT2.
We next tested whether the increased transcription of PPARs was sufficient to induce cubilin expression or whether the epigenetic modifiers also influenced the activation state of PPAR.
Hence, we tested whether the increased HMOX1 induction in BRD4 knockdown resulted in a decreased ROS level and an enhanced cell survival.
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