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To further strengthen our hypothesis that the p-ATM-IKK γ interaction status was subjective to ROS levels, resistant A549 cells were exposed to increasing doses of cisplatin (0 80 μM; 1 h) and H2O2 (0–20 mM; 1 h) in independent experimental setups taking into consideration that the concentrations of H2O2 used strongly mimicked the amount of ROS produced at different doses of cisplatin.
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However, most MRSA strains show high-level resistance to oxacillin, although low-level resistant strains are emerging (20 ).
This indicates that the low level resistant strain had a more stable sakacin P resistance phenotype than the high level resistant strain.
Despite the induction of the mpt, the two low level resistant strains studied in our laboratory showed 1,000 times more resistance phenotype than their respective wild-type strains.
Furthermore, in depth characterization of the quinolone resistance mechanisms as well as the whole process of becoming a high-level resistant mutant were also a matter of concern.
Different Ciprofloxacin concentrations selected different low level resistant mutants, and high level resistant mutants emerged from low level resistant mutants if stressed further by Ciprofloxacin.
The two low level resistant mutants had different molecular mechanisms.
Passage with a higher drug concentration of compound 2 selected higher level resistant viruses with a double mutant L26I + A30T.
These assays are powerful tools when attempting to determine the clinical implications of these low level resistant virions after the administration of single-dose nevirapine.
This contradicts our previous observation which showed more stable phenotype of the high level sakacin P-resistant strains of L. monocytogenes L40 and EGDe than the low level resistant strains [20].
Consequently, in the French context, adding the possibility of 3 different levels of macrolide-susceptibility (susceptible, low-level resistant, and highly resistant) would have limited influence on the predictions.
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