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In fact, worms exposed to the RCM-protected biouptake layer show virtually the same HOC concentrations as those measured in the control worm samples.
We find that virulence attenuation in the LF82Δhfq mutant is independent of rpoS and rpoE (Figure 4D), demonstrating that Hfq acts to control worm colonization and killing by a different, yet uncharacterized, genetic pathway.
Adding D-βHB to the culture medium yielded a roughly 50% increase in L-βHB dehydrogenase activity in control worm extracts that was almost completely blocked by RNAi knockdown of F55E10.6.
Synchronized worm populations were developed and grown on EV up to either day 1 or 9 of adulthood and transferred onto hsf-1 RNAi bacteria for 4 days (hsf-1 RNAi treatments: either days 1 5 or days 9 13 of adulthood, control worm groups were grown on EV bacteria up to either day 5 or 13 of adulthood).
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In the NH4Cl trained control, worms were starved for 1 h before being transferred to 100 mM NH4Cl CTX plates and starved for 1 h before testing.
We flew a daf-16 mutant and control worms to determine if the effects of spaceflight on C. elegans are mediated by DAF-16.
In the benzaldehyde trained control, worms were starved for 1 h before being transferred to new plates to which 2 μL 100% benzaldehyde was added to the lid, after which they were conditioned for 1 h before testing.
In control worms, intact ventral and dorsal cords were observed at all ages.
The animals carried about 50% more α-KG in their cells than did control worms.
In control worms, a continuous, intact line of GFP fluorescence is seen running along both the ventral and dorsal nerve cords on opposite sides of the animal.
In control worms, fluorescent neuronal cell bodies extending long processes are clearly visible in the head (6 neurons) and tail (2 neurons) of the animal.
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