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The FTT1149 mutant demonstrated no increased LD50 in as much as a dose of 10 CFU uniformly killed mice, but the mean time to death was significantly prolonged (Figure 1B).
The ΔatmA ΔxprG double mutant demonstrated no staining for the nonstarved culture and approximately 50% TUNEL and PI nuclear staining after starvation.
In addition to this both the K262E and K268E mutants demonstrated no change in activity.
Compared to wild type, the pmt1 and pmt4 mutants demonstrated no changes in the activity of the secreted enzymes urease or phospholipase B (data not shown), both of which have been linked to virulence of C. neoformans.
In the present study we found that SCHU S4 gpX, sodC, mdaB, and ahpC mutants demonstrated no increased LD50 although ahpC showed a significant prolonged time to death at a challenge dose of 10 CFU (Figure 1B).
er single mutants demonstrated no inflorescence stem vascular cell division defects (Fig. 8A) or secondary growth defects, as er hypocotyls were the same size as wild type (Fig. 8B).
Surprisingly, however, the mutant strain demonstrated no statistically significant differences in susceptibility to Hst-5 in vitro.
The record demonstrates no such thing.
Initial levels of L2 were also comparable among the different mutants again demonstrating no defects in L2 levels in the virus particles or in cell binding (Fig. 6B, lanes 1 5).
As occurred with the previous two deletion mutants, we could demonstrate no Ego1 requirement for relocating Gln3-Myc from the nucleus to the cytoplasm when glutamine was added to re-feed the nitrogen-starved and nitrogen-limited cultures.
Direct sequencing of all five exons demonstrated no mutant alleles in any of the patients.
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CEO of Professional Science Editing for Scientists @ prosciediting.com