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However, since we did not perform a comprehensive analysis of inflammation in our mice, we cannot provide a definitive answer to this hypothesis.
However, since Th17 cells are most abundant in naïve mice we cannot completely rule out whether that cytokine is derived from pre-existing CCR6+ memory cells.
Because there is no report for RIM1-overexpressed mice, we cannot discuss the effect of upregulated RIM1 protein which is derived from SCRAPPER deficiency.
Although we did not observe an obvious Notch phenotype in the Neur1&2DKO mice, we cannot exclude a possible role in the fine regulation of Notch ligands.
Although we have not observed gross alterations of the cerebellum in RhoE gt/gt mice, we cannot rule out that molecular changes in these cells in the RhoE null mice could be responsible for some of the effects.
Because of the low number (n = 5) of available mice, we cannot claim that homozygous Prep1i/i females are sterile, but we have never observed pregnancies in mouse Prep1i/i females.
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Because we cannot know Matrin 3 levels or activity in the developing DGAP105 heart, or the activity of the Matrin 3-β-Geo fusion protein in the mouse, we cannot categorically distinguish between gain- and a loss-of-function models for the mouse or human MATR3 mutations.
As the SPAK243A/243A mice used in this study ablate SPAK activity in all tissues of the mouse, we cannot rule out that the effects on blood pressure seen in the SPAK knock-in mice could in part result from non-renal (e.g. colon, brain, blood vessels) effects.
In this study we compared terminally sick mice to 6 8 week old mice therefore we cannot exclude the possibility that some of the observed changes may also be age related.
Although we did not notice any significant changes of IL-7R expression in Prep1i/i hypomorphic mice [3], we cannot exclude that such changes can occur in Pbx1NT TG mice.
"We can cure a lot of diseases in mice that we cannot cure yet in humans, so there is always a big gap between mice and humans.
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