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By inserting an extra chromosome into mouse embryos (they used mouse Chromosome 16, a portion of which is analogous to human Chromosome 21), they produced a mouse that exhibited many of the characteristics of Down syndrome.
Another mouse that exhibited this behaviour actually died during a home cage drinking session, possibly due to morphine overdose.
Mice were inspected daily and each mouse that exhibited erythema and/or paw swelling in one or more limbs was assigned to an imaging or treatment study.
Each mouse that exhibited erythema and/or swelling of one or more paws was randomly assigned to a treatment or control group and therapy was started.
In the series of the gravid mice analyzed in this study we came across a gravid mouse that exhibited low fluorescence signal at 12.5 dpc) as compared to age-matched control gravid mice).
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Furthermore, unlike the pirouette mouse that exhibits thinning of all stereocilia rows, we observe a specific thinning of the mechanosensitive shorter rows only.
One example is the Pax2 and Pax8 double mutant mouse that exhibits a complete lack of kidney formation, due to an increase in apoptosis during metanephros development.
To this end, Mutel et al. (Mutel et al., 2011) recently generated an inducible liver-specific G6pc-null mouse that exhibits a normal survival rate compared with G6pc−/− mice.
Secondly, a cohort of mice that exhibited impaired object memory retrieval after intra-CA1 muscimol later acquired spatial memory in the MWM comparable to that of control mice.
This was due to scopolamine-treated 5-HTR4 KO mice that exhibited increased swim speed [drug effect: F 1,14) = 4.67, p = 0.05] while WT mice did not [F<1]; (Fig. 2B, right-hand side).
Meanwhile, the percent alternation was indistinguishable between BACE1+/− and wild-type mice at 6 or 15 18 months of age, demonstrating that BACE1+/− mice were normal in spatial working memory function in contrast to BACE1−/− mice that exhibited poor spontaneous alternation performance in the Y-maze in our previous studies [7], [9].
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