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However, not all of the phenotypes of C/EBPα−/− mouse were reversed suggesting that there are also unique C/EBP family member functions.
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Next, the test was repeated, however the horizontal orientation of the mouse was reversed, such that the mouse's dorsal aspect and the raised edge of the lid were toward the same side (from the viewer's perspective, the right side in Figure 1B).
Furthermore, hypothalamic inflammatory changes observed in Ames dwarf mice were reversed.
These effects in DKO mice were reversed by in vivo CB2R antagonism, indicating that the atherosclerotic phenotype of DKO mice is mediated via CB2R activation.
This attenuation of the morphine-induced decrease in minute volume in nerve-ligated mice was reversed by treatment with the serotonin 5-HT 4aa receptor antagonist GR125487.
The antinociceptive effect caused by bis-selenide (50 mg/kg, p.o). on the hot plate test in mice was reversed by intrathecal (i.t).
These observations demonstrate that the deficiency of iron uptake in PrPKO mice is reversed by the expression of PrP in the PrP+ mice.
While cerebellar granule cell loss in PrPΔF mice was reversed by neuronal expression of PrP, white matter degeneration was rescued by myelin-specific expression of PrP [36].
The iron deficient phenotype of PrPKO mice is reversed by expressing Wt PrP in the PrPKO background, demonstrating a functional role for PrP in iron uptake and transport.
Two recent studies have shown that the neurological defects in mutant mice are reversed by restoration of MeCP2 expression in neurons, even at late postnatal stages [16], [17], suggesting that gene therapy may be feasible.
Altered glucose metabolism/homeostasis in arsenic-treated ovariectomized mice was reversed by 17β-estradiol supplementation.
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CEO of Professional Science Editing for Scientists @ prosciediting.com