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Heterozygous Esrp2 +/− mice were crossed to generate Esrp2 −/− KO mice, which present with no overt phenotype.
It contrasts with data obtained with constitutive myostatin deficient mice which present a reduction in fat mass.
Kalergis et al. [ 24] demonstrated that expression of IκB-α, an inhibitor of NF-κB, was decreased in Fcγ receptor IIb-deficient mice which present lupus-like symptoms, and the symptoms were reduced by treatment with NF-κB inhibitors.
BMM from C3H/HeJ mice (LPS-hyporesponsive mice, which present a point mutation in the TLR-4 gene), do not respond with proinflammatory cytokine gene upregulation after stimulus with LLO [ 28].
In follow-up work in 3xtg-AD mice, which present with a combined Aβ plaque and NFT pathology, these improvements were correlated with reductions in soluble Aβ and tau (Oddo et al., 2006).
This effect may explain the worst outcome of female mdx mice, which present extensive fibrosis, increased permeability of the sarcolemma, and marked deposition of extracellular matrix components, once they had been suffering a prolonged action of estrogens [ 33].
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Immunohistology revealed that Lodamin dramatically reduced angiogenesis compared with untreated mice which presented numerous large blood vessels with open lumen structures (n = 5).
The proportion of Creb1−/− mice which were present in each litter at the stages collected was also determined.
This onset occurs much later than the phenotypic changes observed in our knock-in mice, which were present as early as 26 weeks.
This is in agreement with our data on the high-copy SOD1 G93A transgenic mice, which also present with early startle-response deficits.
However, even after elimination of the majority of Type II lesions, the variability of the surviving C3HeB/FeJ mouse population was still somewhat higher than that typically observed in BALB/c mice, which only present with Type III lesions.
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