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The impairment of neurogenesis in a mouse model exhibiting progressive amyloid deposition was reflected by a reduction in the number of neural stem cells, progenitor cells and neuroblasts in the dentate gyrus [13].
Here, using geometric morphometrics, we analyzed facial outgrowth and shape change over time in a novel mouse model exhibiting fully penetrant bilateral CL/P.
These results extend previous findings by demonstrating that in a mouse model exhibiting hyper-cholesterolemia and atherosclerosis, marked elevations in serum cholesterol concentrations are induced by PCB-77.
For example, although T cells from many patients diagnosed with autoimmune uveitis respond to immunization with S-ag [51], there is currently no mouse model exhibiting a similar response.
Genetic ablation of IFNβ or its receptor leads to an increased severity of experimental autoimmune encephalomyelitis (EAE) [ 3, 4] a mouse model exhibiting clinical, neuropathological, and immunological disease manifestations of MS [ 5].
We have previously shown that chronic cerebral hypoperfusion increased the amount of filter-trap Aβ in the extracellular-enriched soluble brain fraction of mice overexpressing a mutant form of the human APP [ 22, 51]; in this mouse model exhibiting senile plaques, the neuronal loss and cognitive impairment that were both accelerated by hypoperfusion was explained by the disturbed Aβ metabolism.
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The ARTE10 mouse model exhibits a neuropathological phenotype that mimics several characteristics of human AD.
We have previously reported that a Comt−/− mouse model exhibits a preeclampsia phenotype that is reversed by administration of 2-ME[27].
Given that our LID mouse model exhibits a constitutive serum IGF-1 deficiency (from birth) we could not rule out an accumulating effect of IGF-1 on bone development in these animals.
The APP/PS1KI mouse model exhibits a large heterogeneity of N-truncated Aβ x –42 variants [ 8].
The db/db mouse model exhibits a spontaneous mutation in the leptin receptor gene (Ob-Rb).
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