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These findings suggest that the alopecia in CRF-OE mice share some features as seen in humans.
Overall, GCs from pilocarpine-treated mice share some of the electrophysiological properties with GCs from α-CaMKII hKO mice 15.
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SGCB knockout mice share many of the phenotypic deficiencies of LGMD2E patients.
These KO mice share several mood stabilization-related behavioral and neurochemical characteristics with lithium treatment, favoring the notion that inositol metabolism is involved in the mechanism of Li-induced behavioral changes (Agam et al, 2009).
C. elegans and mice share many homologs that are involved in synaptic structure and function.
Nonetheless, it is interesting that Fmr1 knockout mice and GSK3 knockin mice share the phenotype of impaired social preference.
The phenotypes of the Hi- and Lo-MYC mice share a number of similarities with the human disease.
Taken together, these suggest that humans and mice share a single locus encompassing one gene that may control corpus callosum development.
Therefore, we conclude that the mPer2 mutant mice share the breakdown of the universal organization of resting periods with human depression patients.
Second, mice share genetic similarities with humans.
The db/AD mice share these features.
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