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A large number of genetic disease model mice have been produced by genetic engineering.
However, in our present study, another mammalian model, mice have been used.
Studies using HD model mice have identified many genes whose expression is altered by mutant huntingtin (4– 7).
Muenke model mice have craniofacial phenotypes that vary in penetrance and expressivity depending on genetic background, but do not include obvious middle ear anomalies.
In the MINO model, mice have been engineered to have neoplastic outgrowths from mammary ducts [ 7, 8] while in the MIND model, human DCIS cell lines are transplanted intraductally to mimic the structure of DCIS found in humans [ 9, 10].
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Accordingly, IFN-α production in IBD model mice has been noted in both CD11b+ and CD11c+ dendritic cells in colonic lamina propria [ 60].
Preclinical animal models (mice) have shown potential.
In a lung-infection model, Nlrp3−/− mice have higher bacterial titers and a higher mortality than WT controls.
Thus, rodent models, and particularly mice, have become the most widely used models of human disease.
The mortality associated with the L-arginine model in mice has been reported [ 12].
In a mouse model of ehrlichiosis, immunocompromised mice have persistent infection, and most eventually die (25 ).
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