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The two mouse models, however, are on different genetic backgrounds.
Data from mouse models, however, suggest that there is more to the story.
Analysis of mouse models, however, has supported a role for HDACs in steroid-resistant severe asthma.
Mouse models, however, have long been used to study neuropsychiatric traits.
In human clinical trials and rat models of inflammatory pain, peripherally restricted opioids have repeatedly shown powerful analgesic effects; in some mouse models however, their actions remain unclear.
Mouse models, however, provide limited applicability to genome-wide screens for pathogen or host factors – factors that might influence systemic dissemination following GI colonisation.
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In another mouse model however, n-3 PUFAs could also act negatively, stimulating the symptoms of ALS progression as well as lipid peroxidation compared to control [138].
Based on our in vivo studies, it is clear that [18F]FDG-6-P did not behave as expected within the mouse model; however, the radioactivity at the infection site was elevated more than twofold for infected mice compared with uninfected controls injected with [18F]FDG-6-P and compared with [18F]FDG.
Our LRP1-overexpressing mouse model, however, did not show an increase in the amyloid plaque burden when crossed to PDAPP amyloid model mice [53].
The latter process is not easily evaluated in the mouse model; however, for the virus to reactivate and replicate in mucosal or cutaneous epithelia in latently infected individuals, there needs to be at least some suppression of existing cellular immune responses.
In the R6/2 mouse model, however, doses required to achieve similar concentrations in the brain were toxic, therefore lower doses were used (1 and 5 mg/ml in the drinking water) for assessment, which resulted in a concentration of 12.2 µM of minocycline in the R6/2 brain after 5 days of treatment, very similar to the results in our study.
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