Notwithstanding differences in the mouse models utilized (Mecp2tm1Tam [24], Mecp21lox [25] or Mecp2tm1.1Bird [this report]), the enrichment paradigms (continuous from 4 weeks of age [24], continuous from 3 weeks of age [25] or transient from 3 to 5 weeks of age [this report]) and the methods used to test its effects, EE is capable of eliciting improvement in some RTT like phenotypes.
For example, the majority of mouse models utilize acute allergen challenges in relatively youthful mice and therefore model early-onset disease.
The experiments and the unique mouse models utilized in this study implicate the importance of targeting IL-17A for preventing metastasis associated with metastatic BC.
In addition, the typical rat and mouse models utilized, albeit useful in many ways, do not fully recapitulate human disease [ 16].
Previous studies of excitotoxicity in HD mouse models utilized a wide range of QA doses (4 30 nmol) (Hansson et al., 1999, 2001; MacGibbon et al., 2002; Zeron et al., 2002; Jarabek et al., 2004; Graham et al., 2006; Graham et al., 2009).
Kim et al report their findings with a mouse model utilizing ovalbumin and Aspergillus protease to induce eosinophilic inflammation.
The study assessed the histological effects of perineural injections of propylene glycol and three medical gels in a mouse model utilizing ultrasound guided microinjection techniques.
As an alternative, a mouse model utilizing repeated doses of bleomycin has been proposed to more closely replicate pathological features of IPF in humans (Degryse et al., 2010).
In these studies, we generated a mouse model utilizing the Cre- loxP system to ablate CENP-F protein expression in a cardiomyocyte-specific manner (termed CENP-F −/− hereafter).
