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This result was independently validated by Madsen et al. When tested in a mouse model, these cells can also migrate to brain tumors.

Together with the experiments in the humanized PPARα mouse model, these in vitro observations suggest that subtle differences in the mPPARα and hPPARα receptors contribute to a species-specific PPARα-dependent metabolic response to DEHP.

This suppressive subset showed polymorphonuclear granulocyte morphology and expressed markers CD11b and CD15, but not CD14; in a mouse model, these cells showed a significant increase in ARG activity and affected T-cell proliferation and CD3ζ expression (51, 52).

In the mouse model these cells proved to be effective, but given that BMMC were also effective and did not translate to humans, we see no reason for starting a new human trial based on the mouse results.

Notwithstanding the limitations of this mouse model, these data support our findings in the human endometrium, suggesting factors with a role in initial repair are not reliant upon estrogen for their expression.

Although we failed to observe the changes in the level of autophagy-related proteins (i.e., no activation of LC3-II and Beclin 1) following 6-OHDA injection in our mouse model, these results suggest that changes in the metabolic signals could be common events in sporadic and genetic PD.

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In FHM1 knock-in mouse models these mutations increase the susceptibility for cortical spreading depression (CSD): the underlying mechanism of the migraine aura.

Combined with our transgenic mouse models, these studies suggest that Twist1 and Hand1 may play a growth-inhibitory role in post-natal heart and phosphorylation may release their inhibitory effects leading to hypertrophy.

Similar to Atg7-deficient mouse models, these flies develop large inclusion bodies and accumulate ubiquitinated proteins within neurons, in addition to a shortened life span under unstressed conditions.

Although POH has not been reported in any of the existent mouse models, these heterozygous mice develop heterotopic ossification with increasing age [Huso et al., 2011; Cheeseman et al., 2012].

Although no specific SNPs were tested in the mice model, these studies illustrate the potential importance of the EPAS1 gene in athletic-related phenotypes.

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