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In combination with data from previous smoke inhalation studies with A/J mice, the current data suggest that this model for MS inhalation-induced pulmonary tumorigenesis is reliable and relevant, two crucial requirements towards validation of such a model.
Because of the ultrastructural inclusions evident in axons of the saposin C−/− mice, the current findings indicate cellular effects on axonal transport and secondary retrograde neuronal degeneration.
Together with the sophisticated genetic tools available for manipulating neural circuits in mice, the current approach makes mouse locomotion a powerful system for investigating the neural control of coordinated movement and establishing relationships between neural circuit activity and behavior.
On the basis of our previous findings of increased bone mineral density in nanoparticle-treated mice the current findings have therapeutic relevance and suggest the process of autophagy as a novel potential target for the regulation of bone density.
Although we were able to identify a BSE associated trait that could potentially be used to detect BSE in the presence of scrapie using VM mice, the current study shows that overall scrapie can dominate the phenotype of the disease even if BSE prions propagate in the background, while some phenotypic aspects of BSE may be evident.
To explore the molecular mechanisms underlying this defect in mobilization of BM Lin-/VEGF-R2+ EPCs in spontaneously diabetic mice, the current study aimed to evaluate differential gene expression of 35 genes that were reported to be closely involved in Lin-/VEGF-R2+ EPC mobilization and function.
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Could a less plastically sensitive brain of 8-10 week old mice vs. 6-8 week old mice explain the current null results?
However, in contrast to their work, UNO mice in the current study actually outperformed control mice on a habituation task and a discrimination task.
The difference in life span between Mecp2-single null and Mbd2/Mecp2-double null animals was not seen in a previous report [26] in which mice were on a mixed genetic background, whereas the mice in the current study were on a C57Bl/6 background, indicating the existence of strain-specific modifiers of life span in Mecp2-null mice.
Previously, we showed that Nrxn2α KO mice have no impairments within the passive avoidance test (Dachtler et al., 2014), and, consistent with that finding, Nrxn2α HET mice in the current study had similar retention latencies to WT mice.
Its subtitle, An Introduction to Characterizing Blood Diseases of the Post-Genomic Mouse, alludes to the practicalities of producing designer mice utilising the current detailed knowledge of the murine genome.
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