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Engineered tissues composed of microvessels from diabetic mice display normal PVC coverage and Jagged1/Notch3 gene expression when implanted into non-diabetic hosts.
Indeed, Batf-/ deficient mice display normal Th1, and Th2 response but are deficient in Th17 differentiation, and are resistant to experimental autoimmune encephalitis[63].
At 1-2 months, G2019S-LRRK2 mice display normal numbers of TH+ and Nissl+ nigral neurons suggesting that neuronal loss occurs in a progressive manner (Figure 3B).
G2019S-LRRK2 mice display normal locomotor activity in the open field at 6 and 15 months of age (Figure 5A B).
However, LIGHT-deficient mice display normal immune responses following infection with Mycobacterium tuberculosis [11] or influenza A [12], suggesting that LIGHT may regulate some cellular responses whilst being superfluous for others.
In summary, this study found that both Fmr1 knockout mice and GSK3 knockin mice display normal sociability with a single stimulus mouse but do not display preference for a novel mouse.
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All engrafted W/BF1 mice displayed normal immunologic competence 100 days posttransplantation.
In mice fed with chow, islets of the Elovl6−/− mice displayed normal architecture and β-cell mass compared with those of the wild-type mice.
Similarly, hippocampal CA1 pyramidal cells in mutant mice displayed normal place-related activity in a full-cue environment but showed a reduction in activity upon partial cue removal.
Furthermore, CaMKIV KO mice displayed normal spatial reference memory in the Barnes circular maze.
Wild-type and Shh+/− mice displayed normal digit morphology (Fig. 2A).
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