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Interestingly, TIMP4 was found not to contribute to cardiac response to mechanical stress, as TIMP4−/− mice exhibited comparable cardiac remodeling, dysfunction and myocardial fibrosis compared with the parallel wildtype mice [ 141].
Finally, while C57BL/6 and 129/Sv mice exhibited comparable behavior during FR1 sessions, C57BL/6 mice tended to acquire food-maintained responding faster than 129/Sv counterparts, and exhibited elevated responding during PR testing.
DG/Lck-cre mice exhibited comparable LCMV specific IFN-γ expressing CD4+ and CD8+ T cells to that of littermate controls (Fig. 5E).
The mutant and control mice exhibited comparable performances in quadrant occupancy (Figure 5E), target quadrant occupancy (Figure 5F), and the number of platform crossings (Figure 5G).
Conclusions Sirt1Tg and WT littermate mice exhibited comparable acute histopathological reactions to the systemic injection of MPTP, loss of TH-positive neurons and reactive gliosis.
At the 8-week time point prior to TAM-induced NELF-B deletion, the KO mice exhibited comparable LV function as the control littermates.
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As previously reported [11], [13], wild type and PI3Kγ−/− mice exhibit comparable baseline phosphorylation of both AKT and ERK1/2.
A preferential accumulation of radioactivity was observed in the inflamed extremities of mice injected with SIP L19) and SIP(G11), whereas no preferential antibody accumulation could be detected in mice exhibiting comparable grades of inflammation that had been injected with a SIP antibody of irrelevant specificity in the mouse.
As shown in Figure 5e, compared with control mice (WT ▸ WT), TLR4 KO bone marrow-transplanted WT mice (KO ▸ WT) exhibited comparable levels of hepcidin mRNA expression.
When miR-150−/− mouse pups were exposed to hyperoxia, a moderate protection of the lung structure was noted at P9; however, no protection was evident at P13, where miR-150−/− mice and wild-type mice exhibited a comparable blunting of alveolarization in response to hyperoxia exposure.
Consistent with these findings A1 mice exhibited a comparable increment in weight gain resultant from the high fat diet.
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