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More importantly, replication of the QA23 and QA23CkA10 viruses in mice was clearly evident.
Moreover, the altered immunoreactivity for ATP1B in the DF mice was clearly evident using immunohistochemical methods.
Additionally, a previous investigation indicated that the brain of E17.5 wildtype mice was clearly more developed than those of E18.5 Creb1−/− mice, despite their comparable size [11].
However, in the hair follicle area of the wounded skin, the number of Ki67-positive cells in the periostin−/− mice was clearly decreased to about one-half compared with that for the WT mice (see insets in Fig. 5A and right graph in 5B); whereas in the area of intact skin, no significant difference in the number of Ki67-positive cells was observed (Fig. 5B, left).
SLE development in BAFF-Tg mice was clearly dependent on both NF-κB pathways.
The escape latency of wild type mice was clearly prolonged after isoflurane treatment).
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Nonetheless, the presence of NCIs in injected CamKIIa-208 mice were clearly evident, distinct from the diffuse perikaryal p409-410 previouslyeviously described in this Tg line (Fig. 6d 42.
In PET studies, C6 and HeLa tumors in mice were clearly visualized using [11C]AZT.
The inferior vena cava (IVC) and pulmonary veins of the mice were clearly identified after intravenous injection of the Au DENPs.
The s.c. LS-174T tumors on the rear flank of the mice were clearly visualized by planar γ-scintigraphy (Figure 4a).
Variations in 11C-dLop brain uptake between wild-type and knock-out/cyclosporine-pretreated mice were clearly observed in μPET images and SUVs.
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