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Apart from abnormal movements such as clasping, and mild impairments in gait, these mice are virtually indistinguishable from wild-type mice.
Our initial time course studies are in line with these findings and show that the microgliosis and dopaminergic neurodegeneration in B10.BR mice are virtually resolved respectively by days 4 and 7 post-MPTP injection (Figure 6, right and middle panels, respectively).
The BM cells of mice are virtually exposed to DZNep intermittently, because its concentration in mice plasma is lowered to less than 10% within 30 minutes after administration.
These clinical manifestations of Scn1ad/d and Scn1ad/+ mice are virtually identical to those previously reported in Nav1.1-null mice (14, 15), indicating that mice carrying the floxed Scn1a allele can serve as useful tools for the dissection of the physiologic consequences of Nav1.1 deletion, in genetically defined neuronal subtypes, using the Cre-loxP system.
Similar to the constitutive KO, Dhh-Cre; Erbb3 fl/fl mice are virtually devoid of Schwann cells (Sheean et al., 2014); however, unlike the constitutive KO, Dhh-Cre; Erbb3 fl/fl mice had a normal frequency of bone marrow hematopoietic progenitors.
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Lesion-infiltrated MØ of young ApoE KO mice were virtually all Arg I+ suggesting that they were of the M2 phenotype.
Interestingly however, the serum insulin levels of Nscl-2 mutant mice were virtually normal while ob/ob mice, which are a model of Type II diabetes [25], showed a massive increase in serum insulin concentrations (Fig. 8A).
Swimming speeds of S14G-HN treated and control mice were virtually the same in probe test (data not shown), indicating that locomotion activity was not affected by S14G-HN.
We found that hepatic glycogen in WT mice was virtually absent after 24 hours of fasting whereas RasGrf1 −/− mice maintained significant glycogen levels.
Not surprisingly, the DRG and roots of symptomatic mice were virtually flooded with both macrophages and CD8+ T cells, where DRG sensory neurons were barely observable.
The phenotype of the TGF-β1 and TβRII knockout mice is virtually indistinguishable and is characterized by defective endothelial differentiation resulting in abnormal capillary tube formation [ 61, 62].
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