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To summarize results, evaluations of blood, bone marrow, liver and spleen of S. Typhimurium-infected mice demonstrated active and ongoing hematopoiesis, inflammatory disease, and six of eight characteristics of sHLH in highly infected mice.
Genetic marking experiments using Sox9-Cre/R26R mice demonstrated active contribution of keratinocytes positive for the early HF SC marker Sox9 to the establishment of the SG lineage (Nowak et al, 2008).
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However, a later study using mice demonstrated that active efflux at the BBB mediated by organic anion transporter 3 (Oand) and multidrug resistance protein 4 (Mrp4) also contributes to the low brain penetration [[5]].
Intravital imaging of live tumor-bearing nude mice demonstrated that active TGFβ signaling is heterogeneously distributed in a minority of cancer cells within primary mammary tumors [ 12].
In fact, when compared with sham-operated controls, rapamycin-treated denervated mice demonstrated no significant upregulation in active pAkt and SGK (Fig. 7A).
Active immunization in PDAPP mice demonstrated more effective rescue from cognitive impairment when treatment was started to prevent Aβ pathology compared to mice treated at a later point in life in a reversal trial [ 10].
Assessment in a critical size long-bone defect in immunodeficient mice demonstrated successful bridging of the defect within 4 weeks, with active contribution of the implanted cells.
All mice demonstrated full visual capability.
Three mice demonstrated subarachnoidal hemorrhages.
Related to Figure 1 Intravital analysis of KCs (green) in liver sinusoids (red) in naive F1 mT/mG × LysMcre) mice demonstrating rapidly moving neutrophils and/or monocytes and stationary, but active, KCs.
Active PTK6 was localized at the membrane in mammary gland epithelial cells, and was only detected in wild-type MMTV-ERBB2 mice demonstrating the specificity of the antibody for PTK6.
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