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Microarray analysis was validated in qPCR studies using human postmortem brain tissue and CA1 sector and regional hippocampal dissections obtained from a mouse model of AD/Down syndrome (Ts65Dn mice) and normal disomic (2N) littermates.
They also found several behavioral differences between these mice and normal mice as the animals entered adolescence.
μPET/CT and ex vivo biodistribution studies were performed in CCK2 tumour xenograft-bearing nude mice and normal mice.
They then fed the mutant mice and normal mice a high-fat diet.
METHODS: Mechanisms that regulate the transition from the prereplicative G1 phase of the cell cycle into S phase were compared in EtOH-fed mice and normal pair-fed mice after PH.
In contrast, there was no difference between NR2B mice and normal mice in their response to acutely painful stimuli, such as a heating probe applied to the tail.
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Activity levels and food consumption were similar for obese DES-treated mice and normal-weight controls.
Normal mouse and normal rabbit control IgG in a dilution of 1∶200 were used.
However, both the mice lacking PARP and normal mice treated with PARP blockers showed no decline.
They compared the animals' ability to negotiate a radial-arm water maze, a standard test of cognitive ability, with that of regular J20 mice and of normal mice at 4, 9, and 14 months of age.
EIU was produced in immunosuppressed iNOS−/− mice and C57BL/6 (normal) mice by footpad injection of lipopolysaccharide.
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