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Two models of rodent spinal cord injury were adequately characterized and closely mimicked the results of histological studies.
The "cognitive map" hypothesis (O'Keefe and Nadel, 1978) is one of the most influential models of rodent hippocampal function.
Our study shows that oxidative injury and its triggering mechanisms diverge in different models of rodent central nervous system inflammation.
Finally, we have established rigorous and externally predictive class-specific QSAR models of rodent acute toxicity measured by LD50 values.
The function of interleukin-18 (IL-18) was investigated in pertinent animal models of rodent rheumatoid arthritis (RA) to determine its proinflammatory and monocyte recruitment properties.
These data, when converted to binary "biological" descriptors, were shown previously to improve the accuracy of conventional, chemical descriptor-based QSAR models of rodent carcinogenicity (Zhu et al. 2008).
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In experimental models of rodents developing autoimmune encephalomyelitis or collagen-induced arthritis, IL-17 has been linked to the severity of inflammation in tissues [12, 13].
We present a spatially explicit individual-based model of rodent dynamics, customized for the prairie vole species, Microtus ochrogaster.
Most of these studies have been performed in a model of rodent hyperoxia-induced lung injury, which mimics most of the morphological and functional features of the "new" BPD.
For example, in a model of rodent status epilepticus, VPA markedly decreased neuronal damage in the hippocampal formation and improved neurological and memory functions [8].
BPA-induced apoptosis evasion has been reported previously in HRBECs (3) and in the dimethylbenz[ a]anthracene model of rodent mammary carcinogenesis (19).
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