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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).
We sought to determine whether early exposure to BPA could accelerate mammary carcinogenesis in a dimethylbenzanthracene (DMBA) model of rodent mammary cancer.
The data presented here provide the first evidence that maternal exposure to BPA during lactation increases mammary carcinogenesis in a DMBA-induced model of rodent mammary cancer.
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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.
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