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Since one pathological feature in MSA patients covers selective neuronal loss in the SNc, and the (PLP -αSYN mouse model rePLP -αSYNthis feature, we evaluated whether mousereatmodelhad an effect on numbereplicateseurons.
By adjusting the boundary condition for exit from the PSD membrane domain, from open to reflective, our model replicates this behaviour.
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This model replicates the role of stress in eliciting physiological and behavioral changes that are homologous to a depressive-like syndrome in mice and respects the time frame of onset and efficacy of antidepressant treatment [ 39].
In the present study, we hope to expand on our initial studies to demonstrate that this model replicates the degenerative phenotype in humans through analysis of global gene expression changes.
As the AC5 KO mice exhibit longevity and protection against diabetes, obesity, and cardiovascular disease (Yan et al., 2007, 2014; Lai et al., 2013; Ho et al., 2015) along with enhanced exercise performance demonstrated in the current investigation, this model replicates the human paradigm of healthful aging.
It would appear then, that this model replicates the type of shunt failure in humans and as such, can provide a foundation on which to build and test new shunt designs that negate the more unfortunate host-shunt interactions that occur in the clinical setting.
First, it is unknown to what degree this rat model replicates the human in terms of gene expression and timing of expression with injury and rest.
The numerical results show that our model replicates the averaged behavior of the combined treatment.
In each case the model replicates the pressure signal very accurately.
Although the model replicates the qualitative structure of the experimental data, there are some quantitative differences.
The model replicates the experimental values remarkably well despite the significant number of simplifying assumptions.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com