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The second problem is that the predictions made by discrete-state models can mimic curvilinear ROC curves (e.g. Broder & Shutz, 2009; Malmberg, 2002; Province & Rouder 2012; but see Chen, Starns, & Rotello 2015).
It was shown that these cell models can mimic various topologies of tissue such as cyst or tumor or monolayer.
These deformable cell models can mimic many aspects of real cells such as growth, cell division, apoptosis and attachment to other cells or ECM.
Genetic events in these mouse models can mimic those that are frequently perturbed in human tumors.
Animal models can mimic only certain aspects of the complex symptomatology of ADHD and at best provide feasible hypotheses regarding the underlying causes of specific aspects of ADHD behaviour.
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Furthermore, the model can mimic different neuronal filter properties.
We believe that this model can mimic the pathogenesis of human OA in terms of cartilage degradation after similar traumas.
Below we discuss how the model can mimic the phenotypes of various genetic mutants and transgenic lines, as summarised in Table 1.
No such human model can mimic all of the critical elements present in spontaneous human sepsis.
Thus, the question remains whether this simple model can mimic all tumor initiation.
The cocultured model can mimic to a certain extent the local ovarian steroidogenesis by supporting similar structural integrity of follicles.
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