It is recognized that different models emphasize different aspect of ARDS and that no model fully replicates the histological findings characteristic of human ARDS (i.e., inflammatory infiltrates, thickened alveolar septae, intravascular microthrombosis, and hyaline membrane deposition).
Although no animal model fully replicates the human disease, AD mouse models are useful to investigate different aspects of AD pathology and disease progression.
Thus, current cellular DPR models cannot fully replicate the pattern of intranuclear aggregates found in patient tissue.
Our current understanding of the disease pathogenesis is incomplete and the study of SSc is hindered, at least partially, by a lack of animal models that fully replicate the complex state of human disease.
The human endotoxemia studies described above provide a highly controlled and reproducible experimental setting to explore sepsis biology at the level of the entire transcriptome, but as with all sepsis models, this model does not fully replicate the complex and heterogeneous syndrome seen at the bedside following infection with live microbes [ 25].
As described above, in addition to the rubric questions used for the drafts, term papers were evaluated based on the extent to which the model had been fully replicated, the difficulty of the model, the level of understanding students illustrated in their write up, the quality of the writing, the kind of extension to the model that students had created, and the quality of the extension.
It should be mentioned that the db/db model may not fully replicate T2DM in human, although copy number variation at the leptin receptor gene locus is associated with metabolic traits and the risk of T2DM in human subjects [ 35].
It is a recognized fact that this model does not fully replicate the magnitude of physiologic stress created by trauma or infection [ 13, 14]; however, it gives researchers the opportunity to study the mechanisms underlying the response to systemic inflammation and relevant therapy options without the inter-species differences obscuring the interpretation of the results.
Similarly, while it appears probable that these data clarify the potential mechanisms of SPA-induced lung injury, these experimental models do not fully replicate the biochemical or physiological milieu found in porcine or human lungs.
Although animal models do not fully replicate human malaria, they are invaluable tools for elucidating immune processes that can cause pathology and death [ 14].
The mechanisms responsible for transition to non-alcoholic steatohepatitis are still not completely understood, in part because of the scarcity of animal models that can fully replicate both the histological and metabolic features of human non-alcoholic steatohepatitis [ 8].
