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Future work will need to consider the effectiveness of phages in mixed culture models replicating the "airway microbiome" including widely available and well-characterized PA strains from diverse sources.
Dissecting the complex pathophysiological pathways involved will represent a major challenge, and future experimental paradigms will require the development of more sophisticated functional systems, such as animal models replicating the features seen in patients with DOA+ phenotypes.
TGF-β expression and activity are increased in human RDEB and in mouse models replicating the disorder (Fritsch et al, 2008; Ng et al, 2012; Kuttner et al, 2013; Nystrom et al, 2013).
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Until recently, no laboratory models replicated the former clinical scenario, but the deficiencies in our knowledge are being corrected.
Thus, neither of the two mouse models replicates the severe muscle phenotype and pathology seen in humans.
This illustrates that both models replicate the experimental phenomena, i.e., increasing PW and NoP decreases detection thresholds.
The mouse models replicates the disease course in humans, clinical features and complications of SS and gives researchers insights into the disease pathogenesis.
Yet several challenges remain, including understanding the extent to which well-characterized xenograft models replicate the biology and growth characteristics of patient disease.
These models replicate the chemistry inside of the cells and allow scientists to observe complex interactions between genes, proteins and other cellular components.
These models replicate the metabolic consequences of cholestasis and the pathogenesis of cholangitis but do not provide real insights into BA etiology [ 17].
We have previously shown that primary-tumor derived orthotopic xenograft mouse models replicated the histology, invasive growth, and genetic abnormalities of pediatric brain tumors [ 45, 50].
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