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Until recently, no laboratory models replicated the former clinical scenario, but the deficiencies in our knowledge are being corrected.
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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The models replicate the percentage of men and women in the labor force and the percentage of those who are employed (in part-time and full-time jobs) for both gender and marital status.
All models replicate the observed axisymmetric flow spreading (NRMSE <8%) and capture the cooling of the flow with temperature profiles along radius at 1230 s (NRMSE <0.3%; Fig. 4b).
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].
The present model replicated the clinical realities leading to delays in organ retrieval upon BD.
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