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These models have typically involved the transgenic expression of disease-associated human proteins.
However, automated code generation from high-level models have typically been inefficient compared to hand-crafted code.
As a consequence, models have typically very large dimensions, and hence considerable computational and ill conditioning problems arise.
Landform-evolution models have typically failed to include human actions, or have done so only in a static, scenario-based way.
Climate change models have typically underestimated the amount of sea level rise observed over the past century.
Bioclimatic, or species distribution models, have typically shown the area of suitable climatic habitat for white pine to decrease and/or move northward by the end of the century, with larger changes under higher greenhouse gas emissions scenarios, but the degree of change varies with region (McKenney et al. 2007; Joyce and Rehfledt et al. 2013; Iverson et al. 2008, 2017).
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Understanding of the effects of vegetation on long-term catchment flows is growing, yet incorporation of these effects into hydrological models has typically been empirical and qualitative, or deterministic and quantitative – but at the cost of simplicity.
Prior studies assessing the effects of CCBs in other mouse models of aortic disease, such as the angiotensin-II infusion model, have typically used lower doses of amlodipine, in the range of 1 to 5 mg/kg/day (Chen et al., 2013; Takahashi et al., 2013).
Research adopting the model has typically adopted an experimental procedure, known as the dual task paradigm, to test model effects [ 78, 81].
Astrogliosis in the cuprizone model has typically been characterized using immunohistochemical detection of GFAP (glial fibrillary acidic protein) either to count the number of astrocytes or measure immunoreactivity in a region of interest.
This model has typically been used to analyze protein binding to DNA sites, which may resemble how Crm1 binds to the array of NES peptides in the Rev-RRE complex.
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