Tumorigenesis in c-Myc transgenic mouse models is accelerated if combined with other anti-apoptosis genetic alterations, such as overexpression of Bcl-2 [51] or Bmi1 [52], or disrupting the ARF-MDM2-p53 pathway [53].
Since the relaxation dynamics of the coarse-grained models are accelerated by the smoothed potentials, single numerical factors are introduced to rescale the time scale of the coarse-grained models, respectively.
Of note this is accelerated within the porcine model, starting within 16 hours of the onset of liver damage.
We report the first in vivo imaging study of VEGFR prevalence in atherosclerotic plaques in diabetic vs. non-diabetic atherosclerosis-prone ApoE−/− mice, a model where atherosclerosis is accelerated by diabetes.
This model was improved by accelerating bone production, after the isolation of the most conspicuous histological constituents (inflammatory, bone and adipose tissues) by laser microdisection and purified from them RNA that was used to determine by RT-PCR the gene expression kinetics of the most important growth bone factors.
Here we demonstrate that the POKO mouse is a model of renal disease that is accelerated by high levels of glucose and lipid accumulation.
In conclusion, the healing of a closed fracture in a goat model can be accelerated by a single local administration of rhOP-1.
For the stronger damage conferred by myeloablative therapies the response of the hybrid model can be accelerated by an adaptation of the transition characteristics that makes them more sensitive to changing cell numbers.
Such two ZNN models can be accelerated to finite-time convergence to the time-varying theoretical pseudoinverse.
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