32,380 research outputs found
Computational Methods and Results for Structured Multiscale Models of Tumor Invasion
We present multiscale models of cancer tumor invasion with components at the
molecular, cellular, and tissue levels. We provide biological justifications
for the model components, present computational results from the model, and
discuss the scientific-computing methodology used to solve the model equations.
The models and methodology presented in this paper form the basis for
developing and treating increasingly complex, mechanistic models of tumor
invasion that will be more predictive and less phenomenological. Because many
of the features of the cancer models, such as taxis, aging and growth, are seen
in other biological systems, the models and methods discussed here also provide
a template for handling a broader range of biological problems
Modeling the Role of the Cell Cycle in Regulating Proteus mirabilis Swarm-Colony Development
We present models and computational results which indicate that the spatial
and temporal regularity seen in Proteus mirabilis swarm-colony development is
largely an expression of a sharp age of dedifferentiation in the cell cycle
from motile swarmer cells to immotile dividing cells (also called swimmer or
vegetative cells.) This contrasts strongly with reaction-diffusion models of
Proteus behavior that ignore or average out the age structure of the cell
population and instead use only density-dependent mechanisms. We argue the
necessity of retaining the explicit age structure, and suggest experiments that
may help determine the underlying mechanisms empirically. Consequently, we
advocate Proteus as a model organism for a multiscale understanding of how and
to what extent the life cycle of individual cells affects the macroscopic
behavior of a biological system
A Multiscale Model of Biofilm as a Senescence-Structured Fluid
We derive a physiologically structured multiscale model for biofilm
development. The model has components on two spatial scales, which induce
different time scales into the problem. The macroscopic behavior of the system
is modeled using growth-induced flow in a domain with a moving boundary.
Cell-level processes are incorporated into the model using a so-called
physiologically structured variable to represent cell senescence, which in turn
affects cell division and mortality. We present computational results for our
models which shed light on modeling the combined role senescence and the
biofilm state play in the defense strategy of bacteria
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