Date
Wed, 25 Apr 2012
Time
10:15 - 11:15
Location
OCCAM Common Room (RI2.28)
Speaker
Hye-Won Kang
Organisation
Ohio State University

In this talk, I will introduce stochastic models to describe the state of the chemical networks using continuous-time Markov chains.
First, I will talk about the multiscale approximation method developed by Ball, Kurtz, Popovic, and Rempala (2006). Extending their method, we construct a general multiscale approximation in chemical reaction networks. We embed a stochastic model for a chemical reaction network into a family of models parameterized by a large parameter N. If reaction rate constants and species numbers vary over a wide range, we scale these numbers by powers of the parameter N. We develop a systematic approach to choose an appropriate set of scaling exponents. When the scaling suggests subnetworks have di erent time-scales, the subnetwork in each time scale is approximated by a limiting model involving a subset of reactions and species.

After that, I will briefly introduce Gaussian approximation using a central limit theorem, which gives a model with more detailed uctuations which may be not captured by the limiting models in multiscale approximations.

Next, we consider modeling of a chemical network with both reaction and diffusion.
We discretize the spatial domain into several computational cells and model diffusion as a reaction where the molecule of species in one computational cell moves to the neighboring one. In this case, the important question is how many computational cells we need to use for discretization to get balance between e ective diffusion rates and reaction rates both of which depend on the computational cell size. We derive a condition under which concentration of species converges to its uniform solution exponentially. Replacing a system domain size in this condition by computational cell size in our stochastic model, we derive an upper bound
for the computational cell size.

Finally, I will talk about stochastic reaction-diffusion models of pattern formation. Spatially distributed signals called morphogens influence gene expression that determines phenotype identity of cells. Generally, different cell types are segregated by boundary between
them determined by a threshold value of some state variables. Our question is how sensitive the location of the boundary to variation in parameters. We suggest a stochastic model for boundary determination using signaling schemes for patterning and investigate their effects on the variability of the boundary determination between cells.

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