Lauffenburger Lab: developed a model of cell migration that simulated recent experimental results that had been published by collaborators.
Genetic interaction profiles enabled assembly of a hierarchical model of cell function, including modules corresponding to protein complexes and pathways, biological processes, and cellular compartments.
Along these lines, a novel model of cell cycle progression is proposed in this work.
First, we analyze the reaction-diffusion model of cell growth and substrate consumption in an immobilized commensalystic system.
A model of cell apoptosis was designed by exposure of the cells to a low concentration of hydrogen peroxide.
We describe a biochemical kinetics model of cell cycle control and DNA damage response proteins in order to model cellular responses to radiation exposures.
These data were compared to the power-law-like predictions from the soft glassy model of cell rheology proposed by Fabry et al. [14].
After the model of cell ischemia and hypoxia was established in vitro, cytoprotective effect of DSP on MSC was detected by AO/EB staining.
In order to design optimal battery controls that effect a tradeoff between cell performance (in some sense) and cell life, a model of cell degradation is necessary.
We implement QSS method with BioRica, and illustrate with applications in Biology, the Tyson model of cell cycle, and examples in Engineering.
Six biogeochemical models of differing complexity were coupled with a pre-calibrated two-dimensional hydrodynamic model of Cell 4 and tested against field data.
