In the above model, the cell distribution of P-gp is assumed to be homogeneous in space.
We used our model cell transcript distributions to perform Monte Carlo simulations of microarray experiments comparing samples from two halves of the same cell and from pairs of identical cells.
31, 33, 39, 41 In the cell distribution model, tumor volume is assumed to represent the population of cycling cells plus additional cells that are in various stages of cell death and removal.
We show that this aspect of the fovea-parafovea difference can be explained with the current model
For each model cell we created ~10 20 specific distributions for values of μ in the range 0.50 – ~2.00 (there is an effective upper limit for μ for each model, depending on the transcript number, where the peak becomes too sharp to model effectively), giving us a set of 205 specific distributions.
We have developed a multiphase model of fluid flow, solute transport and cell distribution in a simplified HFMB.
Model simulations are compared with experimental histology data on cell distribution.
The modeled ∑NEP values for the DF49, HDF00 sites (from Wang et al. 2011) were calculated as site-level means unweighted and weighted by the flux probability distribution for the model cells in the footprint area; and at HDF90 as an unweighted mean of model cells over the spatial extent of the ground plots.
Both models are detailed in Text S1 parts 3 and 4 Theoretical studies [10], [17], [40] have noted that the stochastic model employed in our study should result in a cell-cell distribution of protein levels that follows a Gamma distribution (or, for very small protein numbers a related distribution known as the negative binomial distribution [16]).
Comparison of B-cell distribution by TNFi type at 3 months involved a linear mixed model.
