15,393 research outputs found
StochKit-FF: Efficient Systems Biology on Multicore Architectures
The stochastic modelling of biological systems is an informative, and in some
cases, very adequate technique, which may however result in being more
expensive than other modelling approaches, such as differential equations. We
present StochKit-FF, a parallel version of StochKit, a reference toolkit for
stochastic simulations. StochKit-FF is based on the FastFlow programming
toolkit for multicores and exploits the novel concept of selective memory. We
experiment StochKit-FF on a model of HIV infection dynamics, with the aim of
extracting information from efficiently run experiments, here in terms of
average and variance and, on a longer term, of more structured data.Comment: 14 pages + cover pag
A Simple Cellular Automaton Model for Influenza A Viral Infections
Viral kinetics have been extensively studied in the past through the use of
spatially homogeneous ordinary differential equations describing the time
evolution of the diseased state. However, spatial characteristics such as
localized populations of dead cells might adversely affect the spread of
infection, similar to the manner in which a counter-fire can stop a forest fire
from spreading. In order to investigate the influence of spatial
heterogeneities on viral spread, a simple 2-D cellular automaton (CA) model of
a viral infection has been developed. In this initial phase of the
investigation, the CA model is validated against clinical immunological data
for uncomplicated influenza A infections. Our results will be shown and
discussed.Comment: LaTeX, 12 pages, 18 EPS figures, uses document class ReTeX4, and
packages amsmath and SIunit
Lethal Mutagenesis in Viruses and Bacteria
Here we study how mutations which change physical properties of cell proteins
(stability) impact population survival and growth. In our model the genotype is
presented as a set of N numbers, folding free energies of cells N proteins.
Mutations occur upon replications so that stabilities of some proteins in
daughter cells differ from those in parent cell by random amounts drawn from
experimental distribution of mutational effects on protein stability. The
genotype-phenotype relationship posits that unstable proteins confer lethal
phenotype to a cell and in addition the cells fitness (duplication rate) is
proportional to the concentration of its folded proteins. Simulations reveal
that lethal mutagenesis occurs at mutation rates close to 7 mutations per
genome per replications for RNA viruses and about half of that for DNA based
organisms, in accord with earlier predictions from analytical theory and
experiment. This number appears somewhat dependent on the number of genes in
the organisms and natural death rate. Further, our model reproduces the
distribution of stabilities of natural proteins in excellent agreement with
experiment. Our model predicts that species with high mutation rates, tend to
have less stable proteins compared to species with low mutation rate
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