667 research outputs found
A new model for evolution in a spatial continuum
We investigate a new model for populations evolving in a spatial continuum.
This model can be thought of as a spatial version of the Lambda-Fleming-Viot
process. It explicitly incorporates both small scale reproduction events and
large scale extinction-recolonisation events. The lineages ancestral to a
sample from a population evolving according to this model can be described in
terms of a spatial version of the Lambda-coalescent. Using a technique of
Evans(1997), we prove existence and uniqueness in law for the model. We then
investigate the asymptotic behaviour of the genealogy of a finite number of
individuals sampled uniformly at random (or more generally `far enough apart')
from a two-dimensional torus of side L as L tends to infinity. Under
appropriate conditions (and on a suitable timescale), we can obtain as limiting
genealogical processes a Kingman coalescent, a more general Lambda-coalescent
or a system of coalescing Brownian motions (with a non-local coalescence
mechanism).Comment: 63 pages, version accepted to Electron. J. Proba
Coalescent simulation in continuous space:Algorithms for large neighbourhood size
Many species have an essentially continuous distribution in space, in which there are no natural divisions between randomly mating subpopulations. Yet, the standard approach to modelling these populations is to impose an arbitrary grid of demes, adjusting deme sizes and migration rates in an attempt to capture the important features of the population. Such indirect methods are required because of the failure of the classical models of isolation by distance, which have been shown to have major technical flaws. A recently introduced model of extinction and recolonisation in two dimensions solves these technical problems, and provides a rigorous technical foundation for the study of populations evolving in a spatial continuum. The coalescent process for this model is simply stated, but direct simulation is very inefficient for large neighbourhood sizes. We present efficient and exact algorithms to simulate this coalescent process for arbitrary sample sizes and numbers of loci, and analyse these algorithms in detail
A comparison of CFD and full-scale measurement for analysis of natural ventilation
CFD modelling techniques have been used to simulate the coupled external and internal flow in a cubic building with two dominant openings. CFD predictions of the time-averaged cross ventilation flow rates have been validated against full-scale experimental data under various weather conditions in England. RANS model predictions proved reliable when wind directions were near normal to the vent openings. However, when the fluctuating ventilation rate exceeded the mean flow, RANS models were incapable of predicting the total ventilation rate. Improved results are expected by applying more sophisticated turbulence models, such as LES or weighted quasi-steady approximations
Identifying Changes in the Synaptic Proteome of Cirrhotic Alcoholic Superior Frontal Gyrus
Hepatic complications are a common side-effect of alcoholism. Without the detoxification capabilities of the liver, alcohol misuse induces changes in gene and protein expression throughout the body. A global proteomics approach was used to identify these protein changes in the brain. We utilised human autopsy tissue from the superior frontal gyrus (SFG) of six cirrhotic alcoholics, six alcoholics without comorbid disease, and six non-alcoholic non-cirrhotic controls. Synaptic proteins were isolated and used in two-dimensional differential in-gel electrophoresis coupled with mass spectrometry. Many expression differences were confined to one or other alcoholic sub-group. Cirrhotic alcoholics showed 99 differences in protein expression levels from controls, of which half also differed from non-comorbid alcoholics. This may reflect differences in disease severity between the sub-groups of alcoholics, or differences in patterns of harmful drinking. Alternatively, the protein profiles may result from differences between cirrhotic and non-comorbid alcoholics in subjects’ responses to alcohol misuse. Ten proteins were identified in at least two spots on the 2D gel; they were involved in basal energy metabolism, synaptic vesicle recycling, and chaperoning. These post-translationally modified isoforms were differentially regulated in cirrhotic alcoholics, indicating a level of epigenetic control not previously observed in this disorder
The infinitesimal model with dominance
The classical infinitesimal model is a simple and robust model for the
inheritance of quantitative traits. In this model, a quantitative trait is
expressed as the sum of a genetic and a non-genetic (environmental) component
and the genetic component of offspring traits within a family follows a normal
distribution around the average of the parents' trait values, and has a
variance that is independent of the trait values of the parents. In previous
work, Barton et al.(2017), we showed that when trait values are determined by
the sum of a large number of Mendelian factors, each of small effect, one can
justify the infinitesimal model as limit of Mendelian inheritance.
In this paper, we show that the robustness of the infinitesimal model extends
to include dominance. We define the model in terms of classical quantities of
quantitative genetics, before justifying it as a limit of Mendelian inheritance
as the number, M, of underlying loci tends to infinity. As in the additive
case, the multivariate normal distribution of trait values across the pedigree
can be expressed in terms of variance components in an ancestral population and
identities determined by the pedigree. In this setting, it is natural to
decompose trait values, not just into the additive and dominance components,
but into a component that is shared by all individuals within the family and an
independent `residual' for each offspring, which captures the randomness of
Mendelian inheritance. We show that, even if we condition on parental trait
values, both the shared component and the residuals within each family will be
asymptotically normally distributed as the number of loci tends to infinity,
with an error of order 1/\sqrt{M}.
We illustrate our results with some numerical examples.Comment: 62 pages, 8 figure
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