Past Mathematical Biology and Ecology Seminar

5 February 2016

If the abundances of the constituent molecules of a biochemical reaction system  are sufficiently high then their concentrations are typically modelled by a coupled set of ordinary differential equations (ODEs).  If, however, the abundances are low then the standard deterministic models do not provide a good representation of the behaviour of the system and stochastic models are used.  In this talk, I will first introduce both the stochastic and deterministic models.  I will then provide theorems that allow us to determine the qualitative behaviour of the underlying mathematical models from easily checked properties of the associated reaction network.  I will present results pertaining to so-called ``complex-balanced'' models and those satisfying ``absolute concentration robustness'' (ACR).  In particular, I will show how  ACR models, which are stable when modelled deterministically, necessarily undergo an extinction event in the stochastic setting.  I will then characterise the behaviour of these models prior to extinction.

  • Mathematical Biology and Ecology Seminar
4 December 2015

Transmural propagation is a little studied feature of mammalian electrophysiology, this talk reviews our experimental work using different optical techniques to characterise this mode
of conduction under physiological and pathophysiological conditions.

  • Mathematical Biology and Ecology Seminar
27 November 2015

We will discuss how the analysis of a stochastic mean-field model for
synaptic activity can be used to reconstruct some parameters about
neuronal networks.  The method is based on a non-standard analysis of the
Fokker-Planck equation and the asymptotic computation of the spectrum for
the nonself-adjoint operator. Applications concern Up- and Down- states
and bursting activity in neuronal networks.

  • Mathematical Biology and Ecology Seminar
20 November 2015

Simulating the long time and length scales associated with DNA self-assembly
and DNA nanotechnology is not currently feasible with models at an atomic level
of detail. We, therefore, developed oxDNA a coarse-grained representation of
DNA that aims to capture the fundamental structural, thermodynamic and
mechanical properties of double-stranded and single-stranded DNA, which we have
subsequently applied to study a wide variety of DNA biophysical properties and
DNA nanotechnological systems.

  • Mathematical Biology and Ecology Seminar
13 November 2015

Ductal carcinoma is one of the most common cancers among women, and the main cause of death is the formation of metastases. The development of metastases is caused by cancer cells that migrate from the primary tumour site (the mammary duct) through the blood vessels and extravasating they initiate metastasis. In my talk, I present a multi-compartment mathematical model which mimics the dynamics of tumoural cells in the mammary duct, in the circulatory system and in the bone. Using a branching process approach, the model describes the relation between the survival times and the four markers mainly involved in metastatic breast cancer (EPCAM, CD47, CD44 and MET). In particular, the model takes into account the gene expression profile of circulating tumour cells to predict personalised survival probability. Gene expression data of metastatic breast cancer have been used to validate the model. The administration of drugs as bisphosphonates is also included in order to analyse the dynamic changes induced by the therapy.

Stochastic and deterministic processes are merged together to describe cancer progression and obtain personalised survival analysis based on the gene expression levels of each patient. The main aim of the talk is showing that Mathematics can have a strong impact in speeding cancer research, predicting survival probability and selecting the best cancer treatment. 

  • Mathematical Biology and Ecology Seminar
6 November 2015

The first half of the lecture will begin by reviewing what is known about the
neural representation of faces in the primate visual system. How does the
visual system represent the spatial structure of faces, facial identity and
expression? We then discuss how depression is associated with negative
cognitive biases in the recognition of facial expression, whereby depressed
people interpret facial expressions more negatively. The second half of the
lecture presents computer simulations aimed at understanding how these facial
representations may develop through visual experience. We show how neural
representations of expression are linked to particular spatial relationships
between facial features. Building on this, we show how the synaptic connections
in the model may be rewired by visual training to eliminate the negative
cognitive biases seen in depression.

  • Mathematical Biology and Ecology Seminar
30 October 2015

It is well known that stochasticity can play a fundamental role in 
various biochemical processes, such as cell regulatory networks and 
enzyme cascades. Isothermal, well-mixed systems can be adequately 
modeled by Markov processes and, for such systems, methods such as 
Gillespie's algorithm are typically employed. While such schemes are 
easy to implement and are exact, the computational cost of simulating 
such systems can become prohibitive as the frequency of the reaction 
events increases. This has motivated numerous coarse grained schemes, 
where the ``fast'' reactions are approximated either using Langevin 
dynamics or deterministically.  While such approaches provide a good 
approximation for systems where all reactants are present in large 
concentrations,  the approximation breaks down when the fast chemical 
species exist in small concentrations,  giving rise to significant 
errors in the simulation.  This is particularly problematic when using 
such methods to compute statistics of extinction times for chemical 
species, as well as computing observables of cell cycle models.  In this 
talk, we present a hybrid scheme for simulating well-mixed stochastic 
kinetics, using Gillepsie--type dynamics to simulate the network in 
regions of low reactant concentration, and chemical langevin dynamics 
when the concentrations of all species is large.  These two regimes are 
coupled via an intermediate region in which a ``blended'' jump-diffusion 
model is introduced.  Examples of gene regulatory networks involving 
reactions occurring at multiple scales, as well as a cell-cycle model 
are simulated, using the exact and hybrid scheme, and compared, both in 
terms weak error, as well as computational cost.

This is joint work with A. Duncan (Imperial) and R. Erban (Oxford)

  • Mathematical Biology and Ecology Seminar