Past Mathematical Biology and Ecology Seminar

16 February 2018
15:00
Abstract

A wide range of chronic degenerative diseases of mankind result from the accumulation of altered forms of self proteins, resulting in cell toxicity, tissue destruction and chronic inflammatory processes in which the body’s immune system contributes to further cell death and loss of function. A hallmark of these conditions, which include major disease burdens such as Alzheimer’s Disease and type II diabetes, is the formation of long fibrillar polymers that are deposited in expanding tangled masses called plaques. Recently, similarities between these pathological accumulations and physiological mechanisms for organising intracellular space have been recognised, and formal demonstrations that amyloid accumulations form hydrogels have confirmed this link. We are interested in the pathological consequences of amyloid hydrogel formation and in order to study these processes we combine modelling of the assembly process with biophysical measurement of gelation and its cellular consequences.

Please see https://www.eventbrite.co.uk/e/qbiox-colloquium-dunn-school-seminar-hila...

for further details

  • Mathematical Biology and Ecology Seminar
16 February 2018
14:45
Abstract

T cells stimulation by antigen (peptide-MHC, pMHC) initiates adaptive immunity, a major factor contributing to vertebrate fitness. The T cell antigen receptor (TCR) present on the surface of T cells is the critical sensor for the recognition of and response to “foreign" entities, including microbial pathogens and transformed cells. Much is known about the complex molecular machine physically connected to the TCR to initiate, propagate and regulate signals required for cellular activation. However, we largely ignore the physical distribution, dynamics and reaction energetics of this machine before and after TCR binding to pMHC. I will illustrate a few basic notions of TCR signalling and potent quantitative in-cell approaches used to interpret TCR signalling behaviour. I will provide two examples where mathematical formalisation will be welcome to better understand the TCR signalling process.

 

Please see https://www.eventbrite.co.uk/e/qbiox-colloquium-dunn-school-seminar-hila... for further details.

  • Mathematical Biology and Ecology Seminar
16 February 2018
14:00
Abstract

Bacteria swim by rotating semi-rigid helical flagellar filaments, using an ion driven rotary motor embedded in the membrane. Bacteria are too small to sense a spatial gradient and therefore sense changes in time, and use the signals to bias their direction changing pattern to bias overall swimming towards a favourable environment. I will discuss how interdisciplinary research has helped us understand both the mechanism of motor function and its control by chemosensory signals.

Please see https://www.eventbrite.co.uk/e/qbiox-colloquium-dunn-school-seminar-hila...

for details.

  • Mathematical Biology and Ecology Seminar
2 February 2018
14:00
Abstract

The ability of cells to sense and respond to the mechanical properties of their environments is fundamental to cellular behaviour, with stiffness found to be a key control parameter. The physical mechanisms underpinning mechanosensing are, however, not well understood. I here consider the key physical cellular behaviours of active contractility of the internal cytoskeleton and cell growth, coupling these into mechanical models. These models suggest new distinct mechanisms of mechanotransduction in cells and tissues.

  • Mathematical Biology and Ecology Seminar
26 January 2018
14:00
Abstract

I will discuss a new theoretical approach to information and decisions in signalling systems and relate this to new experimental results about the NF-kappaB signalling system. NF-kappaB is an exemplar system that controls inflammation and in different contexts has varying effects on cell death and cell division. It is commonly claimed that it is information processing hub, taking in signals about the infection and stress status of the tissue environment and as a consequence of the oscillations, transmitting higher amounts of information to the hundreds of genes it controls. My aim is to develop a conceptual and mathematical framework to enable a rigorous quantifiable discussion of information in this context in order to follow Francis Crick's counsel that it is better in biology to follow the flow of information than those of matter or energy. In my approach the value of the information in the signalling system is defined by how well it can be used to make the "correct decisions" when those "decisions" are made by molecular networks. As part of this I will introduce a new mathematical method for the analysis and simulation of large stochastic non-linear oscillating systems. This allows an analytic analysis of the stochastic relationship between input and response and shows that for tightly-coupled systems like those based on current models for signalling systems, clocks, and the cell cycle this relationship is highly constrained and non-generic.

  • Mathematical Biology and Ecology Seminar
24 November 2017
14:00
Professor Julia Gog
Abstract

This will be a whistle-stop tour of a few topics on infectious disease modelling, mainly influenza. Topics to include:

  • challenges in capturing dynamics of pathogens with multiple co-circulating strains
  • untangling the 2009 influenza pandemic from medical insurance claims data from the US
  • bioinformatic methods to detect viral packaging signals
  • and a big science project (top secret until the talk!)

Julia will be visiting the Mathematical Institute on sabbatical this term, and hopes this talk will help us find areas of overlapping interests.

  • Mathematical Biology and Ecology Seminar

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