Phase transitions in neurodegenerative disease

Mechanism of Shiga toxin entry into cells

The plasma membrane of cells protects the interior from the environment while permitting signals to be transduced across it and allowing material to be taken in or expelled in a controlled way. Bacteria and viruses have evolved to co-opt signalling and endocytic pathways to invade a cell in order to propagate themselves. Some of these pathways are independent of the cellular endocytic machinery, an example being that used by Ricin, Shiga and Shiga-like bacterial toxins.
 
 Shiga toxin invasion begins when toxin particles in the bulk solution adsorb to the plasma membrane by binding to globotriaosylceramide glyoclipids (Gb3) lipids. They subsequently diffuse around and form clusters. This clustering process takes place over distances much larger than the particle size, and in the absence of direct protein-protein attractive forces. We have used atomistic and mesoscopic simulations to characterise the toxin

Accelerating Coarse-Grained Molecular Simulations

I have developed and maintain a parallel Dissipative Particle Dynamics (DPD) code to perform complex fluid simulations on length and time scales far beyond those attainable with Molecular Dynamics simulations. The code is used under license from the Max Planck Institute, where part of it was developed. It uses the common Message Passing Interface protocol, and its execution shows excellent weak scaling up to 2000 processors. The code has been used in more than a dozen publications, and is in current use at several universities and research institutes. 
 
 I am working with Imperial College London and the University of Southampton to implement the code on a novel computing platform called POETS - Partially-Oriented Event Triggered Systems (www.poets-project.org) which has the potential to speed up DPD simulations by several orders of magnitude. POETS is funded by the UK