Research 

Increasing cell displacement, stress and strain with time as focal adhesions and ventral stress fibres form.

Cells adhere to, and communicate with, their extra-cellular environment (the ECM) by forming focal adhesion complexes. These adhesions mature in tandem with the development of cell cytoskeleton (particularly ventral actomyosin stress fibres in non-motile cells) through intracellular signaling, with signaling cascades also linked to changes in cell function (e.g. proliferating, differentiating, becoming motile). The main focus of my PhD has been on the formulation of a one-dimensional bio-chemo-mechanical continuum model to describe the coupled formation and maturation of ventral stress fibres and cell-substrate (focal) adhesions in non-motile cells in vitro. We consider the intracellular dynamics of various important cytoskeletal, adhesive and signaling proteins (e.g. actin, myosin II, integrins, Rho-kinase etc.) and couple the evolution of each of these to a Kelvin-Voigt viscoelastic description for the cell cytoplasm and for the extra-cellular matrix (ECM). The resultant model has been successfully employed to understand how cells respond to external and intracellular cues in vitro and has been able to replicate various experimentally observed phenomena including demonstrating that stress fibres exhibit non-uniform striation and that cells form weaker stress fibres and focal adhesions on compliant surfaces. The model hence provides a platform for systematic investigation into how cell biochemistry and mechanics influences the growth and development of the cell (and its cytoskeleton) and facilitates prediction of internal cell measurements that are difficult to ascertain experimentally (e.g. stress distribution).

Submitted: G. R. McNicol, M. J. Dalby and P. S. Stewart, A theoretical model for focal adhesion and cytoskeleton development in non-motile cells (available upon request).

When viscous fluid is driven sufficiently rapidly through a flexible-walled tube or channel, self-excited oscillations can arise (which manifest themselves as oscillations in the flexible wall). The oscillations have several physiological applications, including Korotkoff sound generation in sphygmomanometry and in flow past the vocal cords. We develop a model for laminar high-Reynolds-number flow through a long finite-length planar channel, where a segment of one wall is replaced by a membrane of finite mass that is held under longitudinal tension.  Through a combination of numerical and analytical techniques we have been able to characterise the critical conditions required for the onset of these oscillations, have demonstrated that the presence of wall mass leads to a fundamental change in instability mechanism when compared to a wall with no mass and that non-normal interactions between different modes of instability can lead to substantial transient growth of kinetic energy (which increases with wall mass).

IN PREPARATION: G. R. McNicol and P. S. Stewart, Non-modal growth in a finite length collapsible channel flow with a heavy wall (available upon request).

Wetlands...