I completed my PhD and MRes as part of the CoMPLEX program at UCL - a centre for interdisciplinary work at the interface of mathematics, computing, and the life sciences. My work was funded by the British Heart Foundation.
During my PhD, first of all I created a mathematical model of interactions between cells, oxygen and Vascular Endothelial Growth Factor (VEGF) within engineered tissue. I parameterised the model using in vitro data collected by experimental collaborators at UCL.
Secondly, I used the parameterised model to make predictions about how cells should be seeded within engineered tissue in order to increase cell survival and nerve regeneration after injury. It turns out that using a greater number of cells may not always result in better outcomes…
Finally, I created a stochastic model of blood vessel growth in response to VEGF gradients over time, to make further predictions about how cell seeding strategies could impact the direction and rate of vascular growth into engineered tissue.
During my MRes year I completed several shorter research projects:
A study of the relationship between ectopic beat frequency and heart rate variability in ARVC patients
- I created an algorithm to detect ectopic heartbeats from ECG data.
- I then used looked for correlations between heart rate variability parameters, which reflect sympathetic and parasympathetic modulation of the heart rate, and ectopic beat frequency in ARVC patients.
Predicting the rupture risk of brain aneurysms using computational approaches: a HemeLB validation study
- I helped to investigate the impact of different factors on cerebral blood flow simulation results, through the use of patient specific data and the simulation environment HemeLB.
- Simulations were run using the national supercomputer ARCHER. The work helped to identify sources of error, which could have implications for the clinical use of such simulations to quantify the risk of brain aneurysm rupture.
Modelling the impact of vessel stiffening upon arteriolar networks
- I created a mathematical model to investigate the mechanisms behind microvascular rarefaction (reduced microvascular network density).