{'fraction_non_alphanumeric': 0.017570093457943924, 'fraction_numerical': 0.001869158878504673, 'mean_word_length': 5.706766917293233, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
A novel fluid-solid-growth-transport framework for modelling the evolution of arterial disease: application to aneurysms

Arterial diseases affect more than 1 in 20 adults in the world. However, our current knowledge in the mechanisms of arterial disease formation and progression is incomplete and this creates enormous limitations to clinical diagnosis and treatment. The urgent need for a better understanding of arterial pathophysiology motivates different modelling approaches to explore the underlying mechanisms. This thesis focuses on the development of an in silico model which represents the mechanical arterial environment, the transport of chemical species, the biology of arterial wall, and the interaction between them. The concept of chemo-mechano-biology is crucial in this research: mechanical forces and chemical levels of the artery can trigger the cell signalling which in turn affect the biological behaviour of the arterial tissues, in both healthy and diseased states. We present a novel fluid-solid-growth-transport (FSGT) computational framework for modelling arterial disease evolution: it identifies and quantifies the influence of the arterial mechanical and chemical environments on the growth and remodelling (G&R) of vascular constituents, elastin and collagen. 
 
For the development of the proposed computational framework, a conceptual thick-walled fibre-reinforced tube model is firstly introduced to represent a healthy vascular structure, in which the physiological stress distribution is determined by the inclusion of residual stress. Numerical analysis of arterial mechanical response is validated with analytical solutions. The oxygen concentration within the arterial wall is simulated by a diffusion-only analysis, and the oxygen level is altered due to the propagation of thrombus layer. To apply the G&R method in this conceptual model, a prescribed elastin degradation causes the radial enlargement and initiates subsequent collagen adaptation due to the altered mechanical and chemical environments. This workflow is then applied to a 2D axisymmetric fusiform model to demonstrate the spatial variation modelling behaviour of this computational framework. 
Lastly, a sophisticated FSGT framework is applied to a 3D patient-specific aneurysm geometry. Results from this in silico framework can provide insights into the underlying mechanisms of aneurysm evolution with the quantification of mechanical and chemical stimuli. Additionally, this simulation workflow is fully integrated into ANSYS engineering software which would allow its clinical translation by global healthcare technology industries for maximum clinical impact.