Abstract: Failure of peripheral endovascular interventions occurs at the intersec-tion of vascular biology, biomechanics, and clinical decision making. It is our hypothesis that most of the endovascular treatments share the same driving mech-anisms during post-surgical follow-up, and accordingly, a deep understanding of them is mandatory in order to improve the current surgical outcome. This work presents a versatile model of vascular adaptation post vein graft bypass intervention to treat arterial occlusions. The goal is to improve the computational models developed so far by effec-tively modeling the cell-cell and cell-membrane interactions that are recognized to be pivotal elements for the re-organization of the graft’s structure. A numerical method is here designed to combine the best features of an Agent-Based Model and a Partial Differential Equations model in order to get as close as possible to the physiological reality while keeping the implementation both simple and general.

Abstract: Influenza as an emerging infectious diseases poses a formidable challenge to global health due to lack of effective antivirals and continued drug resistance. Traditional antiviral drug-discovery targeting viral surface proteins is susceptible to drug resistance due to selective pressure driven by high antigenic mutation rates. Influenza virus is a host-obligate parasite that activates numerous signaling, regulatory and metabolic pathways at both molecular and cellular levels as the host attempts to fight the infection and the virus challenges to survive but also replicate in a highly efficient manner. In an effort to understand the complex interplay, we developed a comprehensive model of the influenza virus interacting with the host epithelial cell. Commonly activated host signaling pathways such as Protein Kinase C (PKC), Mitogen-activated Protein Kinase (MAPK), and PI3K/AKT were modeled in detail, enabling in silico simulations to determine their effects on viral internalization and replication. Perturbation analysis of the virus-host interactome revealed several previously unknown host targets. Our multiscale model of virus-host interactions has the potential to enable the development of more sophisticated, and potentially more efficient drugs.

Abstract: In this work I reflect on the development of a multiscale simulation approach for forced migration, and present two prototypes which extend the existing Flee agent-based modelling code. These include one extension for parallelizing Flee and one for multiscale coupling. I provide an overview of both extensions and present performance and scalability results of these implementations in a desktop environment.