Mobility experience with a research focus
PhD sandwich; Post Doc
Department of Electrical, Electronic and Information Engineering "Guglielmo Marconi" (DEI)
Project Title: Role of Mavacamten on force generation using electromechanically coupled human atrial model
Brief description: Hypertrophic cardiomyopathy (HCM) is mostly manifested as a disease of the left ventricular, that leaves poor understanding of the pathogenesis of atrial myopathy in HCM. This project includes the characterization of HCM using an in-silico electromechanically coupled human atrial model. The underlying mechanisms by which HCM arrhythmogenic response alters action potential, Ca2+-handling, and the force kinetics at cellular level will be investigated. Based on the HCM model, the project proceeds with the analysis of Mavacamten action on kinetics of force development in human atrial myocytes following the experimental protocol of fast solution switching techniques.
Project Title: In-silico study of stretch-induced arrhythmia susceptibility in human atria
Brief description: The effect of atrial dilation on electrophysiological parameters has been studied with quite controversial results using both experiments and in-silico modelling. This project mainly deals with understanding the mechanisms by which atrial stretch favors the development of substrate for arrhythmia like atrial fibrillation, in particular. The project will deal with various spatial scales of the modelling starting with cellular level and its incorporation into a multicellular 2D tissue patch. Quantification of conduction velocity, effective refractory period, and action potential duration under stretch and its comparison with experimental findings will be part of the project.
Project Title: In Silico Modelling of the Control of Ryanodine Receptors Calcium Release by Cav1.3 Channels in Sinoatrial Node Cells.
Brief description: The sinoatrial node is the primary pacemaker of the heart, determining the heart rate in physiological conditions thanks to its ability to spontaneously fire action potentials. The current understanding sees the interaction between membrane ion channels and intracellular calcium handling as the mechanism originating this phenomenon. However, recent experimental reports have questioned the independence of the so-called “calcium-clock” by showing that Cav1.3 channels block or knock-out prevents calcium release from the sarcoplasmic reticulum. The aim of this project is that of reproducing this finding in a detailed, spatial model of a single sinoatrial node cell to gain further knowledge about the mechanism underlying cardiac pacemaking.
Project Title: Computational investigation of sinus node dysfunction mechanisms: the role of sinoatrial node architecture and electrophysiology.
Brief description: Sinus node dysfunction (SND) is a highly prevalent pathology in the elder population, defined as the inability of the sinoatrial node to meet the heart rate required by the body. Showing usually as bradycardia, among other symptoms, it accounts for about half of the pacemaker implants worldwide. However, despite the burden for both patients and health systems, its causes are still incompletely understood. This project aims at using biophysically detailed tissue models of the sinoatrial node and surrounding atrium to unravel the mechanisms of SND onset and development, by investigating both structural and electrophysiological aspects of atrial driving by the sinoatrial node.
Use of cardiac mathematical models (by software such as Matlab, OpenCARP, CUDA etc). Knowledges about cardiac electrophysiology.
PhD sandwich: 3-12
Post Doc: 3-9