Personal Statement
As a physiologist and pharmacologist, I'm interested in using bioengineering and imaging techniques to address cardiac biophysical inquiries on the origins and effects of arrhythmias. I graduated with honors from Sheffield Hallam University in 2003 with an MSc in Pharmacology and Biotechnology after earning a first-class undergraduate degree in Biology and Chemistry. After that, I worked as a lab manager and research assistant for Professors Denis Noble and Peter Kohl's Oxford Cardiac Mechano-Electric Feedback Group (Department of Physiology, Anatomy and Genetics, University of Oxford). Still working with the same group, I received funding for my DPhil in Cardiac Physiology (2010) thanks to one of the highly sought-after Oxford Overseas Research Scholarships (ORA Award). I also earned a Merit (2008) MBA while doing this (Oxford Brookes University, Business School). After receiving a Winston Churchill Fellowship in Science and Engineering in January 2015, I had the opportunity to work with Professor Emilia Entcheva's at Stony Brook University, New York. This lead to a Winston Churchill Medal in 2016 for contributions in Science and Engineering. I received a highly competitive Sir Henry Dale fellowship from the Wellcome Trust and Royal Society in December 2015 which allowed me to start my own Research Group in the Department of Pharmacology, University of Oxford. My training and research experience from Sheffield and Oxford, which included basic cardiovascular research at the organ, tissue, and cellular levels as well as translational work looking into the causes of arrhythmias, are built upon by my current and future research plans. In 2020, I was awarded the title of Associate Professor by the Medical Sciences Division, University of Oxford.

One of my main strengths is the proven track record of highly productive collaborations, including in a BBSRC-TDRI project during my DPhil studies, post-doctoral research in EU Project PreDICT, present collaborations with scientists in the US (New York, University of Pennsylvania), Europe (University of Maastricht) and the UK (Imperial College, Kings College London, University of Oxford), New Zealand (University of Auckland) as well as supervision of undergraduate and graduate students who have gone on to work in Industry and the NHS.
The projects I have worked on thus far, involve a cross disciplinary approach encompassing areas of physiology, chemistry, biophysics, molecular biology, pharmacology and computational biology. My graduate research at the University of Oxford with Professors Denis Noble and Peter Kohl [Cardiac Electrophysiology and Cardiac Mechano-Electric Feedback lab], was focussed on developing accurate whole heart, structure-function 3D models of the heart to aide pharmacological assessment of drugs and arrhythmias. An area of research closely aligned with scientists at the University of Auckland and several Universities in the US and Europe. The experimental data from my doctoral work has been used to develop and validate cardiac modelling by researchers internationally and has been extensively published, sited. My post-doctoral research at the University of Oxford with Prof Gil Bub and Prof David Paterson, has involved developing novel technologies to study the cardiac-neural axis and arrhythmias using high speed imaging techniques and proteomics. From 2012, I led a pre-clinical study involving Hydroxychloroquine (HCQ). Our research has shown that HCQ can block the pacemaking “funny current” in cardiac sino-atrial nodal cells, funded externally by Oxford Innovation, UK (highly competitive funding). During this study, I had discussions with major Pharmaceutical Companies (GSK, Astra Zeneca, Sanofi, Novartis etc) and productive conversations with the MHRA and CDRD Canada. Our preclinical study highlights the potential re-use of HCQ for certain cardiac conditions at low doses.

Research Overview
My main research interest lies in understanding the underlying causes of arrhythmias, specifically the role for calcium-dysregulation in atrial fibrillation. Calcium ions regulate processes as diverse as cell motility, gene transcription, muscle contraction, exocytosis and numerous proteins are modulated directly/indirectly by calcium. It is becoming increasingly more apparent that alterations in cardiac calcium regulation may be critical in mechanical dysfunction and arrhythmogenesis. To address these questions, funded by the Wellcome Trust and Royal Society in 2015, I moved to set up my own lab in the Department of Pharmacology, University of Oxford. My lab focused on employing state-of-the-art technologies using an interdisciplinary approach to study single cells to cultured atrial tissue to complex, intact tissue models, using high resolution imaging techniques such as electron microscopy, state of the art tissue engineering in order to specifically control calcium signalling and novel microscopy allowing me to image global and sub-cellular events in at high spatio-temporal resolution, furthering our mechanistic understanding with direct relevance to the development of clinical therapies some of these technologies I have created myself. My Sir Henry Dale Project is a truly interdisciplinary project; as such it relies on the collaboration between global groups in several scientific areas.

On going research:
In March 2024 I joined the Department of Pharmacology and Therapeutics. My current research plans build on my training and research experience over the last 20 years involving basic cardiovascular research at the organ, tissue, cellular-levels and translational work in whole animals and patients investigating the causes of arrhythmogenesis of atrial aetiology as well as diseases where sympathetic perturbations have been reported (specifically hypertension and heart failure). I believe that integration of research across levels, combined with direct and multiple level iteration between experimental, theoretical and computational work, is the key to understanding complex physiological systems and pathologies.
The main cause of mortality and morbidity in atrial fibrillation (AF) is inadequate rate or rhythm control with pharmaceutical methods. Anisotropic cellular and subcellular architecture, electrical state, and shape are some of the elements that are necessary to understand the genesis and maintenance of atrial arrhythmias. Studies have indicated that calcium dysregulation plays a significant part in AF. My research employs a multidisciplinary approach, encompassing advanced tissue engineering, optogenetics, conventional electrophysiology, and the creation of novel high-speed optical imaging tools, to enhance our mechanistic knowledge. The findings will contribute to a deeper comprehension of the fundamental biological processes behind sub-cellular calcium signaling and the aetiology of AF, both of which are important for the creation of novel treatment approaches.
Through my graduate studies, postdoctoral research and teaching (Undergraduate and Post-Graduate Lecturing), I have strived to build a foundation in both basic science and translational research, while also developing the ability to cross traditional boundaries between fields of investigation, so that I may pursue an integrative approach, essential in my future career as a scientist striving to improve clinical therapy.

Papers Under Review:

Lysosomal signalling pathways influence heart rhythm, and regulate atrial function
https://www.biorxiv.org/content/10.1101/2024.06.10.597905v3

Activation of IP3R in atrial cardiomyocytes leads to generation of cytosolic cAMP
https://www.biorxiv.org/content/10.1101/2024.03.28.583721v1

Atrial Granules in Atrial Cardiomyocytes as Acidic Calcium Stores
https://www.biorxiv.org/content/10.1101/2024.11.25.625237v1