Personal Statement
David gained a B.Sc. (Hons) in Pharmacology from the University of Leeds (1986) and a cardiovascular-based PhD in Pharmacology at the University of Bath (1990), with industrial placement at Pfizer. He then became Research Associate at the University of Manchester, investigating ion channel electrophysiology in association with SmithKline Beecham (1991-1993). David then worked in Brazil (1993-2002) at several academic institutions including the State University of Rio de Janeiro (Visiting Professor) and the State and Federal Universities of Ceara (Associate Professor, Director of International Affairs) and has since maintained collaborative research links with Brazil.

In 2002 he joined the University of Liverpool (Department of Physiology), investigating mechanisms of acute pancreatitis, with focus on calcium signalling and mitochondrial dysfunction and is currently Senior Lecturer in the Department of Molecular and Clinical Cancer Medicine. David is a Fellow of the British Pharmacological Society, has served on the Executive Committee of the Pancreatic Society of GB&I, as a Councillor of the European Pancreatic Club, is a Faculty member of the Faculty of 1000 (Gastrointestinal Physiology) and a contributor to the Pancreapedia Knowledge Base.

Research Overview
Research is focussed on the elucidation of critical mechanisms that underlie pathophysiological changes in disease, with particular emphasis on cellular injury in acute pancreatitis. Excess alcohol consumption and hypertriglyceridaemia are important triggers of clinical acute pancreatitis. Our studies have demonstrated how alcohol and fatty acids, via non-oxidative metabolism, disrupt calcium signalling leading to mitochondrial dysfunction and cellular toxicity. Central to damage caused by precipitants of acute pancreatitis is formation of the calcium and oxidative stress-dependent mitochondrial permeability transition pore; impaired mitochondrial bioenergetics and rundown of cellular ATP determine cell fate patterns. Mechanisms of organellar dysfunction and cell death are currently being investigated using multiple approaches, including confocal microscopy and Seahorse bioenergetics analysis. Novel approaches to protect mitochondria and prevent cell damage are being assessed, including mitochondrial-targeted MPTP inhibitors and antioxidant compounds. Collaborative studies with colleagues at the Federal University of Ceara, Brazil are directed towards elucidation of mechanisms that underpin acute and chronic pancreatitis, including associated visceral pain and lung injury, and the evaluation of natural products as novel therapeutic options.