David O’Regan
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I graduated from Southampton University in 1985. I embarked upon a surgical career as an SHO in Bath. I became a fellow of the Royal College of Surgeons in Edinburgh (RCSEd) in 1990. I started my out training as a general surgeon on the numbered training program in Oxford. I was encouraged to do Cardiac Surgery by Professor Stephen Westaby and Mr Ravi Pillai. After eighteen months I was appointed to the Royal Brompton Hospital rotation. I have had the privilege of working for Professor Sir Magdi Yacoub. I passed the intercollegiate exam in 1999. I have been a practicing Consultant Cardiac Surgeon since 2001 and have now done over three thousand adult cardiac cases.
I was awarded an Executive MBA with distinction in 2005 as a result of applying a system change to my practice.
I graduated from the Institute of Health Care Executive Patient Safety Officer Program in 2008 and the Nae Bevan Program in 2015 with a NHS Leadership Award in Executive Health Care Leadership.
I was president of the Association of Surgeons in Training (ASiT) in 1999/2000. I established and continue to run the Silver Scalpel Award to identify the best surgical trainer of the land. I have received from ASiT a Silver Medal for outstanding contribution. I am an enthusiastic surgical trainer and I was appointed deputy Director of the Faculty of Surgical Trainers of the RCSEd.in 2016.
Editorial by MedAll Research interests
David has long been interested in the response of the blood vessels to injury and the influence clotting and inflammation play in the ensuing proliferation and migration of vascular smooth muscle cells (VSMC) that may explain the reocclusion of vessels after percutaneous intervention. He proposed that an alternative physiological anticoagulant system, the product of which, activated protein C (aPC) could modulate the responses.
His research towards a Doctor of Medicine, awarded by Imperial College, London, in 2000, found a controllable level of anti-coagulation can be achieved if aPC when combined with low molecular weight heparin (LMWH). It bound to specific to sites on cultured human and rat vascular smooth muscle cells (VSMC) with properties similar to those described for the endothelial protein C receptor (EPCR). However, unlike the aPC/EPCR complex, the anticoagulant activity of aPC when bound to VSMC is maintained.
Furthermore, he also observed that the addition of aPC to VSMC enhances the activity of a number of mitogens. The expression of the putative receptor on VSMC may serve to protect the blood vessel from thrombosis and modulate the response and survival of cells following acute or chronic endothelial injury. This was presented in a plenary session at the International Society of Thrombosis and Haemostasis and led to a British Heart Foundation Grant.
David now works with a renowned Vascular Biology group at the University of Leeds. The research group have described molecular changes in blood vessels peculiar to patients with diabetes. The molecular mechanisms are being investigated and have been published
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