b.6 November 1915 d.27 October 2002
BA Oxon(1937) MRCS LRCP(1940) BM BCh(1940) MA(1947) DM(1950) FRCPath(1964) MRCP(1970) FRCP(1975)
Despite the fact that John O'Brien, known affectionately as 'OB' to his staff, spent his working life principally in district general hospitals he found the time to make a substantial contribution to our understanding of platelet function.
He was born in London and from Westminster school he went to Oxford University to do the preclinical course. He completed his training at St Batholomew's Medical School, London. After house jobs he returned to Oxford, where he obtained a post as assistant pathologist at the Radcliffe Infirmary. Here he trained in haematology with R G Macfarlane [Munk's Roll, Vol. VIII, p.303] and acquired his lifelong interest in the contribution that platelets make to haemostasis and thrombosis. He wrote this DM on the bleeding time, being the only platelet function test then available. Shortly after arriving at Oxford he contracted pulmonary tuberculosis and with typical enthusiasm he produced one of his earliest papers on the effects of that disease on haematological parameters. With Macfarlane and other co-workers he published the first description of Christmas disease (factor IX deficiency), named after the first patient and not the date - 24 December 1952.
From 1945 to 1951 he was a consultant pathologist to the South Devon/East Cornwall Hospital, Plymouth, and from 1951 to 1981 he held a consultant haematology post at St Mary's Hospital in Portsmouth. While performing his busy NHS duties he found time to do work on different aspects of platelet function, ultimately producing 310 scientific papers.
Gaining grants from the Medical Research Council, the British Heart Foundation, the Wellcome Trust and various commercial sources he formed a small team which gave several new graduates, some from overseas, their first taste of research. Together they were amongst the first to study platelet aggregation using interference of light transmission in, the then new tool, the platelet aggregometer. Thus they studied the inhibitory effects of various chemicals on platelet aggregation and, simultaneously with workers elsewhere, published in 1968, the effects of asprin. John was intrigued that the effect of asprin was apparently much greater in vitro than it was in vivo and he returned to this problem later. He researched the effects of many other promising drugs and collaborated with workers at home and abroad in other aspects of haemostasis.
Towards the end of his working life in the NHS he discovered a second form of platelet aggregation which took place in conditions of high shear, as seen in arterial disease. Using a piece of apparatus he had invented he was able to show that this form of aggregation required not only high shear forces but also Von Willebrand's factor antigen and the platelet receptor glycoprotein IIb, IIIa.
When I succeeded him in his consultant post in 1981 he asked if he could carry on in a corner of the laboratory with his assistant for about 18 months. He continued his research for the next 17 years, his last paper being accepted for publication only two years before his death.
He was a member of many national and international learned societies dedicated to haemostasis and thrombosis. He remained an active contributor to their meetings into his seventies and will be missed by a huge number of friends and colleagues all over the world.
John was a sociable man who enjoyed conversation over a good meal accompanied by good wine. His interests included antiques, travel, photography and the English countryside, through which he jogged and only gave up when months before he died he found that young people walking fast were passing him.
(Volume XI, page 428)
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