EAS prizes for young scientists in atherosclerosis research are awarded to Dr. Stefano Romeo and Dr. Giuseppe Daniel Norata. These annual EAS Prizes are awarded to Young Scientists for distinction in published work contributing to the advancement of knowledge in the field of atherosclerosis and linked metabolic disturbances.
The awards will be presented during the 78th EAS Congress in Hamburg, in a special ceremony to take place on Monday, June 21st, 2010 at 17:30; the recipients will deliver a short presentation on their work.
The 2008-2009 prizes are awarded to:
Dr Stefano Romeo at the Institute of Metabolic Science, University of Cambridge, Cambridge, UK
Publication: Romeo S, Yin W, Kozlitina J, Pennacchio LA, Boerwinkle E, Hobbs HH, Cohen JC (2009). Rare loss-of-function mutations in ANGPTL family members contribute to plasma triglyceride levels in humans. J. Clin. Invest.,Jan; 119(1):70-9. Award statement: The analyses carried out by Dr. Romeo are important for two reasons: a) they identify an important pathogenic mechanism modulating circulating triglycerides levels and b) they provide evidence that research strategies focused on resequencing of individuals at the extremes of a complex trait has the potential
to identify common and rare genetic relevant variants. The study highlights the importance of analyzing candidate genes at extremes of complex traits to identify causal variants and, ultimately, potential targets for new drug discovery.
Dr. Giuseppe Danilo Norata at the Department of Pharmacological Sciences, University of Milan, Milan, Italy
Publication: Norata GD, Marchesi P, Pulakazhi Venu VK, Pasqualini F, Anselmo A, Moalli F, Pizzitola
I, Garlanda C, Mantovani A, Catapano AL (2009). Deficiency of the long pentraxin PTX3 promotes vascular inflammation and atherosclerosis. Circulation, 120:699-708.
Award statement: This paper elegantly presents studies into double transgenic mice lacking PTX3 and APO E knock and investigates the atherogenic process. PTX3 deficiency is associated with increased atherosclerosis, increased macrophage accumulation, and inflammation in the atherosclerotic lesions. These results, integrated with the available evidence on the role of PTX3 as cardiovascular biomarker and as atheroprotective agent, raise the possibility that the increased levels of PTX3 in subjects with cardiovascular disease may reflect a protective physiological response that correlates with the severity of the disease.