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Year in review 2013: basic science and epidemiology
  1. Paul Cullinan1,
  2. Clare M Lloyd2
  1. 1Department of Occupational and Environmental Medicine, National Heart and Lung Institute, London, UK
  2. 2Leukocyte Biology, NHLI, Imperial College, London, UK
  1. Correspondence to Dr Paul Cullinan, Department of Occupational and Environmental Medicine, National Heart and Lung Institute, Manresa Road, London SW3 6LR, UK; p.cullinan{at}imperial.ac.uk

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In the second of our reviews of 2013 we reveal our prize winners in the fields of basic science and epidemiology. As before, manuscripts arising from Imperial, Leicester and Oxford are disallowed, not because we would like to level the playing field (nice as this would be) but because of editors’ conflict of interest. If you read to the end we reveal our overall winners in the traditional gold, silver and bronze positions.

Basic science

The Basic Science for the Chest Physician section has proved popular with our readers according to our most recent survey. Although many of these pieces are commissioned to accompany particular articles, we also welcome uncommissioned articles and suggestions for potential subjects from readers. So, if there is an area of basic science that you would like to highlight for the respiratory community, please let us know.

Manuscripts within the basic science sphere incorporated those seeking to understand the molecular mechanism underlying lung diseases as well as those aimed at discovering novel biomarkers and preclinical testing of novel therapeutic pathways. We continue to publish models and systems designed to reflect the broad range of lung diseases that are of interest to the readers of Thorax, including chronic obstructive pulmonary disease (COPD), asthma, idiopathic pulmonary fibrosis (IPF) and cystic fibrosis as well as respiratory infections.

Pulmonary inflammation may occur either as a result of excessive activation of inflammatory pathways or a failure in immune regulation. Several studies this year indicated that inflammation during COPD may occur as a general failure of pulmonary immune regulation, leading to reduced regulatory T cell populations but increased proportions of effector Th cells such as those defined by interleukin 17 (IL-17) secretion.1 ,2 Similarly, aberrant epidermal growth factor receptor activity was shown to be behind the decreased expression of FoxO3A—a negative …

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