Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Congratulations to Mylene Huebecker of the Fran Platt lab and James Bae of the Ming Lei lab who shared last week’s Paton Prize of £250. Mylene’s presentation was entitled ‘Glycosphingolipids relevant to Parkinson’s disease change in normal ageing of the human and mouse brain’ while James spoke about the ‘Development of small molecule PAK1 activators for the treatment of cardiac hypertrophy and ventricular arrhythmias'.

The Paton Prize in the Department of Pharmacology at Oxford is given annually to the leading presentation from year two DPhil students. All second year students are expected to give a presentation of their work to members of the Department.

This year's prize was judged by Professor Chas Bountra from the Nuffield Department of Clinical Medicine, Professor Nicola Sibson of the Department of Oncology and Dr Sri Vasudevan from the Department of Pharmacology

Similar stories

Key cellular channel identified as a brake on lung scarring

Pulmonary fibrosis is a serious and often fatal condition in which lung tissue becomes progressively scarred, stiff, and less able to transfer oxygen into the bloodstream. With limited treatment options and no cure other than lung transplantation, there is an urgent need to understand the biological mechanisms that drive this disease. A new study from the Grimm Group, published in The EMBO Journal, identifies a previously unrecognised protective role for a cellular ion channel called TRPML1 in preventing lung scarring. The research shows that when this channel is absent or non-functional, the lungs develop a fibrosis-like condition marked by excessive accumulation of structural proteins such as collagen and elastin