Patel, Vinood - University of Westminster - Department of Biomedical Sciences

个人简介

1997 PhD - King's College London, London 1992 BSc Pharmacology (Hons) - University of Portsmouth After completing his PhD Vinood continued his research experience by undertaking his post-doctoral studies in the laboratory of Professor Cunningham in the Department of Biochemistry at Wake Forest University School of Medicine, (Winston-Salem, NC, USA). This extensive project involved investigating mechanisms of hepatic mitochondrial ribosome dysfunction in alcoholic liver disease (ALD) using biophysical and proteomic techniques. These studies have led to new avenues in determining the pathology of ALD. His teaching areas at both post-graduate and undergraduate levels include clinical biochemistry, investigative pathology and laboratory investigation. AWARDS AND GRANTS 2006 Awarded UoW PhD research scholarship. 2007 Awarded UoW Cavendish PhD scholarship. 2007 Wellcome Student Scholarship and Nuffield Foundation Scholarship 1997-2003 Supported by National Institute on Alcohol Abuse and Alcoholism (NIAAA). 2013 Saudi Arabian Government PhD scholarship

研究领域

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Alcoholic liver disease is the most prevalent liver disease in the Western world and the leading cause of liver cirrhosis. The prognosis for both severe alcoholic hepatitis and cirrhosis is poor with a death rate of up to 50%. Therefore it is important to understand the early events/key changes arising in the pathogenesis of ALD. The precise mechanisms responsible for ALD are poorly understood, however a number of key events are clearly involved, which we are studying. These include altered mitochondrial function, oxidative stress, acetaldehyde toxicity and nutritional deprivation/abnormal antioxidant regulation. One area related to the above alterations involves understanding the consequences of oxidative stress. Continued alcohol metabolism results in an alteration to the cellular redox state, due to an increase in the reducing equivalent NADH. This imbalance has an immediate effect on corresponding metabolic pathways, such as the TCA cycle and fatty acid metabolism. However, the high levels of NADH are also utilised in the oxidative phosphorylation system, causing increased flux of electron transport, which results in leakage of reactive oxygen species (ROS). Some of the consequences of ROS tissue injury have been determined, such as lipid peroxidation however, ROS involvement in cell death, particularly apoptotic cell death remains to be elucidated. Increased cell death, whether by necrosis or apoptosis is thought to be a prominent factor in the development of ALD.