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Dr Simon Hart
Simon Hart
Reader in Respiratory Medicine
Biography | Graduated from Edinburgh University and trained in respiratory and general medicine in south-east Scotland. PhD in neutrophil and macrophage biology in the MRC Centre for Inflammation Research, followed by an MRC Clinician Scientist fellowship. Lead clinician for the Hull interstitial lung disease and Sarcoidosis services. Participates in the acute general medicine rota at Hull Royal Infirmary. Research interests include the biology of pulmonary fibrosis, interstitial lung diseases, and sarcoidosis. |
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Research Interests | Pulmonary fibrosis Pulmonary fibrosis is a progressive incurable scarring disease of the lungs that affects about 30,000 people in the UK. Development of effective therapies will depend on understanding the biology of lung scarring. Platelet biology and lung fibrosis We have shown that platelets are hyper-active in patients with idiopathic pulmonary fibrosis (IPF). Platelets contain granules rich in growth factors, with the potential to drive fibrosis when platelets are retained and activated in the lungs. We are studying how platelets contribute to pulmonary fibrosis. Steroids and pulmonary fibrosis The PANTHER-IPF clinical trial showed for the first time that steroid-containing treatment regimens unfortunately led to worse outcomes for people with IPF. We wish to harness this unique observation to better understand the roles of corticosteroids in the biology of pulmonary fibrosis. Molecular imaging of the lungs We are developing novel imaging techniques in pulmonary fibrosis, both in the lab (in collaboration with Hull University PET imaging centre) and in the clinic. Symptoms and quality of life We have an ongoing research program into assessing and treating difficult symptoms in pulmonary fibrosis in conjunction with colleagues in palliative medicine at Hull York Medical School. Sarcoidosis About 4,500 people in the UK are diagnosed each year with sarcoidosis, a chronic inflammatory disease that affects the lungs, lymph nodes, eyes, and skin, and sometimes the bones, heart and nervous system. Disabling symptoms such as breathlessness and fatigue lead to impaired quality of life, and loss of work and income, and some patients suffer considerable morbidity and premature death. Pathologically, affected tissues are infiltrated by granulomas composed of macrophages and other immune cells. Current treatments such as steroids temporarily suppress the inflammatory response, but side effects can be personally distressing, disfiguring, and dangerous. Thus, it is important to understand the cellular and molecular drivers of persistent and progressive disease so that patients with sarcoidosis have treatment options that improve or control their disease without causing undesirable side effects. The monocyte/macrophage in sarcoidosis Recent evidence has highlighted key roles for tissue macrophages and their precursors, blood monocytes, in driving sarcoidosis pathology. We are studying immune responses in the blood and lung tissue of patients with sarcoidosis to help understand how the disease is initiated and perpetuated. We are particularly interested in how abnormal function of regulatory (inhibitory) receptors on blood monocytes leads to an overactive immune response in sarcoidosis. Thanks to our funders: SarcoidosisUK British Lung Foundation Sir Jules Thorn Charitable Trust Foundation for Sarcoidosis Research Boehringer Ingelheim Chiesi |
Teaching and Learning | Deputy Academic Program Training Director, North & East Yorkshire and North Lincolnshire Year 3 clinical tutor, respiratory medicine Year 2 respiratory resource session lead Years 1 and 2 lecturer SSIP supervisor and abstract reviewer Hull York Medical School taster sessions for school leavers Host international elective students at Hull York Medical School Host work experience students considering applying for Medicine Former co-lead for academic foundation program at Hull York Medical School Former chair, Hull York Medical School Academic Progress Committee |
Scopus Author ID | 54905889200 |