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Simon P. Hart

Researcher at Hull York Medical School

Publications -  176
Citations -  4771

Simon P. Hart is an academic researcher from Hull York Medical School. The author has contributed to research in topics: Idiopathic pulmonary fibrosis & Phagocytosis. The author has an hindex of 35, co-authored 165 publications receiving 3740 citations. Previous affiliations of Simon P. Hart include Borders General Hospital & Hull and East Yorkshire Hospitals NHS Trust.

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How variation between individuals affects species coexistence

TL;DR: This work incorporates intraspecific variation into a common model of competition and identifies three pathways by which this variation affects coexistence: changes in competitive dynamics because of nonlinear averaging, changes in species' mean interaction strengths because of variation in underlying traits, and effects on stochastic demography.
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Genetic variants associated with susceptibility to idiopathic pulmonary fibrosis in people of European ancestry: a genome-wide association study

TL;DR: The identification of AKAP13 as a susceptibility gene for IPF increases the prospect of successfully targeting RhoA pathway inhibitors in patients with IPF.
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Genome-Wide Association Study of Susceptibility to Idiopathic Pulmonary Fibrosis.

Richard J. Allen, +77 more
TL;DR: The observation that decreased DEPTOR expression associates with increased susceptibility to IPF supports recent studies demonstrating the importance of mTOR signaling in lung fibrosis, and new signals of association implicating KIF15 and MAD1L1 suggest a possible role of mitotic spindle-assembly genes in IPF susceptibility.
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Outcome of Hospitalization for COVID-19 in Patients with Interstitial Lung Disease: An International Multicenter Study

Thomas M Drake, +77 more
TL;DR: Patients with ILD are at increased risk of death from COVID-19, particularly those with poor lung function and obesity, and Stringent precautions should be taken to avoid CO VID-19 in patients with I LD.
Journal Article

CD44 regulates phagocytosis of apoptotic neutrophil granulocytes, but not apoptotic lymphocytes, by human macrophages.

TL;DR: It is demonstrated that phagocytosis of apoptotic neutrophils, but not apoptotic lymphocytes, by human monocyte-derived macrophages is augmented rapidly following ligation of CD44 by bivalent Abs in vitro, suggesting a novel role for CD44 in inflammation and tissue repair.