Posts by Benjamin David Medoff, MD
Research Reveals Novel Molecular Mechanisms Specific to Allergic Asthma
Researchers at Massachusetts General Hospital combine advanced techniques to identify novel pathways and cell interactions associated with allergic asthma.
Aurora Kinase A Inhibitors May Have Therapeutic Value for Idiopathic Pulmonary Fibrosis
Yang Yang, PhD, Benjamin D. Medoff, MD, and colleagues devised a small-molecule screen to identify agents with antifibrotic activity and found an inhibitor of aurora kinase A significantly reduced profibrotic gene expression in human lung fibroblasts, suggesting such agents might treat idiopathic pulmonary fibrosis.
New Target Identified for Treatment of Pulmonary Fibrosis
Rachel S. Knipe, MD, Benjamin D. Medoff, MD, and colleagues have shown in an animal model that an endothelial cell surface receptor, S1PR1, modulates the fibrotic response to lung injury. Agonism of its expression or function may be a novel and effective antifibrotic approach.
Plasma sST2 Provides Prognostic Information in COVID-19 Respiratory Failure
Jehan W. Alladina, MD, and Benjamin D. Medoff, MD, of the Division of Pulmonary and Critical Care Medicine, and colleagues advise that high plasma concentrations of soluble suppression of tumorigenicity-2 may signify persistent lung injury in COVID-19 respiratory failure and the need for continued ventilatory support.
Medical Grand Rounds: Pathogenesis and Management of Respiratory Failure in COVID-19: What We Know So Far
On March 26, 2020, the Department of Medicine held its third virtual Grand Rounds presentation related to COVID-19. Benjamin Medoff, MD, chief of Pulmonary and Critical Care at Massachusetts General Hospital, along with other members of the Greater Boston medical community, presented on respiratory failure in COVID-19, including management, treatment in clinical trials and the need for biomarkers.
The Medoff Laboratory at Massachusetts General Hospital studies the pathogenesis of pulmonary inflammation, specifically the role of T cells in mediating inflammatory lung diseases. Using genetically modified mice in various models of lung disease, as well as translational studies in humans with various lung diseases, we study mechanisms of T cell activation and function in the context of these disorders. As a result of this work, we hope to delineate some of the molecular mechanisms involved in the development of lung inflammation. In addition, we hope to reveal novel aspects of lung immune biology and potential therapeutic targets for these disorders.