M
Michael A. Matthay
Researcher at University of California, San Francisco
Publications - 1063
Citations - 110857
Michael A. Matthay is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Lung injury & Lung. The author has an hindex of 151, co-authored 998 publications receiving 98687 citations. Previous affiliations of Michael A. Matthay include University of California & Cardiovascular Institute of the South.
Papers
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Journal ArticleDOI
The Acute Respiratory Distress Syndrome: Pathogenesis and Treatment
TL;DR: There is no effective pharmacologic therapy, although cell-based therapy and other therapies currently being tested in clinical trials may provide novel treatments for ARDS.
Journal ArticleDOI
Alveolar Fluid Clearance Is Impaired in the Majority of Patients with Acute Lung Injury and the Acute Respiratory Distress Syndrome
TL;DR: In contrast to hydrostatic pulmonary edema, alveolar fluid clearance in patients with acute lung injury and the acute respiratory distress syndrome is impaired in the majority of patients, and maximal alveolars fluid clearance is associated with better clinical outcomes.
Journal ArticleDOI
Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway?
Karim Brohi,Mitchell J. Cohen,Michael T. Ganter,Michael A. Matthay,Robert C. Mackersie,Jean-Francois Pittet +5 more
TL;DR: Early traumatic coagulopathy occurs only in the presence of tissue hypoperfusion and appears to occur without significant consumption of coagulation factors, which is consistent with activated protein C activation and systemic anticoagulation.
Journal ArticleDOI
Interleukin 4, but not interleukin 5 or eosinophils, is required in a murine model of acute airway hyperreactivity.
David B. Corry,Hans G. Folkesson,Martha L. Warnock,David J. Erle,Michael A. Matthay,Jeanine P. Wiener-Kronish,Richard M. Locksley +6 more
TL;DR: These data implicate IL-4 generated during the period of lymphocyte priming with antigen in establishing the cascade of responses required to generate airway hyperractivity to inhaled antigen and suggest a role for IL-5 or eosinophils.
Journal ArticleDOI
Pulmonary dead-space fraction as a risk factor for death in the acute respiratory distress syndrome.
Thomas J. Nuckton,James A Alonso,Richard H Kallet,Brian M. Daniel,Jean-Francois Pittet,Mark D. Eisner,Michael A. Matthay +6 more
TL;DR: Increased dead-space fraction is a feature of the early phase of the acute respiratory distress syndrome and Elevated values are associated with an increased risk of death.