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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.

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Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome.

TL;DR: In patients with acute lung injury and the acute respiratory distress syndrome, mechanical ventilation with a lower tidal volume than is traditionally used results in decreased mortality and increases the number of days without ventilator use.
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The acute respiratory distress syndrome

TL;DR: An overview of the definitions, clinical features, and epidemiology of the acute respiratory distress syndrome is provided and advances in the areas of pathogenesis, resolution, and treatment are discussed.
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An Expanded Definition of the Adult Respiratory Distress Syndrome

TL;DR: An expanded definition of ARDS is proposed that takes into account new knowledge about adult respiratory distress syndrome and its clinical features, physiologic disturbances, prognosis, and pathologic findings.
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Higher versus Lower Positive End-Expiratory Pressures in Patients with the Acute Respiratory Distress Syndrome

TL;DR: In patients with acute lung injury and ARDS who receive mechanical ventilation with a tidal-volume goal of 6 ml per kilogram of predicted body weight and an end-inspiratory plateau-pressure limit of 30 cm of water, clinical outcomes are similar whether lower or higher PEEP levels are used.
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The integrin alpha v beta 6 binds and activates latent TGF beta 1: a mechanism for regulating pulmonary inflammation and fibrosis.

TL;DR: In this article, Latency-Aged Peptide (LAP) was shown to be a ligand for the integrin alpha v beta 6 and that alpha-v beta 6-expressing cells induce spatially restricted activation of TGF beta 1.