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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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Trauma-associated lung injury differs clinically and biologically from acute lung injury due to other clinical disorders.

TL;DR: Patients with trauma-associated lung injury are less acutely and chronically ill than other lung injury patients; however, these baseline clinical differences do not adequately explain their improved outcomes and may be explained by less severe lung epithelial and endothelial injury.
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Severe Sepsis--A New Treatment With Both Anticoagulant and Antiinflammatory Properties

TL;DR: In the last half of the 20th century, the use of antibiotics for the treatment of bacterial infections transformed the practice of medicine, resulting in sharp reductions in morbidity and mortality.
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Plasma Angiopoietin-2 Predicts the Onset of Acute Lung Injury in Critically Ill Patients

TL;DR: Plasma biomarkers such as Ang-2 can improve clinical prediction scores and identify patients at high risk for ALI and emphasize the importance of endothelial injury in the early pathogenesis of ALI.
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Biomarkers in acute lung injury: insights into the pathogenesis of acute lung injury.

TL;DR: Known biomarkers are reviewed in context of their major biologic activity to provide information regarding the mechanisms involved in lung injury and repair and how this may be helpful in identifying and designing future therapeutic targets and strategies and possibly identifying a sensitive and specific biomarker.
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Transfusion-Related Acute Lung Injury: A Review

TL;DR: Treatment is supportive, with a prognosis substantially better than most causes of clinical acute lung injury, and the pathogenesis of TRALI may be explained by a "two-hit" hypothesis.