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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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Age-, sex-, and race-based differences among patients enrolled versus not enrolled in acute lung injury clinical trials*

TL;DR: Older patients are less likely to be enrolled in acute lung injury clinical trials and black patients and their families refused participation more often than white patients, and there is no evidence that women or racial/ethnic minorities are underrepresented in acute Lung Injury clinical trials.
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The utility of clinical predictors of acute lung injury: towards prevention and earlier recognition.

TL;DR: The growing literature on clinical predictors of acute lung injury (including risk factors for specific subgroups) with an emphasis on transfusion-related risk factors and recent research targeting the early identification of high-risk patients and those with early acute lung Injury prior to the onset of respiratory failure are discussed.
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Incorporating Inflammation into Mortality Risk in Pediatric Acute Respiratory Distress Syndrome.

TL;DR: In pediatric acute respiratory distress syndrome, pro- and anti-inflammatory cytokines are strongly associated with mortality, ICU morbidity, and biochemical evidence of endothelial injury and may allow for identification and enrollment of high-risk subgroups for future studies.
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Body temperature and mortality in patients with acute respiratory distress syndrome.

TL;DR: Early in ARDS, fever is associated with improved survival rates and was a significant predictor of 90-day mortality after primary cause of ARDS and score on the Acute Physiology and Chronic Health Evaluation III were adjusted for.
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Decreased expression of both the α1- and α2-subunits of the Na-K-ATPase reduces maximal alveolar epithelial fluid clearance

TL;DR: A small fraction of the normal Na-K-ATPase activity inaired epithelial sodium channel function predisposes to delayed resorption of pulmonary edema and more severe experimental lung injury.