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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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Biomarkers of inflammation, coagulation and fibrinolysis predict mortality in acute lung injury

TL;DR: Despite lung-protective ventilation, abnormalities in plasma levels of markers of inflammation, coagulation and fibrinolysis predict mortality in ALI patients, indicating more severe activation of these biologic pathways in nonsurvivors.
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Timing of Intubation and Clinical Outcomes in Adults With Acute Respiratory Distress Syndrome

TL;DR: Criteria defining the acute respiratory distress syndrome prior to need for positive pressure ventilation are required so that these patients can be enrolled in clinical studies and to facilitate early recognition and treatment of acute ventilation distress syndrome.
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Mesenchymal stem cells for acute lung injury: preclinical evidence.

TL;DR: Several experimental studies have suggested that mesenchymal stem cells may have value for the treatment of clinical disorders, including myocardial infarction, diabetes, acute renal failure, sepsis, and acute lung injury.
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Hypoxia and β2-Agonists Regulate Cell Surface Expression of the Epithelial Sodium Channel in Native Alveolar Epithelial Cells

TL;DR: It is established that hypoxia-induced inhibition of amiloride-sensitive sodium channel activity is mediated by decreased apical expression of ENaC subunits and that β2-agonists reverse this effect by enhancing the insertion of ENc subunits into the membrane of hypoxic alveolar epithelial cells.
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Acute Pulmonary Edema After Lung Transplantation: The Pulmonary Reimplantation Response

TL;DR: Acute pulmonary edema or PRR occurs frequently after lung transplantation and was not associated with a prolonged ischemia time, preoperative pulmonary hypertension, the type of lung transplant, underlying lung disease, or age or sex of recipients.