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.
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Journal ArticleDOI
In vitro and in vivo regulation of transepithelial lung alveolar sodium transport by serine proteases.
Carole Planès,Celine Leyvraz,Tokujiro Uchida,Milena Apostolova Angelova,Grégoire Vuagniaux,Edith Hummler,Michael A. Matthay,Christine Clerici,Bernard C. Rossier +8 more
TL;DR: Results show that endogenous membrane-bound and/or secreted serine proteases such as CAPs regulate alveolar Na+ and fluid transport in vitro and in vivo in rodent lung.
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Pathogenetic and predictive value of biomarkers in patients with ALI and lower severity of illness: results from two clinical trials.
Ashish Agrawal,Hanjing Zhuo,Sandra Brady,Joseph E. Levitt,Jay S. Steingrub,Mark D. Siegel,Graciela J. Soto,Michael W. Peterson,Mark S. Chesnutt,Michael A. Matthay,Kathleen D. Liu +10 more
TL;DR: Future studies should be focused on examining larger numbers of patients with less severe ALI to further test the relative predictive value of plasma and mini-BAL biomarkers for clinically relevant outcomes, including VFDs and mortality, and for their prospective utility in risk stratification for future clinical trials.
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Transforming growth factor-alpha increases alveolar liquid clearance in anesthetized ventilated rats.
TL;DR: TGF-alpha can stimulate in vivoAlveolar liquid clearance at a rate similar to beta-adrenergic stimulation by increasing Na+ uptake by alveolar epithelial type II cells, however, the effect may be mediated by a non-cAMP dependent mechanism.
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Dysfunction of inflammation-resolving pathways is associated with exaggerated postoperative cognitive decline in a rat model of the metabolic syndrome.
Xiao Su,Xiao Su,Xiaomei Feng,Xiaomei Feng,Niccolò Terrando,Yan Yan,Ajay Chawla,Lauren G. Koch,Steven L. Britton,Michael A. Matthay,Mervyn Maze +10 more
TL;DR: Rats with the metabolic syndrome have ineffective inflammation-resolving mechanisms that represent plausible reasons for the exaggerated and persistent PCD.
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Effect of epinephrine on the ability of end-tidal carbon dioxide readings to predict initial resuscitation from cardiac arrest.
TL;DR: Although epinephrine administration may decrease end-tidal CO2 tensions in cardiac arrest, it does so unpredictably in individual patients, and it does not eliminate the predictive value of this measurement.