L
Lewis J. Rubin
Researcher at University of California, San Diego
Publications - 373
Citations - 60316
Lewis J. Rubin is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Pulmonary hypertension & Bosentan. The author has an hindex of 101, co-authored 370 publications receiving 57044 citations. Previous affiliations of Lewis J. Rubin include University of Texas Health Science Center at San Antonio & Silver Spring Networks.
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Nitric oxide inhibits serotonin-induced calcium release in pulmonary artery smooth muscle cells.
TL;DR: No-induced inhibition of the evoked increases in [Ca2+]i and augmentation of Ca2+ sequestration into intracellular stores in PASMC are involved in the mechanisms by which NO causes pulmonary vasodilation.
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Executive Summary: Diagnosis and Management of Pulmonary Arterial Hypertension: ACCP Evidence-Based Clinical Practice Guidelines
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A mitochondrial uncoupler increases KCa currents but decreases KV currents in pulmonary artery myocytes
TL;DR: FCCP increases IK[Ca] by raising [Ca2+]i primarily as a result of Ca2+ release, but decreases IK(V) by a Ca(2+)-independent mechanism, presumably the inhibition of oxidative ATP production.
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Update in pulmonary hypertension 2005.
Marius M. Hoeper,Lewis J. Rubin +1 more
TL;DR: The focus will be entirely on pathogenetic and therapeutic aspects of pulmonary hypertension, although important articles have also been published in other areas of pulmonary vascular disease, including pulmonary embolism and high-altitude pulmonary edema.
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Patients with pulmonary arterial hypertension with and without cardiovascular risk factors: Results from the AMBITION trial
Vallerie V. McLaughlin,Jean-Luc Vachiery,Ronald J. Oudiz,Stephan Rosenkranz,Nazzareno Galiè,Joan Albert Barberà,Adaani E. Frost,Hossein Ardeschir Ghofrani,Andrew J. Peacock,Gérald Simonneau,Lewis J. Rubin,Christiana Blair,Jonathan Langley,Marius M. Hoeper +13 more
TL;DR: Primary analysis set patients with pulmonary arterial hypertension had fewer clinical failure events, higher rates of satisfactory clinical response, and lower rates of permanent study drug withdrawal due to adverse events than ex-primaryAnalysis set patients.