J
James A. Frank
Researcher at University of California, San Francisco
Publications - 60
Citations - 4035
James A. Frank 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 30, co-authored 59 publications receiving 3679 citations. Previous affiliations of James A. Frank include Cardiovascular Institute Hospital & University of California, Berkeley.
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Journal ArticleDOI
Science review: mechanisms of ventilator-induced injury
TL;DR: The completion of the National Institutes of Health-sponsored Acute Respiratory Distress Syndrome Network low tidal volume study means clinicians now have convincing evidence that ventilation with tidal volumes lower than those conventionally used in this patient population reduces the relative risk of mortality by 21%.
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Clinically relevant concentrations of β2-adrenergic agonists stimulate maximal cyclic adenosine monophosphate-dependent airspace fluid clearance and decrease pulmonary edema in experimental acid-induced lung injury
TL;DR: Clinically relevant airspace concentrations of β2-adrenergic agonists stimulate maximal cAMP-dependent airspace fluid clearance in normal lungs and reduce pulmonary edema in acid aspiration-induced lung injury by increasing alveolar fluid clearance and decreasing endothelial permeability.
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Transforming Growth Factor-β1 Decreases Expression of the Epithelial Sodium Channel αENaC and Alveolar Epithelial Vectorial Sodium and Fluid Transport via an ERK1/2-dependent Mechanism
James A. Frank,Jérémie Roux,Hisaaki Kawakatsu,George Su,André Dagenais,Yves Berthiaume,Marybeth Howard,Cecilia M. Canessa,Xiaohui Fang,Dean Sheppard,Michael A. Matthay,Jean-Francois Pittet +11 more
TL;DR: Study of the effect of active TGF-β1 on 22Na+ uptake across monolayers of primary rat and human alveolar type II (ATII) cells indicates that increased TGF -β1 activity in the distal airspaces during ALI promotes alveolars edema by reducingdistal airway epithelial sodium and fluid clearance.
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Claudin-4 augments alveolar epithelial barrier function and is induced in acute lung injury.
TL;DR: It is hypothesized that increased claudin-4 expression early in acute lung injury represents a mechanism to limit pulmonary edema and that the regulation of alveolar epithelialclaudin expression may be a novel target for acute lung injuries therapy.
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Pathogenetic significance of biological markers of ventilator-associated lung injury in experimental and clinical studies.
TL;DR: Data on biological markers of VALI and VILI from both clinical and experimental studies are summarized with an emphasis on markers identified in patients and in the experimental setting to suggest that measurement of some of these biological markers may be of value in diagnosing VALI