Zobrazeno 1 - 10
of 24
pro vyhledávání: '"Carl W. White"'
Autor:
Isabella Annesi-Maesano, Urmila P. Kodavanti, Frank D. Gilliland, Esteban G. Burchard, Christopher Carlsten, Haneen Khreis, Carl W. White, Rob McConnell, George D. Thurston, Steven R. Kleeberger, Erika Garcia, Joan Reibman, Laura S. Van Winkle, John R. Balmes, Jack R. Harkema, Kent E. Pinkerton, Mary B. Rice, Dave B Peden, Tamara Schikowski, Stephanie J. London
Publikováno v:
Annals of the American Thoracic Society
Annals of the American Thoracic Society, vol 17, iss 4
Annals of the American Thoracic Society, vol 17, iss 4
Although it is well accepted that air pollution exposure exacerbates preexisting airway disease, it has not been firmly established that long-term pollution exposure increases the risk of new-onset asthma or chronic obstruction pulmonary disease (COP
Autor:
Xiao Gao, Wenqi He, Fengyi Zhang, Livia A. Veress, Yusi Miao, Jangwoen Lee, Jianing Tang, Zhikai Zhu, Jing Cao, Matthew Brenner, Melody Doosty, Carl W. White, Saijun Qiu, David Mukai, Sari B. Mahon, George Philipopoulos, Zhongping Chen
Publikováno v:
Endoscopic Microscopy XVI.
In this work, we demonstrate the ability to image and quantify airway changes, edema, and epithelial layer separation using OCT and automated tissue boundary identification in the rabbit large airways as early as 30-minutes post-chlorine gas exposure
Sulfur mustard inhalation: mechanisms of injury, alteration of coagulation, and fibrinolytic therapy
Publikováno v:
Annals of the New York Academy of Sciences. 1378:87-95
Acute lung injury due to sulfur mustard (SM) inhalation causes the formation of airway fibrin casts that obstruct airways at multiple levels, leading to acute respiratory failure and death. These pathophysiological effects are seen in rodent models o
Autor:
Rhonda B. Garlick, Raymond C. Rancourt, Matthew D. McGraw, Jaqueline S. Rioux, Livia A. Veress, Carl W. White
Sulfur mustard (SM) is a chemical warfare agent that causes chronic airway remodeling. This study’s objective was to assess for changes to the bronchiolar epithelium after SM exposure to explain its contribution to chronic airway remodeling. Materi
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6a3a866080c2e08b0c71dc82e6390b00
https://europepmc.org/articles/PMC6075598/
https://europepmc.org/articles/PMC6075598/
Autor:
Livia A. Veress, Raymond C. Rancourt, Carl W. White, Jacqueline S. Rioux, Rhonda B. Garlick, Aftab Ahmad, Tara B. Hendry-Hofer
Publikováno v:
Toxicology and Applied Pharmacology. 272:86-95
Sulfur mustard (SM) inhalation causes airway injury, with enhanced vascular permeability, coagulation, and airway obstruction. The objective of this study was to determine whether recombinant tissue factor pathway inhibitor (TFPI) could inhibit this
Autor:
Tara B. Hendry-Hofer, Raymond C. Rancourt, Joan E. Loader, Livia A. Veress, Carl W. White, Heidi C. O'Neill
Publikováno v:
American Journal of Respiratory and Critical Care Medicine. 182:1352-1361
Sulfur mustard (SM) is a frequently used chemical warfare agent, even in modern history. SM inhalation causes significant respiratory tract injury, with early complications due to airway obstructive bronchial casts, akin to those seen after smoke inh
Autor:
Sture Andersson, Tiina M. Asikainen, Riitta Karikoski, Vuokko L. Kinnula, Riika Vähätalo, Marjukka Myllärniemi, Carl W. White, Markku Heikinheimo
Publikováno v:
Neonatology. 99:231-240
Background: Premature birth and respiratory distress syndrome (RDS) are risk factors for disturbed lung development and bronchopulmonary dysplasia (BPD). The molecular mechanisms related to prematurity and BPD remain largely unknown. Epithelial expre
Autor:
Livia A. Veress, Carl W. White, Jacqueline S. Rioux, Rhonda B. Garlick, Raymond C. Rancourt, Aftab Ahmad
Acute lung injury in response to mustard gas (sulfur mustard [SM]) inhalation results in formation of fibrin casts, which obstruct the airway. The objective of this study was to identify fibrinolytic pathways that could be contributing to the persist
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9a1c4144407e5f3c8427cb59e5adcc5f
https://europepmc.org/articles/PMC4189487/
https://europepmc.org/articles/PMC4189487/
Publikováno v:
American Journal of Physiology-Lung Cellular and Molecular Physiology. 283:L573-L584
Increased glucose utilization and hexokinase (HK)-II expression are adaptive features of lung cells exposed to hypoxia or hyperoxia. HK-II is the most regulated isoform of HK. Whether its overexpression could be protective against oxidative stress wa
Publikováno v:
American Journal of Respiratory Cell and Molecular Biology. 25:51-59
The mechanisms whereby lung adaptation to hyperoxia occurs in the newborn period are incompletely understood. Pulmonary surfactant has been implicated in lung protection against hyperoxic injury, and elevated expression of certain surfactant proteins