Gwen S Skloot, MD
- PROFESSOR | Medicine, Pulmonary, Critical Care and Sleep Medicine
Specialties:Sleep Medicine, Pulmonary Medicine
Gwen Skloot, MD, received her medical degree from New York University School of Medicine and completed her residency at The Mount Sinai Hospital. She attended Johns Hopkins Medical Institution in Baltimore, Maryland, for her Pulmonary/Critical Care Fellowship. Since then Dr. Skloot has built a large general pulmonary practice with special expertise in airways disease and asthma. She has facilitated patient referrals from one sub-specialist to another so that care is streamlined and expedited. As Director of the Pulmonary Physiology Laboratory, she has been in charge of expanding the clinical practice, managing the business, and educating pulmonary fellows and residents. Dr. Skloot has instituted a quality assurance program and put in place new qualification standards for pulmonary function technologists so that the laboratory is staffed by individuals with the highest credentials. Dr. Skloot has added to the types of tests that are done in the laboratory, enhancing diagnostic and monitoring capabilities. Dr. Skloot conducts research on airway hyperresponsivness. This parallels her clinical interest in asthma. She has received multiple small grants to pursue this research in an animal model. She has published peer-reviewed articles, invited reviews, and book chapters, and presented work annually at the American Thoracic Society meeting. She is currently studying obesity as a model of airway hyperresponsiveness and has demonstrated that obesity itself, independent of asthma, may be associated with airways dysfunction and may thus be an important sub-population to study. Her current work builds upon this discovery. Dr. Skloot is also fluent in Spanish.
Mount Sinai Study Finds One Quarter of WTC Responders Continue to Have Lung Function Impairment
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Dr. Gwen Skloot discusses the link between asthma and obesity in The Daily News feature The Daily Check Up.
Critical Care Medicine
- Pulmonary Function Tests
MD, New York University
Internship, Internal Medicine, Mount Sinai Hospital
Residency, Internal Medicine, Mount Sinai Hospital
Fellowship, Pulm & Critical Care, Johns Hopkins Hospital
Airway Responsiveness in Asthma
Our laboratory focuses on clinical asthma studies. We hypothesize that hyperresponsiveness is caused by impairment in the ability of inspiration to stretch airway smooth muscle (ASM) -- i.e. impaired bronchodilation. This hypothesis is supported by our finding that sensitivity to the constrictor agent Methacholine is the same in normals and asthmatics when challenge is conducted without deep breaths. It is also known that deep inspiration (DI) prior to a constrictor agent is bronchoprotective in normal subjects. We have shown that this effect relates to inspiratory velocity, i.e. a fast DI is more bronchoprotective than a slow DI. We speculate that in healthy subjects, DI stretches ASM and breaks cross bridges and that cross bridge breakage is enhanced with increased inspiratory velocity. In asthmatics, inflammation may impair this ability. Further protocols will focus on the mechanism of the impaired response to DI in asthma in order to ultimately develop interventions to treat this aspect of hyperresponsiveness.
We have developed an in vitro model to test similar ideas. We hypothesize that stretching guinea pig (GP) tracheal smooth muscle releases a humoral "relaxant" factor [i.e. stretch-induced relaxation (SIR) involves a receptor-mediated mechanism]. The analogous in vivo situation may be the release of a "bronchodilating" substance when a normal subject takes a deep breath. This bronchodilating substance may be decreased in asthma. We have demonstrated that GP tracheal smooth muscle does relax when stretched; this relaxation is enhanced post-carbachol. We have characterized this relaxation response by pharmacokinetic studies. Additional characterization studies are focused on inhibiting the SIR response with agents such as beta-blockers, indomethacin, etc. We have shown that after induction of airway inflammation, the SIR response is reduced. Future protocols will address the mechanism of this reduced response and the relevance to human asthma.