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741. Absence of Atypical Pathogens in Pleural Infection.

作者: John M Wrightson.;Jessica A Wray.;Teresa L Street.;Stephen J Chapman.;Fergus V Gleeson.;Nicholas A Maskell.;Timothy E A Peto.;Najib M Rahman.;Derrick W M Crook.
来源: Chest. 2015年148卷3期e102-e103页

742. Response.

作者: Joseph Cicenia.;Atul C Mehta.;Kazuhiro Yasufuku.
来源: Chest. 2015年148卷3期e100-e101页

743. Correction to Reference in: Socioeconomic Characteristics Are Major Contributors to Ethnic Differences in Health Status in Obstructive Lung Disease: An Analysis of the National Health and Nutrition Examination Survey 2007-2010.

来源: Chest. 2015年148卷3期842页

744. Correction to Figure in: Long-Latency Sensory-Evoked Responses and Prognosis in Cardiac Arrest Survivors.

来源: Chest. 2015年148卷3期842页

745. Correction to Table and References in: Methodologies for the Development of CHEST Guidelines and Expert Panel Reports.

来源: Chest. 2015年148卷3期842页

746. Giants in Chest Medicine: John (Jack) G. Weg, MD, Master FCCP.

作者: Richard S Irwin.;Pamela Goorsky.
来源: Chest. 2015年148卷3期578-579页

747. Beyond the 6-Minute Walk Test for Assessing Pediatric Pulmonary Hypertension: Making Strides Through Combination End Points.

作者: D Dunbar Ivy.;Steven Abman.
来源: Chest. 2015年148卷3期576-577页

748. Can We Alter the Natural History of Silicosis?

作者: Ltc Daniel E Banks.;Fort Sam Houston.;Surinder K Jindal.
来源: Chest. 2015年148卷3期574-576页

749. The Harm of Tobacco Starts Before Birth.

作者: Harold J Farber.
来源: Chest. 2015年148卷3期573-574页

750. Who Gets Early Tracheostomy?: Evidence of Unequal Treatment at 185 Academic Medical Centers.

作者: Joshua J Shaw.;Heena P Santry.
来源: Chest. 2015年148卷5期1242-1250页
Although the benefits of early tracheostomy in patients dependent on ventilators are well established, the reasons for variation in time from intubation to tracheostomy remain unclear. We identified clinical and demographic disparities in time to tracheostomy.

751. Quantitative CT Scanning Analysis of Pure Ground-Glass Opacity Nodules Predicts Further CT Scanning Change.

作者: So Hyeon Bak.;Ho Yun Lee.;Jae-Hun Kim.;Sang-Won Um.;O Jung Kwon.;Joungho Han.;Hong Kwan Kim.;Jhingook Kim.;Kyung Soo Lee.
来源: Chest. 2016年149卷1期180-91页
We sought to determine whether quantitative analysis of lung adenocarcinoma manifesting as a ground-glass opacity (GGO) nodule (GGN) on initial CT scans can predict further CT scanning change or rate of growth.

752. Obesity Hypoventilation Syndrome: Weighing in on Therapy Options.

作者: Amanda Piper.
来源: Chest. 2016年149卷3期856-68页
Obesity hypoventilation syndrome is becoming an increasingly encountered condition both in respiratory outpatient clinics and in hospitalized patients. The health consequences and social disadvantages of obesity hypoventilation syndrome are significant. Unfortunately, the diagnosis and institution of appropriate therapy is commonly delayed when the syndrome is not recognized or misdiagnosed. Positive airway pressure therapy remains the mainstay of treatment and is effective in controlling sleep-disordered breathing and improving awake blood gases in the majority of individuals. Evidence supporting one mode of therapy over another is limited. Both continuous and bilevel therapy modes can successfully improve daytime gas exchange, with adherence to therapy an important modifiable factor in the response to treatment. Despite adherence to therapy, these individuals continue to experience excess mortality primarily due to cardiovascular events compared with those with eucapnic sleep apnea using CPAP. This difference likely arises from ongoing systemic inflammation secondary to the morbidly obese state. The need for a comprehensive approach to managing nutrition, weight, and physical activity in addition to reversal of sleep-disordered breathing is now widely recognized. Future studies need to evaluate the impact of a more aggressive and comprehensive treatment plan beyond managing sleep-disordered breathing. The impact of early identification and treatment of sleep-disordered breathing on the development and reversal of cardiometabolic dysfunction also requires further attention.

753. Targeted Fluid Minimization Following Initial Resuscitation in Septic Shock: A Pilot Study.

作者: Catherine Chen.;Marin H Kollef.
来源: Chest. 2015年148卷6期1462-1469页
IV fluid represents a basic therapeutic intervention for septic shock. Unfortunately, the optimal administration of IV fluid to maximize patient outcomes and prevent complications is largely unknown.

754. Defining the Asthma-COPD Overlap Syndrome in a COPD Cohort.

作者: Borja G Cosio.;Joan B Soriano.;Jose Luis López-Campos.;Myriam Calle-Rubio.;Juan José Soler-Cataluna.;Juan P de-Torres.;Jose M Marín.;Cristina Martínez-Gonzalez.;Pilar de Lucas.;Isabel Mir.;Germán Peces-Barba.;Nuria Feu-Collado.;Ingrid Solanes.;Inmaculada Alfageme.;Ciro Casanova.; .
来源: Chest. 2016年149卷1期45-52页
Asthma-COPD overlap syndrome (ACOS) has been recently described by international guidelines. A stepwise approach to diagnosis using usual features of both diseases is recommended although its clinical application is difficult.

755. Effect of e-Cigarette Use on Cough Reflex Sensitivity.

作者: Peter V Dicpinigaitis.;Alfredo Lee Chang.;Alis J Dicpinigaitis.;Abdissa Negassa.
来源: Chest. 2016年149卷1期161-5页
E-cigarettes (e-cigs) have attained widespread popularity, yet knowledge of their physiologic effects remains minimal. The aim of this study was to evaluate the effect of a single exposure to e-cig vapor on cough reflex sensitivity.

756. OSA Syndrome and Posttraumatic Stress Disorder: Clinical Outcomes and Impact of Positive Airway Pressure Therapy.

作者: Christopher J Lettieri.;Scott G Williams.;Jacob F Collen.
来源: Chest. 2016年149卷2期483-490页
We sought to determine the impact of OSA syndrome (OSAS) on symptoms and quality of life (QoL) among patients with posttraumatic stress disorder (PTSD). In addition, we assessed adherence and response to positive airway pressure (PAP) therapy in this population.

757. Different Craniofacial Characteristics Predict Upper Airway Collapsibility in Japanese-Brazilian and White Men.

作者: Fabiola Schorr.;Fabiane Kayamori.;Raquel P Hirata.;Naury J Danzi-Soares.;Eloisa M Gebrim.;Henrique T Moriya.;Atul Malhotra.;Geraldo Lorenzi-Filho.;Pedro R Genta.
来源: Chest. 2016年149卷3期737-46页
OSA pathogenesis is complex and may vary according to ethnicity. The anatomic component predisposing to OSA is the result of the interaction between bony structure and upper airway soft tissues and can be assessed using passive critical closing pressure (Pcrit). We hypothesized that Japanese-Brazilians and whites present different predictors of upper airway collapsibility, suggesting different causal pathways to developing OSA in these two groups.

758. Health-care Provider Screening and Advice for Smoking Cessation Among Smokers With and Without COPD: 2009-2010 National Adult Tobacco Survey.

作者: Gillian L Schauer.;Anne G Wheaton.;Ann M Malarcher.;Janet B Croft.
来源: Chest. 2016年149卷3期676-84页
Cigarette smoking is the predominant cause of COPD. Quitting can prevent development of and complications from COPD. The gold standard in clinician delivery of smoking cessation treatments is the 5As (ask, advise, assess, assist, arrange). This study assessed prevalence and correlates of self-reported receipt of the 5A strategies among adult smokers with and without COPD.

759. Clinical Characteristics and Outcomes Are Similar in ARDS Diagnosed by Oxygen Saturation/Fio2 Ratio Compared With Pao2/Fio2 Ratio.

作者: Wei Chen.;David R Janz.;Ciara M Shaver.;Gordon R Bernard.;Julie A Bastarache.;Lorraine B Ware.
来源: Chest. 2015年148卷6期1477-1483页
Oxygen saturation as measured by pulse oximetry/Fio2 (SF) ratio is highly correlated with the Pao2/Fio2 (PF) ratio in patients with ARDS. However, it remains uncertain whether SF ratio can be substituted for PF ratio for diagnosis of ARDS and whether SF ratio might identify patients who are systemically different from patients diagnosed by PF ratio.

760. Rhinovirus in the Pathogenesis and Clinical Course of Asthma.

作者: Kyla C Jamieson.;Stephanie M Warner.;Richard Leigh.;David Proud.
来源: Chest. 2015年148卷6期1508-1516页
In healthy individuals, human rhinovirus (HRV) infections are the major cause of the common cold. These are generally uncomplicated infections except for occasional cases of otitis media or sinusitis. In individuals with asthma, however, HRV infections can have a major impact on disease development and progression. HRV-induced wheezing illnesses in early life are a significant risk factor for subsequent development of asthma, and growing evidence supports a role of recurrent HRV infections in the development and progression of several aspects of airway remodeling in asthma. In addition, HRV infections are one of the most common triggers for acute exacerbations of asthma, which represent a major burden to health-care systems around the world. None of the currently prescribed medications for asthma are effective in preventing or reversing asthma development and airway remodeling or are ideal for treating HRV-induced exacerbations of asthma. Thus, a better understanding of the role of HRV in asthma is important if we are to develop more effective therapies. In the past decade, we have gained new insights into the role of HRV infections in the development and progression of airway remodeling as well as a new appreciation for the proinflammatory and host defense responses to HRV infections that may help to regulate susceptibility to asthma exacerbations. This article reviews the current understanding of the role HRV infections play in the pathogenesis of asthma and identifies possible avenues to new therapeutic strategies for limiting the effects of HRV infections in asthma.
共有 32839 条符合本次的查询结果, 用时 4.9130255 秒