Chest
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We have concentrated on the adenovirus as the source of the heightened inflammatory response of the lungs of patients with COPD. We have concentrated in particular on the responses to agents such as lipopolysaccharides and environmental particulates that contaminate the air we breathe, and we have accumulated evidence that the E1A gene of this virus could be the key player in this process. As other intracellular pathogens such as Chlamydia pneumoniae have recently been implicated in the pathogenesis of COPD, our studies on the adenovirus E1A could serve as the model for investigating the interaction between host and extrinsic factors in the chronic progression of this debilitating lung disease.
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To appraise the potential cost-effectiveness of lung cancer screening with CT. ⋯ If screening for lung cancer is effective, it is likely to be cost-effective if the screening process can detect > 50% of cancers at localized stage.
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The health-related quality of life of smokers without COPD and that of ex-smokers has not been defined. If abnormal, the role of small airways disease and that of cough and phlegm have never been evaluated. Therefore, the aim of the study was to explore whether the differences in quality of life between smokers and ex-smokers could be explained by cough and phlegm, differences in pulmonary function tests, or exercise capacity. ⋯ In smokers without COPD, the abnormal SGRQ score is due to the noxious effect of cigarette smoke, resulting in cough and phlegm, independent of its physiologic effects.
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To describe the risk factors for the development of and mortality resulting from acute respiratory failure (ARF) in a large patient population. ⋯ The present study stresses that ARF is common in the ICU (56% of all patients) and that a number of extrapulmonary factors are related to the risk of development of ARF and to mortality rate in these patients.
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COPD continues to cause a heavy health and economic burden both in the United States and around the world. Some of the risk factors for COPD are well-known and include smoking, occupational exposures, air pollution, airway hyperresponsiveness, asthma, and certain genetic variations, although many questions, such as why < 20% of smokers develop significant airway obstruction, remain. Precise definitions of COPD vary and are frequently dependent on an accurate diagnosis of the problem by a physician. ⋯ Furthermore, evidence that COPD represents several different disease processes with potentially different interventions continues to emerge. In most of the world, COPD prevalence and mortality are still increasing and likely will continue to rise in response to increases in smoking, particularly by women and adolescents. Resources aimed at smoking cessation and prevention, COPD education and early detection, and better treatment will be of the most benefit in our continuing efforts against this important cause of morbidity and mortality.