American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Jun 2016
ReviewPrecision Medicine: The New Frontier in Idiopathic Pulmonary Fibrosis.
Precision medicine is defined by the National Institute of Health's Precision Medicine Initiative Working Group as an approach to disease treatment that takes into account individual variability in genes, environment, and lifestyle. There has been increased interest in applying the concept of precision medicine to idiopathic pulmonary fibrosis, in particular to search for genetic and molecular biomarker-based profiles (so called endotypes) that identify mechanistically distinct disease subgroups. The relevance of precision medicine to idiopathic pulmonary fibrosis is yet to be established, but we believe that it holds great promise to provide targeted and highly effective therapies to patients. In this manuscript, we describe the field's nascent efforts in genetic/molecular endotype identification and how environmental and behavioral subgroups may also be relevant to disease management.
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Am. J. Respir. Crit. Care Med. · Jun 2016
ReviewVolatile Anesthetics: Is A New Player Emerging in Critical Care Sedation?
Volatile anesthetic agent use in the intensive care unit, aided by technological advances, has become more accessible to critical care physicians. With increasing concern over adverse patient consequences associated with our current sedation practice, there is growing interest to find non-benzodiazepine-based alternative sedatives. ⋯ However, like all sedatives, volatile agents are capable of deeply sedating patients, which can have respiratory depressant effects and reduce patient mobility. This review seeks to critically appraise current volatile use in critical care medicine including current research, technical consideration of their use, contraindications, areas of controversy, and proposed future research topics.
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Am. J. Respir. Crit. Care Med. · Jun 2016
Interferon-γ-producing Th17.1 Cells are Increased in Sarcoidosis and More Prevalent Than Th1 Cells.
Pulmonary sarcoidosis is classically defined by T-helper (Th) cell type 1 inflammation (e.g., IFN-γ production by CD4(+) effector T cells). Recently, IL-17A-secreting cells have been found in lung lavage, invoking Th17 immunity in sarcoidosis. Studies also identified IL-17A-secreting cells that expressed IFN-γ, but their abundance as a percentage of total CD4(+) cells was either low or undetermined. ⋯ Combined use of surface markers and functional assays to study CD4(+) T cells in sarcoidosis revealed a marked expansion of Th17.1 cells that only produce IFN-γ. These results suggest that Th17.1 cells could be misclassified as Th1 cells and may be the predominant producer of IFN-γ in pulmonary sarcoidosis, challenging the Th1 paradigm of pathogenesis.
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Am. J. Respir. Crit. Care Med. · Jun 2016
Air Pollution and Lung Function in Minority Youth with Asthma in the GALA II & SAGE II Studies.
Adverse effects of exposures to ambient air pollution on lung function are well documented, but evidence in racial/ethnic minority children is lacking. ⋯ Early-life particulate exposures were associated with reduced lung function in Latino and African American children with asthma. This is the first study to report an association between exposure to particulates and reduced lung function in minority children in which racial/ethnic status was measured by ancestry-informative markers.
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Am. J. Respir. Crit. Care Med. · Jun 2016
Increased Dead Space Ventilation Mediates Reduced Exercise Capacity in Systolic Heart Failure.
Patients with chronic heart failure have limited exercise capacity, which cannot be completely explained by markers of cardiac dysfunction. Reduced pulmonary diffusing capacity at rest and excessively high ventilation during exercise are common in heart failure. We hypothesized that the reduced pulmonary diffusing capacity in patients with heart failure would predict greater dead space ventilation during exercise and that this would lead to impairment in exercise capacity. ⋯ Low resting pulmonary diffusing capacity in heart failure is indicative of high dead space ventilation during exercise, leading to excessive and inefficient ventilation. These findings would support the concept of pulmonary vasculopathy leading to altered ventilation perfusion matching (increased dead space) and resultant dyspnea, independent of markers of cardiac function.