American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Dec 2013
Erratum: Procollagen Types I and III Aminoterminal Propeptide Levels during Acute Respiratory Distress Syndrome and in Response to Methylprednisolone Treatment; Prolonged Methylprednisolone Treatment Suppresses Systemic Inflammation in Patients with Unresolving Acute Respiratory Distress Syndrome.
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Am. J. Respir. Crit. Care Med. · Dec 2013
Clinical TrialBeneficial Hemodynamic Effects of Prone Positioning in Patients with Acute Respiratory Distress Syndrome.
The effects of prone positioning during acute respiratory distress syndrome on all the components of cardiac function have not been investigated under protective ventilation and maximal alveolar recruitment. ⋯ In patients with acute respiratory distress syndrome under protective ventilation and maximal alveolar recruitment, prone positioning increased the cardiac index only in patients with preload reserve, emphasizing the important role of preload in the hemodynamic effects of prone positioning.
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Am. J. Respir. Crit. Care Med. · Dec 2013
Randomized Controlled Trial Multicenter StudyLoss of salmeterol bronchoprotection against exercise in relation to ADRB2 Arg16Gly polymorphism and FeNO.
β2-Agonists are the treatment of choice for exercise-induced bronchoconstriction (EIB) and act through specific receptors (ADRB2). Arg16Gly polymorphisms have been shown to affect responses to regular use of β2-agonists. ⋯ The LOB that occurs with chronic long-acting β2-agonists use is not affected by ADRB2 Arg16Gly polymorphisms. High FE(NO) was associated with marked LOB. Use of long-acting β2-agonists before achieving a reduction in FeNO may need to be avoided. Clinical trial registered with www.clinicaltrials.gov (NCT 00595361).
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Am. J. Respir. Crit. Care Med. · Dec 2013
Lungs, Bone Marrow and Adipose Tissue: A Network Approach to the Pathobiology of Chronic Obstructive Pulmonary Disease.
Patients with chronic obstructive pulmonary disease (COPD) often suffer other concomitant disorders, such as cardiovascular diseases and metabolic disorders, that influence significantly (and independently of lung function) their health status and prognosis. Thus, COPD is not a single organ condition, and disturbances of a complex network of interorgan connected responses occur and modulate the natural history of the disease. ⋯ According to the model, the development of COPD, and associated multimorbidities (here we focus on cardiovascular disease as an important example), depend on the manner in which the vascular connected network responds, adapts, or fails to adapt (dictated by the genetic and epigenetic background of the individual) to the inhalation of particles and gases, mainly in cigarette smoke. The caveats and limitations of the hypothesis, as well as the experimental and clinical research needed to test and explore the proposed model, are also briefly discussed.