Alvarez, F.J. (Francisco Javier)

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    What pulmonologists think about the asthma–COPD overlap syndrome
    (Dove Medical Press, 2015) Perez-de-Llano, L. (Luis); Torrego, A. (Alfons); Esteban, C. (Cristóbal); Cosio, B.G. (Borja G.); Ros, J.A. (José Antonio); Casanova, C. (Ciro); Iriberri, M. (Milagros); Garcia-Sidro, P. (Patricia); Cisneros, C. (Carolina); Soler-Cataluña, J.J. (Juan José); Urrutia, I. (Isabel); Calle-Rubio, M. (Miryam); Alcazar, B. (Bernardino); Alvarez, F.J. (Francisco Javier); Izquierdo, J.L. (José Luis); Bazus, T. (Teresa); Perpiña, M. (Miguel); Torres, J.P. (Juan P.) de; Lopez-Viña, A. (Antolín); Entrenas, L.M. (Luis M.); Serrano, J. (José); Miravitlles, M. (Marc); Huerta, A. (Arturo); Plaza, V. (Vicente); Martinez-Moragon, E. (Eva); Lopez-Campos, J.L. (José Luis)
    Background: Some patients with COPD may share characteristics of asthma; this is the so-called asthma–COPD overlap syndrome (ACOS). There are no universally accepted criteria for ACOS, and most treatments for asthma and COPD have not been adequately tested in this population. Materials and methods: We performed a survey among pulmonology specialists in asthma and COPD aimed at collecting their opinions about ACOS and their attitudes in regard to some case scenarios of ACOS patients. The participants answered a structured questionnaire and attended a face-to-face meeting with the Metaplan methodology to discuss different aspects of ACOS. Results: A total of 26 pulmonologists with a mean age of 49.7 years participated in the survey (13 specialists in asthma and 13 in COPD). Among these, 84.6% recognized the existence of ACOS and stated that a mean of 12.6% of their patients might have this syndrome. In addition, 80.8% agreed that the diagnostic criteria for ACOS are not yet well defined. The most frequently mentioned characteristics of ACOS were a history of asthma (88.5%), significant smoking exposure (73.1%), and postbronchodilator forced expiratory volume in 1 second/forced vital capacity ,0.7 (69.2%). The most accepted diagnostic criteria were eosinophilia in sputum (80.8%), a very positive bronchodilator test (69.2%), and a history of asthma before 40 years of age (65.4%). Up to 96.2% agreed that first-line treatment for ACOS was the combination of a long-acting β2-agonist and inhaled steroid, with a long-acting antimuscarinic agent (triple therapy) for severe ACOS. Conclusion: Most Spanish specialists in asthma and COPD agree that ACOS exists, but the diagnostic criteria are not yet well defined. A previous history of asthma, smoking, and not fully reversible airflow limitation are considered the main characteristics of ACOS, with the most accepted first-line treatment being long-acting β2-agonist/inhaled corticosteroids.
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    Molecular and physiological events in respiratory muscles and blood of rats exposed to inspiratory threshold loading
    (2014) Galdiz, J.B. (Juan Bautista); Sabaté-Brescó, M. (Marina); Barreiro, E. (Esther); Alvarez, F.J. (Francisco Javier); Domínguez-Álvarez, M. (Marisol); Casadevall, C. (Carme); Gea, J. (Joaquim); Vilà-Ubach, M. (Mònica)
    High-intensity exercise induces oxidative stress and inflammatory events in muscles. Tumor necrosis factor (TNF)-α may alter muscle protein metabolism or promote muscle regeneration. We hypothesized that a program of noninvasive chronic inspiratory loading of different intensities induces a differential pattern of physiological, molecular, and cellular events within rat diaphragms. Antioxidants and TNF-α blockade may influence those events. In the diaphragm, gastrocnemius, and blood of rats exposed to high-intensity inspiratory threshold loads (2 hour every 24 hours for 14 days), with and without treatment with N-acetyl cysteine or infliximab (anti-TNF-α antibody), inflammatory cells and cytokines, superoxide anion production, myogenesis markers, and muscle structure were explored. In all animals, maximum inspiratory pressure (MIP) and body weight were determined. High-intensity inspiratory loading for 2 weeks caused a decline in MIP and body weight, and in the diaphragm induced a reduction in fast-twitch fiber proportions and sizes, whereas inflammatory cells and cytokine levels, including TNF-α immunohistochemical expression, superoxide anion, internal nuclei counts, and markers of myogenesis were increased. Blockade of TNF-α improved respiratory muscle function and structure, and animal weight, and, in the diaphragm, reduced inflammatory cell numbers and superoxide anion production drastically while inducing larger increases in protein and messenger RNA levels and immunohistochemical expression of TNF-α, internal nuclei, and markers of muscle regeneration. Blunting of TNF-α also induced a reduction in blood inflammatory cytokines and superoxide anion production. We conclude that TNF-α synthesized by inflammatory cells or myofibers could have differential effects on muscle structure and function in response to chronic, noninvasive, high-intensity inspiratory threshold loading.