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Barreiro E.,Muscle and Respiratory System Research Unit | Barreiro E.,Institute Salud Carlos III | Fermoselle C.,Muscle and Respiratory System Research Unit | Fermoselle C.,Institute Salud Carlos III | And 8 more authors.
Free Radical Biology and Medicine | Year: 2013

Respiratory conditions such as chronic obstructive pulmonary disease (COPD) are associated with a greater risk for lung cancer (LC). Oxidative stress and inflammation are involved in LC pathophysiology. Studies conducted so far have focused solely on lung tumor parenchyma and not the airways. We explored levels of local and systemic oxidative stress and inflammation within normal bronchial epithelium and blood of patients with lung cancer (n=52), with and without COPD, and in control subjects (COPD and non-COPD, n=21). In normal bronchial epithelium specimens (bronchoscopy) and blood from patients with similar smoking history (LC-COPD and LC) and control subjects (both COPD and non-COPD), redox balance and inflammatory markers were measured (ELISA and immunoblotting). All subjects were clinically evaluated. Absence of malignant cells within the bronchial specimens was always pathologically confirmed. Bronchial levels of protein carbonylation, MDA-protein adducts, antioxidants, TNF-α, interferon-γ, TGF-β, and VEGF and blood levels of superoxide anion, oxidatively damaged DNA and proteins, TNF-α, interferon-γ, TGF-β, VEGF, and neutrophils were significantly greater in all LC patients compared to control subjects. Systemic levels of oxidatively damaged DNA, superoxide anion, and TNF-α and bronchial levels of TGF-β and TNF-α showed high sensitivity and specificity for LC among patients. Regardless of the presence of an underlying respiratory condition (COPD), protein oxidation, oxidatively damaged DNA, and inflammation were remarkably increased in the normal airways and blood of patients with LC. Furthermore, the potential predictive value for LC development of these molecular events warrants attention and should be explored in future larger longitudinal studies. © 2013 Elsevier Inc. Source

Gimeno-Santos E.,Hospital del Mar Research Institute IMIM | Gimeno-Santos E.,CIBER ISCIII | Gimeno-Santos E.,University of Barcelona | Gimeno-Santos E.,Ramon Llull University | And 22 more authors.
COPD: Journal of Chronic Obstructive Pulmonary Disease | Year: 2014

Background: Abnormalities of autonomic function have been reported in patients with chronic obstructive pulmonary disease. The effect of the exercise training in heart rate recovery (HRR) has not been established in patients with COPD. Objective: To assess the effects of 8-weeks' endurance training program on parasympathetic nervous system response measured as heart rate recovery in a sample of moderate-to-severe COPD patients. Methods: We recruited a consecutive sample of patients with COPD candidates to participate in a pulmonary rehabilitation program from respiratory outpatient clinics of a tertiary hospital. HRR was calculated, before and after training, as the difference in heart rate between end-exercise and one minute thereafter (HRR1) in a constant-work rate protocol. Results: A total of 73 COPD patients were included: mean (SD) age 66 (8) years, median (P25-P75) post-bronchodilator FEV1 39 (29-53)%. The prevalence of slow HRR1 (≤12 beats) at baseline was 63%, and was associated with spirometric severity (mean FEV1 35% in slow HRR1 vs 53 in normal HRR1, p < 0.001). After 8-weeks training, HRR1 improved from mean (SD) 10 (7) to 12 (7) beats (p = 0.0127). Multivariate linear regression models showed that the only variable related to post-training HRR1 was pre-training HRR1 (p < 0.001). Conclusions: These results suggest that training enhances HRR in patients with moderate-to-severe COPD. HRR is an easy tool to evaluate ANS such that it may be a useful clinical marker of parasympathetic nervous system response in patients with COPD. © 2013 Informa Healthcare USA, Inc. Source

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