Carlos Sanz Simón

Site of Mitochondrial Reactive Oxygen Species Production in Skeletal Muscle of Chronic Obstructive Pulmonary Disease and Its Relationship with Exercise Oxidative Stress

Exercise triggers skeletal muscle oxidative stress in patients with chronic obstructive pulmonary disease (COPD). The objective of this research was to study the specific sites of reactive oxygen species (ROS) production in mitochondria isolated from skeletal muscle of patients with COPD and its relationship with local oxidative stress induced by exercise. Vastus lateralis biopsies were obtained in 16 patients with COPD (66 ± 10 yr; FEV(1), 54 ± 12% ref) and in 14 control subjects with normal lung function who required surgery because of lung cancer (65 ± 7 yr; FEV(1), 91 ± 14% ref) at rest and after exercise. In these biopsies we isolated mitochondria and mitochondrial membrane fragments and determined in vitro mitochondrial oxygen consumption (Mit

Effect of pentoxifylline on the inhibition of surfactant synthesis induced by TNF-alpha in human type II pneumocytes.

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o(2)) and ROS production before and after inhibition of complex I (rotenone), complex II (stigmatellin), and complex III (antimycin-A). We related the in vitro ROS production during state 3 respiration), which mostly corresponds to the mitochondria respiratory state during exercise, with skeletal muscle oxidative stress after exercise, as measured by thiobarbituric acid reactive substances.State 3 Mit

El museo de educación como recurso pedagógico: Blended Learning. Un Proyecto de formación B-Learning sobre las técnicas Freinet en la actualidad

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El retrato de Franco, el de José Antonio y el crucifijo. Construcción de la identidad nacional en los escolares de posguerra

o(2) was similar in patients with COPD and control subjects (191 ± 27 versus 229 ± 46 nmol/min/mg; P = 0.058), whereas H(2)O(2) production was higher in the former (147 ± 39 versus 51 ± 8 pmol/mg/h; P < 0.001). The addition of complexI, II, and III inhibitors identify complex III as the main site of H(2)O(2) release by mitochondria in patients with COPD and in control subjects. The mitochondrial production of H(2)O(2) in state 3 respiration was related (r = 0.69; P < 0.001) to postexercise muscle thiobarbituric acid reactive substance levels. Our results show that complex III is the main site of the enhanced mitochondrial H(2)O(2) production that occurs in skeletal muscle of patients with COPD, and the latter appears to contribute to muscle oxidative damage.

Francisco Giner de los Ríos y su legado pedagógico

BACKGROUND There is evidence in the literature that the incidence of pulmonary complications and mortality is fair enough in patients with lower pulmonary function than conventionally accepted. In this article, we validate in patients with low baseline lung function (ie, FEV(1) or diffusing capacity of the lung for carbon monoxide [DLCO] < 80%) an algorithm to evaluate anatomic lung surgery in patients with low predicted postoperative lung function (ie, either FEV(1)-postoperative estimated [ppo] or DLCO-ppo < 40% or both between 30% and 40% predicted) if peak oxygen uptake (VO(2)peak)-ppo > 10 mL/kg/min. METHODS We prospectively studied 126 consecutive patients evaluated for anatomic resection of lung tumors by thoracotomy. RESULTS Ninety-two patients were operated on: age 67 (8 SD) years; FEV(1) 63 (14)% pp; DLCO 71 (19)% pp; VO(2)peak 71 (19)% predicted; and 2-year Kaplan-Meier conditional probability of survival (CPS) 0.62 (0.06). Thirty-day perioperative mortality was 6.4%. Thirty-four patients were not functionally fit, or rejected the procedure: age 69 (8) years; FEV(1) 58 (16)% predicted; DLCO 67 (26)% predicted; VO(2)peak 66 (16)% predicted. In this group, 2-year CPS was 0.18 (0.08), P < .01. Subgroups A (FEV(1)-ppo and DLCO-ppo > 40% predicted) and B (either FEV(1)-ppo or DLCO-ppo < 40% predicted or both between 30% and 40% predicted) were comparable in terms of perioperative morbidity; however, they were different in terms of 30-day mortality (A, 1/53 [1.9%]; B, 5/37 [13.5%]; P = .047; relative risk, 7.2; 95% CI 1.1-27.7). The survival functions of both subgroups were significantly different (P < .01) from nonsurgical subjects. CONCLUSIONS Adherence to the proposed algorithm results in a reasonable preoperative mortality in patients with low preoperative lung function. Although perioperative mortality is significantly higher when predicted postoperative lung function is low, 2-year survival of patients is better than if such patients had not undergone surgery.