172 research outputs found

    “Sagra Musicale Umbra”. Continuación y final

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    Los conciertos de la XIIIª “Sacra Musicale Umbra”.

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    Los tres estilos de Goffredo Petrassi.

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    Los Ballets del “Festival de los dos Mundos”.

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    Notas del Extranjero: Venecia y la Música Joven

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    Concurso Internacional de Composición 1958

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    Ecos del 33° Festival Mundial de Música Contemporánea de la SIMC.

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    Alterações musculares na doença pulmonar obstrutiva crônica

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    Aumentou recentemente o interesse da comunidade científica nas causas da intolerância ao exercício em pacientes com doença pulmonar obstrutiva crônica (DPOC). Além do desuso imposto principalmente pela inatividade física, há evidências de alterações no músculo esquelético do portador de DPOC Esta revisão expõe sucintamente as principais alterações muculoesqueléticas encontradas nos portadores de DPOC, dando ênfase a estudos referentes às alterações funcionais, estruturais e bioenergéticas. A perda de força muscular ocorre principalmente nos membros inferiores; a força muscular se mantém nos membros superiores em função do grande número de atividades de vida diária exercidas com a parte superior do corpo. Alguns pacientes com DPOC também apresentam diminuição da área de secção transversal tanto de braço quanto de coxa. A literatura descreve ainda diminuição de enzimas oxidativas, manutenção de enzimas glicolíticas e redução de fosfocreatina muscular,resultando em perda da capacidade aeróbia. Além da diminuição crônica do condicionamento, fatores como desnutrição, miopatia causada pelo uso crônico de corticostróides, redução dos hormônios anabólicos e do metabolismo de aminoácidos, inflamação e estresse oxidativo estão envolvidos na patogênese das alterações musculares. Os fatores determinantes dessas disfunções ainda não estão totalmente esclarecidos. Estratégias como exercício físico, estimulação elétrica neuromuscular, suplementação com anabolizantes e com creatina e terapia antioxidante são racionais para o tratamento das alterações musculares.Intolerance to exercise in COPD patients has recently drawn increased attention, as muscular changes have been suggested to be the main factor responsible for the physical impairment. In addition to deconditioning related to physical inactivity, there are evidences of skeletal muscle changes in these patients. This article briefly reviews the skeletal muscle dysfunction in patients with COPD, underlining muscular functional, structural, and bioenergetic changes. Loss of muscle strength occurs mainly in lower limbs; muscle strength remains near to normal in upper limbs probably due to daily-life activities being performed by the upper body. Some patients with COPD present reduced arm and leg muscle crossectional area. There are evidences that oxidative and phosphocreatine capacity is reduced with normal glicolitic enzymes concentration, resulting in poor aerobic capacity. Malnutrition, miopaty caused by chronic use of corticosteroids, reduced anabolic hormones, deconditioning, reduced aminoacids metabolism, local or systemic inflammation, and oxidative stress, may contribute to the pathogenesis of skeletal muscle dysfunction in COPD. The decisive factors of this dysfunction are not still totally explained. Strategies as exercise, neuromuscular electrical stimulation, supplementation with anabolic agents and creatine, and antioxidant therapy, are rationale for the muscle abnormalities management

    Factors associated with the minimal clinically important difference for health-related quality of life after physical conditioning in patients with COPD

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    OBJECTIVE: To identify factors associated with the minimal clinically important difference (MCID) for health-related quality of life (HRQoL) after physical conditioning in patients with COPD. METHODS: Thirty-five patients were submitted to a 12-week program of physical conditioning (strength training plus low-intensity aerobic exercise). Body composition, incremental treadmill test results, endurance treadmill test results, six-minute walk test results, peripheral muscle strength, MIP, baseline dyspnea index (BDI) and Saint George's Respiratory Questionnaire (SGRQ) scores were assessed at baseline and after the program, thus allowing the variations (Δ) to be calculated. The MCID for HRQoL was defined as a reduction of > 4% in the SGRQ total score. Subjects who responded to the program, achieving the MCID for HRQoL, were allocated to the responders (R) group (n = 24), and the remainder were allocated to the non-responders (NR) group (n = 11). RESULTS: The values obtained for the following variables were significantly higher in group R than in group NR (p 4% no escore total do SGRQ. Os pacientes que responderam ao treinamento, apresentando DCSQV, foram alocados no grupo respondedores (R; n = 24), e os demais pacientes foram alocados no grupo não-respondedores (NR; n = 11). RESULTADOS: Os seguintes resultados foram significativamente maiores no grupo R que no grupo NR (p < 0,05): VEF1 (1,48 ± 0,54 L vs. 1,04 ± 0,34 L), VEF1/CVF (47,9 ± 11,7% vs. 35,5 ± 10,7%), PaO2 (74,1 ± 9,7 mmHg vs. 65,0 ± 8,9mmHg) e ΔBDI [mediana (interquartil); 2,0 (0,0-3,5) vs. 0,0 (0,0-1,0)]. Houve correlação significativa (p < 0,01) de ΔSGRQ-sintomas (r = 0,44), ΔSGRQ-atividade (r = 0,62) e ΔSGRQ-total (r = 0,60) com ΔBDI. Após regressão logística, apenas ΔBDI foi selecionado como determinante da DCSQV. CONCLUSÕES: A DCSQV após o condicionamento físico está associada principalmente à redução da dispneia nos pacientes com DPOC. Portanto, são necessárias estratégias de tratamento visando interromper o ciclo dispneia-sedentarismo-dispneia nesses pacientes.Universidade Federal de São Paulo (UNIFESP)UNESP Faculdade de Medicina de Botucatu Hospital das ClínicasUNESP Faculdade de Medicina de BotucatuUNIFESPSciEL

    Predictors of health status do not change over three-year periods and exacerbation makes difference in chronic obstructive pulmonary disease

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    <p>Abstract</p> <p>Background</p> <p>The association between disease markers and health status (HS) overtime is unclear. The aim of this study was to verify the predictors of HS at baseline and after three years in Chronic Obstructive Pulmonary Disease (COPD) patients.</p> <p>Methods</p> <p>Ninety-five consecutive COPD patients (66% male, age = 67 ± 9 y, FEV<sub>1 </sub>= 58 ± 23%) underwent the following evaluations at baseline and after three years: body composition, pulse oximetry (SpO<sub>2</sub>), six-minute walk distance (6MWD), Modified edical Research Council dyspnea scale (MMRC) and Saint George's Respiratory Questionnaire (SGRQ). The Charlson comorbidity index and BODE index were calculated. COPD exacerbations during the follow-up were evaluated. At baseline, age, gender, smoking, SpO<sub>2</sub>, BODE index or its components (BMI, MMRC, FEV<sub>1 </sub>and 6MWD), and Charlson index were included in a multiple linear regression analysis with the baseline SGRQ total score as the dependent variable. After three years, we included the final values of the variables plus the number of exacerbations and the final SGRQ total score as the dependent variable.</p> <p>Results</p> <p>SGRQ total score (42 ± 19% <it>vs </it>44 ± 19%; p = 0.041) and activity domain (52 ± 21% <it>vs </it>60 ± 22%; p < 0.001) deteriorated during follow-up. At baseline, BODE index was selected as a predictor of SGRQ total score (R<sup>2 </sup>= 0.46; p < 0.001); after three years, BODE index and age were the predictors (R<sup>2 </sup>= 0.49; p < 0.001). When the BODE index was replaced by its variables, MMRC was selected as the only variable associated with the SGRQ total score (R<sup>2 </sup>= 0.58; p < 0.001). After three years, MMRC, FEV<sub>1 </sub>and number of exacerbations were selected as predictors of SGRQ total score (R<sup>2 </sup>= 0.63; p < 0.001).</p> <p>Conclusion</p> <p>HS deteriorated significantly over the three-year period and the predictors of HS do not change over time. BODE index and dyspnea were predictors at baseline and after three years. Exacerbation was also a predictor of HS after three years.</p> <p>Trial Registration</p> <p>ClinicalTrials.gov: <a href="http://www.clinicaltrials.gov/ct2/show/NCT00605540">NCT00605540</a></p
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