8 research outputs found

    Comparação de variáveis cardiorrespiratórias máximas entre a corrida em piscina funda e a corrida em esteira

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    The aim of this study was to compare the maximal cardiorespiratory responses between deep water running (DWR) and treadmill running (TR). Five young women performed two maximal tests (DWR and TR), with progressive loads, until subjects’ exhaustion. Oxygen uptake (VO2) and minute ventilation (Ve) were evaluated trough a KB1-C gas analyzer (AEROSPORT) and heart rate (HR), trough a S610 frequencemeter (POLAR). Paired t-test was used, with p < 0.05 (SPSS 13.0). The results obtained in DWR for maximal effort were significantly lower than TR for variables VO2, Ve and HR. This lower behavior probably occurred due the hydrostatic effects from aquatic environment and the different muscular recruitment pattern. It can be concluded that DWR, when compared to TR, in a maximal effort protocol, causes a smaller cardiorespiratory demand for studied variables in young women.O objetivo deste estudo foi comparar as respostas cardiorrespiratórias máximas entre a corrida em piscina funda (CPF) e a corrida em esteira (CE). Cinco mulheres jovens realizaram dois testes máximos (CPF e CE), realizados com cargas progressivas, até a exaustão dos sujeitos. O consumo de oxigênio (VO2) e a ventilação minuto (Ve) foram avaliados através de um analisador de gases KB1-C (AEROSPORT) e a freqüência cardíaca (FC), através de um freqüêncímetro S610 (POLAR). Utilizou-se Teste t pareado, com p < 0,05 (SPSS 13.0). Os resultados obtidos na CPF para o máximo esforço foram significativamente menores que na CE para as variáveis VO2, Ve e FC. Esse menor comportamento provavelmente ocorreu devido aos efeitos hidrostáticos do meio aquático e ao diferente padrão de recrutamento muscular. Pode-se concluir que a CPF, quando comparada à CE, em protocolo de esforço máximo, causa uma menor demanda cardiorrespiratória para as variáveis estudadas em mulheres jovens

    Induction of oxidative stress in rat brain by the metabolites accumulating in maple syrup urine disease

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    Maple syrup urine disease (MSUD) is an inherited disorder caused by deficiency of branched-chain l-2-keto acid dehydrogenase complex activity. Affected patients present severe brain dysfunction manifested as convulsions, coma, psychomotor delay and mental retardation. However, the underlying mechanisms of these neurological findings are virtually unknown. In this study, we tested the in vitro effect of l-leucine, l-isoleucine and l-valine, the amino acids accumulating in MSUD, on the lipid peroxidation parameters chemiluminescence and thiobarbituric acid-reactive substances (TBA-RS), as well as on total radical-trapping antioxidant potential (TRAP) and total antioxidant reactivity (TAR) in cerebral cortex from 30-day-old rats. l-Leucine significantly increased chemiluminescence and TBA-RS measurements and markedly decreased TRAP and TAR values. l-Isoleucine increased chemiluminescence and decreased TRAP measurements, but TAR and TBA-RS levels were not altered by the amino acid. Finally, TRAP measurement was diminished by l-valine. The results indicate a stimulation of lipid peroxidation and a reduction of brain capacity to efficiently modulate the damage associated with an increased production of free radicals by the branched-chain amino acids (BCAAs) accumulated in MSUD. It is therefore tempting to speculate that oxidative stress may be implicated in the brain damage found in MSUD patients

    Schistosoma mansoni infection as a trigger to collapsing glomerulopathy in a patient with high-risk APOL1 genotype.

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    BackgroundSchistosoma mansoni schistosomiasis (SM) remains a public health problem in Brazil. Renal involvement is classically manifested as a glomerulopathy, most often membranoproliferative glomerulonephritis or focal and segmental glomerulosclerosis. We report a case of collapsing glomerulopathy (CG) associated with SM and high-risk APOL1 genotype (HRG).Case reportA 35-year-old male was admitted for hypertension and an eight-month history of lower-limb edema, foamy urine, and increased abdominal girth. He had a recent diagnosis of hepatosplenic SM, treated with praziquantel, without clinical improvement. Laboratory tests revealed serum creatinine 1.89mg/dL, blood urea nitrogen (BUN) 24mg/dL, albumin 1.9g/dL, cholesterol 531mg/dL, low-density lipoprotein 426mg/dL, platelets 115000/mm3, normal C3/C4, antinuclear antibody (ANA), rheumatoid factor (RF), and antineutrophil cytoplasmic antibodies (ANCA), negative serologies for hepatitis C virus (HCV) and human immunodeficiency virus (HIV), HBsAg negative and AntiHBc IgG positive, no hematuria or leukocyturia, 24 hour proteinuria 6.56g and negative serum and urinary immunofixation. Kidney biopsy established the diagnosis of CG. A treatment with prednisone was started without therapeutic response, progressing to end-stage kidney disease 19 months later. Molecular genetics investigation revealed an HRG.ConclusionsThis is the first report of CG associated with SM in the setting of an HRG. This case highlights the two-hit model as a mechanism for CG pathogenesis, where the high-risk APOL1 genotype exerts a susceptibility role and SM infection serves as a trigger to CG
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