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-Background -Severe Acute Liver Failure (ALF) is a life-threatening clinical syndrome characterized by hepatocyte necrosis, loss of hepatic architecture, and impairment of liver functions. One of the main causes of ALF is hepatotoxicity from chemical agents, which damage hepatocytes and result in increase of reactive oxygen species. The vitamin E isoform is the one with the strongest biological antioxidant activity. Objective -To evaluate the antioxidant effect of vitamin E in this ALF model. Methods -We used 56 rats (mean weight of 300 g) divided into eight groups, four groups assessed at 24 hours and 4 assessed at 48 hours after induction: control group (CO); Vitamin E (Vit. E); Thioacetamide (TAA) and Thioacetamide + Vitamina E (TAA+Vit.E). Rats were submitted to injections of thioacetamide (400 mg/kg i.p.) at baseline and 8 hours later. Vitamin E (100 mg/kg ip) was administered 30 minutes after the second dose of thioacetamide. The 48-hour group rats received two additional doses of vitamin E (24h and 36h). At 24h or 48 hours after the administration of the first dose of TAA, rats were weighed and anesthetized and their blood sampled for evaluation of liver integrity through enzymes aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Liver tissue was sampled for assessment of lipid peroxidation (LPO) by the technique TBARS, antioxidant enzymes SOD, CAT, GPx and GST activity, levels of the NO 2 /NO 3 and histology by H&E in two times. The results were expressed as mean ± standard deviation and statistically analyzed by ANOVA followed by Student-Newman-Keuls, with P<0.05 considered as significant. The histopathological evaluation showed a decrease in liver injury (necrosis and inflammation) in both studied times. Conclusion -These results suggest that vitamin E was able to protect the liver from lesions caused by thioacetamide. HEADINGS -Acute liver failure. Thioacetamide. Oxidative stress. Antioxidants.

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Nonalcoholic steatohepatitis (NASH) is a disease with a high incidence worldwide, but its diagnosis and treatment are poorly managed. In this study, NASH pathophysiology and DNA damage biomarkers were investigated in mice with NASH treated and untreated with melatonin (MLT). C57BL/6 mice were fed a methionine-and choline-de cient (MCD) diet for four weeks to develop NASH. Melatonin was administered at 20 mg/kg during the last two weeks. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were measured, and hepatic tissue was dissected for histological analysis, evaluation of lipoperoxidation, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), as well as nuclear factor-erythroid 2 (Nrf2), tumor necrosis factor alpha (TNF-α), inducible nitric oxide synthase (iNOS), and tumor necrosis factor alpha (TGF-β) expression by immunohistochemistry.DNA damage was evaluated using Comet assay, while a micronucleus test in bone marrow was performed to assess the genomic instability associated with the disease. Melatonin decreased AST and ALT, liver in ammatory processes, balloonization and brosis in mice with NASH, decreasing TNF-α, iNOS, and TGF-β, as well as oxidative stress, shown by reducing lipoperoxidation, and intensifying Nrf2 expression. The SOD and GPx activities were increased while CAT was decreased by treatment with MLT.Although the micronucleus frequency was not increased in mice with NASH, a protective effect on DNA was observed with MLT treatment in blood and liver tissues using Comet assay. As conclusions, MLT slows down the progression of NASH, reducing hepatic oxidative stress and in ammatory processes, inhibiting DNA damage via anti-in ammatory and antioxidant actions.

The aim of the present study was to compare the responses of blood pressure, heart rate, and rate-pressure product of hypertensive women using beta-blockers with healthy controls during resistance exercise (by the end of the concentric phase of the contractions) and in the postexercise period (5 and 30 minutes after). Ten untrained normotensive women (N) and 10 mildly hypertensive females receiving 40 mg/day of propanolol (H) were selected. Three sets of 10 repetitions at 80% of 10 repetitions maximum with 30 s rest interval were performed on the leg press exercise. The H group exhibited lower systolic blood pressure after the second set compared with N. Heart rate and rate-pressure product were lower in H in all analyzed periods compared with N. Propanolol attenuates the cardiovascular response to a leg press resistance exercise in mildly hypertensive women.

Introdução. Na atenção básica do Sistema Único de Saúde (SUS) poucos são os relatos de reabilitação domiciliar do paciente pós Acidente Vascular Cerebral (AVC). Objetivos. Relatar casos de reabilitação domiciliar de adultos acometidos por AVC na atenção básica, em uma área de abrangência de uma Estratégia Saúde da Família (ESF). Método. Dados de diagnóstico clínico, comorbidades, número de sessões, condutas e avaliação fisioterapêuticas, sinais vitais antes e após as sessões e efeitos adversos foram coletados a partir de prontuários de pacientes, acometidos por AVC, em um ESF no município de Cachoeira do Sul–RS, Brasil. Para análise dos dados foi utilizado o teste T de Student para comparar a diferença entre os sinais vitais antes e após a intervenção fisioterapêutica. Resultados. Foram avaliados 4 prontuários de pacientes com diagnóstico clínico de AVC; de ambos os sexos e de idade média de 66,25±11,79 anos. O diagnóstico fisioterapêutico mais encontrado foi hemiparesia, alterações do equilíbrio e redução da funcionalidade. As condutas de reabilitação domiciliar mais prevalentes foram treino de marcha, alongamentos, exercícios ativos; orientações ao paciente e cuidadores e prescrição de exercícios físicos e exercícios respiratórios/ventilatórios. Não foi observado nenhum efeito adverso grave durante os atendimentos. Apenas um paciente não apresentou elevação dos sinais vitais após as sessões de reabilitação domiciliar. Conclusão. A reabilitação domiciliar na atenção básica pública de pacientes com AVC é factível, eficaz e variável quanto às condutas e avaliações adotadas. O fisioterapeuta desempenha papel importante e amplo no contexto clínico do atendimento domiciliar do paciente acometido por AVC.

Nonalcoholic steatohepatitis (NASH) is a disease with a high incidence worldwide, but its diagnosis and treatment are poorly managed. In this study, NASH pathophysiology and DNA damage biomarkers were investigated in mice with NASH treated and untreated with melatonin (MLT). C57BL/6 mice were fed a methionine- and choline-deficient (MCD) diet for four weeks to develop NASH. Melatonin was administered at 20 mg/kg during the last two weeks. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were measured, and hepatic tissue was dissected for histological analysis, evaluation of lipoperoxidation, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), as well as nuclear factor-erythroid 2 (Nrf2), tumor necrosis factor alpha (TNF-α), inducible nitric oxide synthase (iNOS), and tumor necrosis factor alpha (TGF-β) expression by immunohistochemistry. DNA damage was evaluated using Comet assay, while a micronucleus test in bone marrow was performed to assess the genomic instability associated with the disease. Melatonin decreased AST and ALT, liver inflammatory processes, balloonization and fibrosis in mice with NASH, decreasing TNF-α, iNOS, and TGF-β, as well as oxidative stress, shown by reducing lipoperoxidation, and intensifying Nrf2 expression. The SOD and GPx activities were increased while CAT was decreased by treatment with MLT. Although the micronucleus frequency was not increased in mice with NASH, a protective effect on DNA was observed with MLT treatment in blood and liver tissues using Comet assay. As conclusions, MLT slows down the progression of NASH, reducing hepatic oxidative stress and inflammatory processes, inhibiting DNA damage via anti-inflammatory and antioxidant actions.