Swimming exercise modifies oxidative stress in skeletal and cardiac muscles of diabetic rats

Introduction: Oxidative stress is a key factor leading to the deterioration of diabetes. Oxidative stress exacerbates diabetes and induction of the activity of the antioxidant system may be required to prevent this effect. Objetive: The aim of the present study was to evaluate the redox state in the skeletal and cardiac muscles in a diabetes rat model subjected to swimming exercise for 4 weeks. Methods: Wistar rats were divided into four groups: untrained control (C), trained control (T), untrained alloxan-induced diabetes (D), and trained alloxan-induced diabetes (TD). The redox state of the skeletal and cardiac muscles was assessed by analyzing TBARS, -SH groups, H2O2 production, and SOD and catalase activity. The total number of cardiomyocytes and the total area of collagen fibers in the cardiac muscle were measured by histomorphometry. Results: In the Soleus muscles, the TD group showed increased H2O2 levels and catalase activity compared to the T group, and SOD activity compared to the D group. Regarding the red gastrocnemius, the TD group presented higher SOD and lower catalase activities than the D group. Regarding the cardiac muscle, the TD group presented lower TBARS and higher levels of -SH groups and catalase activity than the D group. Swimming exercise decreased hyperglycemia and reduced pathology, as evidenced by the reduced number of cardiomyocytes and the area of collagen fibers. Conclusion: Swimming exercise in diabetic rats controlled hyperglycemia and oxidative damage, and the reduced fibrosis in the cardiac muscle of diabetic rats

Frequency of Fabry disease in male and female haemodialysis patients in Spain

<p>Abstract</p> <p>Background</p> <p>Fabry disease (FD), an X-linked lysosomal storage disorder, is caused by a reduced activity of the lysosomal enzyme α-galactosidase A. The disorder ultimately leads to organ damage (including renal failure) in males and females. However, heterozygous females usually present a milder phenotype with a later onset and a slower progression.</p> <p>Methods</p> <p>A combined enzymatic and genetic strategy was used, measuring the activity of α-galactosidase A and genotyping the α-galactosidase A gene (<it>GLA</it>) in dried blood samples (DBS) of 911 patients undergoing haemodialysis in centers across Spain.</p> <p>Results</p> <p><it>GLA </it>alterations were found in seven unrelated patients (4 males and 3 females). Two novel mutations (p.Gly346AlafsX347 and p.Val199GlyfsX203) were identified as well as a previously described mutation, R118C. The R118C mutation was present in 60% of unrelated patients with <it>GLA </it>causal mutations. The D313Y alteration, considered by some authors as a pseudo-deficiency allele, was also found in two out of seven patients.</p> <p>Conclusions</p> <p>Excluding the controversial D313Y alteration, FD presents a frequency of one in 182 individuals (0.55%) within this population of males and females undergoing haemodialysis. Moreover, our findings suggest that a number of patients with unexplained and atypical symptoms of renal disease may have FD. Screening programmes for FD in populations of individuals presenting severe kidney dysfunction, cardiac alterations or cerebrovascular disease may lead to the diagnosis of FD in those patients, the study of their families and eventually the implementation of a specific therapy.</p

O Programa de Cidades Históricas : por uma política integrada de preservação do patrimônio cultural urbano

O Programa de Cidades Históricas (PCH), implementado a partir de 1973, foi o primeiro programa federal que investiu recursos para a recuperação do patrimônio cultural urbano. Implementado pelo Ministério do Planejamento, buscava o desenvolvimento econômico das cidades históricas e dialogava com outros assuntos em pauta naquele momento, como o desenvolvimento urbano e regional e o turismo cultural. Tinha em sua concepção uma mudança na maneira de abordar as cidades históricas: a partir do entendimento da cidade como produtora de capital, o patrimônio cultural geraria desenvolvimento econômico pelo seu consumo para a atividade turística. De 1973 a 1979, foram investidos 17,3 milhões de dólares, realizando-se 143 obras em monumentos (85% dos investimentos); 8 cursos de qualificação de mão de obra nos três níveis (superior, intermediário e operário); 7 planos urbanísticos; 6 obras em espaços públicos (urbanos); e 10 ações de tipos diversos. Nossa análise busca entender essa política a partir do seu processo de formulação e implementação, no período de 1972 a 1979. Pretende, nesse sentido: a) avaliar as relações de poder em jogo durante a construção e a implementação do programa; b) compreender o grau de sucesso que o programa obteve na construção de um Sistema Nacional de Patrimônio Cultural, analisando sua articulação junto aos estados e outros órgãos federais; e c) avaliar o papel do programa enquanto indutor de novas práticas institucionais no campo da preservação do patrimônio cultural, especialmente com relação ao Iphan e aos estados federativos brasileiros.The Historic Cities Program (PCH: 1973-1979) was the first federal program that has invested resources to the recovery of the urban cultural heritage. Implemented by the Ministry of Planning, sought economic development of historic towns and dialogued with other items on the agenda at the time, such as urban and regional development and cultural tourism. It brought a change in the way of approach the historic towns: from the understanding of the city as a producer of capital, heritage would generate economic development through its consume by the tourism. From 1973 to 1979 it was invested 17.3 million dollars, performing 143 works on monuments (85% of investments); 8 hand-to-work training courses in three levels (top, middle and working class); 7 urban plans; 6 works in public spaces (urban); and 10 shares of various types. Our analysis seeks to understand this policy from its formulation and implementation in the period from 1972 to 1979. The aim, in this sense, is: a) to assess the power relations at play during construction and implementation of the Program; b) to understand the degree of success that the program achieved in building a national system, analyzing its relationship with states and other federal agencies; and c) to evaluate the role of Program while inducing new institutional practices in the field of preservation of cultural heritage, especially with regard to Iphan

Genomics and epidemiology for gastric adenocarcinomas (GE4GAC): a Brazilian initiative to study gastric cancer

Abstract Gastric cancer (GC) is the fifth most common type of cancer worldwide with high incidences in Asia, Central, and South American countries. This patchy distribution means that GC studies are neglected by large research centers from developed countries. The need for further understanding of this complex disease, including the local importance of epidemiological factors and the rich ancestral admixture found in Brazil, stimulated the implementation of the GE4GAC project. GE4GAC aims to embrace epidemiological, clinical, molecular and microbiological data from Brazilian controls and patients with malignant and pre-malignant gastric disease. In this letter, we summarize the main goals of the project, including subject and sample accrual and current findings

Inducible Nitric Oxide Synthase in Heart Tissue and Nitric Oxide in Serum of Trypanosoma cruzi-Infected Rhesus Monkeys: Association with Heart Injury

Chagas disease, a neglected tropical disease caused by the protozoan Trypanosoma cruzi, afflicts from 8 to 15 million people in the Latin America. Chronic chagasic cardiomyopathy (CCC) is the most frequent manifestation of Chagas disease. Currently, patient management only mitigates CCC symptoms. The pathogenic factors leading to CCC remain unknown; therefore their comprehension may contribute to develop more efficient therapies. In patients, high nitric oxide (NO) levels have been associated with CCC severity. In T. cruzi-infected mice, NO, mainly produced via inducible nitric oxide synthase (iNOS/NOS2), is proposed to work in parasite control. However, the participation of iNOS/NOS2 and NO in T. cruzi control and heart injury has been questioned. Here, infected rhesus monkeys and iNOS/NOS2-deficient mice were used to explore the participation of iNOS/NOS2-derived NO in heart injury in T. cruzi infection. Chronically infected monkeys presented electrical abnormalities, myocarditis and fibrosis, resembling the spectrum of human CCC. Moreover, cardiomyocyte lesion correlated with iNOS/NOS2+ cells infiltrating the cardiac tissue. Our findings support that parasite-driven iNOS/NOS2+ cells accumulation in the cardiac tissue and NO overproduction contribute to cardiomyopathy severity, mainly disturbing the pathway involved in electrical synchrony in T. cruzi infection