1,752 research outputs found

    The influence of the level of physical activity and human development in the quality of life in survivors of stroke

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    <p>Abstract</p> <p>Background</p> <p>The association between physical activity and quality of life in stroke survivors has not been analyzed within a framework related to the human development index. This study aimed to identify differences in physical activity level and in the quality of life of stroke survivors in two cities differing in economic aspects of the human development index.</p> <p>Methods</p> <p>Two groups of subjects who had suffered a stroke at least a year prior to testing and showed hemiplegia or hemiparesis were studied: a group from Belo Horizonte (BH) with 48 people (51.5 ± 8.7 years) and one from Montes Claros (MC) with 29 subjects (55.4 ± 8.1 years). Subsequently, regardless of location, the groups were divided into Active and Insufficiently Active so their difference in terms of quality of life could be analyzed.</p> <p>Results</p> <p>There were no significant differences between BH and MCG when it came to four dimensions of physical health that were evaluated (physical functioning, physical aspect, pain and health status) or in the following four dimensions of mental health status (vitality, social aspect, emotional aspect and mental health). However, significantly higher mean values were found in Active when compared with Insufficiently Active individuals in various measures of physical health (physical functioning 56.2 ± 4.4 vs. 47.4 ± 6.9; physical aspect 66.5 ± 6.5 vs. 59.1 ± 6.7; pain 55.9 ± 6.2 vs. 47.7 ± 6.0; health status 67.2 ± 4.2 vs. 56.6 ± 7.8) (arbitrary units), and mental health (vitality 60.9 ± 6.8 vs. 54.1 ± 7.2; social aspect 60.4 ± 7.1 vs. 54.2 ± 7.4; emotional aspect 64.0 ± 5.5 vs. 58.1 ± 6.9; mental health status 66.2 ± 5.5 vs. 58.4 ± 7.5) (arbitrary units).</p> <p>Conclusions</p> <p>Despite the difference between the cities concerning HDI values, no significant differences in quality of life were found between BH and MCG. However, the Active group showed significantly better results, confirming the importance of active lifestyle to enhance quality of life in stroke survivors.</p

    Dietary sulfur amino acid restriction upregulates DICER to confer beneficial effects

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    Dietary restriction (DR) improves health and prolongs lifespan in part by upregulating type III endoribonuclease DICER in adipose tissue. In this study, we aimed to specifically test which missing dietary component was responsible for DICER upregulation. Methods: We performed a nutrient screen in mouse preadipocytes and validated the results in vivo using different kinds of dietary interventions in wild type or genetically modified mice and worms, also testing the requirement of DICER on the effects of the diets. Results: We found that sulfur amino acid restriction (i.e., methionine or cysteine) is sufficient to increase Dicer mRNA expression in preadipocytes. Consistently, while DR increases DICER expression in adipose tissue of mice, this effect is blunted by supplementation of the diet with methionine, cysteine, or casein, but not with a lipid or carbohydrate source. Accordingly, dietary methionine or protein restriction mirrors the effects of DR. These changes are associated with alterations in serum adiponectin. We also found that DICER controls and is controlled by adiponectin. In mice, DICER plays a role in methionine restriction-induced upregulation of Ucpl in adipose tissue. In C. elegans, DR and a model of methionine restriction also promote DICER expression in the intestine (an analog of the adipose tissue) and prolong lifespan in a DICER-dependent manner. Conclusions: We propose an evolutionary conserved mechanism in which dietary sulfur amino acid restriction upregulates DICER levels in adipose tissue leading to beneficial health effects29124135CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQCOORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL DE NÍVEL SUPERIOR - CAPESFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESP305069/2015-2; 304995/2014-288887.143923/2017-002017/01184-9; 2017/07975-8; 2017/22057-5; 2015/03292-8; 2012/07259-7; 2016/02207-0; 2010/52557-0; 2015/01316-7; 2012/50558-5; 2015/19530-5We thank Elzira Elisabeth Saviani and Emanoel Cabral for valuable technical support. We thank the National Institute of Science and Technology on Photonics Applied to Cell Biology (INFABIC) at the Universidade Estadual de Campinas to provide access to microscopes, the Caenorhabditis Genetics Center (CGC) for worms and Dr. Amy Pasquinelli for the dcr-1 RNAi clone. CGC is funded by NIH Office of Research Infrastructure Programs ( P40 OD010440 ). We thank Carmen Perrone for sharing the composition of the methionine restriction diet, for valuable discussion and for sharing samples of rats exposed to methionine restriction. This study was funded by grants of the Fundação de Amparo à Pesquisa do Estado de São Paulo ( 2017/01184-9 , 2017/07975-8 , 2017/22057-5 , 2015/03292-8 , 2012/07259-7 , 2016/02207-0 , 2010/52557-0 , 2015/01316-7 , 2012/50558-5 and 2015/19530-5 ), Conselho Nacional de Desenvolvimento Científico e Tecnológico ( 305069/2015-2 and 304995/2014-2 ) and the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - German Academic Exchange Service ( PROBRAL - 88887.143923/2017-00 )

    Effects of Ibuprofen intake in muscle damage, body temperature and muscle power in Paralympic powerlifting athletes

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    The aim of this study is to evaluate the effect of ingesting ibuprofen on post-workout recovery of muscle damage, body temperature and muscle power indicators in Paralympic powerlifting athletes. The study was carried out with eight Paralympic powerlifting athletes (aged 27.0 ± 5.3 years and 79.9 ± 25.5 kg of body mass) competing at the national level, with a minimum training experience of 12 months, who all submitted to two experimental conditions: Ibuprofen (2 × 00 mg) and control. The maximal isometric force of the upper limbs and rate of force development, thermography, and serum biochemical analyzes of creatine kinase, lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase were measured before, after, 24 h after and 48 h after the intervention. Maximal isometric force only decreased in the placebo condition, which increased back to baseline levels, while no substantial decline in baseline force was seen in the ibuprofen condition, although no effect for exercise condition was detected. After the exercise, the rate of force development decreased significantly for both conditions and did not exceed baseline levels again after 48 h. Muscle temperature decreased significantly at 48-h post-exercise in the placebo condition, when compared with the previous day of measurement; and deltoid muscle temperature at 48-h post-exercise was higher with the ibuprofen condition. Although the results indicate some positive effects of ibuprofen use, they do not enable a clear statement regarding its positive effects on muscle function and muscle damage. Ibuprofen seems to have caused a delay in the anti-inflammatory response following exercise.publishedVersio

    Hydrogen peroxide production regulates the mitochondrial function in insulin resistant muscle cells: Effect of catalase overexpression

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    AbstractThe mitochondrial redox state plays a central role in the link between mitochondrial overloading and insulin resistance. However, the mechanism by which the ROS induce insulin resistance in skeletal muscle cells is not completely understood. We examined the association between mitochondrial function and H2O2 production in insulin resistant cells. Our hypothesis is that the low mitochondrial oxygen consumption leads to elevated ROS production by a mechanism associated with reduced PGC1α transcription and low content of phosphorylated CREB. The cells were transfected with either the encoded sequence for catalase overexpression or the specific siRNA for catalase inhibition. After transfection, myotubes were incubated with palmitic acid (500μM) and the insulin response, as well as mitochondrial function and fatty acid metabolism, was determined. The low mitochondrial oxygen consumption led to elevated ROS production by a mechanism associated with β-oxidation of fatty acids. Rotenone was observed to reduce the ratio of ROS production. The elevated H2O2 production markedly decreased the PGC1α transcription, an effect that was accompanied by a reduced phosphorylation of Akt and CREB. The catalase transfection prevented the reduction in the phosphorylated level of Akt and upregulated the levels of phosphorylated CREB. The mitochondrial function was elevated and H2O2 production reduced, thus increasing the insulin sensitivity. The catalase overexpression improved mitochondrial respiration protecting the cells from fatty acid-induced, insulin resistance. This effect indicates that control of hydrogen peroxide production regulates the mitochondrial respiration preventing the insulin resistance in skeletal muscle cells by a mechanism associated with CREB phosphorylation and β-oxidation of fatty acids

    MYBL1 rearrangements and MYB amplification in breast adenoid cystic carcinomas lacking the MYB–NFIB fusion gene

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    Breast adenoid cystic carcinoma (AdCC), a rare type of triple-negative breast cancer, has been shown to be driven by MYB pathway activation, most often underpinned by the MYB–NFIB fusion gene. Alternative genetic mechanisms, such as MYBL1 rearrangements, have been reported in MYB–NFIB-negative salivary gland AdCCs. Here we report on the molecular characterization by massively parallel sequencing of four breast AdCCs lacking the MYB–NFIB fusion gene. In two cases, we identified MYBL1 rearrangements (MYBL1–ACTN1 and MYBL1–NFIB), which were associated with MYBL1 overexpression. A third AdCC harboured a high-level MYB amplification, which resulted in MYB overexpression at the mRNA and protein levels. RNA-sequencing and whole-genome sequencing revealed no definite alternative driver in the fourth AdCC studied, despite high levels of MYB expression and the activation of pathways similar to those activated in MYB–NFIB-positive AdCCs. In this case, a deletion encompassing the last intron and part of exon 15 of MYB, including the binding site of ERG-1, a transcription factor that may downregulate MYB, and the exon 15 splice site, was detected. In conclusion, we demonstrate that MYBL1 rearrangements and MYB amplification probably constitute alternative genetic drivers of breast AdCCs, functioning through MYBL1 or MYB overexpression. These observations emphasize that breast AdCCs probably constitute a convergent phenotype, whereby activation of MYB and MYBL1 and their downstream targets can be driven by the MYB–NFIB fusion gene, MYBL1 rearrangements, MYB amplification, or other yet to be identified mechanisms. Copyright © 2017 Pathological Society of Great Britain and Ireland

    Kinin B(1) receptor deficiency leads to leptin hypersensitivity and resistance to obesity

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    OBJECTIVE-Kinins mediate pathophysiological processes related to hypertension, pain, and inflammation through the activation of two G-protein-coupled receptors, named B(1) and B(2). Although these peptides have been related to glucose homeostasis, their effects on energy balance are still unknown.RESEARCH DESIGN and METHODS-Using genetic and pharmacological strategies to abrogate the kinin B(1) receptor in different animal models of obesity, here we present evidence of a novel role for kinins in the regulation of satiety and adiposity.RESULTS-Kinin B(1) receptor deficiency in mice (B(1)(-/-)) resulted in less fat content, hypoleptinemia, increased leptin sensitivity, and robust protection against high-fat diet-induced weight gain. Under high-fat diet, B(1)(-/-) also exhibited reduced food intake, improved lipid oxidation, and increased energy expenditure. Surprisingly, B(1) receptor deficiency was not able to decrease food intake and adiposity in obese mice lacking leptin (ob/ob-B(1)(-/-)). However, ob/ob-B(1)(-/-) mice were more responsive to the effects of exogenous leptin on body weight and food intake, suggesting that B(1) receptors may be dependent on leptin to display their metabolic roles. Finally, inhibition of weight gain and food intake by B(1) receptor ablation was pharmacologically confirmed by long-term administration of the kinin B(1) receptor antagonist SSR240612 to mice under high-fat diet.CONCLUSIONS-Our data suggest that kinin B(1) receptors participate in the regulation of the energy balance via a mechanism that could involve the modulation of leptin sensitivity.Universidade Federal de São Paulo, Dept Biophys, BR-04023062 São Paulo, BrazilUniv Mogi das Cruzes, Mogi Das Cruzes, BrazilUniversidade Federal de São Paulo, Dept Physiol, BR-04023062 São Paulo, BrazilSanofi Aventis, Montpellier, FranceUniversidade Federal de São Paulo, Dept Med, BR-04023062 São Paulo, BrazilInst Natl Sante & Rech Med, Dept Renal & Cardiac Remodeling, U858 I2MR, Toulouse, FranceUniv Toulouse 3, Inst Med Mol Rangueil, F-31062 Toulouse, FranceInst Natl Rech Agron AgroParisTech, UMR914 Nutr Physiol & Ingest Behav, Paris, FranceMax Delbruck Ctr Mol Med, Berlin, GermanyUniversidade Federal de São Paulo, Dept Biophys, BR-04023062 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Physiol, BR-04023062 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Med, BR-04023062 São Paulo, BrazilWeb of Scienc

    Wild dogs at stake: deforestation threatens the only Amazon endemic canid, the short-eared dog (Atelocynus microtis)

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    The persistent high deforestation rate and fragmentation of the Amazon forests are the main threats to their biodiversity. To anticipate and mitigate these threats, it is important to understand and predict how species respond to the rapidly changing landscape. The short-eared dog Atelocynus microtis is the only Amazon-endemic canid and one of the most understudied wild dogs worldwide. We investigated short-eared dog habitat associations on two spatial scales. First, we used the largest record database ever compiled for short-eared dogs in combination with species distribution models to map species habitat suitability, estimate its distribution range and predict shifts in species distribution in response to predicted deforestation across the entire Amazon (regional scale). Second, we used systematic camera trap surveys and occupancy models to investigate how forest cover and forest fragmentation affect the space use of this species in the Southern Brazilian Amazon (local scale). Species distribution models suggested that the short-eared dog potentially occurs over an extensive and continuous area, through most of the Amazon region south of the Amazon River. However, approximately 30% of the short-eared dog's current distribution is expected to be lost or suffer sharp declines in habitat suitability by 2027 (within three generations) due to forest loss. This proportion might reach 40% of the species distribution in unprotected areas and exceed 60% in some interfluves (i.e. portions of land separated by large rivers) of the Amazon basin. Our local-scale analysis indicated that the presence of forest positively affected short-eared dog space use, while the density of forest edges had a negative effect. Beyond shedding light on the ecology of the short-eared dog and refining its distribution range, our results stress that forest loss poses a serious threat to the conservation of the species in a short time frame. Hence, we propose a re-assessment of the short-eared dog's current IUCN Red List status (Near Threatened) based on findings presented here. Our study exemplifies how data can be integrated across sources and modelling procedures to improve our knowledge of relatively understudied species

    Genetic events in the progression of adenoid cystic carcinoma of the breast to high-grade triple-negative breast cancer

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    Adenoid cystic carcinoma of the breast is a rare histologic type of triple-negative breast cancer with an indolent clinical behavior, often driven by the MYB-NFIB fusion gene. Here we sought to define the repertoire of somatic genetic alterations in two adenoid cystic carcinomas associated with high-grade triple-negative breast cancer. The different components of each case were subjected to copy number profiling and massively parallel sequencing targeting all exons and selected regulatory and intronic regions of 488 genes. Reverse transcription PCR and fluorescence in situ hybridization were employed to investigate the presence of the MYB-NFIB translocation. The MYB-NFIB fusion gene was detected in both adenoid cystic carcinomas and their associated high-grade triple-negative breast cancer components. Whilst the distinct components of both cases displayed similar patterns of gene copy number alterations, massively parallel sequencing analysis revealed intra-tumor genetic heterogeneity. In case 1, progression from the trabecular adenoid cystic carcinoma to the high-grade triple-negative breast cancer was found to involve clonal shifts with enrichment of mutations affecting EP300, NOTCH1, ERBB2 and FGFR1 in the high-grade triple-negative breast cancer. In case 2, a clonal KMT2C mutation was present in the cribriform adenoid cystic carcinoma, solid adenoid cystic carcinoma and high-grade triple-negative breast cancer components, whereas a mutation affecting MYB was present only in the solid and high-grade triple-negative breast cancer areas and additional three mutations targeting STAG2, KDM6A and CDK12 were restricted to the high-grade triple-negative breast cancer. In conclusion, adenoid cystic carcinomas of the breast with high-grade transformation are underpinned by MYB-NFIB fusion gene, and, akin to other forms of cancer, may be constituted by a mosaic of cancer cell clones at diagnosis. The progression from adenoid cystic carcinoma to high-grade triple-negative breast cancer of no special type may involve the selection of neoplastic clones and/ or the acquisition of additional genetic alterations
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