Obesity is a disease that has become a serious public health issue worldwide, and chronic stressors, which are a problem for modern society, cause neuroendocrine changes with alterations in food intake. Obesity and chronic stress are associated with the development of cardiovascular diseases and metabolic disorders. In this study, a rat model was used to evaluate the effects of a hypercaloric diet plus chronic restraint stress on the serum leptin and lipids levels and on the weight of specific adipose tissue (mesenteric, MAT; subcutaneous, SAT and visceral, VAT). Wistar rats were divided into the following 4 groups: standard chow (C), hypercaloric diet (HD), stress plus standard chow (S), and stress plus hypercaloric diet (SHD). The animals in the stress groups were subjected to chronic stress (placed inside a 25 cm × 7 cm plastic tube for 1h per day, 5 days per week for 6 weeks). The following parameters were evaluated: the weight of the liver, adrenal glands and specific adipose tissue; the delta weight; the Lee index; and the serum levels of leptin, corticosterone, glucose, total cholesterol, and triglycerides. The hypercaloric diet induced obesity in rats, increasing the Lee index, weight, leptin, triglycerides, and cholesterol levels. The stress decreased weight gain even in animals fed a hypercaloric diet but did not prevent a significant increase in the Lee index. However, an interaction between the independent factors (hypercaloric diet and stress) was observed, which is demonstrated by the increased serum leptin levels in the animals exposed to both protocols.

Objectives: It is know that repeated exposure to opiates impairs spatial learning and memory and that the hippocampus has important neuromodulatory effects after drug exposure and withdrawal symptoms. Thus, the aim of this investigation was to assess hippocampal levels of BDNF, oxidative stress markers associated with cell viability, and TNF-alpha in the short, medium and long term after repeated morphine treatment in early life. Methods: Newborn male Wistar rats received morphine (morphine group) or saline (control group), 5 ug in the mid-scapular area (s.c.), starting on postnatal day 8 (P8), once daily for 7 days, and neurochemical parameters were assessed in the hippocampus on postnatal days 16 (P16), 30 (P30), and 60 (P60). BDNF and TNF-alpha levels were analyzed through ELISA. Cell viability and cell damage were analyzed in dissected hippocampus with or without H2O2 damage. Superoxide dismutase (SOD) activity was determined using RANSOD kit; Glutathione peroxidase (GPx) activity was determined as described by Wendel (1981), with some modifications; reactive species production by chemical oxidation of Dichlorodihydrofluorescein (DCFH) was evaluated in according method described by Sriram et al (1987); total Thiol level was evaluated in according method described by Aksenov and Markesbery (2001). The data analysis and interactions were evaluated using two-way ANOVA (morphine, age, morphine*age) followed by the Student-Newman-Keuls (SNK) method when indicated. The between group differences were considered significant at P<0.05. The number of animals was 4-7/group/age for each assay. Results: The two way ANOVA showed no effect of age (P = 0.327), but there is effect of morphine (P = 0.042), and interaction between age and morphine treatment (P = 0.049) in BDNF levels. In the TNFalpha levels, showed effects of age (P = 0.036), of morphine treatment (P = 0.011), and no interaction between age and morphine treatment (P = 0.275). There is effect of morphine treatment (P = 0.01), no effect of age (P = 0.127) and no interaction between age and morphine treatment in the superoxide dismutase activity (P = 0.144); effect of age (P<0.001), no effects of morphine treatment (P = 0.624) and no interactions between age and morphine treatment in the glutathione peroxidase activity (P = 0.164); in the thiol levels was also observed effect of age (P = 0.041), no effects of morphine treatment (P = 0.178) and no interactions between age and morphine treatment (P = 0.254); there is effect of age (P<0.001), no effects of treatment (P = 0.541) and no interactions between age and morphine treatment in the analysis of reactive species production (P = 0.715). In the MTT assay, there are no interactions between age and morphine treatment and H2O2-induced cellular damage (P = 0.887), between morphine and age (P = 0.880) and between morphine and H2O2-induced cellular damage (P = 0.200). However, there is effect of H2O2-induced cellular damage (P<0.001), and interaction between age and H2O2-induced cellular damage (P = 0.034), and no eff...

Objetivou-se avaliar a adaptação à universidade e a sua relação com a ocorrência de Transtornos Mentais Comuns (TMC) em graduandos de enfermagem. Estudo analítico, transversal, com abordagem quantitativa dos dados, realizado com 92 graduandos de enfermagem de uma Instituição Federal de Ensino Superior de Minas Gerais. Para coleta de dados foram utilizados um questionário sociodemográfico e acadêmico, o Questionário de Vivências Acadêmicas-reduzido (QVA-r) e o Self-Reporting Questionnaire(SRQ-20). Observou-sebom nível de adaptação entre os participantes, commelhores escores nadimensão Carreira e escores inferiores na dimensão Pessoal. Encontrou-se um indicativo de TMC de 43,5% e uma correlação inversa com adaptação à universidade, indicando que quanto melhor a adaptação, menor a probabilidade de TMC. Os achados evidenciaram que o processo de adaptação à universidade está relacionado à saúde mental dos graduandos e indicam a necessidade de intervenções direcionadas à adaptação acadêmica como estratégia de promoção da saúde.

No abstract

No abstract

No abstract

Manganese (Mn) is an essential element for human health. However, at high concentrations Mn may be neurotoxic. Mn accumulates in astrocytes, affecting their redox status. In view of the high antioxidant and anti-inflammatory properties of the exotic Brazilian fruit açaí (Euterpe oleracea Mart.), its methanolic extract was obtained by solid-phase extraction (SPE). This açaí extract showed considerable anthocyanins content and direct antioxidant capacity. The açaí extract scavenged 2,2-diphenyl-1-picrylhydrazyl radicals (DPPH•) with an EC₅₀ of 19.1 ppm, showing higher antioxidant activity compared to butylated hydroxytoluene (BHT), but lower than ascorbic acid and quercetin. This obtained açaí extract also attenuated Mn-induced oxidative stress in primary cultured astrocytes. Specifically, the açaí extract at an optimal and nutritionally relevant concentration of 0.1 μg/ml prevented Mn-induced oxidative stress by (1) restoring GSH/GSSG ratio and net glutamate uptake, (2) protecting astrocytic membranes from lipid peroxidation, and (3) decreasing Mn-induced expression of erythroid 2-related factor (Nrf2) protein. A larger quantity of açaí extract exacerbated the effects of Mn on these parameters except with respect to lipid peroxidation assessed by means of F₂-isoprostanes. These studies indicate that at nutritionally relevant concentration, anthocyanins obtained from açaí protect astrocytes against Mn neurotoxicity, but at high concentrations, the "pro-oxidant" effects of its constituents likely prevail. Future studies may be profitably directed at potential protective effects of açaí anthocyanins in nutraceutical formulations.

SANTOS, V.S. Açaí (Euterpe oleracea Mart.) as an important source of potentially bioavailable essential chemical elements and neuroprotective effect of its extract on Manganese induced neurotoxicity in astrocytes. 2014. 135 f. Thesis (Ph.D., Doctoral).