Effects of Vaccination Against the H1N1 Virus on BDNF and TNF-α Plasma Levels in Pregnant Women.

BACKGROUND: Vaccination is a widespread strategy to protect women and their children during fetal development. However, there is a lack of knowledge about potential effects of H1N1 vaccination on concentration of cytokines that are important to mother's central nervous system functions and fetal neurodevelopment. OBJECTIVE: The main purpose of the present study was to evaluate such interaction. The specific goals were to study the effects of vaccination against the H1N1 virus on plasma levels of the Brain Derived Neurotrophic Factor(BDNF), Tumor Necrosis Factor-α (TNF-α) and TNF-α Receptors 1 and 2 (sTNFR1; sTNFR2), in different periods of gestation. METHODS: Data were obtained during the period of 6 months in 2010, from a sample of 94 pregnant women who were using the health care service of Conceição do Mato Dentro, a rural area in the state of Minas Gerais, Brazil. Seventeen women were in the first trimester of pregnancy, forty were in the second trimester and 37 were in the third trimester. Each of these groups was divided into two subgroups as follows: immunized against the H1N1 virus (I) and non-immunized (NI). Plasma concentrations of BDNF, TNF-α, sTNFR1 and sTNFR2 were measured using the sandwich ELISA. RESULTS: There was no difference in cytokine or neurotrophic factor levels evaluated between groups I and NI in any trimesters. CONCLUSION: These results show that the recommendation of vaccination against the H1N1 virus for all pregnant women as a public health measure could be considered safe, regarding aspects related to the role played by neurotrophin and cytokine, such as those of CNS development and immunological functions.

Biodegradable seeds of holmium don't change neurological function after implant in brain of rats.

AIM: To evaluate the surgical procedure and parenchymal abnormalities related to implantation of ceramic seeds with holmium-165 in rats' brain. BACKGROUND: An effective method of cancer treatment is brachytherapy in which radioactive seeds are implanted in the tumor, generating a high local dose of ionizing radiation that can eliminate tumor cells while protecting the surrounding healthy tissue. Biodegradable Ho166-ceramic-seeds have been addressed recently. METHODS AND MATERIALS: The experiments in this study were approved by the Ethics Committee on Animal Use at the Federal University of Ouro Preto, protocol number 2012/034. Twenty-one adult Fischer rats were divided into Naive Group, Sham Group and Group for seed implants (ISH). Surgical procedures for implantation of biodegradable seeds were done and 30 days after the implant radiographic examination and biopsy of the brain were performed. Neurological assays were also accomplished to exclude any injury resulting from either surgery or implantation of the seeds. RESULTS: Radiographic examination confirmed the location of the seeds in the brain. Neurological assays showed animals with regular spontaneous activity. The histological analysis showed an increase of inflammatory cells in the brain of the ISH group. Electron microscopy evidenced cytoplasmic organelles to be unchanged. Biochemical analyzes indicate there was neither oxidative stress nor oxidative damage in the ISH brain. CAT activity showed no difference between the groups as well as lipid peroxidation measured by TBARS. CONCLUSIONS: The analysis of the data pointed out that the performed procedure is safe as no animal showed alterations of the neurological parameters and the seeds did not promote histological architectural changes in the brain tissue.

Oxidative effects on lung inflammatory response in rats exposed to different concentrations of formaldehyde.

The formaldehyde (FA) is a crosslinking agent that reacts with cellular macromolecules such as proteins, nucleic acids and molecules with low molecular weight such as amino acids, and it has been linked to inflammatory processes and oxidative stress. This study aimed to analyze the oxidative effects on pulmonary inflammatory response in Fischer rats exposed to different concentrations of FA. Twenty-eight Fischer rats were divided into 4 groups (N = 7). The control group (CG) was exposed to ambient air and three groups were exposed to different concentrations of FA: 1% (FA1%), 5% (FA5%) and 10% (FA10%). In the Bronchoalveolar Lavage Fluid (BALF), the exposure to a concentration of 10% promoted the increase of inflammatory cells compared to CG. There was also an increase of macrophages and lymphocytes in FA10% and lymphocytes in FA5% compared to CG. The activity of NADPH oxidase in the blood had been higher in FA5% and FA10% compared to CG. The activity of superoxide dismutase enzyme (SOD) had an increase in FA5% and the activity of the catalase enzyme (CAT) showed an increase in FA1% compared to CG. As for the glutathione system, there was an increase in total glutathione (tGSH), reduced glutathione (GSH) and oxidized glutathione (GSSG) in FA5% compared to CG. The reduced/oxidized glutathione ratio (GSH/GSSG) had a decrease in FA5% compared to CG. There was an increase in lipid peroxidation compared to all groups and the protein carbonyl formation in FA10% compared to CG. We also observed an increase in CCL2 and CCL5 chemokines in the treatment groups compared to CG and in serum there was an increase in CCL2, CCL3 and CCL5 compared to CG. Our results point out to the potential of formaldehyde in promoting airway injury by increasing the inflammatory process as well as by the redox imbalance.

Analysis of liver fragment subjected to autologous transplant at rat's retroperitoneum.

BACKGROUND: To investigate the regeneration process of autologous implants of liver on the retroperitoneum. METHODS: Thirty male Fisher rats were used divided in to group 1 (G1): studied 60 d after surgery; group 2 (G2): studied 90 d after surgery; group 3 (G3): studied 180 d after surgery; and group C (GC): animals without surgery. Hepatic fragment was processed for histologic and biochemical analysis. RESULTS: There was inflammatory infiltrate, diffuse hydropic degeneration, necrosis, and moderate fibrosis that reduced in direct relation to the postsurgical time. The concentration of albumin was different between GC and G1 and between G1 and G3 (P = 0.0007). The Catalase (CAT) was related to the time of surgery with GC being different when compared with G1, G2, and G3 (P < 0.0001). The oxidative stress measured through the thiobarbituric acid reactive substances lipid peroxidation was different between the GC and the G2 groups (P = 0.0381). CONCLUSIONS: The analysis made showed hepatic regeneration in the fragment subjected to autologous transplant at the retroperitoneum.

Exposure to cigarette smoke during pregnancy causes redox imbalance and histological damage in lung tissue of neonatal mice.

Smoking during pregnancy is directly associated with numerous serious conditions, such as premature birth, low birth weight, and perinatal mortality. We quantitatively evaluated histological inflammatory alterations, oxidative damage by lipid peroxidation, the activity of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) in the lungs of mice exposed to cigarette smoke during pregnancy. Eight female and four male mice were mated for five days. Pregnant female mice were randomly allocated to the control group or to the cigarette smoke group (n = 8) in which they were exposed to 12 cigarettes per day in an exposure chamber, three times a day for 21 days. The control group (CG; n = 8) was kept in the exposure chamber for the same duration, but without exposure to cigarette smoke. Six newborn mice from both groups were weighed 24 hours after birth and then euthanized. Lung tissue was collected and subjected to histomorphometric and biochemical analyses. The cigarette smoke group showed a significant reduction in snout-vent length compared to the control group. Histomorphometric analysis indicated increased alveolar septal thickness and a larger alveolar lumen in mice exposed to cigarette smoke than in mice in the control group. We observed increased alveolar inflammatory infiltrate, decreased SOD activity, and significantly higher oxidative damage in the cigarette smoke group. Our data indicate that cigarette smoke exposure during pregnancy decreases body length at birth, changes lung tissue, and causes redox imbalance and histological damage in newborn mice.

High dietary salt decreases antioxidant defenses in the liver of fructose-fed insulin-resistant rats.

In this study we investigated the hypothesis that a high-salt diet to hyperinsulinemic rats might impair antioxidant defense owing to its involvement in the activation of sodium reabsorption to lead to higher oxidative stress. Rats were fed a standard (CON), a high-salt (HS), or a high-fructose (HF) diet for 10 weeks after which, 50% of the animals belonging to the HF group were switched to a regimen of high-fructose and high-salt diet (HFS) for 10 more weeks, while the other groups were fed with their respective diets. Animals were then euthanized and their blood and liver were examined. Fasting plasma glucose was found to be significantly higher (approximately 50%) in fructose-fed rats than in the control and HS rats, whereas fat liver also differed in these animals, producing steatosis. Feeding fructose-fed rats with the high-salt diet triggered hyperinsulinemia and lowered insulin sensitivity, which led to increased levels of serum sodium compared to the HS group. This resulted in membrane perturbation, which in the presence of steatosis potentially enhanced hepatic lipid peroxidation, thereby decreasing the level of antioxidant defenses, as shown by GSH/GSSG ratio (HFS rats, 7.098±2.1 versus CON rats, 13.2±6.1) and superoxide dismutase (HFS rats, 2.1±0.05 versus CON rats, 2.3±0.1%), and catalase (HFS rats, 526.6±88.6 versus CON rats, 745.8±228.7 U/mg ptn) activities. Our results indicate that consumption of a salt-rich diet by insulin-resistant rats may lead to regulation of sodium reabsorption, worsening hepatic lipid peroxidation associated with impaired antioxidant defenses.

Vildagliptin ameliorates oxidative stress and pancreatic beta cell destruction in type 1 diabetic rats.

BACKGROUND AND AIMS: It is believed that oxidative stress plays a role in the pathogenesis of diabetes mellitus. Several strategies have been developed with the objective of minimizing diabetic complications. Among these, inhibitors of dipeptidyl peptidase-IV (DPP-IV), which act by blocking degradation of incretin hormones, glucagon-like peptide hormone (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), have been the focus of many studies. It is known that, among the effects of incretins, we highlight its insulinotropic and cytoprotective effects on pancreatic ß-cells. The objective of this study was to evaluate the possible protective effects of treatment with vildagliptin, a DPP-IV inhibitor, in ß-cells in an experimental model of type 1 diabetes induced by streptozotocin (STZ). METHODS: Rats were treated for 4 weeks with vildagliptin at concentrations of 5 and 10 mg/kg. In order to observe the pancreatic damage and the possible protective effects of vildagliptin treatment, we measured stress markers TBARS and protein carbonyl, antioxidant enzymes SOD and catalase, and analyzed pancreatic histology. RESULTS: The treatment was effective in modulating stress in pancreatic tissue, both by reducing levels of stress markers as well as by increasing activity of SOD and catalase. After analyzing the pancreatic histology, we found that vildagliptin was also able to preserve islets and pancreatic ß-cells, especially at the concentration of 5 mg/kg. CONCLUSION: Thus, our results suggest that vildagliptin ameliorates oxidative stress and pancreatic beta cell destruction in type 1 diabetic rats. However, to evaluate the real potential of this medication in type 1 diabetes, further studies are needed.

Correlação entre a pressão expiratória máxima (pemáx) e pico de fluxo expiratório máximo (pfe) em indivíduos saudáveis / Correlation between maximal expiratory pressure (mpe) and maximal expiratory flow peak (mefp) in healthy individuals

Introdução: A prova de função pulmonar é um recurso que tem colaborado com a validação científica da fisioterapia respiratória. Ela é capaz de estimar, entre outras variáveis, as alterações dos volumes e capacidades pulmonares, e/ ou as alterações da força dos músculos respiratórios. A mensuração da força é realizada através do manovacuômetro, no qual se obtém a pressão expiratória máxima (PEmáx.). Outra forma de avaliar a função pulmonar é a medida do pico de fluxo expiratório (PFE). Objetivos: Investigar a correlação entre a PEmáx. e PFE, em indivíduos saudáveis. Métodos: O estudo foi realizado na Universidade Severino Sombra. Oitenta e um voluntários de ambos os sexos, 55 do sexo feminino (22,69 ± 0,41 anos), e 26 do sexo masculino (23,11 ± 3,51 anos) participaram deste estudo. Um questionário respiratório foi aplicado para investigar parâmetros clínicos. Todos os indivíduos realizaram exame de manovacuometria e medidor de PFE, em posição ortostática. Os dados foram expressos como média ± erro padrão da média. Resultados: Uma correlação positiva foi encontrada entre a PEmáx. e PFE (r = 0,43; r2 = 0,18, p <0,001). Foi estimada a equação de regressão linear (PFE = 2,93 + 148,07 x PEmáx.), e os valores normais estimados foram apresentados em uma tabela. Conclusões: Este estudo mostra a influência da força dos músculos expiratórios no PFE em vias aéreas, e sugeriu uma equação para estimar a função ventilatória normal, na prática clínica.

Introduction: The pulmonary function is a feature that has collaborated with the scientific validation of respiratory therapy. It is able to estimate, among other variables, changes in lung volumes and capacities, and/or changes in respiratory muscle strength. The measurement of force is obtained by the manometer, through which one can obtain the maximum expiratory pressure (MEP). Another way to assess lung function is by the measurement of expiratory flow peak (EFP). Objectives: To investigate the correlation between MEP and EFP in healthy individuals (patients). Methods: This study was developed at the Severino Sombra University. Eighty-one volunteers of both sexes, 55 females (22.69 ± 0.41 years) and 26 males (23.11 ± 3.51 years) participated in this study. A respiratory questionnaire was applied to investigate clinical parameters. All individuals underwent manometer examination and flow peak measurement, in the standing position. Data were expressed as mean ± standard error of mean. Results: A positive correlation was found between MEP and EFP (r = 0.43, r2 = 0.18, p <0.001). The linear regression equation was estimated (PEF = 148.07 + 2.93 x MEP) and normal values were presented in a table. Conclusions: This study shows the influence of expiratory muscle strength in EFP in the airways, and suggested an equation to estimate the normal ventilating function in clinical practice.

Salt overload in fructose-fed insulin-resistant rats decreases paraoxonase-1 activity.

Paraoxonase 1 (PON1) is a HDL-associated esterase/lactonase and its activity is inversely related to the risk of cardiovascular diseases. The aim of the present study was to evaluate the effect of a high-salt diet on serum PON1 activity in fructose-fed insulin-resistant rats. Adult male Fischer rats were initially divided into two groups. Control (CON), which received a normal salt diet and drinking water throughout the study; high fructose (HF), which received a normal salt diet and 20% fructose supplemented drinking water. After 10 weeks, half of the animals from HF group were randomly switched to a high-salt diet and 20% fructose supplemented drinking water (HFS) for more 10 weeks. Serum PON1 activity was determined by synthetic substrate phenyl acetate. HFS rats showed markedly decreased PON1 activity (HFS rats, 44.3 ± 14.4 g/dL versus CON rats, 64.4 ± 13.3 g/dL, P < 0.05) as compared to controls. In parallel, the level of oxidative stress, as indicated by thiobarbituric acid reactive substances (TBARS), was increased in HFS rats by 1.2-fold in the liver in relation to controls and was negatively correlated with PON activity. Differential leukocyte counts in blood showed a significant change in lymphocytes and monocytes profile. In conclusion, these results show that PON1 activity is decreased in fructose-fed insulin-resistant rats on a high-salt diet, which may be associated with increased oxidative stress, leading to inflammation.