Analysis of total arsenic content in purchased rice from Ecuador

Natural and anthropogenic sources contribute to arsenic contamination in water and human food chain in Andean countries. Human exposure to arsenic via rice consumption is of great concern in countries where this crop is the dominant staple food, and limited information is available on the arsenic contamination on rice in Ecuador. This work was to contribute to the lack of knowledge analysing total arsenic by hydride generation-atomic absorption spectrometry in the samples of white, brown and parboiled rice purchased in Ecuadorian markets and produced in the two main rice wetlands in Ecuador, Guayas and Los Ríos, were carried out. For the samples from Guayas, arsenic concentration in white, brown and parboiled rice were 0.174 ± 0.014, 0.232 ± 0.021, and 0.186 ± 0.017 mg/kg respectively, whereas samples of white rice from Los Ríos showed a total arsenic level of 0.258 ± 0.037 mg/kg. This last arsenic concentration exceeds recommended maximum permissible limit by the FAO/WHO. Obtained data have available to estimate the Ecuadorian dietary exposure revealing serious health risk for population.S

NUEVAS HERRAMIENTAS MULTIMEDIA DE FORMACIÓN E INFORMACIÓN APLICADAS A LA EDUCACIÓN AMBIENTAL. DOS EJEMPLOS DE BUENAS PRÁCTICAS

La irrupción de Internet ha puesto en crisis, sin que nos demos cuenta, las formas clásicas de trabajo enseñanza-aprendizaje entre el alumno y el profesor. Una de las características de la Red es su carácter de sistema de difusión de información y de comunicación abierta. No hace falta contar con grandes infraestructuras. No es necesario un centro de cálculo como el que tienen nuestras universidades, no hacen falta espacios físicos (aulas) para reunirse. Ahora, en la red, una persona con una formación adecuada, puede subirse a la tarima, cualquiera puede tomar la tiza y utilizar la pizarra para explicar. En la red cualquier estudiante puede encontrar un espacio web para publicar información, cualquiera puede crear un espacio de comunicación (foros, listas de distribución de correos, salas de charlas, etc.). Cualquiera puede conseguir espacios de almacenamiento para depositar apuntes, exámenes, prácticas, etc. Incluso, cualquiera puede acceder a herramientas y le permiten hacer docencia a través de la red

La enseñanza de las ciencias químicas en las e-learning de las universidades españolas y su adaptación al EEES

SIN FINANCIACIÓNNo data 200

Hypothalamic kappa opioid receptor mediates both diet‐induced and melanin concentrating hormone–induced liver damage through inflammation and endoplasmic reticulum stress

The opioid system is widely known to modulate the brain reward system and thus affect the behavior of humans and other animals, including feeding. We hypothesized that the hypothalamic opioid system might also control energy metabolism in peripheral tissues. Mice lacking the kappa opioid receptor (κOR) and adenoviral vectors overexpressing or silencing κOR were stereotaxically delivered in the lateral hypothalamic area (LHA) of rats. Vagal denervation was performed to assess its effect on liver metabolism. Endoplasmic reticulum (ER) stress was inhibited by pharmacological (tauroursodeoxycholic acid) and genetic (overexpression of the chaperone glucose‐regulated protein 78 kDa) approaches. The peripheral effects on lipid metabolism were assessed by histological techniques and western blot. We show that in the LHA κOR directly controls hepatic lipid metabolism through the parasympathetic nervous system, independent of changes in food intake and body weight. κOR colocalizes with melanin concentrating hormone receptor 1 (MCH‐R1) in the LHA, and genetic disruption of κOR reduced melanin concentrating hormone–induced liver steatosis. The functional relevance of these findings was given by the fact that silencing of κOR in the LHA attenuated both methionine choline–deficient, diet‐induced and choline‐deficient, high‐fat diet–induced ER stress, inflammation, steatohepatitis, and fibrosis, whereas overexpression of κOR in this area promoted liver steatosis. Overexpression of glucose‐regulated protein 78 kDa in the liver abolished hypothalamic κOR‐induced steatosis by reducing hepatic ER stress. Conclusions:: This study reveals a novel hypothalamic–parasympathetic circuit modulating hepatic function through inflammation and ER stress independent of changes in food intake or body weight; these findings might have implications for the clinical use of opioid receptor antagonists. (Hepatology 2016;64:1086‐1104

Hypothalamic kappa opioid receptor mediates both diet- and MCH-induced liver damage through inflammation and ER stress

The opioid system is widely known to modulate the brain reward system and thus affect human and animal behaviour, including feeding. We hypothesized that the hypothalamic opioid system might also control energy metabolism in peripheral tissues. Mice lacking the kappa opioid receptor (κOR) and adenoviral vectors over-expressing or silencing κOR were stereotaxically delivered in the lateral hypothalamic area (LHA) of rats. Vagal denervation was performed to assess its effect on liver metabolism. ER stress was inhibited by pharmacological (tauroursodeoxycholic acid - TUDCA) and genetic (over-expression of the chaperone glucose-regulated protein 78 kDa - GRP78) approaches. The peripheral effects on lipid metabolism were assessed by histological techniques and Western blot. We show that in the LHA, κOR directly controls hepatic lipid metabolism via the parasympathetic nervous system, independent of changes in food intake and body weight. κOR colocalizes with melanin concentrating hormone receptor (MCH-R1) in the LHA and genetic disruption of κOR reduced MCH-induced liver steatosis. The functional relevance of these findings was given by the fact that silencing of κOR in the LHA attenuated both methionine choline-deficient diet- and choline deficient-high fat diet-induced ER stress, inflammation, steatohepatitis and fibrosis, whereas over-expression of κOR in this area promoted liver steatosis. Over-expression of the GRP78 in the liver abolished hypothalamic κOR-induced steatosis by reducing hepatic ER stress. CONCLUSIONS: Overall, this study reveals a novel hypothalamic-parasympathetic circuit modulating hepatic function via inflammation and ER stress independent of changes in food intake or body weight. These findings might have implications for the clinical use of opioid receptor antagonists. This article is protected by copyright. All rights reserved