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Aran : Ua identitat incomòda. Discorsi sus era identitat aranesa en Internet. Reaccions ath projècte de Lei de Vegueries.
- Vila Parcerisa, Mònica
Analisi des discorsi sus era identitat aranesa en Internet pendent era polemica pera aprobacion deth Projècte de Lei de Vegueries, en hereuèr de 2010. A trauès der estudi d'aguesti discorsi s'identifiquen quini son es principaus trèits identitaris damb es quaus se definissen es aranesi., Anàlisi dels discursos sobre la identitat aranesa a Internet durant la polèmica per l'aprovació del Projecte de Llei de Vegueries, el mes de febrer de 2010. A través de l'estudi d'aquests discursos s'identifiquen quins són els principals trets identitaris amb els quals es defineixen els aranesos., Análisis de los discursos sobre la identidad aranesa en Internet durante la polémica por la aprobación del Proyecto de Ley de Veguerías, el mes de febrero de 2010. A través del estudio de estos discursos se identifican cuáles son los principales rasgos identitarios con los que se definen los araneses., This paper analyses the discourses on Aranese identity on the Internet throughout the controversy over the adoption of the Vegueries Law, on February 2010. Through the study of these discourses are identified the main identitary traits with which Aranese define themselves.
See at: http://hdl.handle.net/10609/6762
- Raemdonck, Anne Van
This article looks at the way culture is represented in 3 commonly used course books of Dutch as a foreign language. According to the author, everyday culture of the regions where Dutch is spoken, is presented from a nationalistic point of view, i.e. it is limited to either cultural, historical and social aspects of The Netherlands or cultural, historical and social aspects of the Flemish Community in Belgium. The existence of the other region or country where the same language is spoken is not only ignored but at times even portrayed wrongfully which has its logically negative effect upon the students" interpretation and can lead to prejudice and the teachers using those course books.
See at: http://hdl.handle.net/2445/59613
Drug-induced lipotoxicity: lipodystrophy associated with HIV-1 infection and antiretroviral treatment.
A subset of HIV-1-infected patients undergoing antiretroviral treatment develops a lipodystrophy syndrome. It is characterized by loss of peripheral subcutaneous adipose tissue (face, limbs, buttocks), visceral fat accumulation, and, in some cases, lipomatosis, especially in the dorsocervical area. In addition, these patients show metabolic alterations reminiscent of the metabolic syndrome, particularly dyslipidemia and insulin resistance. These alterations lead to enhanced cardiovascular risk in patients and favor the development of diabetes. Although a complex combination of HIV-1 infection and drug treatment-related events triggers the syndrome, lipotoxicity appears to contribute to the development of the syndrome. Active lipolysis in subcutaneous fat, combined with impaired fat storage capacity in the subcutaneous depot, drive ectopic deposition of lipids, either in the visceral depot or in nonadipose sites. Both hepatic steatosis and increased lipid content in skeletal muscle take place and surely contribute to systemic metabolic alterations, especially insulin resistance. Pancreatic function may also be affected by the exposure to high levels of fatty acids; together with direct effects of antiretroviral drugs, this may contribute to impaired insulin release and a prodiabetic state in the patients. Addressing lipotoxicity as a pathogenic actor in the lipodystrophy syndrome should be considered in strategies for treating and/or preventing the morphological alterations and systemic metabolic disturbances associated with lipodystrophy.
In this study we examined the effect of the statin atorvastatin on the Akt/GSK-3beta pathway. Our findings indicate that atorvastatin treatment for 15 days inhibited pressure overload-induced cardiac hypertrophy and prevented nuclear translocation of GATA4 and c-Jun and AP-1 DNA-binding activity. In addition, atorvastatin treatment prevented the increase in the phosphorylation of Akt and GSK-3beta caused by cardiac hypertrophy, and this effect correlated with an increase in protein levels of phosphatase and tensin homolog on chromosome 10 (PTEN), which negatively regulates the phosphoinositide-3 kinase/Akt pathway. To test whether the inhibitory effect of atorvastatin on Akt and GSK-3beta phosphorylation was direct we performed in vitro studies using embryonic rat heart-derived H9c2 cells, human AC16 cardiomyoblasts and neonatal rat cardiomyocytes. Preincubation of cells with atorvastatin prevented Akt/GSK-3beta phosphorylation by different hypertrophic stimuli without affecting PTEN protein levels. However, atorvastatin prevented endogenous reactive oxygen species (ROS) generation and PTEN oxidation, a process that correlates with its inactivation, suggesting that atorvastatin prevents ROS-induced PTEN inactivation in acute treatments. These findings point to a new potential anti-hypertrophic effect of statins, which can prevent activation of the Akt/GSK-3beta hypertrophic pathway by modulating PTEN activation by different mechanisms in chronic and acute treatments.
Targeted knockdown of Cerkl, a retinal dystrophy gene, causes mild affectation of the retinal ganglion cell layer.
In order to approach the function of the retinal dystrophy CERKL gene we generated a novel knockout mouse model by cre-mediated targeted deletion of the Cerkl first exon and proximal promoter. The excised genomic region (2.3kb) encompassed the first Cerkl exon, upstream sequences including the proximal promoter and the initial segment of the first intron. The Cerkl-/- mice were viable and fertile. The targeted Cerkl deletion resulted in a knockdown more than a knockout model, given that alternative promoters (unreported at that time) directed basal expression of Cerkl (35%). In situ hybridizations and immunohistochemistry showed that this remnant expression was moderate in the photoreceptors and weak in the ganglion and inner cell layers. Morphological characterization of the Cerkl-/- retinas did not show any gross structural changes, even at 12 months of age. However, some clear and consistent signals of gliosis and retinal stress were detected by the statistically significant increase of i) the glial fibrillary antigen protein (GFAP) expression, and ii) apoptosis, as detected by TUNEL. Remarkably, consistent non-progressive perturbation (from birth up to 12 months of age) of ganglion cells was supported by the decrease of the Brn3a marker expression as well as the reduced oscillatory potentials in the electroretinographic recordings. In conclusion, the Cerkl-/- knockdown shows a mild retinal phenotype, with increased levels of cellular stress and apoptosis indicators, and clear signs of functional alteration at the ganglion cell layer, but no detectable morphological changes.
To determine to what extent lipoprotein lipase activity in the liver of the newborn rat depends on milk ingestion, its changes were studied during different nutritional conditions. Newborns were placed with nurse rats with or without ligated nipples and they were killed at 0,8 or 24 h of life. Lipoprotein lipase in newborns liver was characterized by its inhibition in the presence of 1.0 M NaCl, its specific elution at 1.5 M NaCl on heparin-Sepharose 4B column and its requirement for serum in the assay mixture to manifest its activity. In fed animals lipoprotein lipase activity and triacylglycerol content in liver as well as circulating triacylglycerols and ketone bodies increased progressively after birth. When newborns were kept starved the change in enzyme activity was significantly enhanced, whereas the increase found after birth in the other parameters disappeared. Starvation produced reduction in circulating RIA-insulin levels in the newborn rats. Results show that liver lipoprotein lipase activity in the newborn rat is controlled by a mechanism which resembles that of the enzyme in the adult heart and indicate that its presence facilitates the uptake by the liver of fatty acids from circulating triacylglycerols for their oxidation rather than deposit.
Coordinate induction of Na(+)-dependent transport systems and Na+,K(+)-ATPase in the liver of obese Zucker rats.
Solute uptake into liver plasma membrane vesicles from either lean or obese Zucker rats was monitored. D-Glucose and L-leucine uptakes at physiological concentrations of the substrate were not different in lean and obese Zucker rats. In agreement with a previous report (Ruiz et al. (1991) Biochem. J. 280, 367-372) L-alanine uptake was significantly enhanced in those preparations from obese animals. Na(+)-coupled uridine transport was markedly enhanced also in obese rats. The effect was due to an increase in Vmax (5.5 +/- 0.6 vs. 2.1 +/- 0.2 pmol/mg protein per 3 s, P 0.01) without any significant change in Km (11.0 +/- 2.8 vs. 9.0 +/- 2.7 microM for obese and lean rats, respectively). Na+,K(+)-ATPase activity was also higher in liver plasma membrane vesicles from rat liver and it correlated with a higher amount of alpha 1-subunit protein in both, plasma membrane vesicles and homogenates from obese rat livers. In summary, in the hypertrophic liver of obese Zucker rats a coordinate induction of several Na(+)-dependent transport systems occurs and, in order to sustain the metabolic pressure associated with this adaptation, a significant induction of the Na+,K(+)-ATPase expression is also found. These data also provide new evidence for regulation of the recently characterized Na(+)-dependent nucleoside transporter.
Up-regulation of liver system A for neutral amino acid transport in euglycemic hyperinsulinemic rats.
To determine the role of insulin on the in vivo modulation of liver system A activity, we used the euglycemic hyperinsulinemic clamp coupled to the measurement of solute uptakes into plasma membrane vesicles partially purified from livers of hyperinsulinemic rats and their saline-infused controls. The clamp was performed in chronically catheterized rats, either in the fasted state, 24 h after surgery (Group I), or after 3 days of recovery (Group II). System A activity, measured as the MeAIB-inhibitable L-alanine uptake, was selectively induced by hyperinsulinemia, although the effect was much greater in Group II than in Group I rats (137% vs. 24% over the basal values, respectively). This might be explained by the higher basal levels found in those liver plasma membrane vesicles from Group I fasted animals. Hyperinsulinemia also decreased blood amino acids but to a similar extent in both experimental groups. This suggests that amino acid depletion by itself may not cause up-regulation of system A. Other transport activities involved in neutral amino acid transport (Systems ASC, N and L) were not modified by the clamp. The induction of system A cannot be explained by changes in the dissipation rate of the Na+ transmembrane gradient, because the differences between insulin- and saline-infused rats remained even when the electrochemical Na+ gradient was disrupted in the presence of monensin. Thus, hyperinsulinemia might induce an increase in the number of transporters inserted into the plasma membrane.
Effect of epidermal growth factor (EGF) on gluconeogenesis in isolated rat hepatocytes. Dependency on the red-ox state of the substrate.
It was found that EGF decreased both the basal- and the glucagon-stimulated gluconeogenesis from lactate alone or from a high lactate/pyruvate ratio and that it enhanced both the basal- and the glucagon-inhibited glucose synthesis from pyruvate alone or from a low lactate/pyruvate ratio. These findings demonstrate that the effect of both EGF and glucagon on glucose production by isolated hepatocytes depends on the red-ox state of the substrate.
Early alterations in energy metabolism in the hippocampus of APPswe/PS1dE9 mouse model of Alzheimer's disease.
The present study had focused on the behavioral phenotype and gene expression profile of molecules related to insulin receptor signaling in the hippocampus of 3 and 6 month-old APPswe/PS1dE9 (APP/PS1) transgenic mouse model of Alzheimer's disease (AD). Elevated levels of the insoluble Aß (1-42) were detected in the brain extracts of the transgenic animals as early as 3 months of age, prior to the Aß plaque formation (pre-plaque stage). By the early plaque stage (6 months) both the soluble and insoluble Aß (1-40) and Aß (1-42) peptides were detectable. We studied the expression of genes related to memory function (Arc, Fos), insulin signaling, including insulin receptor (Insr), Irs1 and Irs2, as well as genes involved in insulin growth factor pathways, such as Igf1, Igf2, Igfr and Igfbp2. We also examined the expression and protein levels of key molecules related to energy metabolism (PGC1-a, and AMPK) and mitochondrial functionality (OXPHOS, TFAM, NRF1 and NRF2). 6 month-old APP/PS1 mice demonstrated impaired cognitive ability, were glucose intolerant and showed a significant reduction in hippocampal Insr and Irs2 transcripts. Further observations also suggest alterations in key cellular energy sensors that regulate the activities of a number of metabolic enzymes through phosphorylation, such as a decrease in the Prkaa2 mRNA levels and in the pAMPK (Thr172)/Total APMK ratio. Moreover, mRNA and protein analysis reveals a significant downregulation of genes essential for mitochondrial replication and respiratory function, including PGC-1a in hippocampal extracts of APP/PS1 mice, compared to age-matched wild-type controls at 3 and 6 months of age. Overall, the findings of this study show early alterations in genes involved in insulin and energy metabolism pathways in an APP/PS1 model of AD. These changes affect the activity of key molecules like NRF1 and PGC-1a, which are involved in mitochondrial biogenesis. Our results reinforce the hypothesis that the impairments in both insulin signaling and energy metabolism precede the development of AD amyloidogenesis.