24 research outputs found

    Políticas medioambientales en institutos de investigación: Un análisis aplicado a la investigación de ámbito sanitario en España

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    El objetivo principal de este trabajo es estudiar las políticas medioambientales en institutos de investigación y los factores que influyen en su adopción. A tal fin se analizan las principales características de las políticas medioambientales de los Institutos de investigación más relevantes en ámbito sanitario en España, que son en su mayoría fundaciones públicas dedicadas a la investigación médica. Para alcanzar el objetivo anteriormente descrito, se plantea un doble enfoque de análisis. En primer lugar, se analizan las principales variables económico-financieras y organizativas de una muestra integrada por 35 institutos públicos de investigación españoles en ámbito sanitario. Asimismo, se recaba información acerca de las políticas medioambientales adoptadas por estas organizaciones y se realiza un análisis de las mismas. En segundo lugar, se profundiza en un caso de estudio para analizar uno de los institutos de investigación de la muestra a través la realización de entrevistas semi-estructuradas a 4 de sus profesionales.<br /

    Cytokine pathway disruption in a mouse model of schizophrenia induced by Munc18-1a overexpression in the brain

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    Background: An accumulating body of evidence points to the significance of neuroinflammation and immunogenetics in schizophrenia, and an imbalance of cytokines in the central nervous system (CNS) has been suggested to be associated with the disorder. Munc18-overexpressing mice (Munc18-OE) have provided a model for the study of the alterations that may underlie the symptoms of subjects with schizophrenia. The aim of the present study was to elucidate the involvement of neuroinflammation and cytokine imbalance in this model. Methods: Cytokines were evaluated in the cortex and the striatum of Munc18-OE and wild-type (WT) mice by enzyme-linked immunosorbent assay (ELISA). Protein levels of specific microglia and macrophage, astrocytic and neuroinflammation markers were quantified by western blot in the cortex and the striatum of Munc18-OE and WT mice. Results: Each cytokine evaluated (Interferon-gamma (IFN-γ), Tumor Necrosis Factor-alpha (TNF-α), Interleukin-2 (IL-2) and CCL2 chemokine) was present at higher levels in the striatum of Munc18-OE mice than WT. Cortical TNF-α and IL-2 levels were significantly lower in Munc18-OE mice than WT mice. The microglia and macrophage marker CD11b was lower in the cortexes of Munc18-OE mice than WT, but no differences were observed in the striatum. Glial Fibrillary Acidic Protein (GFAP) and Nuclear Factor-kappaB (NF-κB)p65 levels were not different between the groups. Interleukin-1beta (IL-1β) and IL-6 levels were beneath detection limits. Conclusions: The disrupted levels of cytokines detected in the brain of Munc18-OE mice was found to be similar to clinical reports and endorses study of this type for analysis of this aspect of the disorder. The lower CD11b expression in the cortex but not in the striatum of the Munc18-OE mice may reflect differences in physiological activity. The cytokine expression pattern observed in Munc18-OE mice is similar to a previously published model of schizophrenia caused by maternal immune activation. Together, these data suggest a possible role for an immune imbalance in this disorder

    Cross-modal correspondences in non-human mammal communication

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    For both humans and other animals, the ability to combine information obtained through different senses is fundamental to the perception of the environment. It is well established that humans form systematic cross-modal correspondences between stimulus features that can facilitate the accurate combination of sensory percepts. However, the evolutionary origins of the perceptual and cognitive mechanisms involved in these cross-modal associations remain surprisingly underexplored. In this review we outline recent comparative studies investigating how non-human mammals naturally combine information encoded in different sensory modalities during communication. The results of these behavioural studies demonstrate that various mammalian species are able to combine signals from different sensory channels when they are perceived to share the same basic features, either be- cause they can be redundantly sensed and/or because they are processed in the same way. Moreover, evidence that a wide range of mammals form complex cognitive representations about signallers, both within and across species, suggests that animals also learn to associate different sensory features which regularly co-occur. Further research is now necessary to determine how multisensory representations are formed in individual animals, including the relative importance of low level feature-related correspondences. Such investigations will generate important insights into how animals perceive and categorise their environment, as well as provide an essential basis for understanding the evolution of multisensory perception in humans

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    Cytokine pathway disruption in a mouse model of schizophrenia induced by Munc18-1a overexpression in the brai

    Cytokine pathway disruption in a mouse model of schizophrenia induced by Munc18-1a overexpression in the brain

    Get PDF
    Background: An accumulating body of evidence points to the significance of neuroinflammation and immunogenetics in schizophrenia, and an imbalance of cytokines in the central nervous system (CNS) has been suggested to be associated with the disorder. Munc18-overexpressing mice (Munc18-OE) have provided a model for the study of the alterations that may underlie the symptoms of subjects with schizophrenia. The aim of the present study was to elucidate the involvement of neuroinflammation and cytokine imbalance in this model. Methods: Cytokines were evaluated in the cortex and the striatum of Munc18-OE and wild-type (WT) mice by enzyme-linked immunosorbent assay (ELISA). Protein levels of specific microglia and macrophage, astrocytic and neuroinflammation markers were quantified by western blot in the cortex and the striatum of Munc18-OE and WT mice. Results: Each cytokine evaluated (Interferon-gamma (IFN-gamma), Tumor Necrosis Factor-alpha (TNF-alpha), Interleukin-2 (IL-2) and CCL2 chemokine) was present at higher levels in the striatum of Munc18-OE mice than WT. Cortical TNF-alpha and IL-2 levels were significantly lower in Munc18-OE mice than WT mice. The microglia and macrophage marker CD11b was lower in the cortexes of Munc18-OE mice than WT, but no differences were observed in the striatum. Glial Fibrillary Acidic Protein (GFAP) and Nuclear Factor-kappaB (NF-kappa B)p65 levels were not different between the groups. Interleukin-1beta (IL-1 beta) and IL-6 levels were beneath detection limits. Conclusions: The disrupted levels of cytokines detected in the brain of Munc18-OE mice was found to be similar to clinical reports and endorses study of this type for analysis of this aspect of the disorder. The lower CD11b expression in the cortex but not in the striatum of the Munc18-OE mice may reflect differences in physiological activity. The cytokine expression pattern observed in Munc18-OE mice is similar to a previously published model of schizophrenia caused by maternal immune activation. Together, these data suggest a possible role for an immune imbalance in this disorder.The study was supported by Spanish MINECO (SAF2009-08460) and the Basque Government (IT616-13) to JJM. Experiments were performed in DS's laboratory. CC was supported by the Caja Madrid Foundation and the Parkinson's Disease Foundation. DS's laboratory was supported by NIDA07418 and DA10154 and the Parkinson's, Simons and JPB Foundations

    The NA62 Gigatracker pixel detector system

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    The silicon tracker for the NA62 experiment has to provide both a time resolution of 150 ps rms and a space resolution of about 100 mu m rms. These challenging specifications require the development of a new readout electronics in order to address the problem of measuring the tracks arrival time with such a high channel density. Moreover, the high particle density (up to 1.5 MHz/mm(2) in the center and 0.8-1 GHz in total) requires a high speed measurement and data transmission in order to keep the dead time below 1%. (C) 2009 Elsevier B.V. All rights reserved

    Discovery and Functional Assessment of Gene Variants in the Vascular Endothelial Growth Factor Pathway

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    Angiogenesis is a host-mediated mechanism in disease pathophysiology. The vascular endothelial growth factor (VEGF) pathway is a major determinant of angiogenesis, and a comprehensive annotation of the functional variation in this pathway is essential to understand the genetic basis of angiogenesis-related diseases. We assessed the allelic heterogeneity of gene expression, population specificity of cis expression quantitative trait loci (eQTLs), and eQTL function in luciferase assays in CEU and YRI HapMap lymphoblastoid cell lines (LCLs) in 23 resequenced genes. Among 356 cis-eQTLs, 155 and 174 were unique to CEU and YRI, respectively, and 27 were shared between CEU and YRI. Two cis-eQTLs provided mechanistic evidence for two GWAS findings. Five eQTLs were tested for function in luciferase assays and the effect of two KRAS variants was concordant with the eQTL effect. Two eQTLs found in each of PRKCE, PIK3C2A, and MAP2K6, could predict 44, 37 and 45% of the variance in gene expression, respectively. This is the first analysis focusing on the pattern of functional genetic variation of the VEGF pathway genes in CEU and YRI populations and providing mechanistic evidence for genetic association studies of diseases for which angiogenesis plays a pathophysiologic role

    Neuroblastoma in Spain : Linking the national clinical database and epidemiological registries - A study by the Joint Action on Rare Cancers

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    Altres ajuts: Ministerio de Sanidad; Universitat de València; Sociedad Española de Oncología Pediátrica; Fundación de Oncología Infantil Enriqueta Villavecchia.Purpose: Linkage between clinical databases and population-based cancer registries may serve to evaluate European Reference Networks' (ERNs) activity, by monitoring the proportion of patients benefiting from these and their impact on survival at a population level. To test this, a study targeting neuroblastoma (Nb) was conducted in Spain by the European Joint Action on Rare Cancers. Material and methods: Subjects: Nb cases, incident 1999-2017, aged < 15 years. Linkage included: Spanish Neuroblastoma Clinical Database (NbCDB) (1217 cases); Spanish Registry of Childhood Tumours (RETI) (1514 cases); and 10 regional population-based registries (RPBCRs) which cover 33% of the childhood population (332 cases). Linkage was semiautomatic. We estimated completeness, incidence, contribution, deficit, and 5-year survival in the databases and specific subsets. Results: National completeness estimates for RETI and NbCDB were 91% and 72% respectively, using the Spanish RPBCRs on International Incidence of Childhood Cancer (https://iicc.iarc.fr/) as reference. RPBCRs' specific contribution was 1.6%. Linkage required manual crossover in 54% of the semiautomatic matches. Five-year survival was 74% (0-14 years) and 90% (0-18 months). Conclusions: All three databases were incomplete as regards Spain as a whole and should therefore be combined to achieve full childhood cancer registration. A unique personal patient identifier could facilitate such linkage. Most children have access to Nb clinical trials. Consolidated interconnections between the national registry and clinical registries (including ERNs and paediatric oncology clinical groups) should be established to evaluate outcomes
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