996 resultados para Superior Nervous Functions


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El present projecte de fi de carrera té com a objectiu principal el desenvolupament d’un servei criptogràfic per a la plataforma JADE, perquè es puguin implementar agents mòbils autoprotegits. Aquest objectiu s’ha aconseguit dotant les plataformes amb un parell de claus asimètriques i facilitant a l’agent funcions que utilitzen la clau privada de la plataforma entre un gran ventall de funcions criptogràfiques diferents.

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L'objectiu d'aquest projecte ha estat generalitzar i integrar la funcionalitat de dos projectes anteriors que ampliaven el tractament que oferia el Magma respecte a les matrius de Hadamard. Hem implementat funcions genèriques que permeten construir noves matrius Hadamard de qualsevol mida per a cada rang i dimensió de nucli, i així ampliar la seva base de dades. També hem optimitzat la funció que calcula el nucli, i hem desenvolupat funcions que calculen la invariant Symmetric Hamming Distance Enumerator (SH-DE) proposada per Kai-Tai Fang i Gennian Gei que és més sensible per a la detecció de la no equivalència de les matrius Hadamard.

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Within the last few years, several reports have revealed that cell transplantation can be an effective way to replace lost neurons in the central nervous system (CNS) of patients affected with neurodegenerative diseases. Concerning the retina, the concept that newborn photoreceptors can integrate the retina and restore some visual functions was univocally demonstrated recently in the mouse eye (MacLaren et al. 2006) and remains to be achieved in human. These results pave the way to a standard approach in regenerative medicine aiming to replace lost photoreceptors. With the discovery of stem cells a great hope has appeared towards elaborating protocols to generate adequate cells to restore visual function in different retinal degeneration processes. Retinal stem cells (RSCs) are good candidates to repair the retina and are present throughout the retina development, including adulthood. However, neonatal mouse RSCs derived from the radial glia population have a different potential to proliferate and differentiate in comparison to adult RSCs. Moreover, we observed that adult mouse RSCs, depending on the culture conditions, have a marked tendency to transform, whereas neonatal RSCs show subtle chromosome abnormalities only after extensive expansion. These characteristics should help to identify the optimal cell source and culture conditions for cell transplantation studies. These results will be discussed in light of other studies using RSCs as well as embryonic stem cells. Another important factor to consider is the host environment, which plays a crucial role for cell integration and which was poorly studied in the normal and the diseased retina. Nonetheless, important results were recently generated to reconsider cell transplantation strategy. Perspectives to enhance cell integration by manipulating the environment will also be presented.

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MicroRNAs (miRNAs) have been shown to play important roles in both brain development and the regulation of adult neural cell functions. However, a systematic analysis of brain miRNA functions has been hindered by a lack of comprehensive information regarding the distribution of miRNAs in neuronal versus glial cells. To address this issue, we performed microarray analyses of miRNA expression in the four principal cell types of the CNS (neurons, astrocytes, oligodendrocytes, and microglia) using primary cultures from postnatal d 1 rat cortex. These analyses revealed that neural miRNA expression is highly cell-type specific, with 116 of the 351 miRNAs examined being differentially expressed fivefold or more across the four cell types. We also demonstrate that individual neuron-enriched or neuron-diminished RNAs had a significant impact on the specification of neuronal phenotype: overexpression of the neuron-enriched miRNAs miR-376a and miR-434 increased the differentiation of neural stem cells into neurons, whereas the opposite effect was observed for the glia-enriched miRNAs miR-223, miR-146a, miR-19, and miR-32. In addition, glia-enriched miRNAs were shown to inhibit aberrant glial expression of neuronal proteins and phenotypes, as exemplified by miR-146a, which inhibited neuroligin 1-dependent synaptogenesis. This study identifies new nervous system functions of specific miRNAs, reveals the global extent to which the brain may use differential miRNA expression to regulate neural cell-type-specific phenotypes, and provides an important data resource that defines the compartmentalization of brain miRNAs across different cell types.

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El modelo americano de financiación universitaria no está centrado en la subvención directa de las Universidades sino en facilitar recursos a los estudiantes. Tanto la Unión como los Estados financian a los estudiantes directamente –mediante ayudas y becas- como indirectamente, a través de beneficios fiscales. El sistema es extremadamente complejo y tiene carencias en términos de equidad, eficiencia y neutralidad, pero, en definitiva, las Universidades americanas disponen de suficientes recursos para trabajar con eficacia y los estudiantes encuentran el modo –becas, préstamos y beneficios fiscales- de financiar buena parte de sus gastos educativos. El sistema español de Educación superior está en el polo opuesto. Programas de becas infradotados, precios universitarios simbólicos, programas de préstamos educativos marginales y ausencia de beneficios fiscales. Las Universidades públicas reciben sus recursos de los contribuyentes, a través de los presupuestos autonómicos, pero si se elige una Universidad privada el estudiante ha de pagar derechos de matrícula más elevados –puesto que sus programas no reciben soporte financiero público- al mismo tiempo que financia el sistema público mediante el abono de sus deudas tributarias. En el ordenamiento vigente se atribuye la principal responsabilidad en lo relativo a política universitaria a las Comunidades autónomas. ¿Qué podrían aprender los Gobiernos autonómicos del modelo americano, sin repetir sus errores? Tres lecciones sencillas: (1) Reducir los créditos presupuestarios a fondo perdido e incrementar los precios públicos, y las becas para los estudiantes de rentas bajas; (2) Crear un único beneficio fiscal, no más, en forma de deducción autonómica reembolsable en el IRPF, del 20% de lo invertido en Educación superior.; (3) Crear Programas de Ayuda al Mérito para todos los estudiantes con mejores resultados académicos en forma de cheque universitario para invertir en cualquier institución del sistema, ya sea de iniciativa estatal o social. Estas tres políticas contribuirían a incrementar los recursos financieros de todas las Universidades, y a mejorar la financiación de los estudiantes –en particular de quienes tienen más necesidades y condiciones para el estudio- al mismo tiempo que se refuerza la libertad de elección de Universidad. En dos palabras, mejoraría la eficacia y la equidad del conjunto del sistema.

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L'objectiu d'aquesta recerca és l'estudi de l'evolució del límit superior del bosc en la vessant sud dels Pirineus, concretament a l'àrea dels Plaus de Boldís-Montarenyo (Lladorre, Pallars Sobirà). S'han usat diferents fonts i metodologies amb cobertures temporals diverses. Per una banda s'ha emprat la pedoantracologia, per tal d'analitzar el carbons incorporats en el sòl. Per altra banda, s'ha treballat amb Sistemes d'Informació Geogràfica; també s'han consultat fonts escrites i orals. S'ha dut a terme una anàlisi complexa d'aquesta evolució entesa com el resultat de la interacció entre natura i societat, amb un ús essencialment ramader, durant els últims 6.000 anys.

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In rats, neonatal treatment with monosodium L-glutamate (MSG) induces several metabolic and neuroendocrine abnormalities, which result in hyperadiposity. No data exist, however, regarding neuroendocrine, immune and metabolic responses to acute endotoxemia in the MSG-damaged rat. We studied the consequences of MSG treatment during the acute phase response of inflammatory stress. Neonatal male rats were treated with MSG or vehicle (controls, CTR) and studied at age 90 days. Pituitary, adrenal, adipo-insular axis, immune, metabolic and gonadal functions were explored before and up to 5 h after single sub-lethal i.p. injection of bacterial lipopolysaccharide (LPS; 150 microg/kg). Our results showed that, during the acute phase response of inflammatory stress in MSG rats: (1) the corticotrope-adrenal, leptin, insulin and triglyceride responses were higher than in CTR rats, (2) pro-inflammatory (TNFalpha) cytokine response was impaired and anti-inflammatory (IL-10) cytokine response was normal, and (3) changes in peripheral estradiol and testosterone levels after LPS varied as in CTR rats. These data indicate that metabolic and neroendocrine-immune functions are altered in MSG-damaged rats. Our study also suggests that the enhanced corticotrope-corticoadrenal activity in MSG animals could be responsible, at least in part, for the immune and metabolic derangements characterizing hypothalamic obesity.

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Abstract : Auditory spatial functions are of crucial importance in everyday life. Determining the origin of sound sources in space plays a key role in a variety of tasks including orientation of attention, disentangling of complex acoustic patterns reaching our ears in noisy environments. Following brain damage, auditory spatial processing can be disrupted, resulting in severe handicaps. Complaints of patients with sound localization deficits include the inability to locate their crying child or being over-loaded by sounds in crowded public places. Yet, the brain bears a large capacity for reorganization following damage and/or learning. This phenomenon is referred as plasticity and is believed to underlie post-lesional functional recovery as well as learning-induced improvement. The aim of this thesis was to investigate the organization and plasticity of different aspects of auditory spatial functions. Overall, we report the outcomes of three studies: In the study entitled "Learning-induced plasticity in auditory spatial representations" (Spierer et al., 2007b), we focused on the neurophysiological and behavioral changes induced by auditory spatial training in healthy subjects. We found that relatively brief auditory spatial discrimination training improves performance and modifies the cortical representation of the trained sound locations, suggesting that cortical auditory representations of space are dynamic and subject to rapid reorganization. In the same study, we tested the generalization and persistence of training effects over time, as these are two determining factors in the development of neurorehabilitative intervention. In "The path to success in auditory spatial discrimination" (Spierer et al., 2007c), we investigated the neurophysiological correlates of successful spatial discrimination and contribute to the modeling of the anatomo-functional organization of auditory spatial processing in healthy subjects. We showed that discrimination accuracy depends on superior temporal plane (STP) activity in response to the first sound of a pair of stimuli. Our data support a model wherein refinement of spatial representations occurs within the STP and that interactions with parietal structures allow for transformations into coordinate frames that are required for higher-order computations including absolute localization of sound sources. In "Extinction of auditory stimuli in hemineglect: space versus ear" (Spierer et al., 2007a), we investigated auditory attentional deficits in brain-damaged patients. This work provides insight into the auditory neglect syndrome and its relation with neglect symptoms within the visual modality. Apart from contributing to a basic understanding of the cortical mechanisms underlying auditory spatial functions, the outcomes of the studies also contribute to develop neurorehabilitation strategies, which are currently being tested in clinical populations.

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In the literature the outcome of contests is either interpreted as win probabilities or as shares of the prize. With this in mind, we examine two approaches to contest success functions. In the first we analyze the implications of contestants' incomplete information concerning the "type" of the contest administrator. While in the case of two contestants this approach can rationalize prominent contest success functions, we show that it runs into difficulties when there are more agents. Our second approach interprets contest success functions as sharing rules and establishes a connection to bargaining and claims problems which is independent of the number of contestants. Both approaches provide foundations for popular contest success functions and guidelines for the definition of new ones. Keywords: Endogenous Contests, Contest Success Function. JEL Classification: C72 (Noncooperative Games), D72 (Economic Models of Political Processes: Rent-Seeking, Elections), D74 (Conflict; Conflict Resolution; Alliances).

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The majority of diseases in the retina are caused by genetic mutations affecting the development and function of photoreceptor cells. The transcriptional networks directing these processes are regulated by genes such as nuclear hormone receptors. The nuclear hormone receptor gene Rev-erb alpha/Nr1d1 has been widely studied for its role in the circadian cycle and cell metabolism, however its role in the retina is unknown. In order to understand the role of Rev-erb alpha/Nr1d1 in the retina, we evaluated the effects of loss of Nr1d1 to the developing retina and its co-regulation with the photoreceptor-specific nuclear receptor gene Nr2e3 in the developing and mature retina. Knock-down of Nr1d1 expression in the developing retina results in pan-retinal spotting and reduced retinal function by electroretinogram. Our studies show that NR1D1 protein is co-expressed with NR2E3 in the outer neuroblastic layer of the developing mouse retina. In the adult retina, NR1D1 is expressed in the ganglion cell layer and is co-expressed with NR2E3 in the outer nuclear layer, within rods and cones. Several genes co-targeted by NR2E3 and NR1D1 were identified that include: Nr2c1, Recoverin, Rgr, Rarres2, Pde8a, and Nupr1. We examined the cyclic expression of Nr1d1 and Nr2e3 over a twenty-four hour period and observed that both nuclear receptors cycle in a similar manner. Taken together, these studies reveal a novel role for Nr1d1, in conjunction with its cofactor Nr2e3, in regulating transcriptional networks critical for photoreceptor development and function.

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Cerebral microangiopathy (CMA) has been associated with executive dysfunction and fronto-parietal neural network disruption. Advances in magnetic resonance imaging allow more detailed analyses of gray (e.g., voxel-based morphometry-VBM) and white matter (e.g., diffusion tensor imaging-DTI) than traditional visual rating scales. The current study investigated patients with early CMA and healthy control subjects with all three approaches. Neuropsychological assessment focused on executive functions, the cognitive domain most discussed in CMA. The DTI and age-related white matter changes rating scales revealed convergent results showing widespread white matter changes in early CMA. Correlations were found in frontal and parietal areas exclusively with speeded, but not with speed-corrected executive measures. The VBM analyses showed reduced gray matter in frontal areas. All three approaches confirmed the hypothesized fronto-parietal network disruption in early CMA. Innovative methods (DTI) converged with results from conventional methods (visual rating) while allowing greater spatial and tissue accuracy. They are thus valid additions to the analysis of neural correlates of cognitive dysfunction. We found a clear distinction between speeded and nonspeeded executive measures in relationship to imaging parameters. Cognitive slowing is related to disease severity in early CMA and therefore important for early diagnostics.

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Generalized multiresolution analyses are increasing sequences of subspaces of a Hilbert space H that fail to be multiresolution analyses in the sense of wavelet theory because the core subspace does not have an orthonormal basis generated by a fixed scaling function. Previous authors have studied a multiplicity function m which, loosely speaking, measures the failure of the GMRA to be an MRA. When the Hilbert space H is L2(Rn), the possible multiplicity functions have been characterized by Baggett and Merrill. Here we start with a function m satisfying a consistency condition which is known to be necessary, and build a GMRA in an abstract Hilbert space with multiplicity function m.

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PURPOSE: Several studies observed a female advantage in the prognosis of cutaneous melanoma, for which behavioral factors or an underlying biologic mechanism might be responsible. Using complete and reliable follow-up data from four phase III trials of the European Organisation for Research and Treatment of Cancer (EORTC) Melanoma Group, we explored the female advantage across multiple end points and in relation to other important prognostic indicators. PATIENTS AND METHODS: Patients diagnosed with localized melanoma were included in EORTC adjuvant treatment trials 18832, 18871, 18952, and 18961 and randomly assigned during the period of 1984 to 2005. Cox proportional hazard models were used to calculate hazard ratios (HRs) and 95% CIs for women compared with men, adjusted for age, Breslow thickness, body site, ulceration, performed lymph node dissection, and treatment. RESULTS: A total of 2,672 patients with stage I/II melanoma were included. Women had a highly consistent and independent advantage in overall survival (adjusted HR, 0.70; 95% CI, 0.59 to 0.83), disease-specific survival (adjusted HR, 0.74; 95% CI, 0.62 to 0.88), time to lymph node metastasis (adjusted HR, 0.70; 95% CI, 0.51 to 0.96), and time to distant metastasis (adjusted HR, 0.69; 95% CI, 0.59 to 0.81). Subgroup analysis showed that the female advantage was consistent across all prognostic subgroups (with the possible exception of head and neck melanomas) and in pre- and postmenopausal age groups. CONCLUSION: Women have a consistent and independent relative advantage in all aspects of the progression of localized melanoma of approximately 30%, most likely caused by an underlying biologic sex difference.