95 resultados para Alberto Méndez


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Eterio Pajares, Raquel Merino y José Miguel Santamaría (eds.)

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Eterio Pajares, Raquel Merino y José Miguel Santamaría (eds.)

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Eterio Pajares, Raquel Merino y José Miguel Santamaría (eds.)

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Raquel Merino Álvarez, José Miguel Santamaría, Eterio Pajares (eds.)

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La teleoperación o telerobótica es un campo de la robótica que se basa en el control remoto de robots esclavo por parte de un usuario encargado de gobernar, mediante un dispositivo maestro, la fuerza y movimiento del robot. Sobre dicho usuario recaen también las tareas de percepción del entorno, planificación y manipulación compleja. Concretamente se pretende desarrollar el control software necesario para teleoperar un manipulador esclavo, Kuka Lightweigh mediante un dispositivo háptico Phamton Omni, que se comporta como maestro, sin que afecten las diferencias dinámicas y estructurales existentes entre ambos dispositivos, aportando información adicional al operador para facilitar la operación. La principal motivación de la evolución de esta tecnología se debe a la necesidad de realizar trabajos en entornos hostiles, de difícil acceso, o perjudiciales para la salud del usuario.

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En este proyecto, enmarcado dentro del campo de la web semántica, se ha desarrollado un sistema llamado littera que permite la federación de depósitos de datos enlazados. Dicho sistema permite consultar depósitos del dominio de la literatura de forma unificada a través de una interfaz web, así como construir colaborativamente un nuevo depósito de datos abiertos y enlazados.

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It is with deep conviction and satisfaction that we have accepted the invitation to take part in this meeting, an occasion which enables us to reflect together on such a delicate and important question and at the same time to get to know our mutual environments,different geographically and culturally often distant but drawn to face together problems of European dimensions, such as the question of youth employment.

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Ponencia invitado en el congreso internacional XII congreso AEISAD."El Factor Humano: Cuando la diferencia la marcan las personas" 25/10/2012 San Sebastián - Coeditado por: Juan Aldaz Arregui, Alberto Dorado Suárez, Pedro Jesús Jiménez Martín, Anna Vilanova Soler

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El objeto del presente artículo consiste en realizar una breve exposición de los aspectos innovadores puestos en marcha en la Escuela Universitaria de Estudios Empresariales de San Sebastián recientemente, en relación tanto a aspectos docentes como de gestión.

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El presente artículo es uno de los resultados derivados de la participación de sus autores, profesores adscritos a la Escuela Universitaria de Estudios Empresariales y a la Escuela Universitaria Politécnica de Donostia-San Sebastián, en el equipo responsable del Proyecto de Investigación "Integración de Sistemas de Gestión Medioambiental en las empresas del Territorio Histórico de Gipuzkoa: Generación de herramientas innovadoras", aprobado en el marco del Programa Red Guipuzcoana de Ciencia, Tecnología e Innovación de la Diputación Foral de Gipuzkoa el bienio 2004-2006.

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The role of Na+ fluxes through voltage-gated sodium channels in the regulation of sperm cell function remains poorly understood. Previously, we reported that several genes encoding voltage-gated Na+ channels were expressed in human testis and mature spermatozoa. In this study, we analyzed the presence and function of the TTX-resistant VGSC a subunit Na(v)1.8 in human capacitated sperm cells. Using an RT-PCR assay, we found that the mRNA of the gene SCN10A, that encode Na-v1.8, was abundantly and specifically expressed in human testis and ejaculated spermatozoa. The Na-v1.8 protein was detected in capacitated sperm cells using three different specific antibodies against this channel. Positive immunoreactivity was mainly located in the neck and the principal piece of the flagellum. The presence of Na-v1.8 in sperm cells was confirmed by Western blot. Functional studies demonstrated that the increases in progressive motility produced by veratridine, a voltage-gated sodium channel activator, were reduced in sperm cells preincubated with TTX (10 mu M), the Na-v1.8 antagonist A-803467, or a specific Na-v1.8 antibody. Veratridine elicited similar percentage increases in progressive motility in sperm cells maintained in Ca2+-containing or Ca2+-free solution and did not induce hyperactivation or the acrosome reaction. Veratridine caused a rise in sperm intracellular Na+, [Na+](i), and the sustained phase of the response was inhibited in the presence of A-803467. These results verify that the Na+ channel Na-v1.8 is present in human sperm cells and demonstrate that this channel participates in the regulation of sperm function.

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Pannexin1 (Panx1) is a plasma membrane channel permeable to relatively large molecules, such as ATP. In the central nervous system (CNS) Panx1 is found in neurons and glia and in the immune system in macrophages and T-cells. We tested the hypothesis that Panx1-mediated ATP release contributes to expression of Experimental Autoimmune Encephalomyelitis (EAE), an animal model for multiple sclerosis, using wild-type (WT) and Panx1 knockout (KO) mice. Panx1 KO mice displayed a delayed onset of clinical signs of EAE and decreased mortality compared to WT mice, but developed as severe symptoms as the surviving WT mice. Spinal cord inflammatory lesions were also reduced in Panx1 KO EAE mice during acute disease. Additionally, pharmacologic inhibition of Panx1 channels with mefloquine (MFQ) reduced severity of acute and chronic EAE when administered before or after onset of clinical signs. ATP release and YoPro uptake were significantly increased in WT mice with EAE as compared to WT non-EAE and reduced in tissues of EAE Panx1 KO mice. Interestingly, we found that the P2X7 receptor was upregulated in the chronic phase of EAE in both WT and Panx1 KO spinal cords. Such increase in receptor expression is likely to counterbalance the decrease in ATP release recorded from Panx1 KO mice and thus contribute to the development of EAE symptoms in these mice. The present study shows that a Panx1 dependent mechanism (ATP release and/or inflammasome activation) contributes to disease progression, and that inhibition of Panx1 using pharmacology or gene disruption delays and attenuates clinical signs of EAE.