D. Miguel Allué Salvador: una biografía ejemplar que revela una larga vida dedicada al trabajo y singularmente a la enseñanza.

Biografía, reconocimientos y méritos de D. Miguel Allué Salvador tras su muerte y una vida dedicada a la enseñanza..

De la caça-recol·lecció a l’agricultura i ramaderia: una aproximació a la dieta i l’explotació dels recursos forestals a partir del registre arqueobotànic

Estudi elaborat a partir d’una estada a l’Institut of Archaeology de la University College of London i a jaciments arqueològics espanyols. L’objectiu ha estat l’aprenentatge del mètode carpològic a través de l’anàlisi de fruit i llavors recuperades a jaciments de cronologies paleolítiques i l’estudi de les col·leccions de referència de Institute of Archaeology. Els jaciments analitzats han estat el Molí del Salt (Vimbodí, Tarragona) i Atapuerca (Burgos). L’estudi de mostres carpològiques de jaciments Neolítics d’una regió del Nord de Xina han permès l’apropament previ a restes de cronologies més recents dels primers agricultors i ramaders.

Estudi i millora del sistema d'administració i gestió acadèmica SAGA

Els centres d'ensenyament secundari que depenen del Departament d'Ensenyament, ja siguin públics o concertats, disposen d'un aplicatiu comú d'administració i gestió acadèmica anomenat SAGA. Actualment aquest sistema és d¿ús únicament de gestió, estant tancat a qualsevol interacció per part de membres de la comunitat educativa que no sigui direcció, professorat o personal d'administració. La intenció d'aquest treball és detectar mancances i/o deficiències del sistema existent, corregint-lo i obrint-lo a la resta de comunitat educativa, concretament als pares o tutors legals dels alumnes del centre. La intenció d'aquest treball és facilitar aquesta interacció tant de les persones que actualment treballen ja amb aquest sistema com de les susceptibles de poder-hi treballar en un futur.

Creació d'un sistema d'informació geogràfica de carreteres : problema logístic de l'empresa Vall Companys Grup

En la logística de Vall Companys Grup, un problema fonamental que cal resoldre és el de la situació geogràfica de tots els elements que participen en la logística, com ara fàbriques, granges, camions i magatzems; a més, se n'han d'estudiar les interrelacions per a aconseguir un aprofitament òptim dels recursos disponibles. Per a resoldre aquest problema, l'eina adequada seria un sistema d'informació geogràfica (SIG). En aquest projecte s'estudia què és un SIG i els conceptes que engloba, i se'n presenta un de comercial: Geomedia Professional 5.2. Fent servir aquest producte, s'ha construït un prototipus que estableix les bases per a poder resoldre el problema de logística de Vall Companys Grup i que mostra les potencialitats de Geomedia Professional 5.2.

Creació d'un sistema d'informació geogràfica de carreteres : Problema logístic de l'empresa Vall Companys Grup

En la logística de Vall Companys Grup, un problema fonamental a resoldre és el de la situació geogràfica de tots els elements que participen en la logística, com són fàbriques, granges, camions i magatzems; i estudiar les seves interrelacions per aconseguir un aprofitament òptim dels recursos disponibles. Per resoldre aquest problema, l'eina adequada seria un Sistema d'Informació Geogràfica (SIG).

Oral administration of the KATP channel opener diazoxide ameliorates disease progression in a murine model of multiple sclerosis

Background Multiple Sclerosis (MS) is an acquired inflammatory demyelinating disorder of the central nervous system (CNS) and is the leading cause of nontraumatic disability among young adults. Activated microglial cells are important effectors of demyelination and neurodegeneration, by secreting cytokines and others neurotoxic agents. Previous studies have demonstrated that microglia expresses ATP-sensitive potassium (KATP) channels and its pharmacological activation can provide neuroprotective and anti-inflammatory effects. In this study, we have examined the effect of oral administration of KATP channel opener diazoxide on induced experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. Methods Anti-inflammatory effects of diazoxide were studied on lipopolysaccharide (LPS) and interferon gamma (IFNy)-activated microglial cells. EAE was induced in C57BL/6J mice by immunization with myelin oligodendrocyte glycoprotein peptide (MOG35-55). Mice were orally treated daily with diazoxide or vehicle for 15 days from the day of EAE symptom onset. Treatment starting at the same time as immunization was also assayed. Clinical signs of EAE were monitored and histological studies were performed to analyze tissue damage, demyelination, glial reactivity, axonal loss, neuronal preservation and lymphocyte infiltration. Results Diazoxide inhibited in vitro nitric oxide (NO), tumor necrosis factor alpha (TNF-¿) and interleukin-6 (IL-6) production and inducible nitric oxide synthase (iNOS) expression by activated microglia without affecting cyclooxygenase-2 (COX-2) expression and phagocytosis. Oral treatment of mice with diazoxide ameliorated EAE clinical signs but did not prevent disease. Histological analysis demonstrated that diazoxide elicited a significant reduction in myelin and axonal loss accompanied by a decrease in glial activation and neuronal damage. Diazoxide did not affect the number of infiltrating lymphocytes positive for CD3 and CD20 in the spinal cord. Conclusion Taken together, these results demonstrate novel actions of diazoxide as an anti-inflammatory agent, which might contribute to its beneficial effects on EAE through neuroprotection. Treatment with this widely used and well-tolerated drug may be a useful therapeutic intervention in ameliorating MS disease.

Calcium homeostasis in the central nervous system: adaptation to neurodegeneration.

Here we review the results of our recent studies on neurodegeneration together with data on cerebral calcium precipitation in animal models and humans. A model that integrates the diversity of mechanisms involved in neurodegeneration is presented and discussed based on the functional relevance of calcium precipitation.

Glibenclamide enhances neurogenesis and improves long-term functional recovery after transient focal cerebral ischemia

Glibenclamide is neuroprotective against cerebral ischemia in rats. We studied whether glibenclamide enhances long-term brain repair and improves behavioral recovery after stroke. Adult male Wistar rats were subjected to transient middle cerebral artery occlusion (MCAO) for 90 minutes. A low dose of glibenclamide (total 0.6mg) was administered intravenously 6, 12, and 24 hours after reperfusion. We assessed behavioral outcome during a 30-day follow-up and animals were perfused for histological evaluation. In vitro specific binding of glibenclamide to microglia increased after pro-inflammatory stimuli. In vivo glibenclamide was associated with increased migration of doublecortin-positive cells in the striatum toward the ischemic lesion 72 hours after MCAO, and reactive microglia expressed sulfonylurea receptor 1 (SUR1) and Kir6.2 in the medial striatum. One month after MCAO, glibenclamide was also associated with increased number of NeuN-positive and 5-bromo-2-deoxyuridine-positive neurons in the cortex and hippocampus, and enhanced angiogenesis in the hippocampus. Consequently, glibenclamide-treated MCAO rats showed improved performance in the limb-placing test on postoperative days 22 to 29, and in the cylinder and water-maze test on postoperative day 29. Therefore, acute blockade of SUR1 by glibenclamide enhanced long-term brain repair in MCAO rats, which was associated with improved behavioral outcome.

Molecular Mechanisms of Acute Brain Injury and Ensuing Neurodegeneration

Injury to the central nervous system (CNS), including stroke, traumatic brain injury andspinal cord injury, cause devastating and irreversible damage and loss of function. Forexample, stroke affects very large patient populations, results in major suffering for the patients and their relatives, and involves a significant cost to society. CNS damage implies disruption of the intricate internal circuits involved in cognition, the sensory-motor functions, and other important functions. There are currently no treatments available to properly restore such lost functions. New therapeutic proposals will emerge from an understanding of the interdependence of molecular and cellular responses to CNS injury, in particular the inhibitory mechanisms that block regeneration and those that enhanceneuronal plasticity...

Microglia, Calcification and Neurodegenerative Diseases

Neurodegeneration is a complex process involving different cell types andneurotransmitters. A common characteristic of neurodegenerative disorders such asAlzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis, Huntington’s disease (HD) and Amyotrophic Lateral Sclerosis (ALS) is the occurrence of a neuroinflammatoryreaction in which cellular processes involving glial cells (mainly microglia and astrocytes) and T cells are activated in response to neuronal death. This inflammatory reaction has recently received attention as an unexpected potential target for the treatment of these diseases.Microglial cells have a mesenchymal origin, invade the central nervous system (CNS)prenatally (Chan et al., 2007b) and are the resident macrophages in the CNS (Ransohoff &Perry, 2009). They comprise approximately 10-20% of adult glia and serve as the CNS innateimmune system. In neurodegenerative diseases, microglia is activated by misfoldedproteins. In the case of AD, amyloid- (A ) peptides accumulate extracellularly and activate the microglia locally. In the case of PD, ALS and HD, the misfolded proteins accumulate intracellularly but are still associated with activation of the microglia (Perry et al., 2010). Reactive microglia in the substantia nigra and striatum of PD brains have been described, and increased levels of proinflammatory cytokines and inducible nitric oxide synthase havebeen detected in these brain regions, providing evidence of a local inflammatory reaction (Hirsch & Hunot, 2009). The injection of lipopolysaccharide (a potent microglia activator) into the substantia nigra produces microglial activation and the death of dopaminergic cells. These findings support the hypothesis that microglial activation and neuroinflammationcontribute to PD pathogenesis (Herrera et al., 2000)...

Alteraciones biológicas de la madera: el estudio de los materiales constructivos del yacimiento de Pleta de l'Estall Serrer (Valle del Madriu, Andorra)

El análisis antracológico, dendrológico y tafonómico de tres estructuras pastoriles de época moderna del yacimiento de Pleta de l’Estall Serrer (valle delMadriu, Andorra) situado a 1.980mde altitud, nosmuestra una presencia casi absoluta del pino tipo negro y la presencia puntual de taxones arbustivos como las ericáceas. Se trata de especies típicas en un bosque subalpino de pino negro. La presencia casi absoluta del pino, nos ha permitido observar diferentes alteraciones de la madera que nos han proporcionado una gran información sobre el uso de la madera, sobre todo las alteraciones por microorganismos. Hemos podido distinguir varios tipos de alteraciones causadas tanto por insectos xilófagos e hifas de hongos. Además, hemos identificado algunos individuos de termitas subterráneas tanto vivas como carbonizadas. Las primeras son termitas que atacan la madera arqueológica durante los procesos postdeposicionales y las termitas carbonizadas seguramente fueron la causa del deterioro de las estructuras y su posterior destrucción a través de su incendio.

Targeting microglial KATP channels to treat neurodegenerative diseases: a mitochondrial issue

Neurodegeneration is a complex process involving different cell types and neurotransmitters. A common characteristic of neurodegenerative disorders is the occurrence of a neuroinflammatory reaction in which cellular processes involving glial cells, mainly microglia and astrocytes, are activated in response to neuronal death. Microglia do not constitute a unique cell population but rather present a range of phenotypes closely related to the evolution of neurodegeneration. In a dynamic equilibrium with the lesion microenvironment, microglia phenotypes cover from a proinflammatory activation state to a neurotrophic one directly involved in cell repair and extracellular matrix remodeling. At each moment, the microglial phenotype is likely to depend on the diversity of signals from the environment and of its response capacity. As a consequence, microglia present a high energy demand, for which the mitochondria activity determines the microglia participation in the neurodegenerative process. As such, modulation of microglia activity by controlling microglia mitochondrial activity constitutes an innovative approach to interfere in the neurodegenerative process. In this review, we discuss the mitochondrial KATP channel as a new target to control microglia activity, avoid its toxic phenotype, and facilitate a positive disease outcome.

Targeting microglial KATP channels to treat neurodegenerative diseases: a mitochondrial issue

Neurodegeneration is a complex process involving different cell types and neurotransmitters. A common characteristic of neurodegenerative disorders is the occurrence of a neuroinflammatory reaction in which cellular processes involving glial cells, mainly microglia and astrocytes, are activated in response to neuronal death. Microglia do not constitute a unique cell population but rather present a range of phenotypes closely related to the evolution of neurodegeneration. In a dynamic equilibrium with the lesion microenvironment, microglia phenotypes cover from a proinflammatory activation state to a neurotrophic one directly involved in cell repair and extracellular matrix remodeling. At each moment, the microglial phenotype is likely to depend on the diversity of signals from the environment and of its response capacity. As a consequence, microglia present a high energy demand, for which the mitochondria activity determines the microglia participation in the neurodegenerative process. As such, modulation of microglia activity by controlling microglia mitochondrial activity constitutes an innovative approach to interfere in the neurodegenerative process. In this review, we discuss the mitochondrial KATP channel as a new target to control microglia activity, avoid its toxic phenotype, and facilitate a positive disease outcome.

Glibenclamide enhances neurogenesis and improves long-term functional recovery after transient focal cerebral ischemia

Glibenclamide is neuroprotective against cerebral ischemia in rats. We studied whether glibenclamide enhances long-term brain repair and improves behavioral recovery after stroke. Adult male Wistar rats were subjected to transient middle cerebral artery occlusion (MCAO) for 90 minutes. A low dose of glibenclamide (total 0.6mg) was administered intravenously 6, 12, and 24 hours after reperfusion. We assessed behavioral outcome during a 30-day follow-up and animals were perfused for histological evaluation. In vitro specific binding of glibenclamide to microglia increased after pro-inflammatory stimuli. In vivo glibenclamide was associated with increased migration of doublecortin-positive cells in the striatum toward the ischemic lesion 72 hours after MCAO, and reactive microglia expressed sulfonylurea receptor 1 (SUR1) and Kir6.2 in the medial striatum. One month after MCAO, glibenclamide was also associated with increased number of NeuN-positive and 5-bromo-2-deoxyuridine-positive neurons in the cortex and hippocampus, and enhanced angiogenesis in the hippocampus. Consequently, glibenclamide-treated MCAO rats showed improved performance in the limb-placing test on postoperative days 22 to 29, and in the cylinder and water-maze test on postoperative day 29. Therefore, acute blockade of SUR1 by glibenclamide enhanced long-term brain repair in MCAO rats, which was associated with improved behavioral outcome.