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Selected AbstractsInduction of rapid, activity-dependent neuronal,glial remodelling in the adult rat hypothalamus in vitroEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2003Sarah L. Langle Abstract The hypothalamic oxytocinergic system offers a remarkable model of morphological plasticity in the adult because its neurons and astrocytes undergo mutual remodelling in relation to differing physiological conditions. Among various factors involved in such plasticity, oxytocin (OT) itself appears of primary importance as its central administration resulted in morphological changes similar to those brought on by physiological stimuli. In the present study, we applied OT on acute hypothalamic slices from adult rats that included the supraoptic nucleus. Using ultrastructural morphometric analyses, we found that it induced a significant reduction of astrocytic coverage of OT neurons, leaving their surfaces directly juxtaposed, to an extent similar to that detected in vivo under conditions like lactation. These neuronal,glial changes were rapid and reversible, occurring within a few hours, and specifically mediated via OT receptors. They were potentiated by oestrogen and depended on calcium mobilization and de novo protein synthesis. Moreover, they depended on concurrent neuronal activation brought on by hyperosmotic stimulation or blockade of inhibitory GABAergic neurotransmission; they were inhibited by blockade of glutamatergic receptors. Taken together, our observations show that intrahypothalamic release of OT affects not only neuronal activation of the OT system but its morphological plasticity as well. Moreover, the activity dependence of the OT-induced changes strongly suggests that astrocytes can sense the level of activity of adjacent neurons and/or afferent input and this can subsequently act as a signal to bring on the neuronal and glial conformational changes. [source] Comparative assessment of two distributed watershed models with application to a small watershedHYDROLOGICAL PROCESSES, Issue 11 2006Latif Kalin Abstract Distributed watershed models are beneficial tools for the assessment of management practices on runoff and water-induced erosion. This paper evaluates, by application to an experimental watershed, two promising distributed watershed-scale sediment models in detail: the Kinematic Runoff and Erosion (KINEROS-2) model and the Gridded Surface Subsurface Hydrologic Analysis (GSSHA) model. The physics behind each model are to some extent similar, though they have different watershed conceptualizations. KINEROS-2 was calibrated using three rainfall events and validated over four separate rainfall events. Parameters estimated by this calibration process were adapted to GSSHA. With these parameters, GSSHA generated larger and retarded flow hydrographs. A 30% reduction in both plane and channel roughness in GSSHA along with the assumption of Green-Ampt conductivity KG-A = Ks, where Ks is the saturated conductivity, resulted in almost identical hydrographs. Sediment parameters not common in both models were calibrated independently of KINEROS-2. A comparative discussion of simulation results is presented. Even though GSSHA's flow component slightly overperformed KINEROS-2, the latter outperformed GSSHA in simulations for sediment transport. In spite of the fact that KINEROS-2 is not geared toward continuous-time simulations, simulations performed with both models over a 1 month period generated comparable results. Copyright © 2006 John Wiley & Sons, Ltd. [source] Satellite communications: the contribution of the 5th framework programme and future perspectivesINTERNATIONAL JOURNAL OF SATELLITE COMMUNICATIONS AND NETWORKING, Issue 1 2004Bernard Barani Abstract The telecommunication sector is of key importance for the European economy. Digitization, secure broadband access and mobility are expected to shift an ever-growing proportion of the economy on line, thus creating new markets and business opportunities. With the eEurope 2002 and eEurope 2005 initiatives, the European Union has initiated a number of policy actions aiming at favouring the rapid introduction of innovative communication systems, services and applications. Research and development, as supported under the IST programme of the Union, is closely associated to the overall policy picture. The IST programme is notably instrumental in supporting, with a longer-term approach, key policy orientations such as the pervasive introduction of low cost broadband access, introduction of advanced mobile systems, or migration of networks towards the next generation of Internet protocol, IPv6. Satellite communication form an integral part of this diversified communication landscape, and has also been significantly supported under the 5th Framework Programme. Even if the problematic of the satcom industry are to some extent similar to those of the terrestrial players (e.g. catalysing take up of broadband and advanced mobile markets), the strategies followed by the satcom sector differ from those followed by the terrestrial players. This paper review the current technological approaches of the satcom industry, their relevance in the context of the policy goals of the Union, and how they have been supported under the IST programme. It also introduces briefly how co-ordination with ESA work has been achieved, and the perspectives for further support, notably under the now starting 6th Framework Programme. Copyright © 2004 John Wiley & Sons, Ltd. [source] Brain-derived neurotrophic factor stimulates the transcriptional and neuroprotective activity of myocyte-enhancer factor 2C through an ERK1/2-RSK2 signaling cascadeJOURNAL OF NEUROCHEMISTRY, Issue 3 2007Yupeng Wang Abstract Neurotrophin activation of myocyte-enhancer factor (MEF) 2C is one of the strongest pro-survival signaling pathways in developing neurons. To date, neurotrophin stimulation of MEF2C has been largely attributed to its direct phosphorylation by extracellular signal-regulated kinase (ERK) 5. Because MEF2C is not directly phosphorylated by ERK1/2 in vitro, it is generally assumed that the ERK1/2 signaling cascade does not regulate MEF2C. Surprisingly, we discovered that ERK1/2 are required for both the transcriptional and neuroprotective activity of MEF2C in cortical neurons stimulated by brain-derived neurotrophic factor. ERK1/2 stimulation of MEF2C is mediated by p90 ribosomal S6 kinase 2 (RSK2), a Ser/Thr protein kinase downstream of ERK1/2. RSK2 strongly phosphorylates purified recombinant MEF2C protein in vitro. Furthermore, RSK2 can directly phosphorylate MEF2C on S192, a consensus RSK2-phosphorylation site located in the transactivation domain of MEF2C. Substitution of S192 with a non-phosphorylatable alanine diminishes both the transcriptional and neuroprotective activity of MEF2C to an extent similar to mutation on S387, an established activating phosphorylation site. Together, our data identifies ERK1/2-RSK2 signaling as a novel mechanism by which neurotrophins activate MEF2C and promote neuronal survival. [source] Inflammatory arthritis in caspase 1 gene,deficient mice: Contribution of proteinase 3 to caspase 1,independent production of bioactive interleukin-1,ARTHRITIS & RHEUMATISM, Issue 12 2009Leo A. B. Joosten Objective Caspase 1, a known cysteine protease, is a critical component of the inflammasome. Both caspase 1 and neutrophil serine proteases such as proteinase 3 (PR3) can process pro,interleukin-1, (proIL-1,), a crucial cytokine linked to the pathogenesis of rheumatoid arthritis. This study was undertaken to establish the relative importance of caspase 1 and serine proteases in mouse models of acute and chronic inflammatory arthritis. Methods Acute and chronic arthritis were induced in caspase 1,/, mice, and the lack of caspase 1 was investigated for its effects on joint swelling, cartilage metabolism, and histopathologic features. In addition, caspase 1 activity was inhibited in mice lacking active cysteine proteases, and the effects of dual blockade of caspase 1 and serine proteases on arthritis severity and histopathologic features were evaluated. Results Surprisingly, caspase 1,/, mice, in a model of acute (neutrophil-dominated) arthritis, developed joint swelling to an extent similar to that in wild-type control mice. Joint fluid concentrations of bioactive IL-1, were comparable in caspase 1,/, mice and controls. In contrast, induction of chronic arthritis (characterized by minimal numbers of neutrophils) in caspase 1,/, mice led to reduced joint inflammation and less cartilage damage, implying a caspase 1,dependent role in this process. In mice lacking neutrophil serine PR3, inhibition of caspase 1 activity resulted in decreased bioactive IL-1, concentrations in the synovial tissue and less suppression of chondrocyte anabolic function. In addition, dual blockade of both PR3 and caspase 1 led to protection against cartilage and bone destruction. Conclusion Caspase 1 deficiency does not affect neutrophil-dominated joint inflammation, whereas in chronic arthritis, the lack of caspase 1 results in reduced joint inflammation and cartilage destruction. These findings suggest that inhibitors of caspase 1 are not able to interfere with the whole spectrum of IL-1, production, and therefore such inhibitors may be of therapeutic value only in inflammatory conditions in which limited numbers of neutrophils are present. [source] 2-Phenylmelatonin: A Partial Agonist at Enteric Melatonin ReceptorsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 4 2000Maria Grazia Santagostino-Barbone The effect of the melatonin receptor ligand, 2-phenylmelatonin, has been assessed in isolated strips of the guinea-pig proximal colon. 2-Phenylmelatonin (0.01 nM-1 ,M) caused a concentration-dependent contractile response. The potency value (,log EC50) was 9.3±1.0. The maximum effect was 25±4% of that elicited by the maximally effective concentration (0.3 ,M) of 5-HT and 43±3% of that by the maximally effective concentration (10 ,M) of melatonin. When used as an antagonist, 2-phenylmelatonin (0.01 nM and 0.1 nM) concentration-dependently inhibited melatonin-induced contractions with depression of the maximum response by 25% and 54%, respectively. Higher (1 nM) 2-phenylmelatonin concentrations failed to antagonize melatonin-induced response. Prazosin (0.3 ,M), a selective antagonist of melatonin MT3 sites, antagonized melatonin-induced contractions to an extent similar to that induced by 0.01 nM 2-phenylmelatonin (with 30% reduction of the maximum effect to melatonin). The combination of 0.3 ,M prazosin and 0.01 nM 2-phenylmelatonin caused antagonism similar in extent to that caused by each individual antagonist. 2-Phenylmelatonin at subnanomolar concentrations behaves as an antagonist of melatonin-induced contractile responses while at nanomolar/micromolar concentrations it behaves as a weak contractile agonist. [source] | ||||||||||||||||