Robustness of optimal channel reservation using handover prediction in multiservice wireless networks

The aim of our study is to obtain theoretical limits for the gain that can be expected when using handover prediction and to determine the sensitivity of the system performance against different parameters. We apply an average-reward reinforcement learning approach based on afterstates to the design of optimal admission control policies in mobile multimedia cellular networks where predictive information related to the occurrence of future handovers is available. We consider a type of predictor that labels active mobile terminals in the cell neighborhood a fixed amount of time before handovers are predicted to occur, which we call the anticipation time. The admission controller exploits this information to reserve resources efficiently. We show that there exists an optimum value for the anticipation time at which the highest performance gain is obtained. Although the optimum anticipation time depends on system parameters, we find that its value changes very little when the system parameters vary within a reasonable range. We also find that, in terms of system performance, deploying prediction is always advantageous when compared to a system without prediction, even when the system parameters are estimated with poor precision. © Springer Science+Business Media, LLC 2012.The authors would like to thank the reviewers for their valuable comments that helped to improve the quality of the paper. This work has been supported by the Spanish Ministry of Education and Science and European Comission (30% PGE, 70% FEDER) under projects TIN2008-06739-C04-02 and TIN2010-21378-C02-02 and by Comunidad de Madrid through project S-2009/TIC-1468.Martínez Bauset, J.; Giménez Guzmán, JM.; Pla, V. (2012). Robustness of optimal channel reservation using handover prediction in multiservice wireless networks. 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Functional and neurometabolic asymmetry in SHR and WKY rats following vasoactive treatments

A lateralized distribution of neuropeptidase activities in the frontal cortex of normotensive and hypertensive rats has been described depending on the use of some vasoactive drugs and linked to certain mood disorders. Asymmetrical neuroperipheral connections involving neuropeptidases from the left or right hemisphere and aminopeptidases from the heart or plasma have been suggested to play a role in this asymmetry. We hypothesize that such asymmetries could be extended to the connection between the brain and physiologic parameters and metabolic factors from plasma and urine. To assess this hypothesis, we analyzed the possible correlation between neuropeptidases from the left and right frontal cortex with peripheral parameters in normotensive (Wistar Kyoto [WKY]) rats and hypertensive rats (spontaneously hypertensive rats [SHR]) untreated or treated with vasoactive drugs such as captopril, propranolol and L-nitro-arginine methyl ester. Neuropeptidase activities from the frontal cortex were analyzed fluorometrically using arylamide derivatives as substrates. Physiological parameters and metabolic factors from plasma and urine were determined using routine laboratory techniques. Vasoactive drug treatments differentially modified the asymmetrical neuroperipheral pattern by changing the predominance of the correlations between peripheral parameters and central neuropeptidase activities of the left and right frontal cortex. The response pattern also differed between SHR and WKY rats. These results support an asymmetric integrative function of the organism and suggest the possibility of a different neurometabolic response coupled to particular mood disorders, depending on the selected vasoactive drug.This work was supported by the Ministry of Science and Innovation through project no. SAF 2008 04685 C02 01

Intracellular pathways regulating ciliary beating of rat brain ependymal cells

The mammalian brain ventricles are lined with ciliated ependymal cells. As yet little is known about the mechanisms by which neurotransmitters regulate cilia beat frequency (CBF).Application of 5-HT to ependymal cells in cultured rat brainstem slices caused CBF to increase. 5-HT had an EC50 of 30 μM and at 100 μM attained a near-maximal CBF increase of 52.7 ± 4.1 % (mean ± s.d.) (n= 8).Bathing slices in Ca2+-free solution markedly reduced the 5-HT-mediated increase in CBF. Fluorescence measurements revealed that 5-HT caused a marked transient elevation in cytosolic Ca2+ ([Ca2+]c) that then slowly decreased to a plateau level. Analysis showed that the [Ca2+]c transient was due to release of Ca2+ from inositol 1,4,5-trisphosphate (IP3)-sensitive stores; the plateau was probably due to extracellular Ca2+ influx through Ca2+ release-activated Ca2+ (CRAC) channels.Application of ATP caused a sustained decrease in CBF. ATP had an EC50 of about 50 μM and 100 μM ATP resulted in a maximal 57.5 ± 6.5 % (n= 12) decrease in CBF. The ATP-induced decrease in CBF was unaffected by lowering extracellular [Ca2+], and no changes in [Ca2+]c were observed. Exposure of ependymal cells to forskolin caused a decrease in CBF. Ciliated ependymal cells loaded with caged cAMP exhibited a 54.3 ± 7.5 % (n= 9) decrease in CBF following uncaging. These results suggest that ATP reduces CBF by a Ca2+-independent cAMP-mediated pathway.Application of 5-HT and adenosine-5′-O-3-thiotriphosphate (ATP-γ-S) to acutely isolated ciliated ependymal cells resulted in CBF responses similar to those of ependymal cells in cultured slices suggesting that these neurotransmitters act directly on these cells.The opposite response of ciliated ependymal cells to 5-HT and ATP provides a novel mechanism for their active involvement in central nervous system signalling