High performance binary LDPC-coded OFDM systems over indoor PLC channels

Power line communication (PLC) technology is actually among the most renowned technologies for home environments due to their low-cost installation opportunities. In this study, the bit error rate (BER) performances of binary low-density parity check (LDPC) coded orthogonal frequency-division multiplexing (OFDM) systems have been considered over indoor PLC channels. Performances comparison of diverse soft and hard decision LDPC decoder schemes such as Min-Sum (MS), weighted bit flipping (WBF), gradient descent bit-flip (GDBF), noisy gradient descent bit-flip (NGDBF) and its few variants including the single-bit NGDBF (S-NGDBF), multi-bit NGDBF (M-NGDBF) and smoothed-multi-bit NGDBF (SM-NGDBF) decoders were examined in the modeled network. To evaluate the BER performance analyses three different PLC channel scenarios were generated by using new and more realistic PLC channel model proposal were also employed. All of the simulations performed in Canete’s PLC channel model showed that remarkable performance improvement can be achieved by using short-length LDPC codes. Especially, the improvements are striking when the MS or SM-NGDBF decoding algorithms are employed on the receiver side

EXPRESSION DU RECEPTEUR ALPHA 1 DE LA GLYCINE DANS L'OVOCYTE DE XENOPE (MODIFICATIONS DES PROPRIETES BIOPHYSIQUES LORS DE SON EXPRESSION A FORTE DENSITE)

LA GLYCINE, NEUROTRANSMETTEUR INHIBITEUR DU SYSTEME NERVEUX CENTRAL, AGIT PAR L'INTERMEDIAIRE D'UN RECEPTEUR CANAL DE SELECTIVITE ANIONIQUE. LE RECEPTEUR DE LA GLYCINE (GLYR) A UNE STRUCTURE PENTAMERIQUE (32). CES GLYRS S'ORGANISENT EN DENSITES POSTSYNAPTIQUES GRACE A LEUR ANCRAGE AU CYTOSQUELETTE PAR LA GEPHYRINE. L'EXPRESSION DU GLYR 1 DANS L'OVOCYTE DE XENOPE FORME UN GLYR FONCTIONNEL DONT LA DENSITE DEPEND DE LA QUANTITE D'ADNC INJECTEE. LA SUREXPRESSION DE GLYR FAIT AUGMENTER D'UN FACTEUR 5 L'AFFINITE APPARENTE POUR LA GLYCINE D'UNE PARTIE DE LA POPULATION DE GLYR. CETTE MEILLEURE EFFICACITE DE LA GLYCINE PEUT ETRE EXPLIQUEE PAR LA FORMATION A FORTE DENSITE D'AGREGATS DE GLYRS POUVANT INTERAGIR ENTRE EUX. POUR VERIFIER CETTE HYPOTHESE J'AI COMPARE LES PROPRIETES BIOPHYSIQUES DU CANAL GLYR A DIFFERENTS NIVEAUX D'EXPRESSION. CES TRAVAUX ONT MONTRE QUE LE CANAL GLYR, INDEPENDAMMENT DE SA DENSITE, PRESENTE PLUSIEURS ETATS CONDUCTEURS. A FAIBLE EXPRESSION LES VALEURS DE CONDUCTANCES VARIENT ENTRE 3,3 ET 77 PS AVEC UNE DOMINANCE A 12 PS. A FORTE EXPRESSION, EN PLUS DES CONDUCTANCES PRECEDENTES, S'EN AJOUTENT D'AUTRES ALLANT JUSQU'A 343 PS, ET LA CONDUCTANCE DOMINANTE TEND VERS 80 PS. LA DISTRIBUTION DES SOUS-ETATS DE CONDUCTANCE EN FONCTION DE LA CONCENTRATION DE L'AGONISTE MONTRE QUE LES CONDUCTANCES DE GRANDES VALEURS PEUVENT ETRE OBTENUES SOIT PAR SATURATION DES SITES RECEPTEURS A FAIBLE EXPRESSION, SOIT PAR AUGMENTATION DE LA DENSITE DES GLYRS. DE L'ANALYSE DE LA SELECTIVITE DES DEUX POPULATIONS DE CANAUX JE MONTRE QUE LES PETITES ET LES GRANDES CONDUCTANCES PEUVENT ETRE ASSOCIEES A DES CONFORMATIONS DU CANAL AYANT UN DIAMETRE RESPECTIF DE PETIT OU GROS CALIBRE. CES DONNEES SONT EN FAVEUR DE L'EXISTENCE D'INTERACTIONS ENTRE LES GLYRS IMPLIQUES DANS DES AGREGATS, CE QUI EST CONFIRME PAR L'INHIBITION SELECTIVE PAR LE PH ALCALIN (8,6) DES GRANDES CONDUCTANCES OBSERVEES A FORTE DENSITE DE GLYR.STRASBOURG-Sc. et Techniques (674822102) / SudocSudocFranceF

A Role for Xanthurenic Acid in the Control of Brain Dopaminergic Activity

Xanthurenic acid (XA) is a metabolite of the kynurenine pathway (KP) synthetized in the brain from dietary or microbial tryptophan that crosses the blood-brain barrier through carrier-mediated transport. XA and kynurenic acid (KYNA) are two structurally related compounds of KP occurring at micromolar concentrations in the CNS and suspected to modulate some pathophysiological mechanisms of neuropsychiatric and/or neurodegenerative diseases. Particularly, various data including XA cerebral distribution (from 1 µM in olfactory bulbs and cerebellum to 0.1-0.4 µM in A9 and A10), its release, and interactions with G protein-dependent XA-receptor, glutamate transporter and metabotropic receptors, strongly support a signaling and/or neuromodulatory role for XA. However, while the parent molecule KYNA is considered as potentially involved in neuropsychiatric disorders because of its inhibitory action on dopamine release in the striatum, the effect of XA on brain dopaminergic activity remains unknown. Here, we demonstrate that acute local/microdialysis-infusions of XA dose-dependently stimulate dopamine release in the rat prefrontal cortex (four-fold increase in the presence of 20 µM XA). This stimulatory effect is blocked by XA-receptor antagonist NCS-486. Interestingly, our results show that the peripheral/intraperitoneal administration of XA, which has been proven to enhance intra-cerebral XA concentrations (about 200% increase after 50 mg/kg XA i.p), also induces a dose-dependent increase of dopamine release in the cortex and striatum. Furthermore, our in vivo electrophysiological studies reveal that the repeated/daily administrations of XA reduce by 43% the number of spontaneously firing dopaminergic neurons in the ventral tegmental area. In the substantia nigra, XA treatment does not change the number of firing neurons. Altogether, our results suggest that XA may contribute together with KYNA to generate a KYNA/XA ratio that may crucially determine the brain normal dopaminergic activity. Imbalance of this ratio may result in dopaminergic dysfunctions related to several brain disorders, including psychotic diseases and drug dependence

Xanthurenic Acid Binds to Neuronal G-Protein-Coupled Receptors That Secondarily Activate Cationic Channels in the Cell Line NCB-20

<div><p>Xanthurenic acid (XA) is a metabolite of the tryptophan oxidation pathway through kynurenine and 3-hydroxykynurenine. XA was until now considered as a detoxification compound and dead-end product reducing accumulation of reactive radical species. Apart from a specific role for XA in the signaling cascade resulting in gamete maturation in mosquitoes, nothing was known about its functions in other species including mammals. Based upon XA distribution, transport, accumulation and release in the rat brain, we have recently suggested that XA may potentially be involved in neurotransmission/neuromodulation, assuming that neurons presumably express specific XA receptors. Recently, it has been shown that XA could act as a positive allosteric ligand for class II metabotropic glutamate receptors. This finding reinforces the proposed signaling role of XA in brain. Our present results provide several lines of evidence in favor of the existence of specific receptors for XA in the brain. First, binding experiments combined with autoradiography and time-course analysis led to the characterization of XA binding sites in the rat brain. Second, specific kinetic and pharmacological properties exhibited by these binding sites are in favor of G-protein-coupled receptors (GPCR). Finally, in patch-clamp and calcium imaging experiments using NCB-20 cells that do not express glutamate-induced calcium signals, XA elicited specific responses involving activation of cationic channels and increases in intracellular Ca²⁺ concentration. Altogether, these results suggest that XA, acting through a GPCR-induced cationic channel modulatory mechanism, may exert excitatory functions in various brain neuronal pathways.</p> </div

Reversal potential of XA-induced responses in the cell-attached configuration.

<p>The membrane patch was recorded in the NMDG-Cl condition and stimulated by a ramp potential protocol (−70 to 90 mV, 600 ms duration) at a frequency of 0.2 Hz. <b>A</b>: Membrane patch current traces recorded at different membrane potentials (Vm) as indicated in the figure. The colored vertical lines 1 to 5 indicate the different steps of the Er variations. The dashed lines represent the zero current level for each current trace. <b>B</b>: Time evolution of the Er value obtained by the ramp potential stimulation protocol during the XA response given in <b>A</b> (control current was subtracted). <b>C</b>: Frequency histogram of the Er values obtained during the XA response. The distribution was best fitted by the sum of 5 Gaussians with parameter values of: mean Er = −23.2, −9.6, 0.8, 12.6 and 20.3 mV, standard deviation σ = 6.3, 2.1, 3.6, 2.1 and 2.3 and amplitude = 3.0, 5.6, 8.4, 23.8 and 20.4 respectively. <b>D</b>: I–V relationship of the XA-induced current recorded at the times indicated by numbers 1 to 5 in <b>A</b>. The reversal potential for each I–V curve is indicated by dashed vertical lines (1 to 5). <b>E</b>: Mean data (± SEM) of the reversal potential classes (Er1 to Er5) obtained from the different XA responses. In parenthesis are given the number of time a given Er class was observed overall the XA responses. ***: p<0.001.</p

Saturation curve showing specific binding of [³H]XA displaced by 1 mM non-radioactive XA on crude synaptosomal membranes from rat brain.

<p>TB: total binding; NSB: non-specific binding; SB: specific binding. Non-linear regression lines with GraphPad Prism Program; R² = 0.78. Each point is the mean±SD of three experiments made in triplicate at each concentration. Kd = 0.74 µM; Bmax = 7.5 pmoles/mg protein.</p

Pharmacological characteristics of XA responses recorded in the cell-attached mode from differentiated NCB-20 cells.

<p><b>A</b> and <b>B</b>: Agonistic action of XT-21 and NCS-482, and inhibition by NCS-486 of XA, XT-21 and NCS-482 responses. Note the absence of effect of NCS-486 when applied alone (<b>B</b>). Horizontal bars represent periods of drug application as indicated. <b>C</b>: Statistical data of mean response amplitude (± SEM) obtained with XA, XT-21 and NCS-482 (6, 7 and 4 cells respectively) applied at concentrations as indicated. <b>D</b>: Inhibition of the agonist-induced responses by NCS-486 20 µM (12 cells). The mean of agonist responses (control) was set at 100%.</p

XA-induced GTP-γ-S binding characteristics. A

<p>and <b>B</b> show the optimal concentration level of GDP and MgCl₂ respectively that induce maximal GTP-γ-S binding in the presence of a fixed concentration of XA (5 µM). <b>C</b>: EC₅₀ of GTP-γ-S binding to crude synaptosomal membranes from rat brain in the presence of increased XA concentrations from 0.5 to 50 µM. Non-linear fitting using the GraphPad Prism program, each experimental point was the mean±SEM of three results obtained in triplicate at each concentration.</p

Effects of amino acid neurotransmitters, selected XA-related analogues and compounds of the kynurenine pathway on XA binding sites.

<p>Each compound was tested at 200 µM concentration in the presence of radioactive XA. Displacement of radioactive XA induced by 200 µM XA was arbitrarily set at 100%. Result values are the mean of 3 experiments performed in triplicate±SEM.</p