Comprehensive comparison of a current-source and a voltage-source converter for three-phase EV fast battery chargers

This paper presents a comprehensive comparison of a current-source converter and a voltage-source converter for three-phase electric vehicle (EV) fast battery chargers. Taking into account that the current-source converter (CSC) is a natural buck-type converter, the output voltage can assume a wide range of values, which varies between zero and the maximum instantaneous value of the power grid phase-to-phase voltage. On the other hand, taking into account that the voltage-source converter (VSC) is a natural boost-type converter, the output voltage is always greater than the maximum instantaneous value of the power grid phase-to-phase voltage, and consequently, it is necessary to use a dc-dc buck-type converter for applications as EV fast battery chargers. Along the paper is described in detail the principle of operation of both the CSC and the VSC for EV fast chargers, as well as the main equations of the power theory and current control strategies. The comparison between both converters is mainly established in terms of the total harmonic distortion of the grid current and the estimated efficiency for a range of operation between 10 kW and 50 kW.

Measuring end-to-end delay in real-time auralisation systems

One of the major challenges in the development of an immersive system is handling the delay between the tracking of the user’s head position and the updated projection of a 3D image or auralised sound, also called end-to-end delay. Excessive end-to-end delay can result in the general decrement of the “feeling of presence”, the occurrence of motion sickness and poor performance in perception-action tasks. These latencies must be known in order to provide insights on the technological (hardware/software optimization) or psychophysical (recalibration sessions) strategies to deal with them. Our goal was to develop a new measurement method of end-to-end delay that is both precise and easily replicated. We used a Head and Torso simulator (HATS) as an auditory signal sensor, a fast response photo-sensor to detect a visual stimulus response from a Motion Capture System, and a voltage input trigger as real-time event. The HATS was mounted in a turntable which allowed us to precisely change the 3D sound relative to the head position. When the virtual sound source was at 90º azimuth, the correspondent HRTF would set all the intensity values to zero, at the same time a trigger would register the real-time event of turning the HATS 90º azimuth. Furthermore, with the HATS turned 90º to the left, the motion capture marker visualization would fell exactly in the photo-sensor receptor. This method allowed us to precisely measure the delay from tracking to displaying. Moreover, our results show that the method of tracking, its tracking frequency, and the rendering of the sound reflections are the main predictors of end-to-end delay.

QRS Voltage-Duration Product in the Identification of Left Ventricular Hypertrophy in Spontaneously Hypertensive Rats

OBJECTIVE - Evaluation of the performance of the QRS voltage-duration product (VDP) for detection of left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHR). METHODS - Orthogonal electrocardiograms (ECG) were recorded in male SHR at the age of 12 and 20 weeks, when systolic blood pressure (sBP) reached the average values of 165±3 mmHg and 195±12 mmHg, respectively. Age- and sex- matched normotensive Wistar Kyoto (WKY) rats were used as controls. VDP was calculated as a product of maximum QRS spatial vector magnitude and QRS duration. Left ventricular mass (LVM) was weighed after rats were sacrificed. RESULTS - LVM in SHR at 12 and 20 weeks of age (0.86±0.05 g and 1.05±0.07 g, respectively) was significantly higher as compared with that in WKY (0.65±0.07 g and 0.70±0.02 g). The increase in LVM closely correlated with the sBP increase. VDP did not reflect the increase in LVM in SHR. VDP was lower in SHR as compared with that in WKY, and the difference was significant at the age of 20 weeks (18.2mVms compared with 10.7mVms, p<0.01). On the contrary, a significant increase in the VDP was observed in the control WKY at the age of 20 weeks without changes in LVM. The changes in VDP were influenced mainly by the changes in QRSmax. CONCLUSION - LVM was not the major determinant of QRS voltage changes and consequently of the VDP. These data point to the importance of the nonspatial determinants of the recorded QRS voltage in terms of the solid angle theory.

Effect of rufinamide on gating properties of voltage-gated sodium channel Na(v)1.7

Background: Voltage-gated sodium channels (Nav1.x) are important players in chronic pain. A particular interest has grown in Nav1.7, expressed in nociceptors, since mutations in its gene are associated to two inherited pain syndromes or insensitivity to pain. Rufinamide, a drug used to treat refractory epilepsy such as the Lennox-Gastaut syndrome, has been shown to reduce the number of action potentials in cortical neurons without completely blocking Na channels. Aim: The goal of this study was to investigate the effect of rufinamide on Nav1.7 current. Methods and results: Whole-cell patch clamp experiments were performed using HEK293 cells stably expressing Nav1.7. Rufinamide significantly decreased peak sodium current by 28.3, 21.2 and 12.5% at concentrations of 500, 100 and 50μM respectively (precise EC50 could not be calculated since higher rufinamide concentrations could not be achieved in physiological buffer solution). No significant difference on the V1/2 of voltage-dependence of activation was seen; however a shift in the steady-state inactivation curve was observed (-82.6 mV to -88.8 mV and -81.8 to -87.6 mV for 50 and 100 μM rufinamide respectively, p <0.005). Frequency-dependent inhibition of Nav1.7 was also influenced by the drug. One hundred μM rufinamide reduced the peak sodium current (in % of the peak current taken at the first sweep of a train of 50) from 90.8 to 80.8% (5Hz), 88.7 to 71.8% (10 Hz), 69.1 to 49.2% (25 Hz) and 22.3 to 9.8% (50 Hz) (all p <0.05). Onset of fast inactivation was not influenced by the drug since no difference in the time constant of current decay was observed. Conclusion: In the concentration range of plasma level in human treated for epilepsy, 15 μM, rufinamide only minimally blocks Nav1.7. However, it stabilizes the inactivated state and exerts frequencydependent inhibition of Nav1.7. These pharmacological properties may be of use in reducing ectopic discharges as a causal and symptom related contributor of neuropathic pain syndrome.

Regulation of the voltage-gated sodium channel Nav1.7 by ubiquitin ligase Nedd4-2

Background and aim: Neuropathic pain (NP) is a frequent and disabling disorder occurring as a consequence of a direct lesion of the nervous system and recurrently associated with a positive shift toward nervous system excitability. Peripheral nerve activity is mainly carried by voltage-gated sodium channels (VGSC), with Nav1.7 isoform being an important candidate since loss of function mutations of its gene is associated with congenital inability to experience pain. Interestingly, ubiquitin ligases from the Nedd4 family are well known proteins that regulate the turnover of many membrane proteins such as VGSC and we showed Nedd2-2 is downregualted in experimental models of chronic pain. The aim of this study was to investigate the importance of Nedd4-2 in the modulation of Nav1.7 at the membrane. Methods: In vitro: whole cell patch clamp on HEK293 cell line stably expressing Nav1.7 was used to record sodium currents (INa), where the peak current of INa reflects the quantity of functional Nav1.7 expressed at the membrane. The possibility that Nedd4-2 modulates the currents was assessed by investigating the effect of its cotransfection on INa. Biotinylation of cell surface was used to isolate membrane-targeted Nav1.7. Furthermore, as the interaction between Nedd4-2 and Nav isoforms was previously reported to rely on an xPPxYx sequence (PY-motif), we mutated this latter to study its impact in the specific interaction between Nav1.7 and Nedd4-2. GST-fusion proteins composed of the Nav1.7 c terminal 66 amino acids (wild-type or PY mutated) and GST were used to pull-down Nedd4-2 from lysates. Results: Co-transfection of Nav1.7 with Nedd4-2 reduced the Nav1.7 current amplitude by ~80% (n = 36, p <0.001), without modifying the biophysical properties of INa. In addition, we show that the quantity of Nav1.7 at the membrane was decreased when Nedd4-2 was present. This effect was dependent on the PY-motif since mutations in this sequence abolished the down-regulatory effect of Nedd4-2. The importance of this motif was further confirmed by pull down experiments since the PY mutant completely eliminate the interaction with Nedd4-2. Perspectives: Altogether, these results point to the importance of Nedd4-2 as a Nav1.7 regulator through cell surface modulation of this sodium channel. Further experiments in freshly dissociated neurons from wild type and Scn1bflox/Nedd4-2Cre mice are needed to confirm in vivo these preliminary data.

Use-dependent block of the voltage-gated Na+ channel by tetrodotoxin and saxitoxin: Effect of pore mutations that change ionic selectivity.

Voltage-gated Na(+) channels (NaV channels) are specifically blocked by guanidinium toxins such as tetrodotoxin (TTX) and saxitoxin (STX) with nanomolar to micromolar affinity depending on key amino acid substitutions in the outer vestibule of the channel that vary with NaV gene isoforms. All NaV channels that have been studied exhibit a use-dependent enhancement of TTX/STX affinity when the channel is stimulated with brief repetitive voltage depolarizations from a hyperpolarized starting voltage. Two models have been proposed to explain the mechanism of TTX/STX use dependence: a conformational mechanism and a trapped ion mechanism. In this study, we used selectivity filter mutations (K1237R, K1237A, and K1237H) of the rat muscle NaV1.4 channel that are known to alter ionic selectivity and Ca(2+) permeability to test the trapped ion mechanism, which attributes use-dependent enhancement of toxin affinity to electrostatic repulsion between the bound toxin and Ca(2+) or Na(+) ions trapped inside the channel vestibule in the closed state. Our results indicate that TTX/STX use dependence is not relieved by mutations that enhance Ca(2+) permeability, suggesting that ion-toxin repulsion is not the primary factor that determines use dependence. Evidence now favors the idea that TTX/STX use dependence arises from conformational coupling of the voltage sensor domain or domains with residues in the toxin-binding site that are also involved in slow inactivation.

PHOTO STORE : Galeria virtual d'imatges

Ofereix a l'usuari la possibilitat de crear la seva pròpia galeria virtual d'imatges, i de classificar-les en àlbums dividits en categories per oferir una catalogació molt més específica. Els àlbums els subdividim públics per aque qualsevol visitant del web (registrat o no) pugui tenir la possibilitat d'accedir-hi,visualitzar i imprimir les fotos; o privats per a l'ús exclusiu de l'usuari que els publica.

Study of conformational changes of ASIC1a by voltage-clamp fluorometry

Le fonctionnement du système nerveux est sensible aux variations de la concentration d'acide. Une acidification des tissus peut se produire pendant une activité neuronale intense ou dans des situations physiopathologiques telles que l'inflammation ou les lésions cérébrales. Les canaux ioniques sensibles à l'acide (ASIC) sont activés par acidification et jouent un rôle important dans la détection des changements d'acide. Les ASICs contribuent à la dégénérescence neuronale après une lésion cérébrale, puisque leur inhibition limite la lésion neuronale. L'acidification induite par une inflammation du tissu nerveux conduit à des stimuli de douleur, qui sont détectés par ces canaux. En effet, les toxines qui bloquent spécifiquement les ASICs montrent des effets analgésiques dans des modèles animaux. La structure 3D d'ASIC peut être comparée à une main qui tient une boule entre son pouce et le doigt. Les différents domaines d'ASIC sont appelés doigt, pouce, jointure, boule-ß et paume. Les domaines transmembranaires représentent le poignet de cette main. Mon projet de thèse vise à décrire les mouvements survenant sur ce canal pendant son activité. A cet effet, j'ai utilisé une technique combinée qui permet la mesure des mouvements en temps réel durant l'activité du canal. J'ai montré les réarrangements des domaines extracellulaires pendant l'activité ASIC. Ces mouvements sont transmis au pore du canal, ou ils contrôlent sa fermeture et ouverture. La direction de ces mouvements a été évaluée pour les domaines doigt et jointure, et nous avons montré qu'ils s'éloignent de la boule-ß lors de l'acidification. J'ai également été en mesure de décrire les mouvements qui se produisent dans la poche acidique, une zone qui est considérée comme importante, car elle représente le site de liaison de certaines toxines de venin qui agissent sur les ASICs. J'ai ainsi pu montrer que les domaines doigt et le pouce qui forment la poche acidique se rapprochent l'un de l'autre pendant l'activation du canal. Ces résultats sont en accord avec des observations précédentes réalisées sur les ASICs par d'autres chercheurs. Enfin, cette analyse approfondie permet d'améliorer les connaissances sur le contrôle de l'activité ASIC; de plus, les mécanismes trouvés ici sont probablement partagés entre les canaux de la famille à laquelle appartiennent les ASICs. -- Les acid-sensing ion channels (ASICs) sont des canaux sodiques ouverts par les protons et principalement exprimés dans le système nerveux. Ils sont impliqués dans la détection des protons dans de nombreux états physiologiques et pathologiques comme l'ischémie et la perception de la douleur. La structure cristalline de l'isoforme ASIC1 de poulet a été déterminée dans l'état désensibilisé et ouvert. Les études fonctionnelles indiquent que la protonation des résidus clés dans la boucle extracellulaire déclenche des changements de conformation conduisant à l'ouverture du canal. Cependant, les mécanismes moléculaires qui relient la protonation à l'ouverture et la fermeture du canal n'ont pas encore été clarifiés. Dans cette étude, nous avons utilisé la voltage-clamp fluorimétrie (VCF) pour révéler les mouvements de l'activité associée qui se produisent dans les différents domaines de l'ASICla. Les fluorophores positionnés dans le pouce, la paume, le doigt, l'articulation et dans les domaines de l'entrée du pore extracellulaire ont montré des signaux de VCF liés à des changements de conformation au cours de l'activité du canal. La synchronisation des changements de fluorescence indique une séquence complexe de mouvements en fonction du pH. La cinétique de la fluorescence et des signaux de courant ont été comparés les uns aux autres afin de déterminer si le mouvement détecté par le signal de fluorescence correspond à une transition fonctionnelle définie du canal. Certains des résidus testés se sont révélés être étroitement liés à la désensibilisation du canal ou au rétablissement après la désensibilisation. En outre, nous avons trouvé qu'un tryptophane endogène de la boule-ß diminue le signal de fluorescence des sondes positionnées dans les domaines doigt et jointure. L'augmentation observée de ces signaux indique que ces domaines s'éloignent à une distance à partir de la boucle de la boule-ß. Sur la base de ce principe, nous avons généré des paires Trp-Cys « quencher», dans lequel le Cys est utilisé comme site d'ancrage pour attacher le fluorophore. Ensuite, nous avons évalué les changements de conformation qui se produisent au niveau de la poche acide, une zone importante pour la fonction et la régulation d'ASIC. Les signaux de fluorescence indiquent un mouvement de l'hélice supérieure du pouce vers le doigt et une rotation de la boule-ß dans le sens horaire. L'analyse de la cinétique indique que les mouvements des sous-domaines qui composent la poche acide se produisent pendant la désensibilisation du canal. Mon projet de doctorat représente la première analyse approfondie des changements conformationnels dépendants de l'activité des ASICs et fournit des informations sur les mécanismes de contrôle de l'activité du canal qui sont probablement partagés avec d'autres canaux proches.

p.L1612P, a novel voltage-gated sodium channel Nav1.7 mutation inducing a cold sensitive paroxysmal extreme pain disorder.

BACKGROUND: Mutations in the SCN9A gene cause chronic pain and pain insensitivity syndromes. We aimed to study clinical, genetic, and electrophysiological features of paroxysmal extreme pain disorder (PEPD) caused by a novel SCN9A mutation. METHODS: Description of a 4-generation family suffering from PEPD with clinical, genetic and electrophysiological studies including patch clamp experiments assessing response to drug and temperature. RESULTS: The family was clinically comparable to those reported previously with the exception of a favorable effect of cold exposure and a lack of drug efficacy including with carbamazepine, a proposed treatment for PEPD. A novel p.L1612P mutation in the Nav1.7 voltage-gated sodium channel was found in the four affected family members tested. Electrophysiologically the mutation substantially depolarized the steady-state inactivation curve (V1/2 from -61.8 ± 4.5 mV to -30.9 ± 2.2 mV, n = 4 and 7, P < 0.001), significantly increased ramp current (from 1.8% to 3.4%, n = 10 and 12) and shortened recovery from inactivation (from 7.2 ± 5.6 ms to 2.2 ± 1.5 ms, n = 11 and 10). However, there was no persistent current. Cold exposure reduced peak current and prolonged recovery from inactivation in wild-type and mutated channels. Amitriptyline only slightly corrected the steady-state inactivation shift of the mutated channel, which is consistent with the lack of clinical benefit. CONCLUSIONS: The novel p.L1612P Nav1.7 mutation expands the PEPD spectrum with a unique combination of clinical symptoms and electrophysiological properties. Symptoms are partially responsive to temperature but not to drug therapy. In vitro trials of sodium channel blockers or temperature dependence might help predict treatment efficacy in PEPD.

Large-Area Photo-Mosaics Using Global Alignment and Navigation Data

Seafloor imagery is a rich source of data for the study of biological and geological processes. Among several applications, still images of the ocean floor can be used to build image composites referred to as photo-mosaics. Photo-mosaics provide a wide-area visual representation of the benthos, and enable applications as diverse as geological surveys, mapping and detection of temporal changes in the morphology of biodiversity. We present an approach for creating globally aligned photo-mosaics using 3D position estimates provided by navigation sensors available in deep water surveys. Without image registration, such navigation data does not provide enough accuracy to produce useful composite images. Results from a challenging data set of the Lucky Strike vent field at the Mid Atlantic Ridge are reported

Ubiquitylation of voltage-gated sodium channels.

Ion channel proteins are regulated by different types of posttranslational modifications. The focus of this review is the regulation of voltage-gated sodium channels (Navs) upon their ubiquitylation. The amiloride-sensitive epithelial sodium channel (ENaC) was the first ion channel shown to be regulated upon ubiquitylation. This modification results from the binding of ubiquitin ligase from the Nedd4 family to a protein-protein interaction domain, known as the PY motif, in the ENaC subunits. Many of the Navs have similar PY motifs, which have been demonstrated to be targets of Nedd4-dependent ubiquitylation, tagging them for internalization from the cell surface. The role of Nedd4-dependent regulation of the Nav membrane density in physiology and disease remains poorly understood. Two recent studies have provided evidence that Nedd4-2 is downregulated in dorsal root ganglion (DRG) neurons in both rat and mouse models of nerve injury-induced neuropathic pain. Using two different mouse models, one with a specific knockout of Nedd4-2 in sensory neurons and another where Nedd4-2 was overexpressed with the use of viral vectors, it was demonstrated that the neuropathy-linked neuronal hyperexcitability was the result of Nav1.7 and Nav1.8 overexpression due to Nedd4-2 downregulation. These studies provided the first in vivo evidence of the role of Nedd4-2-dependent regulation of Nav channels in a disease state. This ubiquitylation pathway may be involved in the development of symptoms and diseases linked to Nav-dependent hyperexcitability, such as pain, cardiac arrhythmias, epilepsy, migraine, and myotonias.

Regulation of the cardiac voltage-gated sodium channel Nav1.5 : regulation of Nav1.5 by ubiquitin-protein ligases of the Nedd4/Nedd4-like family and characterisation of two novel mutations in the gene encoding Nav1.5 (SCN5A) implicated in the Brugada syndrome triggered by fever

Abstract: The genesis of the cardiac action potential, which accounts for the cardiac contraction, is due to the sodium current INa mediated by the voltage-gated sodium channel Nav1.5. Several cardiac arrhythmias such as the Brugada syndrome are known te be caused by mutations in SCN5A, the gene encoding Nav1.5. Studies of these mutations allowed a better understanding of biophysical and functional properties of Nav1.5. However, only few investigations have been performed in order to understand the regulation of Nav1.5. During my thesis, I investigated different mechanisms of regulation of Nav1.5 using a heterologous expression system, HEK293 cells, coupled with a technique of sodium current recording: the patch clamp in whole cell configuration. In previous studies it has been shown that an enzyme of the Nedd4 family (Nedd4-2) regulates an epithelial sodium channel via the interaction with PY-motifs present in the latter. Interestingly, Nav1.5 contains a similar PY-motif, which motivated us to study the role of Nedd4-2 expressed in heart for the regulation of Nav1.5. In a second study, we investigated the implication of two Nav1.5 mutants, which were either less functional or net functional (Nav1.5 R535X and Nav1.5 L325R respectively) implied in the genesis of the Brugada syndrome by fever. Our results established two mechanisms implied in Nav1.5 regulation. The first one implies that following the interaction between the PY-motif of Nav1.5 and Nedd4- 2 Nav1.5 is ubiquitinated by Nedd4-2. This ubiquitination leads to the internalization of Nav1 .5. The second mechanism is a phenomenon called the "dominant negative" effect of Nav1.5 L325R on Nay1.5 where the decrease of 'Na is potentially due to the retention of Nav1.5 by Nav1.5 L325R in an undefined intracellular compartment. These studies defined two mechanisms of Nav1.5 regulation, which could play an important role for the genesis of cardiac arrhythmias where molecular processes are still poorly understood. Résumé La genèse du potentiel d'action cardiaque, permettant la contraction cardiaque, est due au courant sodique INa issu des canaux sodiques cardiaques dépendants du voltage Nav1.5. Nombreuses arythmies cardiaques telles que le syndrome de Brugada sont connues pour être liées à des mutations du gène SCN5A, codant pour Nav1.5. L'étude de ces mutations a permis une meilleure compréhension des propriétés structurelles et fonctionnelles de Nav1.5 et leurs implications dans la genèse de ces pathologies. Néanmoins peu d'études ont été menées afin de comprendre les mécanismes de régulation de Nav1.5. Mon travail de thèse a consisté à étudier des mécanismes de régulation de Nav1.5 en utilisant un système d'expression hétérologue, les cellules HEK293, couplé à une technique d'enregistrement des courants sodiques, le "patch clamp" en configuration cellule entière. La présence sur Nav1.5 d'un motif-PY similaire à ceux nécessaires pour la régulation d'un canal épithélial sodique par une enzyme de la famille de Nedd4, nous a amenée à étudier le rôle de ces ubiquitine-ligases, en particulier Nedd4-2, dans la régulation de Nav1.5. La seconde étude s'est intéressée aux conséquences de deux mutations de SCN5A codant pour deux mutants peu ou pas fonctionnels (Nav1.5 L325R et Nav1.5 R535X respectivement) retrouvées chez des patients présentant un syndrome de Brugada exacerbé par un état fébrile. Nos résultats ont permis d'établir deux mécanismes de régulation de Nav1.5 L'un par Nedd4-2 qui implique rubiquitination de Nav1.5 par cette ligase suite à l'interaction entre le motif-PY de Nav1.5 et Nedd4-2. Cette modification déclenche l'internalisation du canal impliquée dans la diminution d'INa. Le second mécanisme quant à lui est un effet "dominant négatif" de Nav1.5 L325R sur Nav1.5 aboutissant à une diminution d'INa suite à la séquestration intracellulaire potentielle de Nav1.5 par Nav1.5 L325R. Ces études ont mis en évidence deux mécanismes de régulation de Nav1.5 pouvant jouer un rôle majeur dans la genèse et/ou l'accentuation des arythmies cardiaques dont les processus moléculaires au sein des cardiomyocytes, impliquant des modifications du courant sodiques, sont encore mal compris. Résumé destiné à un large public La dépolarisation électrique de la membrane des cellules cardiaques permet la contraction du coeur. La génèse de cette activité électrique est due au courant sodique issu d'un type de canal à sodium situé dans la membrane des cellules cardiaques. De nombreuses pathologies provoquant des troubles du rythme cardiaque sont issues de mutations du gène qui code pour ce canal à sodium. Ces canaux mutants, entrainant diverses pathologies cardiaques telles que le syndrome de Brugada, ont été largement étudiées. Néanmoins, peu de travaux ont été réalisés sur les mécanismes de régulation de ce canal à sodium non muté. Mon travail de thèse a consisté à étudier certains des mécanismes de régulation de ce canal à sodium en utilisant une technique permettant l'enregistrement des courants sodiques issus de l'expression de ces canaux à sodium à la membrane de cellules mammifères. La présence sur ce canal à sodium d'une structure spécifique, similaire à celle nécessaire pour la régulation d'un canal épithélial à sodium par une enzyme appelée Nedd4-2, nous a amenée à étudier le rôle de cette enzyme dans la régulation de ce canal à sodium. La seconde étude s'est intéressée aux rôles de deux mutations du gène codant pour ce canal à sodium retrouvées chez des patients présentant un syndrome de Brugada exacerbé par la fièvre. Nos résultats nous ont permis d'établir deux mécanismes de régulation de ce canal à sodium diminuant le courant sodique l'un par l'action de l'enzyme Nedd4-2, suite à son interaction avec ce canal, qui modifie ce canal à sodium (ubiquitination) diminuant de ce fait la densité membranaire du canal. L'autre par un mécanisme suggérant un effet négatif de l'un des canaux mutants sur l'expression à la membrane du canal à sodium non muté. Ces études ont mis en évidence deux mécanismes de régulation de ce canal à sodium pouvant jouer un rôle majeur dans la genèse et/ou l'accentuation des troubles du rythme cardiaques dont les mécanismes cellulaires sont encore incompris.

Two methods for voltage sag source location

This paper presents and compares two approaches to estimate the origin (upstream or downstream) of voltage sag registered in distribution substations. The first approach is based on the application of a single rule dealing with features extracted from the impedances during the fault whereas the second method exploit the variability of waveforms from an statistical point of view. Both approaches have been tested with voltage sags registered in distribution substations and advantages, drawbacks and comparative results are presented

A survey on voltage sag events in power systems

This paper aims to survey the techniques and methods described in literature to analyse and characterise voltage sags and the corresponding objectives of these works. The study has been performed from a data mining point of view