A Fault-Tolerant Location Approach for Transient Voltage Disturbance Source Based on Information Fusion

This paper proposed a fault-tolerant approach based on information fusion (IF) to automatically locate the transient voltage disturbance source (TVDS) in smart distribution grids. We first defined three credibility factors that will influence the reliability of the direction-judgments at each power quality monitor (PQM). Then we proposed two rules of influence and a verification factor for the distributed generation (DG) integration. Based on the two sets of direction-judgment criteria, a novel decision-making method with fault tolerance based on the IF theory is proposed for automatic location of the TVDS. Three critical schemes, including credibility fusion, conflict weakening, and correction for DG integration, have been integrated in the proposed fusion method, followed by a reliability evaluation of the location results. The proposed approach was validated on the IEEE 13-node test feeder, and the TVDS location results demonstrated the effectiveness and fault tolerance of the IF based approach

Fault-tolerant location of transient voltage disturbance source for DG integrated smart grid

In this paper, a new fault-tolerant approach based on improved particle swarm optimization (IPSO) is proposed to automatically locate the transient voltage disturbance source (TVDS) for smart grid with distributed generation (DG) integration. We first analyze the influence of the DG integration on the TVDS direction-judgments. Two new credibility indexes, the monitoring-credibility and the partial-credibility, are defined to measure the reliability of direction-judgment result at each power quality monitor (PQM) with consideration of multiple factors, including DG integration, disturbance intensity and fluctuation characteristic. By using these credibility indexes and a newly defined search space, a heuristic searching approach, called IPSO, is then proposed to obtain the optimal solution of the TVDS location. Simulation study is carried out on the IEEE 34 node test feeder, and the results demonstrate that the proposed approach has significantly improved fault-tolerant capability with satisfatory convergence speed

Regulation of photosensation by hydrogen peroxide and antioxidants in C. elegans.

The eyeless C. elegans exhibits robust phototaxis behavior in response to short-wavelength light, particularly UV light. C. elegans senses light through LITE-1, a unique photoreceptor protein that belongs to the invertebrate taste receptor family. However, it remains unclear how LITE-1 is regulated. Here, we performed a forward genetic screen for genes that when mutated suppress LITE-1 function. One group of lite-1 suppressors are the genes required for producing the two primary antioxidants thioredoxin and glutathione, suggesting that oxidization of LITE-1 inhibits its function. Indeed, the oxidant hydrogen peroxide (H2O2) suppresses phototaxis behavior and inhibits the photoresponse in photoreceptor neurons, whereas other sensory behaviors are relatively less vulnerable to H2O2. Conversely, antioxidants can rescue the phenotype of lite-1 suppressor mutants and promote the photoresponse. As UV light illumination generates H2O2, we propose that upon light activation of LITE-1, light-produced H2O2 then deactivates LITE-1 to terminate the photoresponse, while antioxidants may promote LITE-1's recovery from its inactive state. Our studies provide a potential mechanism by which H2O2 and antioxidants act synergistically to regulate photosensation in C. elegans

A Cold-Sensing Receptor Encoded by a Glutamate Receptor Gene

In search of the molecular identities of cold-sensing receptors, we carried out an unbiased genetic screen for cold-sensing mutants in C. elegans and isolated a mutant allele of glr-3 gene that encodes a kainate-type glutamate receptor. While glutamate receptors are best known to transmit chemical synaptic signals in the CNS, we show that GLR-3 senses cold in the peripheral sensory neuron ASER to trigger cold-avoidance behavior. GLR-3 transmits cold signals via G protein signaling independently of its glutamate-gated channel function, suggesting GLR-3 as a metabotropic cold receptor. The vertebrate GLR-3 homolog GluK2 from zebrafish, mouse, and human can all function as a cold receptor in heterologous systems. Mouse DRG sensory neurons ex- prc GluK2, and GluK2 knockdown in these neurons suppresses their sensitivity to cold but not cool temperatures. Our study identifies an evolutionarily conserved cold receptor, revealing that a central chemical receptor unexpectedly functions as a thermal receptor in the periphery