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Search Results: 1 - 10 of 200596 matches for " P. Subburaj "
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Hybrid Fuzzy Controller Based Frequency Regulation in Restructured Power System  [PDF]
P. Anitha, P. Subburaj
Circuits and Systems (CS) , 2016, DOI: 10.4236/cs.2016.76065
Abstract: This paper discusses the implementation of Load Frequency Control (LFC) in restructured power system using Hybrid Fuzzy controller. The formulation of LFC in open energy market is much more challenging; hence it needs an intelligent controller to adapt the changes imposed by the dynamics of restructured bilateral contracts. Fuzzy Logic Control deals well with uncertainty and indistinctness while Particle Swarm Optimization (PSO) is a well-known optimization tool. Abovementioned techniques are combined and called as Hybrid Fuzzy to improve the dynamic performance of the system. Frequency control of restructured system has been achieved by automatic Membership Function (MF) tuned fuzzy logic controller. The parameters defining membership function has been tuned and updated from time to time using Particle Swarm Optimization (PSO). The robustness of the proposed hybrid fuzzy controller has been compared with conventional fuzzy logic controller using performance measures like overshoot and settling time following a step load perturbation. The motivation for using membership function tuning using PSO is to show the behavior of the controller for a wide range of system parameters and load changes. Error based analysis with parametric uncertainties and load changes is tested on a two-area restructured power system.
Integral Performance Criteria Based Analysis of Load Frequency Control in Bilateral Based Market  [PDF]
P. Anitha, P. Subburaj
Circuits and Systems (CS) , 2016, DOI: 10.4236/cs.2016.76086
Abstract: Performance index based analysis is made to examine and highlight the effective application of Particle Swarm Optimization (PSO) to optimize the Proportional Integral gains for Load Frequency Control (LFC) in a restructured power system that operates under Bilateral based policy scheme. Various Integral Performance Criteria measures are taken as fitness function in PSO and are compared using overshoot, settling time and frequency and tie-line power deviation following a step load perturbation (SLP). The motivation for using different fitness technique in PSO is to show the behavior of the controller for a wide range of system parameters and load changes. Error based analysis with parametric uncertainties and load changes are tested on a two-area restructured power system. The results of the proposed PSO based controller show the better performance compared to the classical Ziegler-Nichols (Z-N) tuned PI andFuzzy Rule based PI controller.
Intelligence Based Soft Starting Scheme for the Three Phase Squirrel Cage Induction Motor with Extinction Angle AC Voltage Controller  [PDF]
A. A. Mohamed Faizal, P. Subburaj
Circuits and Systems (CS) , 2016, DOI: 10.4236/cs.2016.79236
Abstract: Whenever a squirrel cage induction motor is started, notable electromechanical torque and current pulsations occur. The adverse effects of starting torque pulsations and high inrush current in induction motor are eliminated using digital power electronic soft starting schemes that guarantee higher degrees of compliance of the requirements of an ideal soft starter for the induction motor. Soft starters are cheap, simple, reliable and occupy less volume. In this paper, an experimental setup of soft starting technique with extinction angle AC voltage controller and a speed and stator current based closed loop scheme is demonstrated using Artificial Neural Network (ANN) and Fuzzy Logic Control (FLC) by the way of MATLAB/SIMULINK based simulation. The ANN based soft starting scheme produces best results in terms of smooth starting torque and least inrush current. The results thus obtained were satisfactory and promising.
Distribution System Reconfiguration for Loss Reduction using Genetic Algorithm
P. Subburaj,K. Ramar,L. Ganesan,P. Venkatesh
Journal of Electrical Systems , 2006,
Abstract: Feeder reconfiguration is defined as altering the topological structures of distribution feeders by changing the open/closed states of the sectionalizing and tie switches. In network reconfiguration for loss reduction, the solution involves a search over relevant radial configuration. In this paper, a method, based on genetic algorithm (GA) to determine the minimum configuration is presented. A genetic algorithm (GA) is a search or optimization algorithm based on the mechanics of natural selection and natural genetics. Since GA is suitable to solve combinatorial optimization problems, it can be successfully applied to problems of loss minimization in distribution systems. Test results are included to show the performance of the proposed method.
A New Approach to Economic Dispatch Problem with Valve Point Loading Using Evolutionary Programming
P. Subburaj,L. Ganesan,K. Ramar,M. Rajkumar
International Journal of Electrical and Power Engineering , 2012,
Abstract: Economic Load Dispatch (ELD) is one of the main functions of modern Energy Management System (EMS), which determines the optimal real power settings of generating units with an objective of minimizing the total fuel cost. In all practical cases, the fuel cost of generators can be represented as a quadratic function of real power generation. In fact, discontinuity may also be observed in thermal power plants due to valve point loading. The conventional optimization methods require the objective functions in continuous differentiable form, therefore they fail to provide global minima. The Evolutionary Computation (EC) methods can handle non-differentiable and non-convex objective functions and give global or near global optimum solutions. Evolutionary Computation methods such as Genetic Algorithm (GA), Evolutionary Programming (EP) are applied to economic dispatch problem. By avoiding the coding and decoding process of transformations in GA, use of EP among other EC methods resulted in less population size and number of iterations. A MATLAB program has been developed for Evolutionary Programming to solve economic load dispatch problem. In this paper EP based ELD problem is solved with stochastic method for competition and selection.
A SOFTWARE RELIABILITY GROWTH MODEL FOR VITAL QUALITY METRICS
R. Subburaj,G. Gopal,P.K. Kapur
South African Journal of Industrial Engineering , 2012,
Abstract: ENGLISH ABSTRACTA Non-Homogenous Poisson Process (NHPP) model whose failure intensity function has the same mathematical form as that of a generalized exponential function was proposed for application as a Software Reliability Growth Model (SRGM). However, in order to facilitate collecting quality metrics pertaining to the degree of imperfect or efficient debugging phenomena and the number of faults left in the software, in this paper the authors propose an extension to the above SRGM. This SRGM enables adequate goodness of fit statistic and predictive validity, even when the software projects witness learning phenomenon of the testing team, either imperfect or perfect or efficient software debugging phenomenon, as well as wide fluctuations in time between failures – either occurring alone or in combinations thereof. AFRIKAANSE OPSOMMING: 'n Nie-homogene Poissonproses (NHPP) waarvan die mislukkingsdigtheidsfunksie soortgelyk is aan 'n algemene eksponensi le funksie word voorgehou as 'n programmatuur-betroubaarheidsgroeimodel (PBGM). Die model lewer toereikende passingsgoedheid en voorspellingsgeldigheid onder uiteenlopende leereienskappe van toetsers, swak of goeie ontfouting van programmatuur, en groot verskille tussen waardes van tyd tussen mislukkings. Die outeurs stel ook voor dat die goedheid van ontfoutingsaksies gemeet word met behulp van 'n uitbreiding van die PBGM-model.
Free radical theory of autoimmunity
Subburaj Kannan
Theoretical Biology and Medical Modelling , 2006, DOI: 10.1186/1742-4682-3-22
Abstract: A hypothetical scheme to explain the damage induced by chemotherapy and associated chronic oxidative stress is proposed on the basis of published literature, experimental data and anecdotal observations. Brief accounts of multidrug resistance, lymphoid malignancy, the cellular and molecular basis of autoimmunity and chronic oxidative stress are assembled to form a basis for the hypothesis and to indicate the likelihood that it is valid in vivo.The argument set forward in this article suggests a possible mechanism for the development of autoimmunity. According to this view, the various sorts of damage induced by chemotherapy have a role in the pattern of drug resistance, which is associated with the initiation of autoimmunity.After exposure to chemotherapeutic drugs, lymphoid cells develop along two distinct pathways. First, a cell population susceptible to the drugs dies by apoptosis or necrosis, depending on the severity of treatment. Secondly, a few cells evolve one or more mechanisms for survival, resisting the damage inflicted by the drugs. It is well known that chemotherapeutic drugs induce tumor cell death via apoptosis through DNA damage, and, in particular, activation of proteolytic enzymes involved in programmed cell death. When one drug fails, various others are tried as parts of a therapeutic regimen. Such drugs kill cancer cells by increasing their sensitivity via alterations in internal mechanisms, a desired outcome for effective chemotherapy. Some tumor cells evolve mechanisms, as yet poorly understood, by which they acquire resistance to structurally and functionally unrelated drugs; this is referred to as multi-drug resistance.Distinct factors contributing to the formation of tumorigenic phenotypes ensure that each malignant cell is unique in terms of activation of oncogenes and inactivation of tumor suppressor genes. Drug-exposed tumor cells are subjected to sustained to oxidative stress and become tolerant to it. During this time window, selection
An ETP model (exclusion-tolerance-progression) for multi drug resistance
Subburaj Kannan
Theoretical Biology and Medical Modelling , 2005, DOI: 10.1186/1742-4682-2-17
Abstract: Based on findings from clinical and experimental studies, a unifying model is proposed to delineate the potential mechanism by which tumor cells progress towards multi drug resistance, resulting in failure of chemotherapy.It is suggested that the evolution of multi drug resistance is a developmentally orchestrated event. Identifying stage-specific time windows during this process would help to identify valid therapeutic targets for the effective elimination of malignancy.The phenomenon of drug resistance is a distinct and multifactorial entity culminating in the failure of therapeutic regimens in clinical oncology. From the clinical perspective, the emergence of drug resistance is determined by the rate of tumor growth, in conjunction with the remission index subsequent to chemotherapy. In contrast, experimental model(s) for studying drug resistance involve either homogeneous cell populations or co-culture models where the time frame ranges from a few days to a week at the most. It is obvious that the biochemical and collective physiological process that coexist in the cancer patient are totally distinct and do not warrant direct comparison with experimental data.A tumor mass encompassing approximately 1011 to 1012 cells is considered a lethal tumor burden. Depending on the sensitivity of a given tumor cell population to anti-neoplastic drug(s) (chemotherapeutic agents), and the dose administered, the effectiveness of the therapy, referred to as "Cell Kill", is determined. "Cell Kill" depends on the inherent susceptibility of the tumor burden. The "Cell Kill" of a given tumor burden varies between 90 % to 99.99%. If we assume that, under the best therapeutic regimen, one round of chemotherapy or radiation therapy would be likely to achieve a 99.99% "cell kill" in a tumor burden of 1011cells, this would reduce the tumor burden to 108 cells. It should be noted that chemotherapy and radiation therapy exert considerable toxic effects on normal cells; because of this fac
Regulatory role of E-NTPase/E-NTPDase in Ca2+/Mg2+ transport via gated channel
Hans M Schreiber, Subburaj Kannan
Theoretical Biology and Medical Modelling , 2004, DOI: 10.1186/1742-4682-1-3
Abstract: In this article it is proposed on the basis of published data that E-NTPase/E-NTPDase could play a role in the influx and efflux of Ca2+and Mg2+ in vivo.Attenuation of extracellular Ca2+ influx by rat cardiac sarcoplasmic anti-E-NTPase antibodies and oligomerization studies on mammalian CD39 conclusively point towards the existence of a new channel in the membrane. Further studies on these properties of the E-NTPase/E-NTPDase may provide detailed mechanisms and identify the potential patho-physiological significance.The mechanism by which [Ca2+]i is increased in excitable cells differs from that obtaining in non-excitable cells. Excitable cells exhibit an action potential, a substantial general depolarization of the plasma membrane, in response to depolarizing stimuli; influx of Ca2+ occurs via plasma membrane Ca2+ channels and/or release from sarco (endo) plasmic reticulum via ryanodine-receptor Ca2+ channels which regulate the excitation – contraction coupling [1,2]. The factors that determine the extent of Ca2+ entry are (i) magnitude of the membrane potential and (ii) magnitude of the transmembrane Ca2+ gradient. These two factors also determine whether Ca2+ or Mg2+ enters and the time (probably milliseconds) that elapses between channel opening and termination of Ca2+ or Mg2+ transport [3].In non-excitable cells, the increase in [Ca2+]i results from influx of Ca2+ across the plasma membrane and Ca2+ release from the endoplasmic reticulum. Ca2+ release from the SER depends on the binding of inositol 1,4,5-triphosphate (InsP3) to its receptor Ca2+channels, and also on Ca2+ binding to ryanodine receptor – Ca2+channels.Ca2+ is removed from the cell by the following means. i: the sarco (endo) plasmic reticular Ca2+ pump ATPase (SERCA), which transports Ca2+ from the cytoplasm into the SER lumen (~70% of the activator Ca2+); ii: The plasma membrane Ca2+ pump ATPase (PMCA), which exports Ca2+ across the plasma membrane (~1% of the activator Ca2+); iii: Mitochondrial C
Structural and molecular basis of interaction of HCV non-structural protein 5A with human casein kinase 1α and PKR
Govindarajan Sudha, Subburaj Yamunadevi, Nidhi Tyagi, Saumitra Das, Narayanaswamy Srinivasan
BMC Structural Biology , 2012, DOI: 10.1186/1472-6807-12-28
Abstract: Serine 232 of NS5A is known to be phosphorylated by human ck1α. A structural model of NS5A peptide containing phosphoacceptor residue Serine 232 bound to ck1α has been generated using the known 3-D structures of kinase-peptide complexes. The substrate interacting residues in ck1α has been identified from the model and these are found to be conserved well in the ck1 family. ck1α – substrate peptide complex has also been used to understand the structural basis of association between ck1α and its other viral stress induced substrate, tumour suppressor p53 transactivation domain which has a crystal structure available.Interaction of NS5A with another human kinase PKR is primarily genotype specific. NS5A from genotype 1b has been shown to interact and inhibit PKR whereas NS5A from genotype 2a/3a are unable to bind and inhibit PKR efficiently. This is one of the main reasons for the varied response to interferon therapy in HCV patients across different genotypes. Using PKR crystal structure, sequence alignment and evolutionary trace analysis some of the critical residues responsible for the interaction of NS5A 1b with PKR have been identified.The substrate interacting residues in ck1α have been identified using the structural model of kinase - substrate peptide. The PKR interacting NS5A 1b residues have also been predicted using PKR crystal structure, NS5A sequence analysis along with known experimental results. Functional significance and nature of interaction of interferon sensitivity determining region and variable region 3 of NS5A in different genotypes with PKR which was experimentally shown are also supported by the findings of evolutionary trace analysis. Designing inhibitors to prevent this interaction could enable the HCV genotype 1 infected patients respond well to interferon therapy.Hepatitis C virus (HCV) which belongs to the family flaviviridae, causes chronic liver disease, liver cirrhosis and hepatocellular carcinoma in humans [1]. Non-structural protein 5A
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