A novel algorithm for feature selection using Harmony Search and its application for non-technical losses detection

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Boosting optimum-path forest clustering through harmony Search and its applications for intrusion detection in computer networks

In this paper we propose a nature-inspired approach that can boost the Optimum-Path Forest (OPF) clustering algorithm by optimizing its parameters in a discrete lattice. The experiments in two public datasets have shown that the proposed algorithm can achieve similar parameters' values compared to the exhaustive search. Although, the proposed technique is faster than the traditional one, being interesting for intrusion detection in large scale traffic networks. © 2012 IEEE.

Multilayer perceptron neural networks training through charged system search and its Application for non-technical losses detection

The non-technical loss is not a problem with trivial solution or regional character and its minimization represents the guarantee of investments in product quality and maintenance of power systems, introduced by a competitive environment after the period of privatization in the national scene. In this paper, we show how to improve the training phase of a neural network-based classifier using a recently proposed meta-heuristic technique called Charged System Search, which is based on the interactions between electrically charged particles. The experiments were carried out in the context of non-technical loss in power distribution systems in a dataset obtained from a Brazilian electrical power company, and have demonstrated the robustness of the proposed technique against with several others nature-inspired optimization techniques for training neural networks. Thus, it is possible to improve some applications on Smart Grids. © 2013 IEEE.

A transgenic model for conditional induction and rescue of portal hypertension reveals a role of VEGF-mediated regulation of sinusoidal fenestrations

Portal hypertension (PH) is a common complication and a leading cause of death in patients with chronic liver diseases. PH is underlined by structural and functional derangement of liver sinusoid vessels and its fenestrated endothelium. Because in most clinical settings PH is accompanied by parenchymal injury, it has been difficult to determine the precise role of microvascular perturbations in causing PH. Reasoning that Vascular Endothelial Growth Factor (VEGF) is required to maintain functional integrity of the hepatic microcirculation, we developed a transgenic mouse system for a liver-specific-, reversible VEGF inhibition. The system is based on conditional induction and de-induction of a VEGF decoy receptor that sequesters VEGF and preclude signaling. VEGF blockade results in sinusoidal endothelial cells (SECs) fenestrations closure and in accumulation and transformation of the normally quiescent hepatic stellate cells, i.e. provoking the two processes underlying sinusoidal capillarization. Importantly, sinusoidal capillarization was sufficient to cause PH and its typical sequela, ascites, splenomegaly and venous collateralization without inflicting parenchymal damage or fibrosis. Remarkably, these dramatic phenotypes were fully reversed within few days from lifting-off VEGF blockade and resultant re-opening of SECs' fenestrations. This study not only uncovered an indispensible role for VEGF in maintaining structure and function of mature SECs, but also highlights the vasculo-centric nature of PH pathogenesis. Unprecedented ability to rescue PH and its secondary manifestations via manipulating a single vascular factor may also be harnessed for examining the potential utility of de-capillarization treatment modalities.

Do we need new personalized emergency telehealth solutions? A survey of 100 emergency department patients and a first report of the swiss limmex emergency wristwatch: an original study

Development of new personal mobile and wireless devices for healthcare has become essential due to our aging population characterized by constant rise in chronic diseases that consequently require a complex treatment and close monitoring. Personal telehealth devices allow patients to adequately receive their appropriate treatment, followup with their doctors, and report any emergency without the need of the presence of any caregivers with them thus increasing their quality of life in a cost-effective fashion. This paper includes a brief overview of personal telehealth systems, a survey of 100 consecutive ED patients aged >65 years, and introduces "Limmex" a new GSM based technology packaged in a wristwatch. Limmex can by a push of a button initiate multiple emergency call and establish mobile communication between the patient and a preselected person, institution, or a search and rescue service. To the best of our knowledge, Limmex is the first of its kind worldwide.

Transgenic system for conditional induction and rescue of chronic myocardial hibernation provides insights into genomic programs of hibernation

A key energy-saving adaptation to chronic hypoxia that enables cardiomyocytes to withstand severe ischemic insults is hibernation, i.e., a reversible arrest of contractile function. Whereas hibernating cardiomyocytes represent the critical reserve of dysfunctional cells that can be potentially rescued, a lack of a suitable animal model has hampered insights on this medically important condition. We developed a transgenic mouse system for conditional induction of long-term hibernation and a system to rescue hibernating cardiomyocytes at will. Via myocardium-specific induction (and, in turn, deinduction) of a VEGF-sequestering soluble receptor, we show that VEGF is indispensable for adjusting the coronary vasculature to match increased oxygen consumption and exploit this finding to generate a hypoperfused heart. Importantly, ensuing ischemia is tunable to a level at which large cohorts of cardiomyocytes are driven to enter a hibernation mode, without cardiac cell death. Relieving the VEGF blockade even months later resulted in rapid revascularization and full recovery of contractile function. Furthermore, we show that left ventricular remodeling associated with hibernation is also fully reversible. The unique opportunity to uncouple hibernation from other ischemic heart phenotypes (e.g., infarction) was used to determine the genetic program of hibernation; uncovering hypoxia-inducible factor target genes associated with metabolic adjustments and induced expression of several cardioprotective genes. Autophagy, specifically self-digestion of mitochondria, was identified as a key prosurvival mechanism in hibernating cardiomyocytes. This system may lend itself for examining the potential utility of treatments to rescue dysfunctional cardiomyocytes and reverse maladaptive remodeling.

Combining series elastic actuation and magneto-rheological damping for the control of agile locomotion

All-terrain robot locomotion is an active topic of research. Search and rescue maneuvers and exploratory missions could benefit from robots with the abilities of real animals. However, technological barriers exist to ultimately achieving the actuation system, which is able to meet the exigent requirements of these robots. This paper describes the locomotioncontrol of a leg prototype, designed and developed to make a quadruped walk dynamically while exhibiting compliant interaction with the environment. The actuation system of the leg is based on the hybrid use of series elasticity and magneto-rheological dampers, which provide variable compliance for natural-looking motion and improved interaction with the ground. The locomotioncontrol architecture has been proposed to exploit natural leg dynamics in order to improve energy efficiency. Results show that the controller achieves a significant reduction in energy consumption during the leg swing phase thanks to the exploitation of inherent leg dynamics. Added to this, experiments with the real leg prototype show that the combined use of series elasticity and magneto-rheologicaldamping at the knee provide a 20 % reduction in the energy wasted in braking the knee during its extension in the leg stance phase.

Analysis of ad hoc routing protocols for emergency and rescue scenarios.

A mobile ad hoc network MANET is a collection of wireless mobile nodes that can dynamically configure a network without a fixed infrastructure or centralized administration. This makes it ideal for emergency and rescue scenarios where information sharing is essential and should occur as soon as possible. This article discusses which of the routing strategies for mobile ad hoc networks: proactive, reactive and hierarchical, have a better performance in such scenarios. Using a real urban area being set for the emergency and rescue scenario, we calculate the density of nodes and the mobility model needed for validation. The NS2 simulator has been used in our study. We also show that the hierarchical routing strategies are beffer suited for this type of scenarios.

Behavior of Ad Hoc routing protocols, analyzed for emergency and rescue scenarios, on a real urban area

A mobile Ad Hoc network (MANET) is a collection of wireless mobile nodes that can dynamically configure a network without a fixed infrastructure or central administration. This makes it ideal for emergency and rescue scenarios, where sharing information is essential and should occur as soon as possible. This article discusses which of the routing strategies for mobile MANETs: proactive, reactive or hierarchical, has a better performance in such scenarios. By selecting a real urban area for the emergency and rescue scenario, we calculated the density of nodes and the mobility model needed for the validation study of AODV, DSDV and CBRP in the routing model. The NS2 simulator has been used for our study. We also show that the hierarchical routing strategies are better suited for this type of scenarios.

Mutations in Drosophila Enabled and Rescue by Human Vasodilator-stimulated Phosphoprotein (VASP) Indicate Important Functional Roles for Ena/VASP Homology Domain 1 (EVH1) and EVH2 Domains

Drosophila Enabled (Ena) was initially identified as a dominant genetic suppressor of mutations in the Abelson tyrosine kinase and, more recently, as a member of the Ena/human vasodilator-stimulated phosphoprotein (VASP) family of proteins. We have used genetic, biochemical, and cell biological approaches to demonstrate the functional relationship between Ena and human VASP. In addition, we have defined the roles of Ena domains identified as essential for its activity in vivo. We have demonstrated that VASP rescues the embryonic lethality associated with loss of Ena function in Drosophila and have shown that Ena, like VASP, is associated with actin filaments and focal adhesions when expressed in cultured cells. To define sequences that are central to Ena function, we have characterized the molecular lesions present in two lethal ena mutant alleles that affected the Ena/VASP homology domain 1 (EVH1) and EVH2. A missense mutation that resulted in an amino acid substitution in the EVH1 domain eliminated in vitro binding of Ena to the cytoskeletal protein zyxin, a previously reported binding partner of VASP. A nonsense mutation that resulted in a C-terminally truncated Ena protein lacking the EVH2 domain failed to form multimeric complexes and exhibited reduced binding to zyxin and the Abelson Src homology 3 domain. Our analysis demonstrates that Ena and VASP are functionally homologous and defines the conserved EVH1 and EVH2 domains as central to the physiological activity of Ena.

Unifying theory of hypoxia tolerance: molecular/metabolic defense and rescue mechanisms for surviving oxygen lack.

We develop a unifying theory of hypoxia tolerance based on information from two cell level models (brain cortical cells and isolated hepatocytes) from the highly anoxia tolerant aquatic turtle and from other more hypoxia sensitive systems. We propose that the response of hypoxia tolerant systems to oxygen lack occurs in two phases (defense and rescue). The first lines of defense against hypoxia include a balanced suppression of ATP-demand and ATP-supply pathways; this regulation stabilizes (adenylates) at new steady-state levels even while ATP turnover rates greatly decline. The ATP demands of ion pumping are down-regulated by generalized "channel" arrest in hepatocytes and by "spike" arrest in neurons. Hypoxic ATP demands of protein synthesis are down-regulated probably by translational arrest. In hypoxia sensitive cells this translational arrest seems irreversible, but hypoxia-tolerant systems activate "rescue" mechanisms if the period of oxygen lack is extended by preferentially regulating the expression of several proteins. In these cells, a cascade of processes underpinning hypoxia rescue and defense begins with an oxygen sensor (a heme protein) and a signal-transduction pathway, which leads to significant gene-based metabolic reprogramming-the rescue process-with maintained down-regulation of energy-demand and energy-supply pathways in metabolism throughout the hypoxic period. This recent work begins to clarify how normoxic maintenance ATP turnover rates can be drastically (10-fold) down-regulated to a new hypometabolic steady state, which is prerequisite for surviving prolonged hypoxia or anoxia. The implications of these developments are extensive in biology and medicine.