Localisation of mobile nodes in wireless networks with correlated in time measurement noise.

Wireless sensor networks are an inherent part of decision making, object tracking and location awareness systems. This work is focused on simultaneous localisation of mobile nodes based on received signal strength indicators (RSSIs) with correlated in time measurement noises. Two approaches to deal with the correlated measurement noises are proposed in the framework of auxiliary particle filtering: with a noise augmented state vector and the second approach implements noise decorrelation. The performance of the two proposed multi model auxiliary particle filters (MM AUX-PFs) is validated over simulated and real RSSIs and high localisation accuracy is demonstrated

A neighborhood-based approach for clustering of linked document collections

This technical report addresses the problem of automatically structuring linked document collections by using clustering. In contrast to traditional clustering, we study the clustering problem in the light of available link structure information for the data set (e.g., hyperlinks among web documents or co-authorship among bibliographic data entries). Our approach is based on iterative relaxation of cluster assignments, and can be built on top of any clustering algorithm (e.g., k-means or DBSCAN). These techniques result in higher cluster purity, better overall accuracy, and make self-organization more robust. Our comprehensive experiments on three different real-world corpora demonstrate the benefits of our approach

Simple Applications of q-Bosons

A deformation of the harmonic oscillator algebra associated with the Morse potential and the SU(2) algebra is derived using the quantum analogue of the anharmonic oscillator. We use the quantum oscillator algebra or $q$-boson algebra which is a generalisation of the Heisenberg-Weyl algebra obtained by introducing a deformation parameter $q$. Further, we present a new algebraic realization of the $q$-bosons, for the case of $q$ being a root of unity, which corresponds to a periodic structure described by a finite-dimensional representation. We show that this structure represents the symmetry of a linear lattice with periodic boundary conditions.Comment: LATEX2e, 10 pages, v2: few misprints corrected, added Journal-re

Carbon monoxide neurotoxicity is triggered by oxidative stress induced by ROS production from three distinct cellular sources

Carbon monoxide (CO) poisoning is one of the leading causes of toxic mortality and morbidity. We have studied the generation of reactive oxygen species in cortical neurons in culture in response to toxic doses of CO exposure. Fluorescence microscopy was used to measure the rate of free radical generation, lipid peroxidation, GSH level and also mitochondrial metabolism. We have found that toxic concentrations of CO released from CORM-401 induced mitochondrial depolarisation and inhibition of NADH dependent respiration to a lesser degree than when compared to ischaemia. Energy collapse was not observed within 40 min of CO exposure. We have found that CO induces the generation of reactive oxygen species resulting in lipid peroxidation and a decrease in GSH via three different mechanisms: from mitochondria during the first minutes of CO exposure, from xanthine oxidase at around 20 min exposure due to energy deprivation, and considerable ROS production from NADPH oxidase in the post CO exposure period (re-oxygenation). Inhibition of these different phases with mitochondrial antioxidants, inhibitors of xanthine oxidase, or NADPH oxidase, protected neurons and astrocytes against CO-induced oxidative stress and cell death. The most profound effect was seen during NADPH oxidase inhibition. Thus, oxidative stress has a remarkably significant role in CO-induced neuronal cell death and preventing its occurrence during reoxygenation is of great importance in the consideration of a positive, neurologically protective therapeutic outcome for CO exposed patients

The Application of Constraint Rules to Data-driven Parsing

In this paper, we show an approach to extracting different types of constraint rules from a dependency treebank. Also, we show an approach to integrating these constraint rules into a dependency data-driven parser, where these constraint rules inform parsing decisions in specific situations where a set of parsing rule (which is induced from a classifier) may recommend several recommendations to the parser. Our experiments have shown that parsing accuracy could be improved by using different sets of constraint rules in combination with a set of parsing rules. Our parser is based on the arc-standard algorithm of MaltParser but with a number of extensions, which we will discuss in some detail

Assessment of ROS Production in the Mitochondria of Live Cells

Production of reactive oxygen species (ROS) in the mitochondria plays multiple roles in physiology, and excessive production of ROS leads to the development of various pathologies. ROS in the mitochondria are generated by various enzymes, mainly in the electron transporvt chain, and it is important to identify not only the trigger but also the source of free radical production. It is important to measure mitochondrial ROS in live, intact cells, because activation of ROS production could be initiated by changes in extramitochondrial processes which could be overseen when using isolated mitochondria. Here we describe the approaches, which allow to measure production of ROS in the matrix of mitochondria in live cells. We also demonstrate how to measure kinetic changes in lipid peroxidation in mitochondria of live cells. These methods could be used for understanding the mechanisms of pathology in a variety of disease models and also for testing neuro- or cardioprotective chemicals

Age-related changes in the energy of human mesenchymal stem cells

Aging is a physiological process that leads to a higher risk for the most devastating diseases. There are a number of theories of human aging proposed, and many of them are directly or indirectly linked to mitochondria. Here, we used mesenchymal stem cells (MSCs) from young and older donors to study age-related changes in mitochondrial metabolism. We have found that aging in MSCs is associated with a decrease in mitochondrial membrane potential and lower NADH levels in mitochondria. Mitochondrial DNA content is higher in aged MSCs, but the overall mitochondrial mass is decreased due to increased rates of mitophagy. Despite the higher level of ATP in aged cells, a higher rate of ATP consumption renders them more vulnerable to energy deprivation compared to younger cells. Changes in mitochondrial metabolism in aged MSCs activate the overproduction of reactive oxygen species in mitochondria which is compensated by a higher level of the endogenous antioxidant glutathione. Thus, energy metabolism and redox state are the drivers for the aging of MSCs/mesenchymal stromal cells

Monomeric alpha-synuclein exerts a physiological role in brain ATP synthase

Misfolded α-synuclein is a key factor in the pathogenesis of Parkinson's disease (PD). However, knowledge about a physiological role for the native, unfolded α-synuclein is limited. Using brains of mice lacking α-, β-, and γ-synuclein, we report that extracellular monomeric α-synuclein enters neurons and localizes to mitochondria, interacts with ATP synthase subunit α, and modulates ATP synthase function. Using a combination of biochemical, live-cell imaging and mitochondrial respiration analysis, we found that brain mitochondria of α-, β-, and γ-synuclein knock-out mice are uncoupled, as characterized by increased mitochondrial respiration and reduced mitochondrial membrane potential. Furthermore, synuclein deficiency results in reduced ATP synthase efficiency and lower ATP levels. Exogenous application of low unfolded α-synuclein concentrations is able to increase the ATP synthase activity that rescues the mitochondrial phenotypes observed in synuclein deficiency. Overall, the data suggest that α-synuclein is a previously unrecognized physiological regulator of mitochondrial bioenergetics through its ability to interact with ATP synthase and increase its efficiency. This may be of particular importance in times of stress or PD mutations leading to energy depletion and neuronal cell toxicity