Calculation of resonances in the Coulomb three-body system with two disintegration channels in the adiabatic hyperspherical approach

The method of calculation of the resonance characteristics is developed for the metastable states of the Coulomb three-body (CTB) system with two disintegration channels. The energy dependence of K-matrix in the resonance region is calculated with the use of the stabilization method. Resonance position and partial widths are obtained by fitting the numerically calculated K(E)-matrix with the help of the generalized Breit-Wigner formula.Comment: Latex, 11 pages with 5 figures and 2 table

Determination Of Dynamic Characteristics Of Heat Fire Detectors

The proposed methods for determining the dynamic characteristics of heat fire detectors in the time and frequency domains, focused on the use of existing thermal chambers. The proposed method for determining the transition function of the detector is implemented as follows. Heat fire detector creates a thermal effect in the form of a linearly increasing function. The response of the output signal to the influence of this type is measured and approximated using the Heaviside function at regular intervals.It is shown that information on the transition function of a heat fire detector can be used to determine its frequency characteristics by approximating it with Heaviside functions at the same time intervals. This method of determining the frequency characteristics will significantly reduce the time to determine them compared to the classical method, and also eliminate the need for additional equipment.As a result of the studies, the choice of the sampling interval was justified on the example of a class A1 heatfire detector and certain sampling intervals for determining their transition function (τ0≤1.05 s), amplitude-frequency characteristic (τ0≤0.27 s) and phase-frequency characteristic (τ0≤2.0 s).The proposed methods for determining the dynamic characteristics of heat fire detectors open up new opportunities for developing methods for monitoring their technical condition. This is because the information about the transition function of the detector can be used in two ways. The first method involves comparing a certain transition function of the detector with an exemplary one. The second method consists in determining other characteristics of the detector based on information about its transient function and comparing them with standard values

Large closed queueing networks in semi-Markov environment and its application

The paper studies closed queueing networks containing a server station and $k$ client stations. The server station is an infinite server queueing system, and client stations are single-server queueing systems with autonomous service, i.e. every client station serves customers (units) only at random instants generated by a strictly stationary and ergodic sequence of random variables. The total number of units in the network is $N$. The expected times between departures in client stations are $(N\mu_j)^{-1}$. After a service completion in the server station, a unit is transmitted to the $j$th client station with probability $p_{j}$ $(j=1,2,...,k)$, and being processed in the $j$th client station, the unit returns to the server station. The network is assumed to be in a semi-Markov environment. A semi-Markov environment is defined by a finite or countable infinite Markov chain and by sequences of independent and identically distributed random variables. Then the routing probabilities $p_{j}$ $(j=1,2,...,k)$ and transmission rates (which are expressed via parameters of the network) depend on a Markov state of the environment. The paper studies the queue-length processes in client stations of this network and is aimed to the analysis of performance measures associated with this network. The questions risen in this paper have immediate relation to quality control of complex telecommunication networks, and the obtained results are expected to lead to the solutions to many practical problems of this area of research.Comment: 35 pages, 1 figure, 12pt, accepted: Acta Appl. Mat

Mechanism of Oxidative Stress in Neurodegeneration

Biological tissues require oxygen to meet their energetic demands. However, the consumption of oxygen also results in the generation of free radicals that may have damaging effects on cells. The brain is particularly vulnerable to the effects of reactive oxygen species due to its high demand for oxygen, and its abundance of highly peroxidisable substrates. Oxidative stress is caused by an imbalance in the redox state of the cell, either by overproduction of reactive oxygen species, or by dysfunction of the antioxidant systems. Oxidative stress has been detected in a range of neurodegenerative disease, and emerging evidence from in vitro and in vivo disease models suggests that oxidative stress may play a role in disease pathogenesis. However, the promise of antioxidants as novel therapies for neurodegenerative diseases has not been borne out in clinical studies. In this review, we critically assess the hypothesis that oxidative stress is a crucial player in common neurodegenerative disease and discuss the source of free radicals in such diseases. Furthermore, we examine the issues surrounding the failure to translate this hypothesis into an effective clinical treatment

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