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

β-Amyloid peptides induce mitochondrial dysfunction and oxidative stress in astrocytes and death of neurons through activation of NADPH oxidase

β-Amyloid (βA) peptide is strongly implicated in the neurodegeneration underlying Alzheimer's disease, but the mechanisms of neurotoxicity remain controversial. This study establishes a central role for oxidative stress by the activation of NADPH oxidase in astrocytes as the cause of βA-induced neuronal death. βA causes a loss of mitochondrial potential in astrocytes but not in neurons. The mitochondrial response consists of Ca2+-dependent transient depolarizations superimposed on a slow collapse of potential. The slow response is both prevented by antioxidants and, remarkably, reversed by provision of glutamate and other mitochondrial substrates to complexes I and II. These findings suggest that the depolarization reflects oxidative damage to metabolic pathways upstream of mitochondrial respiration. Inhibition of NADPH oxidase by diphenylene iodonium or 4-hydroxy-3-methoxy-acetophenone blocks βA-induced reactive oxygen species generation, prevents the mitochondrial depolarization, prevents βA-induced glutathione depletion in both neurons and astrocytes, and protects neurons from cell death, placing the astrocyte NADPH oxidase as a primary target of βA-induced neurodegeneration

Changes in intracellular calcium and glutathione in astrocytes as the primary mechanism of amyloid neurotoxicity

Although the accumulation of the neurotoxic peptide {beta} amyloid ({beta}A) in the CNS is a hallmark of Alzheimer's disease, the mechanism of {beta}A neurotoxicity remains controversial. In cultures of mixed neurons and astrocytes, we found that both the full-length peptide {beta}A (1–42) and the neurotoxic fragment (25–35) caused sporadic cytoplasmic calcium [intracellular calcium ([Ca2+]c)] signals in astrocytes that continued for hours, whereas adjacent neurons were completely unaffected. Nevertheless, after 24 hr, although astrocyte cell death was marginally increased, ~50% of the neurons had died. The [Ca2+]c signal was entirely dependent on Ca2+ influx and was blocked by zinc and by clioquinol, a heavy-metal chelator that is neuroprotective in models of Alzheimer's disease. Neuronal death was associated with Ca2+-dependent glutathione depletion in both astrocytes and neurons. Thus, astrocytes appear to be the primary target of {beta}A, whereas the neurotoxicity reflects the neuronal dependence on astrocytes for antioxidant support

Cross sections for geodesic flows and \alpha-continued fractions

We adjust Arnoux's coding, in terms of regular continued fractions, of the geodesic flow on the modular surface to give a cross section on which the return map is a double cover of the natural extension for the \alpha-continued fractions, for each $\alpha$ in (0,1]. The argument is sufficiently robust to apply to the Rosen continued fractions and their recently introduced \alpha-variants.Comment: 20 pages, 2 figure

Improved linear response for stochastically driven systems

The recently developed short-time linear response algorithm, which predicts the average response of a nonlinear chaotic system with forcing and dissipation to small external perturbation, generally yields high precision of the response prediction, although suffers from numerical instability for long response times due to positive Lyapunov exponents. However, in the case of stochastically driven dynamics, one typically resorts to the classical fluctuation-dissipation formula, which has the drawback of explicitly requiring the probability density of the statistical state together with its derivative for computation, which might not be available with sufficient precision in the case of complex dynamics (usually a Gaussian approximation is used). Here we adapt the short-time linear response formula for stochastically driven dynamics, and observe that, for short and moderate response times before numerical instability develops, it is generally superior to the classical formula with Gaussian approximation for both the additive and multiplicative stochastic forcing. Additionally, a suitable blending with classical formula for longer response times eliminates numerical instability and provides an improved response prediction even for long response times

Expression and modulation of an NADPH oxidase in mammalian astrocytes

Amyloid β peptides generate oxidative stress in hippocampal astrocytes through a mechanism sensitive to inhibitors of the NADPH oxidase [diphenylene iodonium (DPI) and apocynin]. Seeking evidence for the expression and function of the enzyme in primary hippocampal astrocytes, we confirmed the expression of the subunits of the phagocyte NADPH oxidase by Western blot analysis and by immunofluorescence and coexpression with the astrocyte-specific marker glial fibrillary acidic protein both in cultures and in vivo. Functional assays using lucigenin luminescence, dihydroethidine, or dicarboxyfluorescein fluorescence to measure the production of reactive oxygen species (ROS) demonstrated DPI and apocynin-sensitive ROS generation in response to the phorbol ester PMA and to raised [Ca2+]c after application of ionomycin or P2u receptor activation. Stimulation by PMA but not Ca2+ was inhibited by the protein kinase C (PKC) inhibitors staurosporine and hispidin. Responses were absent in transgenic mice lacking gp91phox. Expression of gp91phox and p67phox was increased in reactive astrocytes, which showed increased rates of both resting and stimulated ROS generation. NADPH oxidase activity was modulated by intracellular pH, suppressed by intracellular alkalinization, and enhanced by acidification. The protonophore carbonyl cyanide p-trifluoromethoxyphenylhydrazone suppressed basal ROS generation but markedly increased PMA-stimulated ROS generation. This was independent of mitochondrial ROS production, because it was unaffected by mitochondrial depolarization with rotenone and oligomycin. Thus, the NADPH oxidase is expressed in astrocytes and is functional, activated by PKC and intracellular calcium, modulated by pHi, and upregulated by astrocyte activation. The astrocytic NADPH oxidase is likely to play important roles in CNS physiology and pathology

The Hopf algebra structure of the Z3_3-graded quantum supergroup GLq,j(1∣1)_{q,j}(1|1)

In this work, we give some features of the Z$_3$-graded quantum supergroup

Natural extensions and entropy of α\alpha-continued fractions

We construct a natural extension for each of Nakada's $\alpha$-continued fractions and show the continuity as a function of $\alpha$ of both the entropy and the measure of the natural extension domain with respect to the density function $(1+xy)^{-2}$. In particular, we show that, for all $0 < \alpha \le 1$, the product of the entropy with the measure of the domain equals $\pi^2/6$. As a key step, we give the explicit relationship between the $\alpha$-expansion of $\alpha-1$ and of $\alpha$

The effective bandwidth problem revisited

The paper studies a single-server queueing system with autonomous service and $\ell$ priority classes. Arrival and departure processes are governed by marked point processes. There are $\ell$ buffers corresponding to priority classes, and upon arrival a unit of the $k$th priority class occupies a place in the $k$th buffer. Let $N^{(k)}$, $k=1,2,...,\ell$ denote the quota for the total $k$th buffer content. The values $N^{(k)}$ are assumed to be large, and queueing systems both with finite and infinite buffers are studied. In the case of a system with finite buffers, the values $N^{(k)}$ characterize buffer capacities. The paper discusses a circle of problems related to optimization of performance measures associated with overflowing the quota of buffer contents in particular buffers models. Our approach to this problem is new, and the presentation of our results is simple and clear for real applications.Comment: 29 pages, 11pt, Final version, that will be published as is in Stochastic Model