Scale-Free topologies and Activatory-Inhibitory interactions

A simple model of activatory-inhibitory interactions controlling the activity of agents (substrates) through a "saturated response" dynamical rule in a scale-free network is thoroughly studied. After discussing the most remarkable dynamical features of the model, namely fragmentation and multistability, we present a characterization of the temporal (periodic and chaotic) fluctuations of the quasi-stasis asymptotic states of network activity. The double (both structural and dynamical) source of entangled complexity of the system temporal fluctuations, as an important partial aspect of the Correlation Structure-Function problem, is further discussed to the light of the numerical results, with a view on potential applications of these general results.Comment: Revtex style, 12 pages and 12 figures. Enlarged manuscript with major revision and new results incorporated. To appear in Chaos (2006

Geometric Universality of Currents

We discuss a non-equilibrium statistical system on a graph or network. Identical particles are injected, interact with each other, traverse, and leave the graph in a stochastic manner described in terms of Poisson rates, possibly dependent on time and instantaneous occupation numbers at the nodes of the graph. We show that under the assumption of constancy of the relative rates, the system demonstrates a profound statistical symmetry, resulting in geometric universality of the statistics of the particle currents. This phenomenon applies broadly to many man-made and natural open stochastic systems, such as queuing of packages over the internet, transport of electrons and quasi-particles in mesoscopic systems, and chains of reactions in bio-chemical networks. We illustrate the utility of our general approach using two enabling examples from the two latter disciplines.Comment: 15 pages, 5 figure

Ueber die Einwirkung von Phenylhydrazin auf Chlormalonsäureester

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Stub model for dephasing in a quantum dot

As an alternative to Buttiker's dephasing lead model, we examine a dephasing stub. Both models are phenomenological ways to introduce decoherence in chaotic scattering by a quantum dot. The difference is that the dephasing lead opens up the quantum dot by connecting it to an electron reservoir, while the dephasing stub is closed at one end. Voltage fluctuations in the stub take over the dephasing role from the reservoir. Because the quantum dot with dephasing lead is an open system, only expectation values of the current can be forced to vanish at low frequencies, while the outcome of an individual measurement is not so constrained. The quantum dot with dephasing stub, in contrast, remains a closed system with a vanishing low-frequency current at each and every measurement. This difference is a crucial one in the context of quantum algorithms, which are based on the outcome of individual measurements rather than on expectation values. We demonstrate that the dephasing stub model has a parameter range in which the voltage fluctuations are sufficiently strong to suppress quantum interference effects, while still being sufficiently weak that classical current fluctuations can be neglected relative to the nonequilibrium shot noise.Comment: 8 pages with 1 figure; contribution for the special issue of J.Phys.A on "Trends in Quantum Chaotic Scattering

Examining methods to induce cognitive fatigue

Cognitive fatigue is important to user task productivity and worker safety in critical occupations because it may cause exhaustion and difficulty executing mental tasks leading to increased errors and job related injuries. Activities that require sustained focused attention over time (i.e. vigilance) increase stress and induce cognitive fatigue. In careers where safety is critical, such as aviation, homeland security, and medicine, these errors can lead to serious injury or even death. Therefore, studying this phenomenon is crucial for findings ways to ameliorate these deleterious effects. In order to study cognitive fatigue effects in a laboratory setting researchers need to find effective tasks to induce fatigue. Studies that fail to do so may suffer ceiling effects as participants may not arrive to the study fatigued. Three methods shown to be stressful in the literature, a 15-minute break, a 15-minute vigilance task, and a 30-minute vigilance task were used to induce laboratory fatigue. These three methods were compared to determine their effectiveness of inducing fatigue. Physiological fatigue was determined using ECG, subjective fatigue was determined using self-report stress, task engagement, and anxiety, and cognitive fatigue was determined using performance on a cognitive test designed to measure executive functioning. It was hypothesized that a 30-minute vigilance task would be most effective at inducing fatigue, as errors during vigilance tasks tend to increase over time on watch. Overall self-reported stress and fatigue was rated high in both vigilance tasks, but only the 30-minute task induced cognitive fatigue (decreased performance pre to post on the cognitive task). This finding is unique in the literature, as previous research has tested fatigue effects using subjective measures and not cognitive ones. Researchers who are interested in studying the restoration of cognitive fatigue effects are recommended to use tasks that require sustained focused attention for at least 30-minutes. It is also recommended that future research investigate motivational differences which may have lead to these findings

Differential levels of glutamate dehydrogenase 1 (GLUD1) in Balb/c and C57BL/6 mice and the effects of overexpression of the Glud1 gene on glutamate release in striatum

We have previously shown that overexpression of the Glud1 (glutamate dehydrogenase 1) gene in neurons of C57BL/6 mice results in increased depolarization-induced glutamate release that eventually leads to selective neuronal injury and cell loss by 12 months of age. However, it is known that isogenic lines of Tg (transgenic) mice produced through back-crossing with one strain may differ in their phenotypic characteristics from those produced using another inbred mouse strain. Therefore, we decided to introduce the Glud1 transgene into the Balb/c strain that has endogenously lower levels of GLUD1 (glutamate dehydrogenase 1) enzyme activity in the brain as compared with C57BL/6. Using an enzyme-based MEA (microelectrode array) that is selective for measuring glutamate in vivo, we measured depolarization-induced glutamate release. Within a discrete layer of the striatum, glutamate release was significantly increased in Balb/c Tg mice compared with wt (wild-type) littermates. Furthermore, Balb/c mice released approx. 50–60% of the amount of glutamate compared with C57BL/6 mice. This is similar to the lower levels of endogenous GLUD1 protein in Balb/c compared with C57BL/6 mice. The development of these Glud1-overexpressing mice may allow for the exploration of key molecular events produced by chronic exposure of neurons to moderate, transient increases in glutamate release, a process hypothesized to occur in neurodegenerative disorders.This work was supported by the NSF (National Science Foundation) [grant number EEC-0310723]; NIH/NIDA (National Institutes of Health/National Institute on Drug Abuse) [grant number DA017186]; CEBRA, Phase II, NIA, [grant number AG12993]; NIAAA (National Institute of Alcohol Abuse and Alcoholism) [grant numbers AA11419, AA04732, AA12276]; NSF [grant numbers DBI-9987807, DBI-0352848]; NIDA [grant number DA017186]; NINDS (National Institute of Neurological Disorders and Strokes) [grant number NS39787]; NIMH (National Institute of Mental Health) [grant number MH58414]; NIDA Training [grant number DA022738]; NIDA [grant number DA015088], The Kansas Technology Enterprise Corporation, The Miller, Hedwig and Wilbur Fund, and The University of Kansas Research Development Fund

Differential Levels of Glutamate Dehydrogenase 1 (GLUD1) in Balb/c and C57BL/6 Mice and the Effects of Overexpression of the \u3cem\u3eGlud1\u3c/em\u3e Gene on Glutamate Release in Striatum

We have previously shown that overexpression of the Glud1 (glutamate dehydrogenase 1) gene in neurons of C57BL/6 mice results in increased depolarization-induced glutamate release that eventually leads to selective neuronal injury and cell loss by 12 months of age. However, it is known that isogenic lines of Tg (transgenic) mice produced through back-crossing with one strain may differ in their phenotypic characteristics from those produced using another inbred mouse strain. Therefore, we decided to introduce the Glud1 transgene into the Balb/c strain that has endogenously lower levels of GLUD1 (glutamate dehydrogenase 1) enzyme activity in the brain as compared with C57BL/6. Using an enzyme-based MEA (microelectrode array) that is selective for measuring glutamate in vivo, we measured depolarization-induced glutamate release. Within a discrete layer of the striatum, glutamate release was significantly increased in Balb/c Tg mice compared with wt (wild-type) littermates. Furthermore, Balb/c mice released approx. 50-60% of the amount of glutamate compared with C57BL/6 mice. This is similar to the lower levels of endogenous GLUD1 protein in Balb/c compared with C57BL/6 mice. The development of these Glud1-overexpressing mice may allow for the exploration of key molecular events produced by chronic exposure of neurons to moderate, transient increases in glutamate release, a process hypothesized to occur in neurodegenerative disorders