Agent Based Test and Repair of Distributed Systems

This article demonstrates how to use intelligent agents for testing and repairing a distributed system, whose elements may or may not have embedded BIST (Built-In Self-Test) and BISR (Built-In Self-Repair) facilities. Agents are software modules that perform monitoring, diagnosis and repair of the faults. They form together a society whose members communicate, set goals and solve tasks. An experimental solution is presented, and future developments of the proposed approach are explore

Generalization of the effective Wiener-Ikehara theorem

International audienceWe consider the classical Wiener–Ikehara Tauberian theorem, with a generalized condition of slow decrease and some additional poles on the boundary of convergence of the Laplace transform. In this generality, we prove the otherwise known asymptotic evaluation of the transformed function, when the usual conditions of the Wiener-Ikehara theorem hold. However, our version also provides an effective error term, not known thus far in this generality. The crux of the proof is a proper asymptotic variation of the lemmas of Ganelius and Tenenbaum, also constructed for the sake of an effective version of the Wiener–Ikehara theorem

Agent Based Test and Repair of Distributed Systems

This article demonstrates how to use intelligent agents for testing and repairing a distributed system, whose elements may or may not have embedded BIST (Built-In Self-Test) and BISR (Built-In Self-Repair) facilities. Agents are software modules that perform monitoring, diagnosis and repair of the faults. They form together a society whose members communicate, set goals and solve tasks. An experimental solution is presented, and future developments of the proposed approach are explored

The tricyclic antidepressant desipramine inhibited the neurotoxic, kainate-induced [Ca] increases in CA1 pyramidal cells in acute hippocampal slices.

Kainate (KA), used for modelling neurodegenerative diseases, evokes excitotoxicity. However, the precise mechanism of KA-evoked [Ca2+]i increase is unexplored, especially in acute brain slice preparations. We used [Ca2+]i imaging and patch clamp electrophysiology to decipher the mechanism of KA-evoked [Ca2+]i rise and its inhibition by the tricyclic antidepressant desipramine (DMI) in CA1 pyramidal cells in rat hippocampal slices and in cultured hippocampal cells. The effect of KA was dose-dependent and relied totally on extracellular Ca2+. The lack of effect of dl-2-amino-5-phosphonopentanoic acid (AP-5) and abolishment of the response by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) suggested the involvement of non-N-methyl-d-aspartate receptors (non-NMDARs). The predominant role of the Ca2+-impermeable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors (AMPARs) in the initiation of the Ca2+ response was supported by the inhibitory effect of the selective AMPAR antagonist GYKI 53655 and the ineffectiveness of 1-naphthyl acetylspermine (NASPM), an inhibitor of the Ca2+-permeable AMPARs. The voltage-gated Ca2+ channels (VGCC), blocked by omega-Conotoxin MVIIC+nifedipine+NiCl2, contributed to the [Ca2+]i rise. VGCCs were also involved, similarly to AMPAR current, in the KA-evoked depolarisation. Inhibition of voltage-gated Na+ channels (VGSCs; tetrodotoxin, TTX) did not affect the depolarisation of pyramidal cells but blocked the depolarisation-evoked action potential bursts and reduced the Ca2+ response. The tricyclic antidepressant DMI inhibited the KA-evoked [Ca2+]i rise in a dose-dependent manner. It directly attenuated the AMPA-/KAR current, but its more potent inhibition on the Ca2+ response supports additional effect on VGCCs, VGSCs and Na+/Ca2+ exchangers. The multitarget action on decisive players of excitotoxicity holds out more promise in clinical therapy of neurodegenerative diseases

Causality - Complexity - Consistency: Can Space-Time Be Based on Logic and Computation?

The difficulty of explaining non-local correlations in a fixed causal structure sheds new light on the old debate on whether space and time are to be seen as fundamental. Refraining from assuming space-time as given a priori has a number of consequences. First, the usual definitions of randomness depend on a causal structure and turn meaningless. So motivated, we propose an intrinsic, physically motivated measure for the randomness of a string of bits: its length minus its normalized work value, a quantity we closely relate to its Kolmogorov complexity (the length of the shortest program making a universal Turing machine output this string). We test this alternative concept of randomness for the example of non-local correlations, and we end up with a reasoning that leads to similar conclusions as in, but is conceptually more direct than, the probabilistic view since only the outcomes of measurements that can actually all be carried out together are put into relation to each other. In the same context-free spirit, we connect the logical reversibility of an evolution to the second law of thermodynamics and the arrow of time. Refining this, we end up with a speculation on the emergence of a space-time structure on bit strings in terms of data-compressibility relations. Finally, we show that logical consistency, by which we replace the abandoned causality, it strictly weaker a constraint than the latter in the multi-party case.Comment: 17 pages, 16 figures, small correction

The Disappearing Act of KH 15D: Photometric Results from 1995 to 2004

We present results from the most recent (2002-2004) observing campaigns of the eclipsing system KH 15D, in addition to re-reduced data obtained at Van Vleck Observatory (VVO) between 1995 and 2000. Phasing nine years of photometric data shows substantial evolution in the width and depth of the eclipses. The most recent data indicate that the eclipses are now approximately 24 days in length, or half the orbital period. These results are interpreted and discussed in the context of the recent models for this system put forward by Winn et al. and Chiang & Murray-Clay. A periodogram of the entire data set yields a highly significant peak at 48.37 +/- 0.01 days, which is in accord with the spectroscopic period of 48.38 +/- 0.01 days determined by Johnson et al. Another significant peak, at 9.6 days, was found in the periodogram of the out-of-eclipse data at two different epochs. We interpret this as the rotation period of the visible star and argue that it may be tidally locked in pseudosynchronism with its orbital motion. If so, application of Hut's theory implies that the eccentricity of the orbit is e = 0.65 +/- 0.01. Analysis of the UVES/VLT spectra obtained by Hamilton et al. shows that the v sin(i) of the visible star in this system is 6.9 +/- 0.3 km/sec. Using this value of v sin(i) and the measured rotation period of the star, we calculate the lower limit on the radius to be R = (1.3 +/- 0.1), R_Sun, which concurs with the value obtained by Hamilton et al. from its luminosity and effective temperature. Here we assume that i = 90 degrees since it is likely that the spin and orbital angular momenta vectors are nearly aligned.Comment: 55 pages, 18 figures, 1 color figure, to appear the September issue of the Astronomical Journa

K2-106, a system containing a metal-rich planet and a planet of lower density

Aims: Planets in the mass range from 2 to 15 M? are very diverse. Some of them have low densities, while others are very dense. By measuring the masses and radii, the mean densities, structure, and composition of the planets are constrained. These parameters also give us important information about their formation and evolution, and about possible processes for atmospheric loss. Methods: We determined the masses, radii, and mean densities for the two transiting planets orbiting K2-106

A nemszinaptikus nikotinikus acetilkolin és NMDA receptorok szerepe élettani körülmények között és pathológiás állapotokban = Role of nonsynaptic nicotinic acetylcholine receptors and NMDA receptors in physiological and pathophysiological conditions

A szélütés (stroke) utáni neurodegeneráció a jelenlegi morbiditási és mortalitási mutatók egyik legfontosabb tényezője. Az iszkémiás stroke kezelésében számos ígéretes gyógyszerjelölt molekula vallott kudarcot a klinikai vizsgálatokban. Ennek valószínűleg az az oka, hogy hiányosak ismereteink az iszkémiás kórképek kialakulásának mechanizmusaira vonatkozólag. A legtöbb központi idegrendszerre ható gyógyszert szinaptikusan elhelyezkedő receptorokra vagy transzporterekre fejlesztik annak érdekében, hogy igazán hatékony gyógyszereket tudjunk fejleszteni, figyelembe kell venni, hogy az extraszinaptikus receptorok és transzporterek száma jóval meghaladja a szinaptikusakét, illetve hogy nagyon sok központi idegrendszeri megbetegedés alapja a nemszinaptikus rendszer malfunkciója. Például, a szinaptikus NMDA receptorok aktivációja neuroprotektív hatást fejt ki, míg az extraszinaptikus NMDA receptor aktiváció excitotoxikus hatású. Konkrét javaslataink a gyógyszerfejlesztést illetően: Az NR2B alegységet tartalmazó NMDA receptorok szelektív gátlói (mint például a fluoxetine), és a nátriumcsatorna gátlók egyes típusai; mint neuroprotektív szerek. A nikotinikus agonisták pozitív modulátorai, amelyek a kognitív problémák kezelésében, ill. a dohányzásról való leszokás segítésében lehetnek hasznosak. | Neurodegeneration after a stroke is one of the major causes of present-day morbidity and mortality. There is a long list of neuroprotective compounds that have failed to be clinically useful in the treatment of ischaemic stroke. This is likely due, at least in part, to our inadequate knowledge regarding the core mechanisms of ischaemic diseases. Most “novel” drugs that target the CNS are designed to act on neurotransmitter receptors or transporters that are localised within synapses. To develop the most effective drugs, it is important to remember that there are extrasynaptic receptors and transporters that may outnumber those located within synapses and that, when malfunctioning, may be responsible for several symptoms of CNS disorders. For example, activation of synaptic NMDA receptors is neuroprotective, whereas stimulation of extrasynaptic NMDA receptors causes excitotoxicity. We suggest that future drug development research consider the following: Compounds that are able to selectively inhibit non-synaptic NR2B Glu receptors (such as Fluoxetine), and specific subtypes of sodium channel inhibitors as neuroprotective compounds. Positive modulators of nicotinic acetylcholine receptors. They would be potential drugs in the treatment of memory problems and in smoking cessation