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Mark Brodie

Publications and source records attributed to Mark Brodie.

2 recordsLinked to original sources

Adaptive diagnosis in distributed systems.

Real-time problem diagnosis in large distributed computer systems and networks is a challenging task that requires fast and accurate inferences from potentially huge data volumes. In this paper, we propose a cost-efficient, adaptive diagnostic technique called active probing. Probes are end-to-end test transactions that collect information about the performance of a distributed system. Active probing uses probabilistic reasoning techniques combined with information-theoretic approach, and allows a fast online inference about the current system state via active selection of only a small number of most-informative tests. We demonstrate empirically that the active probing scheme greatly reduces both the number of probes (from 60% to 75% in most of our real-life applications), and the time needed for localizing the problem when compared with nonadaptive (preplanned) probing schemes. We also provide some theoretical results on the complexity of probe selection, and the effect of "noisy" probes on the accuracy of diagnosis. Finally, we discuss how to model the system's dynamics using dynamic Bayesian networks (DBNs), and an efficient approximate approach called sequential multifault; empirical results demonstrate clear advantage of such approaches over "static" techniques that do not handle system's changes.

Algorithms↗

Enduring effects of chronic ethanol in the CNS: basis for alcoholism.

This symposium focused on functional alterations in the mesolimbic dopamine system during the abstinence phase after chronic alcohol intake. Mark Brodie first described his recordings from midbrain slices prepared after chronic alcohol treatment in vivo by daily injection in C57BL/6J mice. No changes were found in the baseline firing frequency of dopaminergic neurones in the VTA (ventral tegmental area), but the excitation produced in these neurones by an acute ethanol challenge was significantly increased in neurons from ethanol-treated mice compared with those from the saline-treated controls. There was also a significant decrease in the inhibitory response to GABA by the dopamine neurones following the chronic ethanol treatment. These data suggest that the timing pattern and mode of ethanol administration may determine the types of changes observed in dopaminergic reward area neurons. Annalisa Muntoni lectured on the relationship between electrophysiological and biochemical in vivo evidence supporting a reduction in tonic activity of dopamine neurons projecting to the nucleus accumbens at various times after suspension of chronic ethanol treatment and morphological changes affecting dopamine neurons in rat VTA. Hilary J. Little then described changes in dopaminergic neurone function in the VTA during the abstinence phase. Decreases in baseline firing were seen at 6 days after withdrawal of mice from chronic ethanol treatment but were not apparent after 2 months abstinence. Increases in the affinity of D1 receptors in the striatum, but not in the cerebral cortex, were seen however up to 2 months after withdrawal. Scott Steffensen then described his studies recording in vivo from GABA containing neurones in the VTA in freely moving rats. Chronic ethanol administration enhanced the baseline activity of these neurones and resulted in tolerance to the inhibition by ethanol of these neurones. His results demonstrated selective adaptive circuit responses within the VTA or in extrategmental structures that regulate VTA-GABA neurone activity.

Alcohol Withdrawal Delirium↗