The ATLAS Level-1 Calorimeter Trigger Achenbach, R; Adragna, P; Andrei, V ...
Journal of instrumentation,
03/2008, Volume:
3, Issue:
3
Journal Article
Peer reviewed
Open access
The ATLAS Level-1 Calorimeter Trigger uses reduced-granularity information from all the ATLAS calorimeters to search for high transverse-energy electrons, photons, τ leptons and jets, as well as high ...missing and total transverse energy. The calorimeter trigger electronics has a fixed latency of about 1 μs, using programmable custom-built digital electronics. This paper describes the Calorimeter Trigger hardware, as installed in the ATLAS electronics cavern.
: This manuscript reviews the proceedings of a symposium organized by Drs. Antonio Noronha and Fulton Crews presented at the 2003 Research Society on Alcoholism meeting. The purpose of the symposium ...was to examine recent findings on when alcohol induced brain damage occurs, e.g., during intoxication and/or during alcohol withdrawal. Further studies investigate specific brain regions (where) and the mechanisms (why) of alcoholic neurodegeneration. The presentations were (1) Characterization of Synaptic Loss in Cerebella of Mature and Senescent Rats after Lengthy Chronic Ethanol Consumption, (2) Ethanol Withdrawal Both Causes Neurotoxicity and Inhibits Neuronal Recovery Processes in Rat Organotypic Hippocampal Cultures, (3) Binge Drinking‐Induced Brain Damage: Genetic and Age Related Effects, (4) Binge Ethanol‐Induced Brain Damage: Involvement of Edema, Arachidonic Acid and Tissue Necrosis Factor α (TNFα), and (5) Cyclic AMP Cascade, Stem Cells and Ethanol. Taken together these studies suggest that alcoholic neurodegeneration occurs through multiple mechanisms and in multiple brain regions both during intoxication and withdrawal.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
This study examines Purkinje neurons of rats aged 1, 10, 18 and 28 months to investigate growth and decline in the magnitude of the dendritic tree, i.e. the number of exterior links (terminal ...segments) per cell. Growth in the mean number of exterior links was observed from 1 to 10 months, decline at 18 months and regrowth at 28 months. At 10, 28, and especially at 18 months, the cell size frequency distribution indicates two groups of cells, one of small and the other of large sized cells. The study also examines the relationship of age to lengths of topologically defined links of various types. For each age group we find that exterior links are longer than interior links (non-terminal or intermediate segments). Analysis of the geometric mean lengths of subtypes of exterior and interior links at maturity (10 months) indicates that they follow a Fibonacci series of link lengths, such that mean lengths of topologically defined types of mean exterior links are either about 13 or 8 microns long, while interior links are about 5 microns long. A sequential growth model for adding exterior links is suggested to illustrate a style of growth which could account for the various mean link lengths and the Fibonacci ratio (1.618) between their lengths. Interior link lengths are also dependent on the generation of exterior links from the sides of pre-existing interior links. If the Strahler branching ratio, Rb, should increase owing to growth of terminals from interior links, then mean interior link length would decline. During a period of regression, mean exterior link lengths become shorter and mean interior link lengths become longer. Changes in mean interior link length are much less affected by changes in Rb during regression than is the situation during growth. Finally, the changes in link lengths dictate that the ratio of mean exterior to mean interior link length increases during growth phases from 1 to 10 and 18 to 28 months, and declines during regression from 10 to 28 months. The lowest values of the ratio of mean exterior to mean interior lengths are found at 1 month. This is the period of most intense growth. During this period, the rate of development of new exterior links outbalances the rate at which the links increase in length.
This article represents a symposium of the 2002 joint meeting of RSA and ISBRA held in San Francisco. Presentations were Neuropathology of alcohol‐related cerebellar damage in humans, by Antony J. ...Harding; Neuropathological evidence of cerebellar damage in an animal model of alcoholism, by Roberta Pentney and Cynthia Dlugos; Understanding cortical‐cerebellar circuits through neuroimaging study of chronic alcoholics, by Peter R. Martin and Mitchell H. Parks; and Functional reorganization of the brain in alcoholism: neuroimaging evidence, by John E. Desmond, S.H. Annabel Chen, Michelle R. Pryor, Eve De Rosa, Adolf Pfefferbaum, and Edith V. Sullivan.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
Pyruvate dehydrogenase complex (PDC) deficiency is an inborn metabolic disorder associated with a variety of neurologic abnormalities. This report describes the development and initial ...characterization of a novel murine model system in which PDC deficiency has been introduced specifically into the developing nervous system. The absence of liveborn male and a roughly 50% reduction in female offspring following induction of the X‐linked mutation indicate that extensive deficiency of PDC in the nervous system leads to pre‐natal lethality. Brain tissue from surviving females at post‐natal days 15 and 35 was shown to have approximately 75% of wild‐type PDC activity, suggesting that a threshold of enzyme activity exists for post‐natal survival. Detailed histological analyses of brain tissue revealed structural defects such as disordered neuronal cytoarchitecture and neuropil fibers in grey matter, and reduced size of bundles and disorganization of fibers in white matter. Many of the histologic abnormalities resemble those found in human female patients who carry mutations in the X‐linked ortholog. These findings demonstrate a requirement for PDC activity within the nervous system for survival in utero and suggest that impaired pyruvate metabolism in the developing brain can affect neuronal migration, axonal growth and cell–cell interactions.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
The ATLAS level-1 calorimeter trigger will utilise a number of advanced technologies, many of which have already been successfully demonstrated. To evaluate the different technologies associated with ...the important areas of high-speed data transport a large demonstrator system has been designed and operated during the last two years, using signals from prototype calorimeters in the ATLAS test-beam. Using this system, inter-crate data transmission and reception have been demonstrated at over 1.4 Gbyte/s, with individual links running at up to 1.6 Gbaud. Operating with 160 Mbit/s signals across a transmission-line backplane, custom transceiver ASICs have achieved inter-module data fanout at peak rates above 800 Mbyte/s. With the addition of further modules, the system was extended to emulate a vertical slice through the ATLAS level-1 calorimeter trigger. We present here the results from these tests, including measurements of bit-error rates across different data paths.
The topological structure of a binary tree is characterized by a measure called tree asymmetry, defined as the mean value of the asymmetry of its partitions. The statistical properties of this ...tree-asymmetry measure have been studied using a growth model for binary trees. The tree-asymmetry measure appears to be sensitive for topological differences and the tree-asymmetry expectation for the growth model that we used appears to be almost independent of the size of the trees. These properties and the simple definition make the measure suitable for practical use, for instance for characterizing, comparing and interpreting sets of branching patterns. Examples are given of the analysis of three sets of neuronal branching patterns. It is shown that the variance in tree-asymmetry values for these observed branching patterns corresponds perfectly with the variance predicted by the used growth model.
It is generally accepted that long term chronic ethanol consumption by young rats will lead to significant losses of cerebellar granule neurons (GN). A recent study in this laboratory showed, ...however, that 40 weeks of chronic ethanol consumption had no effect on the total numbers of GN in aged Fischer 344 rats (F344). The goals of the present study were to determine whether F344 GN were resistant to ethanol toxicity only in aged rats and whether resistance of GN in aged rats to ethanol toxicity occurred only in the F344 strain. To accomplish those goals, young and aged adult F344 and Wistar-Kyoto (WKY) rats were treated chronically with ethanol for 40 weeks during the first or second half of their life span. In each rat the total numbers of GN were estimated with the optical fractionator and the volumes of the GN layer were estimated according to Cavalieri's theorem. After the 40 weeks of ethanol, there were significant age-related differences in the total numbers of GN in the F344 rats. There were also significant strain-related differences in the total numbers of GN and volumes of the GN layer. There were no significant ethanol-related differences, however, in numbers of cerebellar GN or volumes of the GN layer in F344 rats or WKY rats. The results presented here show that consumption of ethanol over long periods of time had no effect on the total numbers of cerebellar GN or the granular layer volumes in young or aged F344 or WKY rats.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ