170 research outputs found

    Parallelism through Digital Circuit Design

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    Two ways to exploit chips with a very large number of transistors are multicore processors and programmable logic chips. Some data parallel algorithms can be executed efficiently on ordinary parallel computers, including multicores. A class of data parallel algorithms is identified which have characteristics that make implementation on multiprocessors inefficient, but they are well suited for direct design as digital circuits. This leads to a programming model called circuit parallelism. The characteristics of circuit parallel algorithms are discussed, and a prototype system for supporting them is described

    The Big Ten

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    The Big Ten

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    Operation Characteristics of the Series System for Electrolytic Refining of Copper

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    In the copper electrolytic refining operation, two main objectives are desired: the first is the production of a metal of desired chemical composition and physical characteristics, and the second is the recovery of the valuable by-products

    Maria Montessori

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    Dr. Maria Montessori was born in Italy in 1870. At the age of 24 she became the first woman to receive a medical degree from the University of Rome. As assistant physician in the psychiatric clinic of the University of Rome, she became interested in the learning ability of mentally and physically atypical children. Her interest in this field was furthered by her reading of the success of Dr. Edward Sequin, a French physician, who was doing extensive work with the education of [people with learning disabilities]. Dr. Montessori founded the Orthophrenic School in Rome in 1898 and carried on much of her early work in this school. She also lectured at the University of Rome on pedagogical anthropology. In 1922 she was named inspector general of all schools in Italy. Her work was interrupted in 1933 because she was not able to accept the type of training the Mussolini regime was imposing on children. She left Italy in 1933 and did not return until 1947. Madame Montessori spent the last of her life speaking and writing about the Montessori method in Spain, India, England, and the Netherlands. Her work was by now accepted for the normal child as well as the mentally handicapped. Dr. Maria Montessori died in 1952 while visiting the Netherlands. The author of this article, Dr. John R. O\u27Donnell, is in his second year on the University of Dayton faculty. He has lectured widely and is looked upon as a resource person in the field of elementary school mathematics, an area in which he has written several books

    Compliance with the New Continuity of Business Enterprise Regulation

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    Many questions unanswered by the new regulation have already been dealt with in these older forms of continuity of enterprise requirements. This article will discuss the major unanswered questions of the new regulation, examine how the older forms of continuity of enterprise have dealt with such issues, and consider the propriety of applying the older-form decisions to the new reorganization-enterprise continuity regulation. The result will be some guidance, although unfortunately no guaranteed methods, on how to avoid being forced to litigate the validity of the regulation itself

    Air Crimes: Perspective from the Cockpit

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    Glutamate Transport Affects Mitochondria And Calcium Signaling In Astrocytic Processes Under Normal And Pathological Conditions

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    ABSTRACT GLUTAMATE TRANSPORT AFFECTS MITOCHONDRIA AND CALCIUM SIGNALING IN ASTROCYTIC PROCESSES UNDER NORMAL AND PATHOLOGICAL CONDITIONS John Charles O’Donnell Michael B. Robinson Mitochondria are responsible for synthesis and metabolism of the primary excitatory neurotransmitter, glutamate, which is cleared from synapses via Na+-dependent transporters on astrocytes. Astrocytic clearance of glutamate is required to prevent excitotoxic neuronal death. Mitochondria also participate in calcium signaling in various cell types. Astrocytic calcium signaling is implicated in neurovascular coupling. Glutamate transport and calcium signaling are central to the function of astrocytic processes that are in turn vital for normal brain function. We recently confirmed that mitochondria are present throughout astrocytic processes. Using confocal microscopy and hippocampal slice cultures along with a variety of biochemical assays, we sought to elucidate the physiological and pathological interactions between mitochondria, glutamate transport, and calcium signaling in astrocytic processes. We found that glutamate uptake is reduced after displacing hexokinase from the voltage-dependent anion channel on the outer mitochondrial membrane, but coimmunoprecipitations between transporter and mitochondrial proteins are not changed. As in neurons, we found that some astrocytic mitochondria are mobile. We provide evidence that neuronal activity, activation of astrocytic glutamate transporters, and subsequent reversal of the Na+/Ca2+ exchanger leads to immobilization of mitochondria near transporters and synapses, where they can oxidize glutamate, buffer ions, and provide ATP. Finally, I found that following transient oxygen/glucose deprivation (a model of ischemia/reperfusion injury), mitochondria in astrocytic processes undergo fragmentation and autophagic degradation, culminating 24 h after insult with an ~50% reduction in mitochondrial size and the percentage of process length occupied by mitochondria. This loss of mitochondria is independent of the accompanying excitotoxic neuropathology, and seems to instead be driven by an extended period of high glutamate uptake. I also identified a previously overlooked distinction between Ca2+ signals in astrocytic processes, showing two populations with different properties based on their anatomical relationship to mitochondria. These Ca2+ signals were greatly increased after mitochondrial loss and were no longer spatially restricted by the remaining mitochondria. In summary, we found that glutamate transport positions mitochondria at sites of activity in astrocytic processes where they shape calcium signals; but glutamate uptake under excitoxic conditions leads to mitochondrial loss and dramatically altered calcium signaling, potentially impacting neuronal injury and recovery
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