222 research outputs found

    Detecting corrupted pages in M replicated large files

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    A file in a distributed database system is replicated on M sites and may contain corrupted pages. Abdel-Ghaffar and El Abbadi gave a detection scheme assuming that the number of corrupted pages f < M l 2. We replace this assumption by a much weaker one, that, for each page, the majority of copies are correct. Our schemes are based on the structure of the Reed-Solomon code, as proposed by Abdel-Ghaffar and El Abbadi for M= 2. © 1997 IEEE.published_or_final_versio

    Optimal competitiveness for the Rectilinear Steiner Arborescence problem

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    We present optimal online algorithms for two related known problems involving Steiner Arborescence, improving both the lower and the upper bounds. One of them is the well studied continuous problem of the {\em Rectilinear Steiner Arborescence} (RSARSA). We improve the lower bound and the upper bound on the competitive ratio for RSARSA from O(logN)O(\log N) and Ω(logN)\Omega(\sqrt{\log N}) to Θ(logNloglogN)\Theta(\frac{\log N}{\log \log N}), where NN is the number of Steiner points. This separates the competitive ratios of RSARSA and the Symetric-RSARSA, two problems for which the bounds of Berman and Coulston is STOC 1997 were identical. The second problem is one of the Multimedia Content Distribution problems presented by Papadimitriou et al. in several papers and Charikar et al. SODA 1998. It can be viewed as the discrete counterparts (or a network counterpart) of RSARSA. For this second problem we present tight bounds also in terms of the network size, in addition to presenting tight bounds in terms of the number of Steiner points (the latter are similar to those we derived for RSARSA)

    Improved Average Complexity for Comparison-Based Sorting

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    This paper studies the average complexity on the number of comparisons for sorting algorithms. Its information-theoretic lower bound is nlgn1.4427n+O(logn)n \lg n - 1.4427n + O(\log n). For many efficient algorithms, the first nlgnn\lg n term is easy to achieve and our focus is on the (negative) constant factor of the linear term. The current best value is 1.3999-1.3999 for the MergeInsertion sort. Our new value is 1.4106-1.4106, narrowing the gap by some 25%25\%. An important building block of our algorithm is "two-element insertion," which inserts two numbers AA and BB, A<BA<B, into a sorted sequence TT. This insertion algorithm is still sufficiently simple for rigorous mathematical analysis and works well for a certain range of the length of TT for which the simple binary insertion does not, thus allowing us to take a complementary approach with the binary insertion.Comment: 21 pages, 2 figure

    Improved Adaptive Group Testing Algorithms with Applications to Multiple Access Channels and Dead Sensor Diagnosis

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    We study group-testing algorithms for resolving broadcast conflicts on a multiple access channel (MAC) and for identifying the dead sensors in a mobile ad hoc wireless network. In group-testing algorithms, we are asked to identify all the defective items in a set of items when we can test arbitrary subsets of items. In the standard group-testing problem, the result of a test is binary--the tested subset either contains defective items or not. In the more generalized versions we study in this paper, the result of each test is non-binary. For example, it may indicate whether the number of defective items contained in the tested subset is zero, one, or at least two. We give adaptive algorithms that are provably more efficient than previous group testing algorithms. We also show how our algorithms can be applied to solve conflict resolution on a MAC and dead sensor diagnosis. Dead sensor diagnosis poses an interesting challenge compared to MAC resolution, because dead sensors are not locally detectable, nor are they themselves active participants.Comment: Expanded version of a paper appearing in ACM Symposium on Parallelism in Algorithms and Architectures (SPAA), and preliminary version of paper appearing in Journal of Combinatorial Optimizatio

    Massive stars as thermonuclear reactors and their explosions following core collapse

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    Nuclear reactions transform atomic nuclei inside stars. This is the process of stellar nucleosynthesis. The basic concepts of determining nuclear reaction rates inside stars are reviewed. How stars manage to burn their fuel so slowly most of the time are also considered. Stellar thermonuclear reactions involving protons in hydrostatic burning are discussed first. Then I discuss triple alpha reactions in the helium burning stage. Carbon and oxygen survive in red giant stars because of the nuclear structure of oxygen and neon. Further nuclear burning of carbon, neon, oxygen and silicon in quiescent conditions are discussed next. In the subsequent core-collapse phase, neutronization due to electron capture from the top of the Fermi sea in a degenerate core takes place. The expected signal of neutrinos from a nearby supernova is calculated. The supernova often explodes inside a dense circumstellar medium, which is established due to the progenitor star losing its outermost envelope in a stellar wind or mass transfer in a binary system. The nature of the circumstellar medium and the ejecta of the supernova and their dynamics are revealed by observations in the optical, IR, radio, and X-ray bands, and I discuss some of these observations and their interpretations.Comment: To be published in " Principles and Perspectives in Cosmochemistry" Lecture Notes on Kodai School on Synthesis of Elements in Stars; ed. by Aruna Goswami & Eswar Reddy, Springer Verlag, 2009. Contains 21 figure

    The Functional DRD3 Ser9Gly Polymorphism (rs6280) Is Pleiotropic, Affecting Reward as Well as Movement

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    Abnormalities of motivation and behavior in the context of reward are a fundamental component of addiction and mood disorders. Here we test the effect of a functional missense mutation in the dopamine 3 receptor (DRD3) gene (ser9gly, rs6280) on reward-associated dopamine (DA) release in the striatum. Twenty-six healthy controls (HCs) and 10 unmedicated subjects with major depressive disorder (MDD) completed two positron emission tomography (PET) scans with [11C]raclopride using the bolus plus constant infusion method. On one occasion subjects completed a sensorimotor task (control condition) and on another occasion subjects completed a gambling task (reward condition). A linear regression analysis controlling for age, sex, diagnosis, and self-reported anhedonia indicated that during receipt of unpredictable monetary reward the glycine allele was associated with a greater reduction in D2/3 receptor binding (i.e., increased reward-related DA release) in the middle (anterior) caudate (p<0.01) and the ventral striatum (p<0.05). The possible functional effect of the ser9gly polymorphism on DA release is consistent with previous work demonstrating that the glycine allele yields D3 autoreceptors that have a higher affinity for DA and display more robust intracellular signaling. Preclinical evidence indicates that chronic stress and aversive stimulation induce activation of the DA system, raising the possibility that the glycine allele, by virtue of its facilitatory effect on striatal DA release, increases susceptibility to hyperdopaminergic responses that have previously been associated with stress, addiction, and psychosis

    Inhibition of Proliferation and Induction of Apoptosis in Multiple Myeloma Cell Lines by CD137 Ligand Signaling

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    BACKGROUND: Multiple myeloma (MM) is a malignancy of terminally-differentiated plasma cells, and the second most prevalent blood cancer. At present there is no cure for MM, and the average prognosis is only three to five years. Current treatments such as chemotherapy are able to prolong a patient's life but rarely prevent relapse of the disease. Even hematopoietic stem cell transplants and novel drug combinations are often not curative, underscoring the need for a continued search for novel therapeutics. CD137 and its ligand are members of the Tumor Necrosis Factor (TNF) receptor and TNF superfamilies, respectively. Since CD137 ligand cross-linking enhances proliferation and survival of healthy B cells we hypothesized that it would also act as a growth stimulus for B cell cancers. METHODOLOGY/PRINCIPAL FINDINGS: Proliferation and survival of B cell lymphoma cell lines were not affected or slightly enhanced by CD137 ligand agonists in vitro. But surprisingly, they had the opposite effects on MM cells, where CD137 ligand signals inhibited proliferation and induced cell death by apoptosis. Furthermore, secretion of the pro-inflammatory cytokines, IL-6 and IL-8 were also enhanced in MM but not in non-MM cell lines in response to CD137 ligand agonists. The secretion of these cytokines in response to CD137 ligand signaling was consistent with the observed activation of the classical NF-kappaB pathway. We hypothesize that the induction of this pathway results in activation-induced cell death, and that this is the underlying mechanism of CD137-induced MM cell death and growth arrest. CONCLUSIONS/SIGNIFICANCE: These data point to a hitherto unrecognized role of CD137 and CD137 ligand in MM cell biology. The selective inhibition of proliferation and induction of cell death in MM cells by CD137 ligand agonists may also warrant a closer evaluation of their therapeutic potential

    High Extracellular Ca2+ Stimulates Ca2+-Activated Cl− Currents in Frog Parathyroid Cells through the Mediation of Arachidonic Acid Cascade

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    Elevation of extracellular Ca2+ concentration induces intracellular Ca2+ signaling in parathyroid cells. The response is due to stimulation of the phospholipase C/Ca2+ pathways, but the direct mechanism responsible for the rise of intracellular Ca2+ concentration has remained elusive. Here, we describe the electrophysiological property associated with intracellular Ca2+ signaling in frog parathyroid cells and show that Ca2+-activated Cl− channels are activated by intracellular Ca2+ increase through an inositol 1,4,5-trisphophate (IP3)-independent pathway. High extracellular Ca2+ induced an outwardly-rectifying conductance in a dose-dependent manner (EC50∼6 mM). The conductance was composed of an instantaneous time-independent component and a slowly activating time-dependent component and displayed a deactivating inward tail current. Extracellular Ca2+-induced and Ca2+ dialysis-induced currents reversed at the equilibrium potential of Cl− and were inhibited by niflumic acid (a specific blocker of Ca2+-activated Cl− channel). Gramicidin-perforated whole-cell recording displayed the shift of the reversal potential in extracellular Ca2+-induced current, suggesting the change of intracellular Cl− concentration in a few minutes. Extracellular Ca2+-induced currents displayed a moderate dependency on guanosine triphosphate (GTP). All blockers for phospholipase C, diacylglycerol (DAG) lipase, monoacylglycerol (MAG) lipase and lipoxygenase inhibited extracellular Ca2+-induced current. IP3 dialysis failed to induce conductance increase, but 2-arachidonoylglycerol (2-AG), arachidonic acid and 12S-hydroperoxy-5Z,8Z,10E,14Z-eicosatetraenoic acid (12(S)-HPETE) dialysis increased the conductance identical to extracellular Ca2+-induced conductance. These results indicate that high extracellular Ca2+ raises intracellular Ca2+ concentration through the DAG lipase/lipoxygenase pathway, resulting in the activation of Cl− conductance
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