2,936 research outputs found

    Sensation of presence and cybersickness in applications of virtual reality for advanced rehabilitation

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    Around three years ago, in the special issue on augmented and virtual reality in rehabilitation, the topics of simulator sickness was briefly discussed in relation to vestibular rehabilitation. Simulator sickness with virtual reality applications have also been referred to as visually induced motion sickness or cybersickness. Recently, study on cybersickness has been reported in entertainment, training, game, and medical environment in several journals. Virtual stimuli can enlarge sensation of presence, but they sometimes also evoke unpleasant sensation. In order to safely apply augmented and virtual reality for long-term rehabilitation treatment, sensation of presence and cybersickness should be appropriately controlled. This issue presents the results of five studies conducted to evaluate visually-induced effects and speculate influences of virtual rehabilitation. In particular, the influence of visual and vestibular stimuli on cardiovascular responses are reported in terms of academic contribution

    An Emerging Role for Epigenetic Dysregulation in Arsenic Toxicity and Carcinogenesis

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    Competing Interests Declaration: The authors declare they have no competing financial interests. Abbreviations: AHCY, S-adenosylhomocysteine hydrolase; APL, acute promyelocytic leukemias; As, inorganic arsenic; AS3MT, arsenic (+3 oxidation state) methyltransferase; ChIP-on-chip, chromatin immunoprecipitation-on-chip; ChIP-seq, chromatin immunoprecipitation-sequencing; DEFB1, defensin, beta 1; DNMTs, DNA methyltransferases; H3K4me3, H3K4 tri-methylation; H3K9me2, H3K9 di-methylation; H3K27me3, H3K27 tri-methylation; HATs, histone acetyltransferases; HDACs, histon

    Incorporating topological information for predicting robust cancer subnetwork markers in human protein-protein interaction network

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    BACKGROUND: Discovering robust markers for cancer prognosis based on gene expression data is an important yet challenging problem in translational bioinformatics. By integrating additional information in biological pathways or a protein-protein interaction (PPI) network, we can find better biomarkers that lead to more accurate and reproducible prognostic predictions. In fact, recent studies have shown that, “modular markers,” that integrate multiple genes with potential interactions can improve disease classification and also provide better understanding of the disease mechanisms. RESULTS: In this work, we propose a novel algorithm for finding robust and effective subnetwork markers that can accurately predict cancer prognosis. To simultaneously discover multiple synergistic subnetwork markers in a human PPI network, we build on our previous work that uses affinity propagation, an efficient clustering algorithm based on a message-passing scheme. Using affinity propagation, we identify potential subnetwork markers that consist of discriminative genes that display coherent expression patterns and whose protein products are closely located on the PPI network. Furthermore, we incorporate the topological information from the PPI network to evaluate the potential of a given set of proteins to be involved in a functional module. Primarily, we adopt widely made assumptions that densely connected subnetworks may likely be potential functional modules and that proteins that are not directly connected but interact with similar sets of other proteins may share similar functionalities. CONCLUSIONS: Incorporating topological attributes based on these assumptions can enhance the prediction of potential subnetwork markers. We evaluate the performance of the proposed subnetwork marker identification method by performing classification experiments using multiple independent breast cancer gene expression datasets and PPI networks. We show that our method leads to the discovery of robust subnetwork markers that can improve cancer classification. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12859-016-1224-1) contains supplementary material, which is available to authorized users

    Klebsiella pneumoniae is able to trigger epithelial-mesenchymal transition process in cultured airway epithelial cells

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    The ability of some bacterial pathogens to activate Epithelial-Mesenchymal Transition normally is a consequence of the persistence of a local chronic inflammatory response or depends on a direct interaction of the pathogens with the host epithelial cells. In this study we monitored the abilities of the K. pneumoniae to activate the expression of genes related to EMT-like processes and the occurrence of phenotypic changes in airway epithelial cells during the early steps of cell infection. We describe changes in the production of intracellular reactive oxygen species and increased HIF-1α mRNA expression in cells exposed to K. pneumoniae infection. We also describe the upregulation of a set of transcription factors implicated in the EMT processes, such as Twist, Snail and ZEB, indicating that the morphological changes of epithelial cells already appreciable after few hours from the K. pneumoniae infection are tightly regulated by the activation of transcriptional pathways, driving epithelial cells to EMT. These effects appear to be effectively counteracted by resveratrol, an antioxidant that is able to exert a sustained scavenging of the intracellular ROS. This is the first report indicating that strains of K. pneumoniae may promote EMT-like programs through direct interaction with epithelial cells without the involvement of inflammatory cells

    The Spin Structure of the Nucleon

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    We present an overview of recent experimental and theoretical advances in our understanding of the spin structure of protons and neutrons.Comment: 84 pages, 29 figure

    Resonances in J/ψϕπ+πJ/\psi \to \phi \pi ^+\pi ^- and ϕK+K\phi K^+K^-

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    A partial wave analysis is presented of J/ψϕπ+πJ/\psi \to \phi \pi ^+\pi ^- and ϕK+K\phi K^+K^- from a sample of 58M J/ψJ/\psi events in the BES II detector. The f0(980)f_0(980) is observed clearly in both sets of data, and parameters of the Flatt\' e formula are determined accurately: M=965±8M = 965 \pm 8 (stat) ±6\pm 6 (syst) MeV/c2^2, g1=165±10±15g_1 = 165 \pm 10 \pm 15 MeV/c2^2, g2/g1=4.21±0.25±0.21g_2/g_1 = 4.21 \pm 0.25 \pm 0.21. The ϕππ\phi \pi \pi data also exhibit a strong ππ\pi \pi peak centred at M=1335M = 1335 MeV/c2^2. It may be fitted with f2(1270)f_2(1270) and a dominant 0+0^+ signal made from f0(1370)f_0(1370) interfering with a smaller f0(1500)f_0(1500) component. There is evidence that the f0(1370)f_0(1370) signal is resonant, from interference with f2(1270)f_2(1270). There is also a state in ππ\pi \pi with M=179030+40M = 1790 ^{+40}_{-30} MeV/c2^2 and Γ=27030+60\Gamma = 270 ^{+60}_{-30} MeV/c2^2; spin 0 is preferred over spin 2. This state, f0(1790)f_0(1790), is distinct from f0(1710)f_0(1710). The ϕKKˉ\phi K\bar K data contain a strong peak due to f2(1525)f_2'(1525). A shoulder on its upper side may be fitted by interference between f0(1500)f_0(1500) and f0(1710)f_0(1710).Comment: 17 pages, 6 figures, 1 table. Submitted to Phys. Lett.

    Measurement of the Branching Fraction of J/psi --> pi+ pi- pi0

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    Using 58 million J/psi and 14 million psi' decays obtained by the BESII experiment, the branching fraction of J/psi --> pi+ pi- pi0 is determined. The result is (2.10+/-0.12)X10^{-2}, which is significantly higher than previous measurements.Comment: 9 pages, 8 figures, RevTex
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