332 research outputs found

    Beating the channel capacity limit for linear photonic superdense coding

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    Dense coding is arguably the protocol that launched the field of quantum communication. Today, however, more than a decade after its initial experimental realization, the channel capacity remains fundamentally limited as conceived for photons using linear elements. Bob can only send to Alice three of four potential messages owing to the impossibility of carrying out the deterministic discrimination of all four Bell states with linear optics, reducing the attainable channel capacity from 2 to log_2 3 \approx 1.585 bits. However, entanglement in an extra degree of freedom enables the complete and deterministic discrimination of all Bell states. Using pairs of photons simultaneously entangled in spin and orbital angular momentum, we demonstrate the quantum advantage of the ancillary entanglement. In particular, we describe a dense-coding experiment with the largest reported channel capacity and, to our knowledge, the first to break the conventional linear-optics threshold. Our encoding is suited for quantum communication without alignment and satellite communication.Comment: Letter: 6 pages, 4 figures. Supplementary Information: 4 pages, 1 figur

    Some additive results on Drazin inverse

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    In this paper, we investigate additive results of the Drazin inverse of elements in a ring R. Under the condition ab = ba, we show that a + b is Drazin invertible if and only if aa^D(a+b) is Drazin invertible, where the superscript D means the Drazin inverse. Furthermore we find an expression of (a + b)^D. As an application we give some new representations for the Drazin inverse of a 2 × 2 block matrix.Supported by the National Natural Science Foundation of China (11361009), the Guangxi Provincial Natural Science Foundation of China (2013GXNSFAA019008), and Science Research Project 2013 of the China-ASEAN Study Center (Guangxi Science Experiment Center) of Guangxi University for Nationalities.Liu, X.; Qin, X.; Benítez López, J. (2015). Some additive results on Drazin inverse. Applied Mathematics - A Journal of Chinese Universities. 30(4):479-490. https://doi.org/10.1007/s11766-015-3333-4S479490304A Ben-Israel, T N E Greville. Generalized Inverses, Theory and Applications, 2nd edition, Springer-Verlag, 2003.S L Campbell, C D Meyer. Generalized Inverses of Linear Transformations, Pitman (Advanced Publishing Program), Boston, MA, 1979.N Castro-González, J J Koliha. Additive perturbation results for the Drazin inverse, Linear Algebra Appl, 2005, 397: 279–297.N Castro-González, E Dopazo, M F Martínez-Serrano. On the Drazin inverse of the sum of two operators and its application to operator matrices, J Math Anal Appl, 2008, 350: 207–215.N Castro-González, M F Martínez-Serrano. Expressions for the g-Drazin inverse of additive perturbed elements in a Banach algebra, Linear Algebra Appl, 2010, 432: 1885–1895.N Castro-González, J J Koliha. New additive results for the Drazin inverse, Proc Roy Soc Edinburgh Sect A, 2004, 134: 1085–1097.M Catral, D D Olesky, P van den Driessche. Block representations of the Drazin inverse of a bipartite matrix, Electron J Linear Algebra, 2009, 18: 98–107.J L Chen, G F Zhuang, Y Wei. The Drazin inverse of a sum of morphisms, Acta Math Sci Ser A Chin Ed, 2009, 29(3): 538–552.D S Cvetković-Ilić, D S Djordjević, Y Wei. Additive results for the generalized Drazin inverse in a Banach algebra, Linear Algebra Appl, 2006, 418, 53–61.D S Cvetković-Ilić. A note on the representation for the Drazin inverse of 2 × 2 block matrices, Linear Algebra Appl, 2008, 429: 242–248.C Deng. The Drazin inverses of sum and difference of idempotents, Linear Algebra Appl, 2009, 430: 1282–1291.C Deng, Y Wei. Characterizations and representations of the Drazin inverse of idempotents, Linear Algebra Appl, 2009, 431: 1526–1538.C Deng, Y Wei. New additive results for the generalized Drazin inverse, J Math Anal Appl, 2010, 370: 313–321.D S Djordjević, P S Stanimirović. On the generalized Drazin inverse and generalized resolvent, Czechoslovak Math J, 2001, 51(126): 617–634.D S Djordjević, Y Wei. Additive results for the generalized Drazin inverse, J Aust Math Soc, 2002, 73: 115–125.D S Djordjević, V Rakočević. Lectures on Generalized inverses, University of Niš, 2008.E Dopazo, M F Martínez-Serrano. Further results on the representation of the Drazin inverse of a 2 × 2 block matrices, Linear Algebra Appl, 2010, 432: 1896–1904.M P Drazin. Pseudo-inverses in associative rings and semiproup, Amer Math Monthly, 1958, 65: 506–514.R E Hartwig, G R Wang, Y Wei. Some additive results on Drazin inverse, Linear Algebra Appl, 2001, 322: 207–217.R E Hartwig, X Li, Y Wei. Representations for the Drazin inverse of a 2×2 block matrix, SIAM J Matrix Anal Appl, 2006, 27: 757–771.Y Liu, C G Cao. Drazin inverse for some partitioned matrices over skew fields, J Nat Sci Heilongjiang Univ, 2004, 24: 112–114.J Ljubisavljević, D S Cvetković-Ilić. Additive results for the Drazin inverse of block matrices and applications, J Comput Appl Math, 2011, 235: 3683–3690.C D Meyer ffixJr, N J Rose. The index and the Drazin inverse of block triangular matrices, SIAM J Appl Math, 1977, 33(1): 1–7.L Wang, H H Zhu, X Zhu, J L Chen. Additive property of Drazin invertibility of elements, arXiv: 1307.1816v1 [math.RA], 2013.H Yang, X Liu. The Drazin inverse of the sum of two matrices and its applications, J Comput Appl Math, 2011, 235: 1412–1417

    Endothelial Cell and Platelet Bioenergetics: Effect of Glucose and Nutrient Composition

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    It has been suggested that cells that are independent of insulin for glucose uptake, when exposed to high glucose or other nutrient concentrations, manifest enhanced mitochondrial substrate oxidation with consequent enhanced potential and generation of reactive oxygen species (ROS); a paradigm that could predispose to vascular complications of diabetes. Here we exposed bovine aortic endothelial (BAE) cells and human platelets to variable glucose and fatty acid concentrations. We then examined oxygen consumption and acidification rates using recently available technology in the form of an extracellular oxygen and proton flux analyzer. Acute or overnight exposure of confluent BAE cells to glucose concentrations from 5.5 to 25 mM did not enhance or change the rate of oxygen consumption (OCR) under basal conditions, during ATP synthesis, or under uncoupled conditions. Glucose also did not alter OCR in sub-confluent cells, in cells exposed to low serum, or in cells treated with added pyruvate. Likewise, overnight exposure to fatty acids of varying saturation had no such effects. Overnight exposure of BAE cells to low glucose concentration decreased maximal uncoupled respiration, but not basal or ATP related oxygen consumption. Labeled glucose oxidation to CO2 increased, but only marginally after high glucose exposure while oleate oxidation to CO2 decreased. Overnight exposure to linolenic acid, but not oleic or linoleic acid increased extracellular acidification consistent with enhanced glycolytic metabolism. We were unable to detect an increase in production of reactive oxygen species (ROS) from BAE cells exposed to high medium glucose. Like BAE cells, exposure of human platelets to glucose did not increase oxygen consumption. As opposed to BAE cells, platelet mitochondria demonstrate less respiratory reserve capacity (beyond that needed for basal metabolism). Our data do not support the concept that exposure to high glucose or fatty acids accelerates mitochondrial oxidative metabolism in endothelial cells or platelets

    Extracellular signal-regulated kinase 1/2 activity is not required in mammalian cells during late G2 for timely entry into or exit from mitosis

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    Author Posting. © American Society for Cell Biology, 2006. This article is posted here by permission of American Society for Cell Biology for personal use, not for redistribution. The definitive version was published in Molecular Biology of the Cell 17 (2006): 5227-5240, doi:10.1091/mbc.E06-04-0284.Extracellular signal-regulated kinase (ERK)1/2 activity is reported to be required in mammalian cells for timely entry into and exit from mitosis (i.e., the G2-mitosis [G2/M] and metaphase-anaphase [M/A] transitions). However, it is unclear whether this involvement reflects a direct requirement for ERK1/2 activity during these transitions or for activating gene transcription programs at earlier stages of the cell cycle. To examine these possibilities, we followed live cells in which ERK1/2 activity was inhibited through late G2 and mitosis. We find that acute inhibition of ERK1/2 during late G2 and through mitosis does not affect the timing of the G2/M or M/A transitions in normal or transformed human cells, nor does it impede spindle assembly, inactivate the p38 stress-activated checkpoint during late G2 or the spindle assembly checkpoint during mitosis. Using CENP-F as a marker for progress through G2, we also show that sustained inhibition of ERK1/2 transiently delays the cell cycle in early/mid-G2 via a p53-dependent mechanism. Together, our data reveal that ERK1/2 activity is required in early G2 for a timely entry into mitosis but that it does not directly regulate cell cycle progression from late G2 through mitosis in normal or transformed mammalian cells.This research was supported by National Institutes of Health Grant GMS-40198 to C.L.R., by National Institutes of Health/National Cancer Institute Grant CA109182, and Samuel Waxman Cancer Research Foundation grants to J.A.A.-G

    Nuclear Translocation of β-Catenin during Mesenchymal Stem Cells Differentiation into Hepatocytes Is Associated with a Tumoral Phenotype

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    Wnt/β-catenin pathway controls biochemical processes related to cell differentiation. In committed cells the alteration of this pathway has been associated with tumors as hepatocellular carcinoma or hepatoblastoma. The present study evaluated the role of Wnt/β-catenin activation during human mesenchymal stem cells differentiation into hepatocytes. The differentiation to hepatocytes was achieved by the addition of two different conditioned media. In one of them, β-catenin nuclear translocation, up-regulation of genes related to the Wnt/β-catenin pathway, such as Lrp5 and Fzd3, as well as the oncogenes c-myc and p53 were observed. While in the other protocol there was a Wnt/β-catenin inactivation. Hepatocytes with nuclear translocation of β-catenin also had abnormal cellular proliferation, and expressed membrane proteins involved in hepatocellular carcinoma, metastatic behavior and cancer stem cells. Further, these cells had also increased auto-renewal capability as shown in spheroids formation assay. Comparison of both differentiation protocols by 2D-DIGE proteomic analysis revealed differential expression of 11 proteins with altered expression in hepatocellular carcinoma. Cathepsin B and D, adenine phosphoribosyltransferase, triosephosphate isomerase, inorganic pyrophosphatase, peptidyl-prolyl cis-trans isomerase A or lactate dehydrogenase β-chain were up-regulated only with the protocol associated with Wnt signaling activation while other proteins involved in tumor suppression, such as transgelin or tropomyosin β-chain were down-regulated in this protocol. In conclusion, our results suggest that activation of the Wnt/β-catenin pathway during human mesenchymal stem cells differentiation into hepatocytes is associated with a tumoral phenotype

    Molecular characterization of a novel ssRNA ourmia-like virus from the rice blast fungus Magnaporthe oryzae

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    In this study we characterize a novel positive and single stranded RNA (ssRNA) mycovirus isolated from the rice field isolate of Magnaporthe oryzae Guy11. The ssRNA contains a single open reading frame (ORF) of 2,373 nucleotides in length and encodes an RNA-dependent RNA polymerase (RdRp) closely related to ourmiaviruses (plant viruses) and ourmia-like mycoviruses. Accordingly, we name this virus Magnaporthe oryzae ourmia-like virus 1 (MOLV1). Although phylogenetic analysis suggests that MOLV1 is closely related to ourmia and ourmia-like viruses, it has some features never reported before within the Ourmiavirus genus. 3' RLM-RACE (RNA ligase-mediated rapid amplification of cDNA ends) and extension poly(A) tests (ePAT) suggest that the MOLV1 genome contains a poly(A) tail whereas the three cytosine and the three guanine residues present in 5' and 3' untranslated regions (UTRs) of ourmia viruses are not observed in the MOLV1 sequence. The discovery of this novel viral genome supports the hypothesis that plant pathogenic fungi may have acquired this type of viruses from their host plants

    Imaging mass spectrometry of intraspecies metabolic exchange revealed the cannibalistic factors of Bacillus subtilis

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    During bacterial cannibalism, a differentiated subpopulation harvests nutrients from their genetically identical siblings to allow continued growth in nutrient-limited conditions. Hypothesis-driven imaging mass spectrometry (IMS) was used to identify metabolites active in a Bacillus subtilis cannibalism system in which sporulating cells lyse nonsporulating siblings. Two candidate molecules with sequences matching the products of skfA and sdpC, genes for the proposed cannibalistic factors sporulation killing factor (SKF) and sporulation delaying protein (SDP), respectively, were identified and the structures of the final products elucidated. SKF is a cyclic 26-amino acid (aa) peptide that is posttranslationally modified with one disulfide and one cysteine thioether bridged to the α-position of a methionine, a posttranslational modification not previously described in biology. SDP is a 42-residue peptide with one disulfide bridge. In spot test assays on solid medium, overproduced SKF and SDP enact a cannibalistic killing effect with SDP having higher potency. However, only purified SDP affected B. subtilis cells in liquid media in fluorescence microscopy and growth assays. Specifically, SDP treatment delayed growth in a concentration-dependent manner, caused increases in cell permeability, and ultimately caused cell lysis accompanied by the production of membrane tubules and spheres. Similarly, SDP but not SKF was able to inhibit the growth of the pathogens Staphylococcus aureus and Staphylococcus epidermidis with comparable IC(50) to vancomycin. This investigation, with the identification of SKF and SDP structures, highlights the strength of IMS in investigations of metabolic exchange of microbial colonies and also demonstrates IMS as a promising approach to discover novel biologically active molecules

    Role of the IL-1 Pathway in Dopaminergic Neurodegeneration and Decreased Voluntary Movement

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    Interleukin-1 (IL-1), a proinflammatory cytokine synthesized and released by activated microglia, can cause dopaminergic neurodegeneration leading to Parkinsons disease (PD). However, it is uncertain whether IL-1 can act directly, or by exacerbating the harmful actions of other brain insults. To ascertain the role of the IL-1 pathway on dopaminergic neurodegeneration and motor skills during aging, we compared mice with impaired [caspase-1 knockout (casp1(-/-))] or overactivated IL-1 activity [IL-1 receptor antagonist knockout (IL-1ra(-/-))] to wild-type (wt) mice at young and middle age. Their motor skills were evaluated by the open-field and rotarod tests, and quantification of their dopamine neurons and activated microglia within the substantia nigra were performed by immunohistochemistry. IL-1ra(-/-) mice showed an age-related decline in motor skills, a reduced number of dopamine neurons, and an increase in activated microglia when compared to wt or casp1(-/-) mice. Casp1(-/-) mice had similar changes in motor skills and dopamine neurons, but fewer activated microglia cells than wt mice. Our results suggest that the overactivated IL-1 pathway occurring in IL-1ra(-/-) mice in the absence of inflammatory interventions (e.g., intracerebral injections performed in animal models of PD) increased activated microglia, decreased the number of dopaminergic neurons, and reduced their motor skills. Decreased IL-1 activity in casp1(-/-) mice did not yield clear protective effects when compared with wt mice. In summary, in the absence of overt brain insults, chronic activation of the IL-1 pathway may promote pathological aspects of PD per se, but its impairment does not appear to yield advantages over wt mice.Funding Agencies|John Curtin School of Medical Research, The Australian National University</p
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