127 research outputs found

    Electronic liquid crystal state in the high-temperature superconductor YBCO(6.45)

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    Electronic phases with symmetry properties matching those of conventional liquid crystals have recently been discovered in transport experiments on semiconductor heterostructures and metal oxides at milli-Kelvin temperatures. We report the spontaneous onset of a onedimensional, incommensurate modulation of the spin system in the high-temperature superconductor YBa2Cu3O6.45 upon cooling below ~150 K, while static magnetic order is absent above 2 K. The evolution of this modulation with temperature and doping parallels that of the in-plane anisotropy of the resistivity, indicating an electronic nematic phase that is stable over a wide temperature range. The results suggest that soft spin fluctuations are a microscopic route towards electronic liquid crystals, and nematic order can coexist with high-temperature superconductivity in underdoped cuprates.Comment: 10 pages, 4+2 figures, includes a "materials and methods" as well as a "supporting text" sectio

    Origin of the Pseudogap in High-Temperature Cuprate Superconductors

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    Cuprate high-temperature superconductors exhibit a pseudogap in the normal state that decreases monotonically with increasing hole doping and closes at x \approx 0.19 holes per planar CuO2 while the superconducting doping range is 0.05 < x < 0.27 with optimal Tc at x \approx 0.16. Using ab initio quantum calculations at the level that leads to accurate band gaps, we found that four-Cu-site plaquettes are created in the vicinity of dopants. At x \approx 0.05 the plaquettes percolate, so that the Cu dx2y2/O p{\sigma} orbitals inside the plaquettes now form a band of states along the percolating swath. This leads to metallic conductivity and below Tc to superconductivity. Plaquettes disconnected from the percolating swath are found to have degenerate states at the Fermi level that split and lead to the pseudogap. The pseudogap can be calculated by simply counting the spatial distribution of isolated plaquettes, leading to an excellent fit to experiment. This provides strong evidence in favor of inhomogeneous plaquettes in cuprates.Comment: 24 pages (4 pages main text plus 20 pages supplement

    Petri Net computational modelling of Langerhans cell Interferon Regulatory Factor Network predicts their role in T cell activation

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    Langerhans cells (LCs) are able to orchestrate adaptive immune responses in the skin by interpreting the microenvironmental context in which they encounter foreign substances, but the regulatory basis for this has not been established. Utilising systems immunology approaches combining in silico modelling of a reconstructed gene regulatory network (GRN) with in vitro validation of the predictions, we sought to determine the mechanisms of regulation of immune responses in human primary LCs. The key role of Interferon regulatory factors (IRFs) as controllers of the human Langerhans cell response to epidermal cytokines was revealed by whole transcriptome analysis. Applying Boolean logic we assembled a Petri net-based model of the IRF-GRN which provides molecular pathway predictions for the induction of different transcriptional programmes in LCs. In silico simulations performed after model parameterisation with transcription factor expression values predicted that human LC activation of antigen-specific CD8 T cells would be differentially regulated by epidermal cytokine induction of specific IRF-controlled pathways. This was confirmed by in vitro measurement of IFN-g production by activated T cells. As a proof of concept, this approach shows that stochastic modelling of a specific immune networks renders transcriptome data valuable for the prediction of functional outcomes of immune responses

    The placenta: phenotypic and epigenetic modifications induced by Assisted Reproductive Technologies throughout pregnancy

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    Expert consensus document: Clinical and molecular diagnosis, screening and management of Beckwith-Wiedemann syndrome: an international consensus statement.

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    Beckwith-Wiedemann syndrome (BWS), a human genomic imprinting disorder, is characterized by phenotypic variability that might include overgrowth, macroglossia, abdominal wall defects, neonatal hypoglycaemia, lateralized overgrowth and predisposition to embryonal tumours. Delineation of the molecular defects within the imprinted 11p15.5 region can predict familial recurrence risks and the risk (and type) of embryonal tumour. Despite recent advances in knowledge, there is marked heterogeneity in clinical diagnostic criteria and care. As detailed in this Consensus Statement, an international consensus group agreed upon 72 recommendations for the clinical and molecular diagnosis and management of BWS, including comprehensive protocols for the molecular investigation, care and treatment of patients from the prenatal period to adulthood. The consensus recommendations apply to patients with Beckwith-Wiedemann spectrum (BWSp), covering classical BWS without a molecular diagnosis and BWS-related phenotypes with an 11p15.5 molecular anomaly. Although the consensus group recommends a tumour surveillance programme targeted by molecular subgroups, surveillance might differ according to the local health-care system (for example, in the United States), and the results of targeted and universal surveillance should be evaluated prospectively. International collaboration, including a prospective audit of the results of implementing these consensus recommendations, is required to expand the evidence base for the design of optimum care pathways

    Sex- and Diet-Specific Changes of Imprinted Gene Expression and DNA Methylation in Mouse Placenta under a High-Fat Diet

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    Changes in imprinted gene dosage in the placenta may compromise the prenatal control of nutritional resources. Indeed monoallelic behaviour and sensitivity to changes in regional epigenetic state render imprinted genes both vulnerable and adaptable
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