2,396 research outputs found

    Out-of-equilibrium physics in driven dissipative coupled resonator arrays

    Get PDF
    Coupled resonator arrays have been shown to exhibit interesting many- body physics including Mott and Fractional Hall states of photons. One of the main differences between these photonic quantum simulators and their cold atoms coun- terparts is in the dissipative nature of their photonic excitations. The natural equi- librium state is where there are no photons left in the cavity. Pumping the system with external drives is therefore necessary to compensate for the losses and realise non-trivial states. The external driving here can easily be tuned to be incoherent, coherent or fully quantum, opening the road for exploration of many body regimes beyond the reach of other approaches. In this chapter, we review some of the physics arising in driven dissipative coupled resonator arrays including photon fermionisa- tion, crystallisation, as well as photonic quantum Hall physics out of equilibrium. We start by briefly describing possible experimental candidates to realise coupled resonator arrays along with the two theoretical models that capture their physics, the Jaynes-Cummings-Hubbard and Bose-Hubbard Hamiltonians. A brief review of the analytical and sophisticated numerical methods required to tackle these systems is included.Comment: Chapter that appeared in "Quantum Simulations with Photons and Polaritons: Merging Quantum Optics with Condensed Matter Physics" edited by D.G.Angelakis, Quantum Science and Technology Series, Springer 201

    Neurodegeneration and Epilepsy in a Zebrafish Model of CLN3 Disease (Batten Disease)

    Get PDF
    The neuronal ceroid lipofuscinoses are a group of lysosomal storage disorders that comprise the most common, genetically heterogeneous, fatal neurodegenerative disorders of children. They are characterised by childhood onset, visual failure, epileptic seizures, psychomotor retardation and dementia. CLN3 disease, also known as Batten disease, is caused by autosomal recessive mutations in the CLN3 gene, 80–85% of which are a ~1 kb deletion. Currently no treatments exist, and after much suffering, the disease inevitably results in premature death. The aim of this study was to generate a zebrafish model of CLN3 disease using antisense morpholino injection, and characterise the pathological and functional consequences of Cln3 deficiency, thereby providing a tool for future drug discovery. The model was shown to faithfully recapitulate the pathological signs of CLN3 disease, including reduced survival, neuronal loss, retinopathy, axonopathy, loss of motor function, lysosomal storage of subunit c of mitochondrial ATP synthase, and epileptic seizures, albeit with an earlier onset and faster progression than the human disease. Our study provides proof of principle that the advantages of the zebrafish over other model systems can be utilised to further our understanding of the pathogenesis of CLN3 disease and accelerate drug discovery

    The Quantum Internet

    Get PDF
    Quantum networks offer a unifying set of opportunities and challenges across exciting intellectual and technical frontiers, including for quantum computation, communication, and metrology. The realization of quantum networks composed of many nodes and channels requires new scientific capabilities for the generation and characterization of quantum coherence and entanglement. Fundamental to this endeavor are quantum interconnects that convert quantum states from one physical system to those of another in a reversible fashion. Such quantum connectivity for networks can be achieved by optical interactions of single photons and atoms, thereby enabling entanglement distribution and quantum teleportation between nodes.Comment: 15 pages, 6 figures Higher resolution versions of the figures can be downloaded from the following link: http://www.its.caltech.edu/~hjkimble/QNet-figures-high-resolutio

    WNT signalling in prostate cancer

    Get PDF
    Genome sequencing and gene expression analyses of prostate tumours have highlighted the potential importance of genetic and epigenetic changes observed in WNT signalling pathway components in prostate tumours-particularly in the development of castration-resistant prostate cancer. WNT signalling is also important in the prostate tumour microenvironment, in which WNT proteins secreted by the tumour stroma promote resistance to therapy, and in prostate cancer stem or progenitor cells, in which WNT-β-catenin signals promote self-renewal or expansion. Preclinical studies have demonstrated the potential of inhibitors that target WNT receptor complexes at the cell membrane or that block the interaction of β-catenin with lymphoid enhancer-binding factor 1 and the androgen receptor, in preventing prostate cancer progression. Some WNT signalling inhibitors are in phase I trials, but they have yet to be tested in patients with prostate cancer

    Study of Bc+B_c^+ decays to the K+Kπ+K^+K^-\pi^+ final state and evidence for the decay Bc+χc0π+B_c^+\to\chi_{c0}\pi^+

    Get PDF
    A study of Bc+K+Kπ+B_c^+\to K^+K^-\pi^+ decays is performed for the first time using data corresponding to an integrated luminosity of 3.0 fb1\mathrm{fb}^{-1} collected by the LHCb experiment in pppp collisions at centre-of-mass energies of 77 and 88 TeV. Evidence for the decay Bc+χc0(K+K)π+B_c^+\to\chi_{c0}(\to K^+K^-)\pi^+ is reported with a significance of 4.0 standard deviations, resulting in the measurement of σ(Bc+)σ(B+)×B(Bc+χc0π+)\frac{\sigma(B_c^+)}{\sigma(B^+)}\times\mathcal{B}(B_c^+\to\chi_{c0}\pi^+) to be (9.83.0+3.4(stat)±0.8(syst))×106(9.8^{+3.4}_{-3.0}(\mathrm{stat})\pm 0.8(\mathrm{syst}))\times 10^{-6}. Here B\mathcal{B} denotes a branching fraction while σ(Bc+)\sigma(B_c^+) and σ(B+)\sigma(B^+) are the production cross-sections for Bc+B_c^+ and B+B^+ mesons. An indication of bˉc\bar b c weak annihilation is found for the region m(Kπ+)<1.834GeV ⁣/c2m(K^-\pi^+)<1.834\mathrm{\,Ge\kern -0.1em V\!/}c^2, with a significance of 2.4 standard deviations.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://lhcbproject.web.cern.ch/lhcbproject/Publications/LHCbProjectPublic/LHCb-PAPER-2016-022.html, link to supplemental material inserted in the reference

    Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

    Get PDF
    Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

    Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

    Get PDF
    This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

    Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

    Get PDF
    Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

    Measurement of the B0 anti-B0 oscillation frequency using l- D*+ pairs and lepton flavor tags

    Full text link
    The oscillation frequency Delta-md of B0 anti-B0 mixing is measured using the partially reconstructed semileptonic decay anti-B0 -> l- nubar D*+ X. The data sample was collected with the CDF detector at the Fermilab Tevatron collider during 1992 - 1995 by triggering on the existence of two lepton candidates in an event, and corresponds to about 110 pb-1 of pbar p collisions at sqrt(s) = 1.8 TeV. We estimate the proper decay time of the anti-B0 meson from the measured decay length and reconstructed momentum of the l- D*+ system. The charge of the lepton in the final state identifies the flavor of the anti-B0 meson at its decay. The second lepton in the event is used to infer the flavor of the anti-B0 meson at production. We measure the oscillation frequency to be Delta-md = 0.516 +/- 0.099 +0.029 -0.035 ps-1, where the first uncertainty is statistical and the second is systematic.Comment: 30 pages, 7 figures. Submitted to Physical Review
    corecore