714 research outputs found

    Local Integrals of Motion for Topologically Ordered Many-Body Localized Systems

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    Many-body localized (MBL) systems are often described using their local integrals of motion, which, for spin systems, are commonly assumed to be a local unitary transform of the set of on-site spin-z operators. We show that this assumption cannot hold for topologically ordered MBL systems. Using a suitable definition to capture such systems in any spatial dimension, we demonstrate a number of features, including that MBL topological order, if present: (i) is the same for all eigenstates; (ii) is robust in character against any perturbation preserving MBL; (iii) implies that on topologically nontrivial manifolds a complete set of integrals of motion must include nonlocal ones in the form of local-unitary-dressed noncontractible Wilson loops. Our approach is well suited for tensor-network methods, and is expected to allow these to resolve highly-excited finite-size-split topological eigenspaces despite their overlap in energy. We illustrate our approach on the disordered Kitaev chain, toric code, and X-cube model.Comment: 5 pages, 1 figur

    Local integrals of motion detection of localization-protected topological order

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    Many-body-localized (MBL) phases can be topologically distinct, but distinguishing these phases using order parameters can be challenging. Here we show how topologically distinct local integrals of motion, variationally parametrized by quantum circuits, can be used to numerically demonstrate the topological inequivalence of MBL phases. We illustrate our approach on a fermionic chain where both topologically distinct MBL phases and benchmark comparisons to order parameters are possible. We also use our approach, augmented by the DMRG-X algorithm, to extract high-energy topological doublets. We describe applying our methods to higher dimensions to identify MBL topological order and topological multiplets hidden by the dense many-body spectrum.Comment: 8 pages, 7 figures; v2: accepted manuscript; v3: typo fixe

    Stromal mesenteric lymph node cells are essential for the generation of gut-homing T cells in vivo

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    T cells primed in the gut-draining mesenteric lymph nodes (mLN) are imprinted to express α4β7-integrin and chemokine receptor CCR9, thereby enabling lymphocytes to migrate to the small intestine. In vitro activation by intestinal dendritic cells (DC) or addition of retinoic acid (RA) is sufficient to instruct expression of these gut-homing molecules. We report that in vivo stroma cells, but not DC, allow the mLN to induce the generation of gut tropism. Peripheral LN (pLN) transplanted into the gut mesenteries fail to support the generation of gut-homing T cells, even though gut-derived DC enter the transplants and prime T cells. DC that fail to induce α4β7-integrin and CCR9 in vitro readily induce these factors in vivo upon injection into mLN afferent lymphatics. Moreover, uniquely mesenteric but not pLN stroma cells express high levels of RA-producing enzymes and support induction of CCR9 on activated T cells in vitro. These results demonstrate a hitherto unrecognized contribution of stromal cell delivered signals, including RA, on the imprinting of tissue tropism in vivo

    Cardiosphere-derived cells demonstrate metabolic flexibility that Is influenced by adhesion status

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    Adult stem cells demonstrate metabolic flexibility that is regulated by cell adhesion status. The authors demonstrate that adherent cells primarily utilize glycolysis, whereas suspended cells rely on oxidative phosphorylation for their ATP needs. Akt phosphorylation transduces adhesion-mediated regulation of energy metabolism, by regulating translocation of glucose transporters (GLUT1) to the cell membrane and thus, cellular glucose uptake and glycolysis. Cell dissociation, a pre-requisite for cell transplantation, leads to energetic stress, which is mediated by Akt dephosphorylation, downregulation of glucose uptake, and glycolysis. They designed hydrogels that promote rapid cell adhesion of encapsulated cells, Akt phosphorylation, restore glycolysis, and cellular ATP levels

    Automated quantum error mitigation based on probabilistic error reduction

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    Current quantum computers suffer from a level of noise that prohibits extracting useful results directly from longer computations. The figure of merit in many near-term quantum algorithms is an expectation value measured at the end of the computation, which experiences a bias in the presence of hardware noise. A systematic way to remove such bias is probabilistic error cancellation (PEC). PEC requires a full characterization of the noise and introduces a sampling overhead that increases exponentially with circuit depth, prohibiting high-depth circuits at realistic noise levels. Probabilistic error reduction (PER) is a related quantum error mitigation method that systematically reduces the sampling overhead at the cost of reintroducing bias. In combination with zero-noise extrapolation, PER can yield expectation values with an accuracy comparable to PEC.Noise reduction through PER is broadly applicable to near-term algorithms, and the automated implementation of PER is thus desirable for facilitating its widespread use. To this end, we present an automated quantum error mitigation software framework that includes noise tomography and application of PER to user-specified circuits. We provide a multi-platform Python package that implements a recently developed Pauli noise tomography (PNT) technique for learning a sparse Pauli noise model and exploits a Pauli noise scaling method to carry out PER.We also provide software tools that leverage a previously developed toolchain, employing PyGSTi for gate set tomography and providing a functionality to use the software Mitiq for PER and zero-noise extrapolation to obtain error-mitigated expectation values on a user-defined circuit.Comment: 11 pages, 9 figure

    Acute Downregulation but Not Genetic Ablation of Murine MCU Impairs Suppressive Capacity of Regulatory CD4 T Cells

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    By virtue of mitochondrial control of energy production, reactive oxygen species (ROS) generation, and maintenance of Ca2+ homeostasis, mitochondria play an essential role in modulating T cell function. The mitochondrial Ca2+ uniporter (MCU) is the pore-forming unit in the main protein complex mediating mitochondrial Ca2+ uptake. Recently, MCU has been shown to modulate Ca2+ signals at subcellular organellar interfaces, thus fine-tuning NFAT translocation and T cell activation. The mechanisms underlying this modulation and whether MCU has additional T cell subpopulationspecific effects remain elusive. However, mice with germline or tissue-specific ablation of Mcu did not show impaired T cell responses in vitro or in vivo, indicating that ‘chronic’ loss of MCU can be functionally compensated in lymphocytes. The current work aimed to specifically investigate whether and how MCU influences the suppressive potential of regulatory CD4 T cells (Treg). We show that, in contrast to genetic ablation, acute siRNA-mediated downregulation of Mcu in murine Tregs results in a significant reduction both in mitochondrial Ca2+ uptake and in the suppressive capacity of Tregs, while the ratios of Treg subpopulations and the expression of hallmark transcription factors were not affected. These findings suggest that permanent genetic inactivation of MCU may result in compensatory adaptive mechanisms, masking the effects on the suppressive capacity of Tregs

    Atomic-scale imaging of emergent order at a magnetic-field-induced Lifshitz transition

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    Funding: UK Engineering and Physical Sciences Research Council, Funder ID: (FUNDREF) 10.13039/501100000266, Grant: EP/L015110/1. UK Engineering and Physical Sciences Research Council, Funder ID:(FUNDREF) 10.13039/501100000266, Grant: EP/R031924/1. Engineering and Physical Sciences Research Council, Funder ID:(FUNDREF) 10.13039/501100000266, Grant: EP/R023751/1. Engineering and Physical Sciences Research Council, Funder ID:(FUNDREF) 10.13039/501100000266, Grant: EP/L017008/1.The phenomenology and radical changes seen in material properties traversing a quantum phase transition have captivated condensed matter research over the past decades. Strong electronic correlations lead to exotic electronic ground states, including magnetic order, nematicity, and unconventional superconductivity. Providing a microscopic model for these requires detailed knowledge of the electronic structure in the vicinity of the Fermi energy, promising a complete understanding of the physics of the quantum critical point. Here, we demonstrate such a measurement at the surface of Sr3Ru2O7. Our results show that, even in zero field, the electronic structure is strongly C2 symmetric and that a magnetic field drives a Lifshitz transition and induces a charge-stripe order. We track the changes of the electronic structure as a function of field via quasiparticle interference imaging at ultralow temperatures. Our results provide a complete microscopic picture of the field-induced changes of the electronic structure across the Lifshitz transition.Publisher PDFPeer reviewe
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