Simulating noise on a quantum processor: interactions between a qubit and resonant two-level system bath

Material defects fundamentally limit the coherence times of superconducting qubits, and manufacturing completely defect-free devices is not yet possible. Therefore, understanding the interactions between defects and a qubit in a real quantum processor design is essential. We build a model that incorporates the standard tunneling model, the electric field distributions in the qubit, and open quantum system dynamics, and draws from the current understanding of two-level system (TLS) theory. Specifically, we start with one million TLSs distributed on the surface of a qubit and pick the 200 systems that are most strongly coupled to the qubit. We then perform a full Lindbladian simulation that explicitly includes the coherent coupling between the qubit and the TLS bath to model the time dependent density matrix of resonant TLS defects and the qubit. We find that the 200 most strongly coupled TLSs can accurately describe the qubit energy relaxation time. This work confirms that resonant TLSs located in areas where the electric field is strong can significantly affect the qubit relaxation time, even if they are located far from the Josephson junction. Similarly, a strongly-coupled resonant TLS located in the Josephson junction does not guarantee a reduced qubit relaxation time if a more strongly coupled TLS is far from the Josephson junction. In addition to the coupling strengths between TLSs and the qubit, the model predicts that the geometry of the device and the TLS relaxation time play a significant role in qubit dynamics. Our work can provide guidance for future quantum processor designs with improved qubit coherence times.Comment: 8 pages, 5 figure

Direct Observation of Field-Induced Incommensurate Fluctuations in a One-Dimensional S=1/2 Antiferromagnet

Neutron scattering from copper benzoate, Cu(C6D5COO)2 3D2O, provides the first direct experimental evidence for field-dependent incommensurate low energy modes in a one-dimensional spin S = 1/2 antiferromagnet. Soft modes occur for wavevectors q=\pi +- dq(H) where dq(H) ~ 2 \pi M(H)/g\mu_B as predicted by Bethe ansatz and spinon descriptions of the S = 1/2 chain. Unexpected was a field-induced energy gap $\Delta(H) \propto H^\alpha$, where $\alpha = 0.65(3)$ as determined from specific heat measurements. At H = 7 T (g\mu_B H/J = 0.52), the magnitude of the gap varies from 0.06 - 0.3 J depending on the orientation of the applied field.Comment: 11 pages, 5 postscript figures, LaTeX, Submitted to PRL 3/31/97, e-mail comments to [email protected]

A Transient Sub-Eddington Black Hole X-ray Binary Candidate in the Dust Lanes of Centaurus A

We report the discovery of a bright X-ray transient, CXOU J132527.6-430023, in the nearby early-type galaxy NGC 5128. The source was first detected over the course of five Chandra observations in 2007, reaching an unabsorbed outburst luminosity of 1-2*10^38 erg/s in the 0.5-7.0 keV band before returning to quiescence. Such luminosities are possible for both stellar-mass black hole and neutron star X-ray binary transients. Here, we attempt to characterize the nature of the compact object. No counterpart has been detected in the optical or radio sky, but the proximity of the source to the dust lanes allows for the possibility of an obscured companion. The brightness of the source after a >100 fold increase in X-ray flux makes it either the first confirmed transient non-ULX black hole system in outburst to be subject to detailed spectral modeling outside the Local Group, or a bright (>10^38 erg/s) transient neutron star X-ray binary, which are very rare. Such a large increase in flux would appear to lend weight to the view that this is a black hole transient. X-ray spectral fitting of an absorbed power law yielded unphysical photon indices, while the parameters of the best-fit absorbed disc blackbody model are typical of an accreting ~10 Msol black hole in the thermally dominant state.Comment: 8 pages, 6 figures, accepted for publication in Ap

Prolyl-4-hydroxylase 3 maintains β-cell glucose metabolism during fatty acid excess in mice

The α-ketoglutarate–dependent dioxygenase, prolyl-4-hydroxylase 3 (PHD3), is an HIF target that uses molecular oxygen to hydroxylate peptidyl prolyl residues. Although PHD3 has been reported to influence cancer cell metabolism and liver insulin sensitivity, relatively little is known about the effects of this highly conserved enzyme in insulin-secreting β cells in vivo. Here, we show that the deletion of PHD3 specifically in β cells (βPHD3KO) was associated with impaired glucose homeostasis in mice fed a high-fat diet. In the early stages of dietary fat excess, βPHD3KO islets energetically rewired, leading to defects in the management of pyruvate fate and a shift from glycolysis to increased fatty acid oxidation (FAO). However, under more prolonged metabolic stress, this switch to preferential FAO in βPHD3KO islets was associated with impaired glucose-stimulated ATP/ADP rises, Ca(2+) fluxes, and insulin secretion. Thus, PHD3 might be a pivotal component of the β cell glucose metabolism machinery in mice by suppressing the use of fatty acids as a primary fuel source during the early phases of metabolic stress

Pathogenomic analyses of Shigella isolates inform factors limiting shigellosis prevention and control across LMICs

Shigella spp. are the leading bacterial cause of severe childhood diarrhoea in low- and middle-income countries (LMICs), are increasingly antimicrobial resistant and have no widely available licenced vaccine. We performed genomic analyses of 1,246 systematically collected shigellae sampled from seven countries in sub-Saharan Africa and South Asia as part of the Global Enteric Multicenter Study (GEMS) between 2007 and 2011, to inform control and identify factors that could limit the effectiveness of current approaches. Through contemporaneous comparison among major subgroups, we found that S. sonnei contributes ≥6-fold more disease than other Shigella species relative to its genomic diversity, and highlight existing diversity and adaptative capacity among S. flexneri that may generate vaccine escape variants in <6 months. Furthermore, we show convergent evolution of resistance against ciprofloxacin, the current WHO-recommended antimicrobial for the treatment of shigellosis, among Shigella isolates. This demonstrates the urgent need to integrate existing genomic diversity into vaccine and treatment plans for Shigella, providing a framework for the focused application of comparative genomics to guide vaccine development, and the optimization of control and prevention strategies for other pathogens relevant to public health policy considerations

Foundations for Open Scholarship Strategy Development, Version 2.1 [Pre-print]

This document aims to agree on a broad, international strategy for the implementation of open scholarship that meets the needs of different national and regional communities but works globally. Scholarly research can be idealised as an inspirational process for advancing our collective knowledge to the benefit of all humankind. However, current research practices often struggle with a range of tensions, in part due to the fact that this collective (or “commons”) ideal conflicts with the competitive system in which most scholars work, and in part because much of the infrastructure of the scholarly world is becoming largely digital. What is broadly termed as Open Scholarship is an attempt to realign modern research practices with this ideal. We do not propose a definition of Open Scholarship, but recognise that it is a holistic term that encompasses many disciplines, practices, and principles, sometimes also referred to as Open Science or Open Research. We choose the term Open Scholarship to be more inclusive of these other terms. When we refer to science in this document, we do so historically and use it as shorthand for more general scholarship. The purpose of this document is to provide a concise analysis of where the global Open Scholarship movement currently stands: what the common threads and strengths are, where the greatest opportunities and challenges lie, and how we can more effectively work together as a global community to recognise and address the top strategic priorities. This document was inspired by the Foundations for OER Strategy Development and work in the FORCE11 Scholarly Commons Working Group, and developed by an open contribution working group. Our hope is that this document will serve as a foundational resource for continuing discussions and initiatives about implementing effective strategies to help streamline the integration of Open Scholarship practices into a modern, digital research culture. Through this, we hope to extend the reach and impact of Open Scholarship into a global context, making sure that it is truly open for all. We also hope that this document will evolve as the conversations around Open Scholarship progress, and help to provide useful insight for both global co-ordination and local action. We believe this is a step forward in making Open Scholarship the norm. Ultimately, we expect the impact of widespread adoption of Open Scholarship to be diverse. We expect novel research practices to accelerate the pace of innovation, and therefore stimulate critical industries around the world. We could also expect to see an increase in public trust of science and scholarship, as transparency becomes more normative. As such, we expect interest in Open Scholarship to increase at multiple levels, due to its inherent influence on society and global economics

Boon, bias or bane? The potential influence of reviewer recommendations on editorial decision-making

No formal investigations have been conducted into the efficacy or potential influence of reviewer recommendations on editorial decisions, and the impact of this on the expectations and behaviour of authors, reviewers and journal editors. This article addresses key questions about this critical aspect of the peer review submission process. We suggest several future steps which could be taken towards improving the review process and make it more transparent, better understood, and fairer for all parties

A ‘Strategy-as-Practice’ exploration of lean construction strategizing

This article was published in the journal, Building Research and Information [© Taylor & Francis (Routledge)] and the definitive version is available at: http://dx.doi.org/10.1080/09613218.2012.655925A growing body of work emerging from the management and organizational studies literature is the ‘Strategy-as-Practice’ (SaP) perspective, which focuses on the ways in which strategy is actually enacted within organizational settings. This perspective is used to examine the diffusion of lean construction. In recent years lean construction has grown in prominence to become one of the primary performative improvement recipes for the construction sector. However, rather than providing a stable strategy around which more collaborative, intelligent and efficient project-based organizations develop, this research reveals how the lean concept transforms during its journey with unintended organizational consequences. An ethnographic case study, informed by SaP, demonstrates how a lean strategy and its effects on organizational practice and culture cannot be understood separately from material and embodied practices and power effects. As well as contributing to the examination of lean construction practice, the findings show how strategy is enacted within construction organizations and the ensuing effects of social power. A new trajectory is opened for research into strategizing within construction organizations, which provides ways to explore actual practices and spaces where strategizing occurs

Glucose utilization via glycogen phosphorylase sustains proliferation and prevents premature senescence in cancer cells.

Metabolic reprogramming of cancer cells provides energy and multiple intermediates critical for cell growth. Hypoxia in tumors represents a hostile environment that can encourage these transformations. We report that glycogen metabolism is upregulated in tumors in vivo and in cancer cells in vitro in response to hypoxia. In vitro, hypoxia induced an early accumulation of glycogen, followed by a gradual decline. Concordantly, glycogen synthase (GYS1) showed a rapid induction, followed by a later increase of glycogen phosphorylase (PYGL). PYGL depletion and the consequent glycogen accumulation led to increased reactive oxygen species (ROS) levels that contributed to a p53-dependent induction of senescence and markedly impaired tumorigenesis in vivo. Metabolic analyses indicated that glycogen degradation by PYGL is important for the optimal function of the pentose phosphate pathway. Thus, glycogen metabolism is a key pathway induced by hypoxia, necessary for optimal glucose utilization, which represents a targetable mechanism of metabolic adaptation

Metabolic Profiling of Hypoxic Cells Revealed a Catabolic Signature Required for Cell Survival

Hypoxia is one of the features of poorly vascularised areas of solid tumours but cancer cells can survive in these areas despite the low oxygen tension. The adaptation to hypoxia requires both biochemical and genetic responses that culminate in a metabolic rearrangement to counter-balance the decrease in energy supply from mitochondrial respiration. The understanding of metabolic adaptations under hypoxia could reveal novel pathways that, if targeted, would lead to specific death of hypoxic regions. In this study, we developed biochemical and metabolomic analyses to assess the effects of hypoxia on cellular metabolism of HCT116 cancer cell line. We utilized an oxygen fluorescent probe in anaerobic cuvettes to study oxygen consumption rates under hypoxic conditions without the need to re-oxygenate the cells and demonstrated that hypoxic cells can maintain active, though diminished, oxidative phosphorylation even at 1% oxygen. These results were further supported by in situ microscopy analysis of mitochondrial NADH oxidation under hypoxia. We then used metabolomic methodologies, utilizing liquid chromatography–mass spectrometry (LC-MS), to determine the metabolic profile of hypoxic cells. This approach revealed the importance of synchronized and regulated catabolism as a mechanism of adaptation to bioenergetic stress. We then confirmed the presence of autophagy under hypoxic conditions and demonstrated that the inhibition of this catabolic process dramatically reduced the ATP levels in hypoxic cells and stimulated hypoxia-induced cell death. These results suggest that under hypoxia, autophagy is required to support ATP production, in addition to glycolysis, and that the inhibition of autophagy might be used to selectively target hypoxic regions of tumours, the most notoriously resistant areas of solid tumours