Performance and structure of single-mode bosonic codes

The early Gottesman, Kitaev, and Preskill (GKP) proposal for encoding a qubit in an oscillator has recently been followed by cat- and binomial-code proposals. Numerically optimized codes have also been proposed, and we introduce new codes of this type here. These codes have yet to be compared using the same error model; we provide such a comparison by determining the entanglement fidelity of all codes with respect to the bosonic pure-loss channel (i.e., photon loss) after the optimal recovery operation. We then compare achievable communication rates of the combined encoding-error-recovery channel by calculating the channel's hashing bound for each code. Cat and binomial codes perform similarly, with binomial codes outperforming cat codes at small loss rates. Despite not being designed to protect against the pure-loss channel, GKP codes significantly outperform all other codes for most values of the loss rate. We show that the performance of GKP and some binomial codes increases monotonically with increasing average photon number of the codes. In order to corroborate our numerical evidence of the cat/binomial/GKP order of performance occurring at small loss rates, we analytically evaluate the quantum error-correction conditions of those codes. For GKP codes, we find an essential singularity in the entanglement fidelity in the limit of vanishing loss rate. In addition to comparing the codes, we draw parallels between binomial codes and discrete-variable systems. First, we characterize one- and two-mode binomial as well as multi-qubit permutation-invariant codes in terms of spin-coherent states. Such a characterization allows us to introduce check operators and error-correction procedures for binomial codes. Second, we introduce a generalization of spin-coherent states, extending our characterization to qudit binomial codes and yielding a new multi-qudit code.Comment: 34 pages, 11 figures, 4 tables. v3: published version. See related talk at https://absuploads.aps.org/presentation.cfm?pid=1351

The Effect of Caffeic Acid Phenethyl Ester (CAPE) on H2O2-Induced Oxidative Stress in Cultured H9c2 Cells Compared to Common Antioxidants

Caffeic Acid Phenethyl Ester (CAPE) is a natural compound that has previously exhibited anti-proliferative, anti-inflammation and antioxidant activities. However, CAPE’s effects have not been fully elucidated in myoblasts under oxidative stress. We compared the effects of 24 hour pretreatment of CAPE to several known antioxidants (caffeic acid, vitamin C, and trolox) in H9c2 cells following oxidative injury by hydrogen peroxide (H2O2). H9c2 cells incubated with H2O2 treatment (100-700 μM, n=4) for 24 hours dose-dependently reduced cell viability (assessed by a cell counting assay). Compared to the reduction in viability from H2O2 500 μM treatment (22 ± 4%), H9c2 cell viability was significantly restored by pretreatment of CAPE (at 10 μM (100 ± 25%); 20 μM (112 ± 15%); 40 μM (109 ± 15%) n=5, p\u3c0.001) and Trolox (at 50 μM (83 ± 10%); 100 μM (89 ± 8%) n=4, p\u3c0.001). In contrast, pretreatment of H9c2 cells with caffeic acid (1-80 μM, n=3) and vitamin C (1000-10,000 μM, n=3) did not restore cell viability following H2O2-induced injury. CAPE’s mechanism was further investigated by measuring reactive oxygen species via a dichlorofluorescin diacetate assay and by evaluating heme oxygenase-1 (HO-1) expression via western blot. Increases in ROS caused by H2O2 500 μM (239 ± 30% of control, n=3) were significantly restored to control by pretreatment of CAPE dose-dependently (n=3, p\u3c0.001). Moreover, CAPE dose-dependently increased HO-1 expression (n=3). These results suggest CAPE can mitigate oxidative stress in H9c2 cells which may involve the induction of HO-1

Synergistic Effects of Methylglyoxal and Hyperglycemia on ROS Generation and the Viability of Cultured H9c2 Myoblast Cells

Heart damage in diabetics may be closely related to the possible synergistic cellular damage from hyperglycemia and increased methylglyoxal levels. This study investigated the effects of glucose and/or methylglyoxal and/or metformin on H9c2 reactive oxygen species (ROS) generation measured by a dichlorofluorescein diacetate (DCFDA) assay and cell viability measured by a cell counting kit-8 assay after various treatments for 24 hours. Glucose treatment (5 mM-40 mM) displayed similar cell viability (n=4) and ROS generation (n=7) when compared to control cells. By contrast, methylglyoxal (5 µM-1400 µM) decreased cell viability at higher concentration (1000 µM (51 ± 8%); 1200 µM (41 ± 5%); 1400 µM (36 ± 8%); all p\u3c0.05, n=5) compared to control cells, which was accompanied by significantly higher ROS generation (1000 µM (167 ± 27%); 1200 µM (204 ± 22%); 1400 µM (201 ± 15%); all p\u3c0.05, n=3). Furthermore, metformin (1 mM-40 mM) reduced methylglyoxal (1200 µM) induced ROS generation and cell death. When H9c2 cells were treated with glucose (25 mM or 40 mM) and different doses of methylglyoxal (600 µM -1400 µM), only higher glucose (40 mM) with different doses of methylglyoxal (600 µM -1400 µM) consistently showed lower cell viability and higher ROS when compared to individual glucose or methylglyoxal. The data suggest that higher concentrations of methylglyoxal, not glucose, induces H9c2 cell damage and metformin can protect cells from the methylglyoxal insult possibly by reduction of ROS production. Moreover, hyperglycemia and methylglyoxal tend to synergistically induce cell damage associated with increased ROS production

High permeability explains the vulnerability of the carbon store in drained tropical peatlands

Tropical peatlands are an important global carbon (C) store but are threatened by drainage for palm oil and wood pulp production. The store's stability depends on the dynamics of the peatland water table, which in turn depend on peat permeability. We found that an example of the most abundant type of tropical peatland—ombrotrophic domes—has an unexpectedly high permeability similar to that of gravel. Using computer simulations of a natural peat dome (NPD) and a ditch-drained peat dome (DPD) we explored how such high permeability affects water tables and peat decay. High permeability has little effect on NPD water tables because of low hydraulic gradients from the center to the margin of the peatland. In contrast, DPD water tables are consistently deep, leaving the upper meter of peat exposed to rapid decay. Our results reveal why ditch drainage precipitates a rapid destabilization of the tropical peatland C store

HDAC-mediated control of ERK- and PI3K-dependent TGF-β-induced extracellular matrix-regulating genes

Histone deacetylases (HDACs) regulate the acetylation of histones in the control of gene expression. Many non-histone proteins are also targeted for acetylation, including TGF-ß signalling pathway components such as Smad2, Smad3 and Smad7. Our studies in mouse C3H10T1/2 fibroblasts suggested that a number of TGF-ß-induced genes that regulate matrix turnover are selectively regulated by HDACs. Blockade of HDAC activity with trichostatin A (TSA) abrogated the induction of a disintegrin and metalloproteinase 12 (Adam12) and tissue inhibitor of metalloproteinases-1 (Timp-1) genes by TGF-ß, whereas plasminogen activator inhibitor-1 (Pai-1) expression was unaffected. Analysis of the activation of cell signalling pathways demonstrated that TGF-ß induced robust ERK and PI3K activation with delayed kinetics compared to the phosphorylation of Smads. The TGF-ß induction of Adam12 and Timp-1 was dependent on such non-Smad signalling pathways and, importantly, HDAC inhibitors completely blocked their activation without affecting Smad signalling. Analysis of TGF-ß-induced Adam12 and Timp-1 expression and ERK/PI3K signalling in the presence of semi-selective HDAC inhibitors valproic acid, MS-275 and apicidin implicated a role for class I HDACs. Furthermore, depletion of HDAC3 by RNA interference significantly down-regulated TGF-ß-induced Adam12 and Timp-1 expression without modulating Pai-1 expression. Correlating with the effect of HDAC inhibitors, depletion of HDAC3 also blocked the activation of ERK and PI3K by TGF-ß. Collectively, these data confirm that HDACs, and in particular HDAC3, are required for activation of the ERK and PI3K signalling pathways by TGF-ß and for the subsequent gene induction dependent on these signalling pathways

Observing Dynamical Phases of a Bardeen-Cooper-Schrieffer Superconductor in a Cavity QED Simulator

In conventional Bardeen-Cooper-Schrieffer (BCS) superconductors, electrons with opposite momenta bind into Cooper pairs due to an attractive interaction mediated by phonons in the material. While superconductivity naturally emerges at thermal equilibrium, it can also emerge out of equilibrium when the system's parameters are abruptly changed. The resulting out-of-equilibrium phases are predicted to occur in real materials and ultracold fermionic atoms but have not yet been directly observed. This work realizes an alternate way to generate the proposed dynamical phases using cavity quantum electrodynamics (cavity QED). Our system encodes the presence or absence of a Cooper pair in a long-lived electronic transition in $^{88}$Sr atoms coupled to an optical cavity and represents interactions between electrons as photon-mediated interactions through the cavity. To fully explore the phase diagram, we manipulate the ratio between the single-particle dispersion and the interactions after a quench and perform real-time tracking of subsequent dynamics of the superconducting order parameter using non-destructive measurements. We observe regimes where the order parameter decays to zero ("phase I"), assumes a non-equilibrium steady-state value ("phase II"), or exhibits persistent oscillations ("phase III") in the form of a self-generated Floquet phase. The capability to emulate these dynamical phases in optical cavities without real Cooper pairs demonstrates that programmable simulators can overcome many challenges faced by traditional approaches. This opens up exciting prospects for quantum simulation, including the potential to engineer unconventional superconductors and to probe beyond mean-field effects like the spectral form factor, and for increasing coherence time for quantum sensing.Comment: Main Text with Supporting Material, 18 pages, 10 figure