SU(2) Cosmological Solitons

We present a class of numerical solutions to the SU(2) nonlinear $\sigma$-model coupled to the Einstein equations with cosmological constant $\Lambda\geq 0$ in spherical symmetry. These solutions are characterized by the presence of a regular static region which includes a center of symmetry. They are parameterized by a dimensionless ``coupling constant'' $\beta$, the sign of the cosmological constant, and an integer ``excitation number'' $n$. The phenomenology we find is compared to the corresponding solutions found for the Einstein-Yang-Mills (EYM) equations with positive $\Lambda$ (EYM$\Lambda$). If we choose $\Lambda$ positive and fix $n$, we find a family of static spacetimes with a Killing horizon for $0 \leq \beta < \beta_{max}$. As a limiting solution for $\beta = \beta_{max}$ we find a {\em globally} static spacetime with $\Lambda=0$, the lowest excitation being the Einstein static universe. To interpret the physical significance of the Killing horizon in the cosmological context, we apply the concept of a trapping horizon as formulated by Hayward. For small values of $\beta$ an asymptotically de Sitter dynamic region contains the static region within a Killing horizon of cosmological type. For strong coupling the static region contains an ``eternal cosmological black hole''.Comment: 20 pages, 6 figures, Revte

Sign problems, noise, and chiral symmetry breaking in a QCD-like theory

The Nambu-Jona-Lasinio model reduced to 2+1 dimensions has two different path integral formulations: at finite chemical potential one formulation has a severe sign problem similar to that found in QCD, while the other does not. At large N, where N is the number of flavors, one can compute the probability distributions of fermion correlators analytically in both formulations. In the former case one finds a broad distribution with small mean; in the latter one finds a heavy tailed positive distribution amenable to the cumulant expansion techniques developed in earlier work. We speculate on the implications of this model for QCD.Comment: 16 pages, 5 figures; Published version with minor changes from the origina

A new basis for Hamiltonian SU(2) simulations

Due to rapidly improving quantum computing hardware, Hamiltonian simulations of relativistic lattice field theories have seen a resurgence of attention. This computational tool requires turning the formally infinite-dimensional Hilbert space of the full theory into a finite-dimensional one. For gauge theories, a widely-used basis for the Hilbert space relies on the representations induced by the underlying gauge group, with a truncation that keeps only a set of the lowest dimensional representations. This works well at large bare gauge coupling, but becomes less efficient at small coupling, which is required for the continuum limit of the lattice theory. In this work, we develop a new basis suitable for the simulation of an SU(2) lattice gauge theory in the maximal tree gauge. In particular, we show how to perform a Hamiltonian truncation so that the eigenvalues of both the magnetic and electric gauge-fixed Hamiltonian are mostly preserved, which allows for this basis to be used at all values of the coupling. Little prior knowledge is assumed, so this may also be used as an introduction to the subject of Hamiltonian formulations of lattice gauge theories.Comment: 27 pages, 11 figure

Aligning Values for Rural Tourism: Tourism on the Solway Coast

Cumbria's Solway coast is 'on the edge' of a number of phenomena: the sea, Cumbria, England, the Lake District and commercial viability as a tourist area. The presentation describes how many of its stakeholders have common goals which can be served by tourism, but so far it has not proved possible to unite these and improve the tourism offer and the popularity of the area

Overcoming exponential volume scaling in quantum simulations of lattice gauge theories

Real-time evolution of quantum field theories using classical computers requires resources that scale exponentially with the number of lattice sites. Because of a fundamentally different computational strategy, quantum computers can in principle be used to perform detailed studies of these dynamics from first principles. Before performing such calculations, it is important to ensure that the quantum algorithms used do not have a cost that scales exponentially with the volume. In these proceedings, we present an interesting test case: a formulation of a compact U(1) gauge theory in 2+1 dimensions free of gauge redundancies. A naive implementation onto a quantum circuit has a gate count that scales exponentially with the volume. We discuss how to break this exponential scaling by performing an operator redefinition that reduces the non-locality of the Hamiltonian. While we study only one theory as a test case, it is possible that the exponential gate scaling will persist for formulations of other gauge theories, including non-Abelian theories in higher dimensions.Comment: 11 pages, 2 figures, Proceedings of the 39th Annual International Symposium on Lattice Field Theory (Lattice 2022), August 8-13 2022, Bonn, German

Amoebozoa possess lineage-specific globin gene repertoires gained by individual horizontal gene transfers

The Amoebozoa represent a clade of unicellular amoeboid organisms that display a wide variety of lifestyles, including free-living and parasitic species. For example, the social amoeba Dictyostelium discoideum has the ability to aggregate into a multicellular fruiting body upon starvation, while the pathogenic amoeba Entamoeba histolytica is a parasite of humans. Globins are small heme proteins that are present in almost all extant organisms. Although several genomes of amoebozoan species have been sequenced, little is known about the phyletic distribution of globin genes within this phylum. Only two flavohemoglobins (FHbs) of D. discoideum have been reported and characterized previously while the genomes of Entamoeba species are apparently devoid of globin genes. We investigated eleven amoebozoan species for the presence of globin genes by genomic and phylogenetic in silico analyses. Additional FHb genes were identified in the genomes of four social amoebas and the true slime mold Physarum polycephalum. Moreover, a single-domain globin (SDFgb) of Hartmannella vermiformis, as well as two truncated hemoglobins (trHbs) of Acanthamoeba castellanii were identified. Phylogenetic evidence suggests that these globin genes were independently acquired via horizontal gene transfer from some ancestral bacteria. Furthermore, the phylogenetic tree of amoebozoan FHbs indicates that they do not share a common ancestry and that a transfer of FHbs from bacteria to amoeba occurred multiple times

Selection of mutants with resistance or diminished susceptibility to ceftazidime/avibactam from ESBL- and AmpC- producing Enterobacteriaceae

Introduction: Difficult Gram-negative infections are increasingly treated with new β-lactamase inhibitor combinations, e.g. ceftazidime/avibactam. Disturbingly, mutations in KPC carbapenemases can confer ceftazidime/avibactam resistance, which is sometimes selected during therapy. We explored whether this risk extended to AmpC and ESBL enzymes. Methods: Mutants were selected by plating AmpC-derepressed strains, ESBL producers and ceftazidime-susceptible controls on agar containing ceftazidime + avibactam (1 or 4 mg/L). MICs were determined by CLSI agar dilution; WGS was by Illumina methodology. Results: Using 2× MIC of ceftazidime + 1 mg/L avibactam, mutants were selected from all strain types at frequencies of 10−7–10−9. Rates diminished to <10−9 with 4 mg/L avibactam or higher MIC multiples, except with AmpC-derepressed Enterobacteriaceae. Characterized mutants (n = 10; MICs 4–64 mg/L) of AmpC-derepressed strains had modifications in ampC, variously giving Arg168Pro/His, Gly176Arg/Asp, Asn366Tyr or small deletions around positions 309–314. Mutants of ESBL producers (n = 19; MICs 0.5–16 mg/L) mostly had changes affecting permeability, efflux or β-lactamase quantity; only one had an altered β-lactamase, with an Asp182Tyr substitution in CTX-M-15, raising the ceftazidime/avibactam MIC, but abrogating other cephalosporin resistance. Mutants of ceftazidime-susceptible strains were not sequenced, but phenotypes suggested altered drug accumulation or, for Enterobacter cloacae only, AmpC derepression. In further experiments, avibactam reduced, but did not abolish, selection of AmpC-derepressed Enterobacteriaceae by ceftazidime. Conclusions: Most mutants of AmpC-derepressed Enterobacteriaceae had structural mutations in ampC; those of ESBL producers mostly had genetic modifications outside β-lactamase genes, commonly affecting uptake, efflux, or β-lactamase quantity. The clinical significance of these observations remains to be determined

AmpC β-lactamase induction by avibactam and relebactam

Background: Diazabicyclooctanes, e.g. avibactam and relebactam, are a new class of β-lactamase inhibitors. Their spectrum includes AmpC enzymes, but it is important to understand whether they also induce these enzymes.  Methods: Levels of ampC mRNA were measured by RT–PCR during 4 h of exposure of Enterobacter cloacae, Citrobacter freundii and Pseudomonas aeruginosa (n = 5 strains per species) to avibactam, relebactam and cefoxitin at 0, 1, 4 and 32 mg/L. The method had low precision compared with conventional specific-activity-based induction assays, which are impracticable for inhibitors. Accordingly, induction was only considered to be significant if induction ratios >10 were found at two consecutive time intervals, with ‘strong induction’ if one or more of these ratios was >100.  Results: Cefoxitin, as expected, gave concentration-dependent induction for all strains, with strong induction for 13/15. At the other extreme, relebactam caused no significant induction for any strain. Avibactam gave strain-variable results, with strong concentration-dependent induction for 2/5 E. cloacae and 2/5 P. aeruginosa, but little or no induction for the other strains, including all the C. freundii strains.  Conclusions: Avibactam, but not relebactam, had some strain-variable ability to induce AmpC enzymes, though at concentrations (32 mg/L) above those reached in the patient