Origin of Spin Incommensurability in Hole-doped S=1 Y2−xCaxBaNiO5\rm Y_{2-x}Ca_x Ba Ni O_5 Chains

Spin incommensurability has been recently experimentally discovered in the hole-doped Ni-oxide chain compound $\rm Y_{2-x}Ca_x Ba Ni O_5$ (G. Xu {\it al.}, Science {\bf 289}, 419 (2000)). Here a two orbital model for this material is studied using computational techniques. Spin IC is observed in a wide range of densities and couplings. The phenomenon originates in antiferromagnetic correlations ``across holes'' dynamically generated to improve hole movement, as it occurs in the one-dimensional Hubbard model and in recent studies of the two-dimensional extended t-J model. The close proximity of ferromagnetic and phase-separated states in parameter space are also discussed.Comment: RevTex, 4 pages, 4 figures (eps

Ferromagnetism in the Hubbard model with orbital degeneracy in infinite dimensions

We study the ferromagnetism due to orbital degeneracy in the Hubbard model in infinite dimensions. The model contains the intraorbital repulsion $U$, the interorbital repulsion $U^\prime$, the exchange $J$ (Hund coupling) and the pair hopping $J^\prime$, where all of them originate from the on-site Coulomb interaction. The ground state of the effective one-site problem was obtained by exact diagonalizations. At the 1/4-filling, we found two insulating phases; one is a ferromagnetic phase with alternating orbital order and the other is antiferromagnetic one with uniform orbital order. If electrons are doped into the 1/4-filling, the ferromagnetic phase still survives and becomes metallic, while the antiferromagnetic phase disappears. This result indicates that the double-exchange mechanism is relevant to stabilize metallic ferromagnetism in infinite dimensions.Comment: 4 pages, Revtex, 3 figures, corrected some typos and references, to be published in Phys. Rev. B (Rapid Communication

Ferromagnetism in the one-dimensional Hubbard model with orbital degeneracy: From low to high electron density

We studied ferromagnetism in the one-dimensional Hubbard model with doubly degenerate atomic orbitals by means of the density-matrix renormalization-group method and obtained the ground-state phase diagrams. It was found that ferromagnetism is stable from low to high (0< n < 1.75) electron density when the interactions are sufficiently strong. Quasi-long-range order of triplet superconductivity coexists with the ferromagnetic order for a strong Hund coupling region, where the inter-orbital interaction U'-J is attractive. At quarter-filling (n=1), the insulating ferromagnetic state appears accompanying orbital quasi-long-range order. For low densities (n<1), ferromagnetism occurs owing to the ferromagnetic exchange interaction caused by virtual hoppings of electrons, the same as in the quarter-filled system. This comes from separation of the charge and spin-orbital degrees of freedom in the strong coupling limit. This ferromagnetism is fragile against variation of band structure. For high densities (n>1), the phase diagram of the ferromagnetic phase is similar to that obtained in infinite dimensions. In this case, the double exchange mechanism is operative to stabilize the ferromagnetic order and this long-range order is robust against variation of the band-dispersion. A partially polarized state appears in the density region 1.68<n<1.75 and phase separation occurs for n just below the half-filling (n=2).Comment: 16 pages, 16 figures, final version, references adde

Comparative genomics of the niche-specific plant pathogen Streptomyces ipomoeae reveal novel genome content and organization

The sweet potato soil rot pathogen Streptomyces ipomoeae differs in disease pathology, host range, and virulence factor production from Streptomyces species that cause scab diseases on potato and other plant hosts. Nevertheless, previous phylogenomic analysis suggested S. ipomoeae and the oldest scab species, Streptomyces scabiei, are derived from a common ancestor. While genomes of scab pathogens have been described in some detail, similar knowledge of S. ipomoeae has been lacking. Here, we performed comparative genomic analyses involving both virulent and avirulent strains of S. ipomoeae, along with other plant-pathogenic and saprophytic Streptomyces spp. The txt gene cluster for the phytotoxin thaxtomin C was found in all virulent strains of S. ipomoeae, but, contrary to scab species, the thaxtomin locus does not appear to reside within a genomic island and has diverged from its scab pathogen counterparts. Increased TTA rare codon usage appears to be a hallmark of S. ipomoeae, and in particular, for its txt locus. The txtR activator gene, which we show here is essential for pathogenicity, appears to be subject to exceptional bldA translational control. Ortholog group searches identified genes found only in virulent S. ipomoeae strains in our analysis, and genome mining revealed secondary metabolite gene clusters of S. ipomoeae, which are not shared with scab species. Overall, we have identified novel aspects of genome organization and gene content consistent with niche development by S. ipomoeae, and the results here will facilitate the elucidation of the mechanisms governing its virulence and ecology

B→η(η′)K(π)B \to \eta(\eta') K(\pi) in the Standard Model with Flavor Symmetry

The observed branching ratios for $B\to K \eta'$ decays are much larger than factorization predictions in the Standard Model (SM). Many proposals have been made to reconcile the data and theoretical predictions. In this paper we study these decays within the SM using flavor U(3) symmetry. If small annihilation amplitudes are neglected, one needs 11 hadronic parameters to describe $B\to PP$ decays where $P$ can be one of the $\pi$, $K$, $\eta$ and $\eta'$ nonet mesons. We find that existing data are consistent with SM with flavor U(3) symmetry. We also predict several measurable branching ratios and CP asymmetries for $B \to K (\pi) \eta(\eta')$, $\eta(\eta')\eta(\eta')$ decays. Near future experiments can provide important tests for the Standard Model with flavor U(3) symmetry.Comment: 13 pages, 4 table

Metallic ferromagnetism: Progress in our understanding of an old strong-coupling problem

Metallic ferromagnetism is in general an intermediate to strong coupling phenomenon. Since there do not exist systematic analytic methods to investigate such types of problems, the microscopic origin of metallic ferromagnetism is still not sufficiently understood. However, during the last two or three years remarkable progress was made in this field: It is now certain that even in the one-band Hubbard model metallic ferromagnetism is stable in dimensions $d=1,$ 2, and $\infty$ on regular lattices and at intermediate values of the interaction $U$ and density $n$. In this paper the basic questions and recent insights regarding the microscopic conditions favoring metallic ferromagnetism in this model are reviewed. These findings are contrasted with the results for the orbitally degenerate case.Comment: 16 pages, 13 figures, latex using vieweg.sty (enclosed); typos corrected; to appear in "Advances in Solid State Physics", Vol. 3

Маркетинг навколишнього середовища

The photophysical properties of silicon semiconductor nanocrystals (SiNCs) are extremely sensitive to the presence of surface chemical defects, many of which are easily produced by oxidation under ambient conditions. The diversity of chemical structures of such defects and the lack of tools capable of probing individual defects continue to impede understanding of the roles of these defects in SiNC photophysics. We use scanning tunneling spectroscopy to study the impact of surface defects on the electronic structures of hydrogen-passivated SiNCs supported on the Au(111) surface. Spatial maps of the local electronic density of states (LDOS) produced by our measurements allowed us to identify locally enhanced defect-induced states as well as quantum-confined states delocalized throughout the SiNC volume. We use theoretical calculations to show that the LDOS spectra associated with the observed defects are attributable to Si-O-Si bridged oxygen or Si-OH surface defects

Lactate signalling regulates fungal β-glucan masking and immune evasion

AJPB: This work was supported by the European Research Council (STRIFE, ERC- 2009-AdG-249793), The UK Medical Research Council (MR/M026663/1), the UK Biotechnology and Biological Research Council (BB/K017365/1), the Wellcome Trust (080088; 097377). ERB: This work was supported by the UK Biotechnology and Biological Research Council (BB/M014525/1). GMA: Supported by the CNPq-Brazil (Science without Borders fellowship 202976/2014-9). GDB: Wellcome Trust (102705). CAM: This work was supported by the UK Medical Research Council (G0400284). DMM: This work was supported by UK National Centre for the Replacement, Refinement and Reduction of Animals in Research (NC/K000306/1). NARG/JW: Wellcome Trust (086827, 075470,101873) and Wellcome Trust Strategic Award in Medical Mycology and Fungal Immunology (097377). ALL: This work was supported by the MRC Centre for Medical Mycology and the University of Aberdeen (MR/N006364/1).Peer reviewedPostprin

Evolutionary Action of Mutations Reveals Antimicrobial Resistance Genes in Escherichia coli

Since antibiotic development lags, we search for potential drug targets through directed evolution experiments. A challenge is that many resistance genes hide in a noisy mutational background as mutator clones emerge in the adaptive population. Here, to overcome this noise, we quantify the impact of mutations through evolutionary action (EA). After sequencing ciprofloxacin or colistin resistance strains grown under different mutational regimes, we find that an elevated sum of the evolutionary action of mutations in a gene identifies known resistance drivers. This EA integration approach also suggests new antibiotic resistance genes which are then shown to provide a fitness advantage in competition experiments. Moreover, EA integration analysis of clinical and environmental isolates of antibiotic resistant of E. coli identifies gene drivers of resistance where a standard approach fails. Together these results inform the genetic basis of de novo colistin resistance and support the robust discovery of phenotype-driving genes via the evolutionary action of genetic perturbations in fitness landscapes