Superconductivity in the Hubbard model with correlated hopping: Slave-boson study

The slave boson mean-field studies of the ground state of the Hubbard model with correlated hopping were performed. The approach qualitatively recovers the exact results for the case of the hopping integral t equal to the correlated hopping integral X. The phase diagram for the strongly correlated state with only singly occupied sites, the weakly correlated state, where single and double occupation is allowed, and for the superconducting state, was determined for any values of X and any electron concentration n. At the half-filled band (n=1) a direct transition from the superconductor to the Mott insulator was found. In the region of strong correlations the superconducting solution is stable for n close to 1, in contrast to the case of weak correlations, in which superconductivity occurs at n close to 0 and n close to 2. We found also that strong correlations change characteristics of the superconducting phase, e.g. the gap in the excitation spectrum has a nonexponential dependence close to the point of the phase transition.Comment: 13 pages, 24 Postscript figures (in 12 files

Phase Diagram of the Extended Hubbard Model with Correlated Hopping Interaction

A one-dimensional model of interacting electrons with on-site $U$, nearest-neighbor $V$, and correlated-hopping interaction $T^{\ast}$ is studied at half-filling using the continuum-limit field theory approach. The ground state phase diagram is obtained for a wide range of coupling constants. In addition to the insulating spin- and charge-density wave phases for large $U$ and $V$, respectively, we identify bond-located ordered phases corresponding to an enhanced Peierls instability in the system for $T^\ast>0$, $|U-2V|<8T^\ast/\pi$ and to a staggered magnetization located on bonds between sites for $T^\ast<0$, $|U-2V|<8|T^\ast|/\pi$. The general ground state phase diagram including insulating, metallic, and superconducting phases is discussed.Comment: 8 pages, 4 eps-figure

Organised Genome Dynamics in the Escherichia coli Species Results in Highly Diverse Adaptive Paths

The Escherichia coli species represents one of the best-studied model organisms, but also encompasses a variety of commensal and pathogenic strains that diversify by high rates of genetic change. We uniformly (re-) annotated the genomes of 20 commensal and pathogenic E. coli strains and one strain of E. fergusonii (the closest E. coli related species), including seven that we sequenced to completion. Within the ∼18,000 families of orthologous genes, we found ∼2,000 common to all strains. Although recombination rates are much higher than mutation rates, we show, both theoretically and using phylogenetic inference, that this does not obscure the phylogenetic signal, which places the B2 phylogenetic group and one group D strain at the basal position. Based on this phylogeny, we inferred past evolutionary events of gain and loss of genes, identifying functional classes under opposite selection pressures. We found an important adaptive role for metabolism diversification within group B2 and Shigella strains, but identified few or no extraintestinal virulence-specific genes, which could render difficult the development of a vaccine against extraintestinal infections. Genome flux in E. coli is confined to a small number of conserved positions in the chromosome, which most often are not associated with integrases or tRNA genes. Core genes flanking some of these regions show higher rates of recombination, suggesting that a gene, once acquired by a strain, spreads within the species by homologous recombination at the flanking genes. Finally, the genome's long-scale structure of recombination indicates lower recombination rates, but not higher mutation rates, at the terminus of replication. The ensuing effect of background selection and biased gene conversion may thus explain why this region is A+T-rich and shows high sequence divergence but low sequence polymorphism. Overall, despite a very high gene flow, genes co-exist in an organised genome

Etude de l'altération du vieillissement de C. elegans par sa flore intestinale

Aging theory holds that populations exposed to higher environmentally imposed mortality evolve faster aging. It has been postulated that the presence of parasites causing high extrinsic mortality may trigger an inducible acceleration of host aging. I tested this hypothesis in a detailed and systematic investigation of how the aging patterns of genetically identical Caenorhabditis elegans can be altered by human opportunistic pathogen or innocuous strains of Escherichia coli. My results suggest that pathogenic bacteria trigger a re-allocation of resources from body maintenance to reproduction and antimicrobial defense, causing faster accumulation of damage and thus faster aging. I also observed that mortality increased at a slower rate in old worms, a phenomenon known as mortality deceleration. I formulated a mathematical model explaining why the deceleration of mortality occurred earlier and at higher levels of mortality when the worms were grown in contact with more virulent bacteria.La théorie du vieillissement soutient que les populations exposées à une mortalité extrinsèque élevée évoluent à vieillir plus vite. Il a été postulé que la présence de parasites peut induire une accélération du vieillissement de l'hôte. J'ai testé cette hypothèse en étudiant comment les profils de vieillissement des Caenorhabditis elegans génétiquement identiques peuvent être changés par des souches d'Escherichia coli de pathogénicité variable. Mes résultats suggèrent que les bactéries pathogènes déclenchent une re-allocation des ressources de l'entretien à la reproduction et à la défense antimicrobienne, entraînant une accumulation de dommages plus rapide et donc un vieillissement plus rapide. J'ai également observé une décélération de mortalité dans de vieux vers. J'ai formulé un modèle mathématique expliquant pourquoi la décélération de la mortalité s'esl produite plus tôt et à des niveaux de mortalité plus élevés pour des vers en contact avec des bactéries plus virulentes.PARIS5-BU Méd.Cochin (751142101) / SudocSudocFranceF

Novel inhibitors of the enzyme activated factor xii (fxiia)

The present invention relates to a bicyclic inhibitor of the coagulation enzyme activated factor XII (FXIIa) comprising or consisting of the peptide (X1)(X2)(X3)n(X4)(X5)(X6)m(X7)(X9)l(X10)(X11)(X12)(X13)(X14)k(X15)(X16), wherein (X1) is present or absent and, if present, is an amino acid; (X2) is an amino acid with a side chain; (X3) is an amino acid and n is between 0 and 3, preferably 0 or 1 and most preferably 0; (X4) is an aliphatic L-amino acid or a cyclic L- amino acid, preferably L, P or an aromatic L-amino acid, and most preferably an aromatic L-amino acid; (X5) is an amino acid; (X6) is an amino acid and m is between 0 and 3, preferably 0 or 1 and most preferably 0; (X7) is an amino acid with a side chain; (X9) is an amino acid and I is between 0 and 3, preferably 0 or 1 and most preferably 0; (X10) is an amino acid; (X11) is an amino acid, preferably Q; (X12) is a hydrophobic L-amino acid, preferably an aliphatic L-amino acid, and is most preferably L; (X13) is an amino acid; (X14) is an amino acid and k is between 0 and 3, preferably 0 or 1 and most preferably 0, (X15) is an amino acid with a side chain; and (X18) is present or absent and, if present, is an amino acid; and wherein the side chains of (X2), (X7) and (X15) are connected via a connecting molecule, said connecting molecule having at least three functional groups, each functional group forming a covalent bond with one of the side chains of (X2), (X7) and (X15)

Modulation of aging profiles in isogenic populations of Caenorhabditis elegans by bacteria causing different extrinsic mortality rates

It has been postulated that the presence of parasites causing high extrinsic mortality may trigger an inducible acceleration of the host aging. We tested this hypothesis using isogenic populations of Caenorhabditis elegans nematodes and different Escherichia coli strains. When exposed to pathogenic bacteria, nematodes showed up to fourfold higher mortality rates, reproduced earlier, produced more H(2)O(2), and accumulated more autofluorescence, than when exposed to an innocuous strain. We also observed that mortality increased at a slower rate in old animals, a phenomenon known as mortality deceleration. Mortality deceleration started earlier in populations dying faster, likely as a consequence of lifelong heterogeneity between individual tendencies to die. Taken together, our results strongly suggest that the high extrinsic mortality imposed by the pathogens results in the modulation of nematodes' life-history traits, including aging and reproduction. This could be an adaptive response aiming at the maximization of Darwinian fitness

Caenorhabditis elegans as a simple model to study phenotypic and genetic virulence determinants of extraintestinal pathogenic Escherichia coli

Caenorhabditis elegans as a simple model to study phenotypic and genotypic determinants of pathogenicity of extraintestinal pathogenic Escherichia coli Virulence of extraintestinal pathogenic Escherichia coli strains in Caenorhabditis elegans Virulence of extraintestinal pathogenic Escherichia coli strains in Caenorhabditis elegans and mice Comparison of the virulence of extraintestinal pathogenic Escherichia coli in Caenorhabditis elegans and miceInternational audienceExtraintestinal pathogenic Escherichia coli (ExPEC) strains cause disease by invading normally sterile niches within the host body, e.g., urinary tract, blood and cerebrospinal fluid. Infections due to ExPEC strains, in particular urinary tract infections, cause considerable morbidity and significant health-care costs. The goal of our study is to evaluate whether Caenorhabditis elegans can be used as a model to study phenotypic and genetic virulence determinants of ExPEC strains. For this purpose, we used a collection of 31 E. coli strains isolated during acute extra-intestinal infections or from the feces of healthy individuals. For all strains, the phylogeny, the presence of ExPEC virulence factors, the resistance to biologically relevant stressors (bile, human serum and lysozyme), the motility, the growth rate, the virulence in C. elegans and in a murine septicaemia model has been established. The results show that there is a strong link between virulence in C. elegans and certain phenotypic and genetic virulence predictors of ExPEC strains determinable in vitro. Furthermore, there is a significant correlation between virulence of different ExPEC strains in C. elegans and in the murine model. Therefore, our results suggest that C. elegans can be used as a model to study virulence determinants of ExPEC strains

Stress-induced in vivo recruitment of human cytotoxic natural killer cells favors subsets with distinct receptor profiles and associates with increased epinephrine levels

Acute stress drives a 'high-alert' response in the immune system. Psychoactive drugs induce distinct stress hormone profiles, offering a sought-after opportunity to dissect the in vivo immunological effects of acute stress in humans. 3,4-methylenedioxymethamphetamine (MDMA), methylphenidate (MPH), or both, were administered to healthy volunteers in a randomized, double-blind, placebo-controlled crossover-study. Lymphocyte subset frequencies, natural killer (NK) cell immune-phenotypes, and changes in effector function were assessed, and linked to stress hormone levels and expression of CD62L, CX3CR1, CD18, and stress hormone receptors on NK cells. MDMA/MPH > MDMA > MPH robustly induced an epinephrine-dominant stress response. Immunologically, rapid redistribution of peripheral blood lymphocyte-subsets towards phenotypically mature NK cells occurred. NK cytotoxicity was unaltered, but they expressed slightly reduced levels of the activating receptor NKG2D. Preferential circulation of mature NK cells was associated with high epinephrine receptor expression among this subset, as well as expression of integrin ligands previously linked to epinephrine-induced endothelial detachment. The acute epinephrine-induced stress response was characterized by rapid accumulation of mature and functional NK cells in the peripheral circulation. This is in line with studies using other acute stressors and supports the role of the acute stress response in rapidly mobilizing the innate immune system to counteract incoming threats