Generalized effective hamiltonian for graphene under non-uniform strain

We use a symmetry approach to construct a systematic derivative expansion of the low energy effective Hamiltonian modifying the continuum Dirac description of graphene in the presence of non-uniform elastic deformations. We extract all experimentally relevant terms and describe their physical significance. Among them there is a new gap-opening term that describes the Zeeman coupling of the elastic pseudomagnetic field and the pseudospin. We determine the value of the couplings using a generalized tight binding model.Comment: 13 pages, 1 figure. Matches published version + 1 footnote added, typos correcte

Reduction in vitro of the minor Fusarium mycotoxin beauvericin employing different strains of probiotic bacteria

The interaction between the minor Fusarium mycotoxins BEA and 13 bacterial strains characteristic of the gastrointestinal tract as Bifidobacterium longum, Bifidobacterium bifidum, Bifidobacterium breve, Bifidobacterium adolescentes, Lactobacillus rhamnosus, Lactobacillus casei-casei, Lactobacillus plantarum, Eubacterium crispatus, Salmonella fecalis, Salmonella termofilus, Lactobacillus ruminis, Lactobacillus casei and Lactobacillus animalis was studied. The fermentations were carried out in the liquid medium of MRS during 4, 12, 16, 24 and 48 h at 37 C, under anaerobic conditions. Levels of BEA in the fermentation liquid, on the cell walls and on the internal part of the cells were determined using liquid chromatography coupled to the mass spectrometry detector (LC-MS/MS). Results showed that the bacteria reduced the concentration of the BEA present in the medium, part of the mycotoxin was adsorbed by cell wall and part internalized by the bacteria. All the bacteria analyzed in this study showed a significant BEA reduction during the fermentation process, in particular the mean diminution resulted variable from 66 to the 83%

Existence and topological stability of Fermi points in multilayered graphene

We study the existence and topological stability of Fermi points in a graphene layer and stacks with many layers. We show that the discrete symmetries (spacetime inversion) stabilize the Fermi points in monolayer, bilayer and multilayer graphene with orthorhombic stacking. The bands near $k=0$ and $\epsilon=0$ in multilayers with the Bernal stacking depend on the parity of the number of layers, and Fermi points are unstable when the number of layers is odd. The low energy changes in the electronic structure induced by commensurate perturbations which mix the two Dirac points are also investigated.Comment: 6 pages, 6 figures. Expanded version as will appear in PR

Effective theory for the Goldstone field in the BCS-BEC crossover at T=0

We perform a detailed study of the effective Lagrangian for the Goldstone mode of a superfluid Fermi gas at zero temperature in the whole BCS-BEC crossover. By using a derivative expansion of the response functions, we derive the most general form of this Lagrangian at the next to leading order in the momentum expansion in terms of four coefficient functions. This involves the elimination of all the higher order time derivatives by careful use of the leading order field equations. In the infinite scattering length limit where conformal invariance is realized, we show that the effective Lagrangian must contain an unnoticed invariant combination of higher spatial gradients of the Goldstone mode, while explicit couplings to spatial gradients of the trapping potential are absent. Across the whole crossover, we determine all the coefficient functions at the one-loop level, taking into account the dependence of the gap parameter on the chemical potential in the mean-field approximation. These results are analytically expressed in terms of elliptic integrals of the first and second kind. We discuss the form of these coefficients in the extreme BCS and BEC regimes and around the unitary limit, and compare with recent work by other authors.Comment: 27 pages. 4 references added, typos corrected, expanded Section III

Type I phosphatidylinositol 4-phosphate 5-kinase controls neutrophil polarity and directional movement

Directional cell movement in response to external chemical gradients requires establishment of front–rear asymmetry, which distinguishes an up-gradient protrusive leading edge, where Rac-induced F-actin polymerization takes place, and a down-gradient retractile tail (uropod in leukocytes), where RhoA-mediated actomyosin contraction occurs. The signals that govern this spatial and functional asymmetry are not entirely understood. We show that the human type I phosphatidylinositol 4-phosphate 5-kinase isoform β (PIPKIβ) has a role in organizing signaling at the cell rear. We found that PIPKIβ polarized at the uropod of neutrophil-differentiated HL60 cells. PIPKIβ localization was independent of its lipid kinase activity, but required the 83 C-terminal amino acids, which are not homologous to other PIPKI isoforms. The PIPKIβ C terminus interacted with EBP50 (4.1-ezrin-radixin-moesin (ERM)-binding phosphoprotein 50), which enabled further interactions with ERM proteins and the Rho-GDP dissociation inhibitor (RhoGDI). Knockdown of PIPKIβ with siRNA inhibited cell polarization and impaired cell directionality during dHL60 chemotaxis, suggesting a role for PIPKIβ in these processes

Dynamic redistribution of raft domains as an organizing platform for signaling during cell chemotaxis

Spatially restricted activation of signaling molecules governs critical aspects of cell migration; the mechanism by which this is achieved nonetheless remains unknown. Using time-lapse confocal microscopy, we analyzed dynamic redistribution of lipid rafts in chemoattractant-stimulated leukocytes expressing glycosyl phosphatidylinositol–anchored green fluorescent protein (GFP-GPI). Chemoattractants induced persistent GFP-GPI redistribution to the leading edge raft (L raft) and uropod rafts of Jurkat, HL60, and dimethyl sulfoxide–differentiated HL60 cells in a pertussis toxin–sensitive, actin-dependent manner. A transmembrane, nonraft GFP protein was distributed homogeneously in moving cells. A GFP-CCR5 chimera, which partitions in L rafts, accumulated at the leading edge, and CCR5 redistribution coincided with recruitment and activation of phosphatidylinositol-3 kinase γ in L rafts in polarized, moving cells. Membrane cholesterol depletion impeded raft redistribution and asymmetric recruitment of PI3K to the cell side facing the chemoattractant source. This is the first direct evidence that lipid rafts order spatial signaling in moving mammalian cells, by concentrating the gradient sensing machinery at the leading edge

Bardeen-Anomaly and Wess-Zumino Term in the Supersymmetric Standard Model

We construct the Bardeen anomaly and its related Wess-Zumino term in the supersymmetric standard model. In particular we show that it can be written in terms of a composite linear superfield related to supersymmetrized Chern-Simons forms, in very much the same way as the Green-Schwarz term in four-dimensional string theory. Some physical applications, such as the contribution to the g-2 of gauginos when a heavy top is integrated out, are briefly discussed.Comment: 21 pages, (plain TeX), CERN.TH-6845/93, DFPD 93/TH/32, UCLA/93/TEP/13, NYU-TH-93/10/01, ENSLAPP-A442/9

Blocking of HIV-1 Infection by Targeting CD4 to Nonraft Membrane Domains

Human immunodeficiency virus (HIV)-1 infection depends on multiple lateral interactions between the viral envelope and host cell receptors. Previous studies have suggested that these interactions are possible because HIV-1 receptors CD4, CXCR4, and CCR5 partition in cholesterol-enriched membrane raft domains. We generated CD4 partitioning mutants by substituting or deleting CD4 transmembrane and cytoplasmic domains and the CD4 ectodomain was unaltered. We report that all CD4 mutants that retain raft partitioning mediate HIV-1 entry and CD4-induced Lck activation independently of their transmembrane and cytoplasmic domains. Conversely, CD4 ectodomain targeting to a nonraft membrane fraction results in a CD4 receptor with severely diminished capacity to mediate Lck activation or HIV-1 entry, although this mutant binds gp120 as well as CD4wt. In addition, the nonraft CD4 mutant inhibits HIV-1 X4 and R5 entry in a CD4+ cell line. These results not only indicate that HIV-1 exploits host membrane raft domains as cell entry sites, but also suggest new strategies for preventing HIV-1 infection