Flavored Gauge-Mediation

The messengers of Gauge-Mediation Models can couple to standard-model matter fields through renormalizable superpotential couplings. These matter-messenger couplings generate generation-dependent sfermion masses and are therefore usually forbidden by discrete symmetries. However, the non-trivial structure of the standard-model Yukawa couplings hints at some underlying flavor theory, which would necessarily control the sizes of the matter-messenger couplings as well. Thus for example, if the doublet messenger and the Higgs have the same properties under the flavor theory, the resulting messenger-lepton couplings are parametrically of the same order as the lepton Yukawas, so that slepton mass-splittings are similar to those of minimally-flavor-violating models and therefore satisfy bounds on flavor-violation, with, however, slepton mixings that are potentially large. Assuming that fermion masses are explained by a flavor symmetry, we construct viable and natural models with messenger-lepton couplings controlled by the flavor symmetry. The resulting slepton spectra are unusual and interesting, with slepton mass-splittings and mixings that may be probed at the LHC. In particular, since the new contributions are typically negative, and since they are often larger for the first- and second-generation sleptons, some of these examples have the selectron or the smuon as the lightest slepton, with mass splittings of a few to tens of GeV.Comment: 16 pages v2: Explicit expressions (which are not needed in the analysis) for the pure Yukawa contributions removed. There was an error in some of these expressions in v1. References adde

Electron and hole g-factors and spin dynamics of negatively charged excitons in CdSe/CdS colloidal nanoplatelets with thick shells

We address spin properties and spin dynamics of carriers and charged excitons in CdSe/CdS colloidal nanoplatelets with thick shells. Magneto-optical studies are performed by time-resolved and polarization-resolved photoluminescence, spin-flip Raman scattering and picosecond pump-probe Faraday rotation in magnetic fields up to 30 T. We show that at low temperatures the nanoplatelets are negatively charged so that their photoluminescence is dominated by radiative recombination of negatively charged excitons (trions). Electron g-factor of 1.68 is measured and heavy-hole g-factor varying with increasing magnetic field from -0.4 to -0.7 is evaluated. Hole g-factors for two-dimensional structures are calculated for various hole confining potentials for cubic- and wurtzite lattice in CdSe core. These calculations are extended for various quantum dots and nanoplatelets based on II-VI semiconductors. We developed a magneto-optical technique for the quantitative evaluation of the nanoplatelets orientation in ensemble

Genetic Diversity and Virulence Potential of Shiga Toxin-Producing Escherichia coli O113:H21 Strains Isolated from Clinical, Environmental, and Food Sources

Shiga toxin-producing Escherichia coli strains of serotype O113:H21 have caused severe human diseases, but they are unusual in that they do not produce adherence factors coded by the locus of enterocyte effacement. Here, a PCR microarray was used to characterize 65 O113:H21 strains isolated from the environment, food, and clinical infections from various countries. in comparison to the pathogenic strains that were implicated in hemolytic-uremic syndrome in Australia, there were no clear differences between the pathogens and the environmental strains with respect to the 41 genetic markers tested. Furthermore, all of the strains carried only Shiga toxin subtypes associated with human infections, suggesting that the environmental strains have the potential to cause disease. Most of the O113:H21 strains were closely related and belonged in the same clonal group (ST-223), but CRISPR analysis showed a great degree of genetic diversity among the O113:H21 strains.French Joint Ministerial Program of R&D against CBRNE RisksFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Food & Drug Adm, Div Microbiol, College Pk, MD 20740 USAFrench Agcy Food Environm & Occupat Hlth & Safety, Lab Food Safety, Maisons Alfort, FranceFood & Drug Adm, Div Mol Biol, Laurel, MD USAUniversidade Federal de São Paulo, Dept Microbiol Immunol & Parasitol, São Paulo, BrazilFed Inst Risk Assessment, Natl Reference Lab Escherichia coli, Berlin, GermanyInst Nacl Enfermedades Infecciosas ANLIS Dr Carlo, Serv Fisiopatogenia, Buenos Aires, DF, ArgentinaUniv Melbourne, Peter Doherty Inst Infect & Immun, Dept Microbiol & Immunol, Melbourne, Vic, AustraliaUniv Adelaide, Res Ctr Infect Dis, Sch Mol & Biomed Sci, Adelaide, SA, AustraliaUniversidade Federal de São Paulo, Dept Microbiol Immunol & Parasitol, São Paulo, BrazilFrench Joint Ministerial Program of R&D against CBRNE Risks: C17609-2Web of Scienc

Numerical study of oscillatory regimes in the Kadomtsev-Petviashvili equation

The aim of this paper is the accurate numerical study of the KP equation. In particular we are concerned with the small dispersion limit of this model, where no comprehensive analytical description exists so far. To this end we first study a similar highly oscillatory regime for asymptotically small solutions, which can be described via the Davey-Stewartson system. In a second step we investigate numerically the small dispersion limit of the KP model in the case of large amplitudes. Similarities and differences to the much better studied Korteweg-de Vries situation are discussed as well as the dependence of the limit on the additional transverse coordinate.Comment: 39 pages, 36 figures (high resolution figures at http://www.mis.mpg.de/preprints/index.html

Electronic localization at mesoscopic length scales: different definitions of localization and contact effects in a heuristic DNA model

In this work we investigate the electronic transport along model DNA molecules using an effective tight-binding approach that includes the backbone on site energies. The localization length and participation number are examined as a function of system size, energy dependence, and the contact coupling between the leads and the DNA molecule. On one hand, the transition from an diffusive regime to a localized regime for short systems is identified, suggesting the necessity of a further length scale revealing the system borders sensibility. On the other hand, we show that the lenght localization and participation number, do not depended of system size and contact coupling in the thermodynamic limit. Finally we discuss possible length dependent origins for the large discrepancies among experimental results for the electronic transport in DNA sample

Dark Matter attempts for CoGeNT and DAMA

Recently, the CoGeNT collaboration presented a positive signal for an annual modulation in their data set. In light of the long standing annual modulation signal in DAMA/LIBRA, we analyze the compatibility of both of these signal within the hypothesis of dark matter (DM) scattering on nuclei, taking into account existing experimental constraints. We consider the cases of elastic and inelastic scattering with either spin-dependent or spin-independent coupling to nucleons. We allow for isospin violating interactions as well as for light mediators. We find that there is some tension between the size of the modulation signal and the time-integrated event excess in CoGeNT, making it difficult to explain both simultaneously. Moreover, within the wide range of DM interaction models considered, we do not find a simultaneous explanation of CoGeNT and DAMA/LIBRA compatible with constraints from other experiments. However, in certain cases part of the data can be made consistent. For example, the modulation signal from CoGeNT becomes consistent with the total rate and with limits from other DM searches at 90% CL (but not with the DAMA/LIBRA signal) if DM scattering is inelastic spin-independent with just the right couplings to protons and neutrons to reduce the scattering rate on xenon. Conversely the DAMA/LIBRA signal (but not CoGeNT) can be explained by spin-dependent inelastic DM scattering.Comment: 20 pages, 9 figure

Interdependency of EGF and GLP-2 Signaling in Attenuating Mucosal Atrophy in a Mouse Model of Parenteral Nutrition

BACKGROUND & AIMS: Total parenteral nutrition (TPN), a crucial treatment for patients who cannot receive enteral nutrition, is associated with mucosal atrophy, barrier dysfunction, and infectious complications. Glucagon-like peptide-2 (GLP-2) and epidermal growth factor (EGF) improve intestinal epithelial cell (IEC) responses and attenuate mucosal atrophy in several TPN models. However, it remains unclear whether these 2 factors use distinct or overlapping signaling pathways to improve IEC responses. We investigated the interaction of GLP-2 and EGF signaling in a mouse TPN model and in patients deprived of enteral nutrition. METHODS: Adult C57BL/6J, IEC-Egfrknock out (KO) and IEC-pik3r1KO mice receiving TPN or enteral nutrition were treated with EGF or GLP-2 alone or in combination with reciprocal receptor inhibitors, GLP-2(3-33) or gefitinib. Jejunum was collected and mucosal atrophy and IEC responses were assessed by histologic, gene, and protein expression analyses. In patients undergoing planned looped ileostomies, fed and unfed ileum was analyzed. RESULTS: Enteral nutrient deprivation reduced endogenous EGF and GLP-2 signaling in mice and human beings. In the mouse TPN model, exogenous EGF or GLP-2 attenuated mucosal atrophy and restored IEC proliferation. The beneficial effects of EGF and GLP-2 were decreased upon Gefitinib treatment and in TPN-treated IEC-EgfrKO mice, showing epidermal growth factor–receptor dependency for these IEC responses. By contrast, in TPN-treated IEC-pi3kr1KO mice, the beneficial actions of EGF were lost, although GLP-2 still attenuated mucosal atrophy. CONCLUSIONS: Upon enteral nutrient deprivation, exogenous GLP-2 and EGF show strong interdependency for improving IEC responses. Understanding the differential requirements for phosphatidylinositol 3-kinase/phosphoAKT (Ser473) signaling may help improve future therapies to prevent mucosal atrophy

Interdependency of EGF and GLP-2 Signaling in Attenuating Mucosal Atrophy in a Mouse Model of Parenteral Nutrition

Background & Aims: Total parenteral nutrition (TPN), a crucial treatment for patients who cannot receive enteral nutrition, is associated with mucosal atrophy, barrier dysfunction, and infectious complications. Glucagon-like peptide-2 (GLP-2) and epidermal growth factor (EGF) improve intestinal epithelial cell (IEC) responses and attenuate mucosal atrophy in several TPN models. However, it remains unclear whether these 2 factors use distinct or overlapping signaling pathways to improve IEC responses. We investigated the interaction of GLP-2 and EGF signaling in a mouse TPN model and in patients deprived of enteral nutrition. Methods: Adult C57BL/6J, IEC-Egfrknock out (KO) and IEC-pik3r1KO mice receiving TPN or enteral nutrition were treated with EGF or GLP-2 alone or in combination with reciprocal receptor inhibitors, GLP-2(3-33) or gefitinib. Jejunum was collected and mucosal atrophy and IEC responses were assessed by histologic, gene, and protein expression analyses. In patients undergoing planned looped ileostomies, fed and unfed ileum was analyzed. Results: Enteral nutrient deprivation reduced endogenous EGF and GLP-2 signaling in mice and human beings. In the mouse TPN model, exogenous EGF or GLP-2 attenuated mucosal atrophy and restored IEC proliferation. The beneficial effects of EGF and GLP-2 were decreased upon Gefitinib treatment and in TPN-treated IEC-EgfrKO mice, showing epidermal growth factorâreceptor dependency for these IEC responses. By contrast, in TPN-treated IEC-pi3kr1KO mice, the beneficial actions of EGF were lost, although GLP-2 still attenuated mucosal atrophy. Conclusions: Upon enteral nutrient deprivation, exogenous GLP-2 and EGF show strong interdependency for improving IEC responses. Understanding the differential requirements for phosphatidylinositol 3-kinase/phosphoAKT (Ser473) signaling may help improve future therapies to prevent mucosal atrophy. Keywords: Total Parenteral Nutrition, EGF, GLP-2, EGFR, PI3K, Mucosal Atroph