1,074 research outputs found

    Natural Supersymmetry at the LHC

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    If the minimal supersymmetric standard model is the solution to the hierarchy problem, the scalar top quark (stop) and the Higgsino should weigh around the electroweak scale such as 200 GeV. A low messenger scale, which results in a light gravitino, is also suggested to suppress the quantum corrections to the Higgs mass parameters. Therefore the minimal model for natural supersymmetry is a system with stop/Higgsino/gravitino whereas other superparticles are heavy. We study the LHC signatures of the minimal system and discuss the discovery potential and methods for the mass measurements.Comment: 19 pages, 6 figures, 1 tabl

    The CMB and the measure of the multiverse

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    In the context of eternal inflation, cosmological predictions depend on the choice of measure to regulate the diverging spacetime volume. The spectrum of inflationary perturbations is no exception, as we demonstrate by comparing the predictions of the fat geodesic and causal patch measures. To highlight the effect of the measure---as opposed to any effects related to a possible landscape of vacua---we take the cosmological model, including the model of inflation, to be fixed. We also condition on the average CMB temperature accompanying the measurement. Both measures predict a 1-point expectation value for the gauge-invariant Newtonian potential, which takes the form of a (scale-dependent) monopole, in addition to a related contribution to the 3-point correlation function, with the detailed form of these quantities differing between the measures. However, for both measures both effects are well within cosmic variance. Our results make clear the theoretical relevance of the measure, and at the same time validate the standard inflationary predictions in the context of eternal inflation.Comment: 28 pages; v2: reference added, some clarification

    Distinguishing among Technicolor/Warped Scenarios in Dileptons

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    Models of dynamical electroweak symmetry breaking usually include new spin-1 resonances, whose couplings and masses have to satisfy electroweak precision tests. We propose to use dilepton searches to probe the underlying structure responsible for satisfying these. Using the invariant mass spectrum and charge asymmetry, we can determine the number, parity, and isospin of these resonances. We pick three models of strong/warped symmetry breaking, and show that each model produces specific features that reflect this underlying structure of electroweak symmetry breaking and cancellations.Comment: Added missing referenc

    Structural analysis of MDM2 RING separates degradation from regulation of p53 transcription activity

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    MDM2–MDMX complexes bind the p53 tumor-suppressor protein, inhibiting p53's transcriptional activity and targeting p53 for proteasomal degradation. Inhibitors that disrupt binding between p53 and MDM2 efficiently activate a p53 response, but their use in the treatment of cancers that retain wild-type p53 may be limited by on-target toxicities due to p53 activation in normal tissue. Guided by a novel crystal structure of the MDM2–MDMX–E2(UbcH5B)–ubiquitin complex, we designed MDM2 mutants that prevent E2–ubiquitin binding without altering the RING-domain structure. These mutants lack MDM2's E3 activity but retain the ability to limit p53â€Čs transcriptional activity and allow cell proliferation. Cells expressing these mutants respond more quickly to cellular stress than cells expressing wild-type MDM2, but basal p53 control is maintained. Targeting the MDM2 E3-ligase activity could therefore widen the therapeutic window of p53 activation in tumors

    Inflammatory cytokines and biofilm production sustain Staphylococcus aureus outgrowth and persistence: A pivotal interplay in the pathogenesis of Atopic Dermatitis

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    Individuals with Atopic dermatitis (AD) are highly susceptible to Staphylococcus aureus colonization. However, the mechanisms driving this process as well as the impact of S. aureus in AD pathogenesis are still incompletely understood. In this study, we analysed the role of biofilm in sustaining S. aureus chronic persistence and its impact on AD severity. Further we explored whether key inflammatory cytokines overexpressed in AD might provide a selective advantage to S. aureus. Results show that the strength of biofilm production by S. aureus correlated with the severity of the skin lesion, being significantly higher (P < 0.01) in patients with a more severe form of the disease as compared to those individuals with mild AD. Additionally, interleukin (IL)-ÎČ and interferon Îł (IFN-Îł), but not interleukin (IL)-6, induced a concentration-dependent increase of S. aureus growth. This effect was not observed with coagulase-negative staphylococci isolated from the skin of AD patients. These findings indicate that inflammatory cytokines such as IL1-ÎČ and IFN-Îł, can selectively promote S. aureus outgrowth, thus subverting the composition of the healthy skin microbiome. Moreover, biofilm production by S. aureus plays a relevant role in further supporting chronic colonization and disease severity, while providing an increased tolerance to antimicrobials

    Mass-Matching in Higgsless

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    Modern extra-dimensional Higgsless scenarios rely on a mass-matching between fermionic and bosonic KK resonances to evade constraints from precision electroweak measurements. After analyzing all of the Tevatron and LEP bounds on these so-called Cured Higgsless scenarios, we study their LHC signatures and explore how to identify the mass-matching mechanism, the key to their viability. We find singly and pair produced fermionic resonances show up as clean signals with 2 or 4 leptons and 2 hard jets, while neutral and charged bosonic resonances are visible in the dilepton and leptonic WZ channels, respectively. A measurement of the resonance masses from these channels shows the matching necessary to achieve S≃0S\simeq 0. Moreover, a large single production of KK-fermion resonances is a clear indication of compositeness of SM quarks. Discovery reach is below 10 fb−1^{-1} of luminosity for resonances in the 700 GeV range.Comment: 28 pages, 18 figure

    Genetically Programmed Differences in Epidermal Host Defense between Psoriasis and Atopic Dermatitis Patients

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    In the past decades, chronic inflammatory diseases such as psoriasis, atopic dermatitis, asthma, Crohn’s disease and celiac disease were generally regarded as immune-mediated conditions involving activated T-cells and proinflammatory cytokines produced by these cells. This paradigm has recently been challenged by the finding that mutations and polymorphisms in epithelium-expressed genes involved in physical barrier function or innate immunity, are risk factors of these conditions. We used a functional genomics approach to analyze cultured keratinocytes from patients with psoriasis or atopic dermatitis and healthy controls. First passage primary cells derived from non-lesional skin were stimulated with pro-inflammatory cytokines, and expression of a panel of 55 genes associated with epidermal differentiation and cutaneous inflammation was measured by quantitative PCR. A subset of these genes was analyzed at the protein level. Using cluster analysis and multivariate analysis of variance we identified groups of genes that were differentially expressed, and could, depending on the stimulus, provide a disease-specific gene expression signature. We found particularly large differences in expression levels of innate immunity genes between keratinocytes from psoriasis patients and atopic dermatitis patients. Our findings indicate that cell-autonomous differences exist between cultured keratinocytes of psoriasis and atopic dermatitis patients, which we interpret to be genetically determined. We hypothesize that polymorphisms of innate immunity genes both with signaling and effector functions are coadapted, each with balancing advantages and disadvantages. In the case of psoriasis, high expression levels of antimicrobial proteins genes putatively confer increased protection against microbial infection, but the biological cost could be a beneficial system gone awry, leading to overt inflammatory disease
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