Decaying Dark Matter from Dark Instantons

We construct an explicit, TeV-scale model of decaying dark matter in which the approximate stability of the dark matter candidate is a consequence of a global symmetry that is broken only by instanton-induced operators generated by a non-Abelian dark gauge group. The dominant dark matter decay channels are to standard model leptons. Annihilation of the dark matter to standard model states occurs primarily through the Higgs portal. We show that the mass and lifetime of the dark matter candidate in this model can be chosen to be consistent with the values favored by fits to data from the PAMELA and Fermi LAT experiments.Comment: 19 pages LaTeX, 3 eps figures. v2,v3: references adde

Towards improved management of coastal submersion crises - CRISMA-WAVE solution as an example of CRISMA Framework application

Coping with various types of natural or man-made hazards the FP7 SECURITY CRISMA project (http://www.crisrnaprojecteu) has designed and developed an experimental software framework allowing building crisis management simulation application. One of the five pilot applications of CRISMA dealing with preparedness to the coastal submersions was developed and implemented using return of experience of the reference Xynthia storm surge event in the Charente Maritime County in France. The paper addresses the generic CRISMA Framework applicability to simulate mitigation effects of a coastal submersion through CRISMA-Wave implementation of a full modelling cycle. The CRISMA-Wave paradigm reflects user needs for simulation of "what-if" scenarios for short and long-term actions and the paper describes in particular its different components : *Simulation of submersion effects at a range of temporal and spatial scales, *Preparedness Planning, *Assessment of impacts depending on scenarios based on options for managing the inundation risks, *Cascading effects and *Evaluation of damages with comparison of submersion defence scenarios based on cost-benefit and multi criteria analysis

Analysis of mixtures using next generation sequencing of mitochondrial DNA hypervariable regions

Aim To apply massively parallel and clonal sequencing (next generation sequencing or NGS) to the analysis of forensic mixed samples. Methods A duplex polymerase chain reaction (PCR) assay targeting the mitochondrial DNA (mtDNA) hypervariable regions I/II (HVI/HVII) was developed for NGS analysis on the Roche 454 GS Junior instrument. Eight sets of multiplex identifier-tagged 454 fusion primers were used in a combinatorial approach for amplification and deep sequencing of up to 64 samples in parallel. Results This assay was shown to be highly sensitive for sequencing limited DNA amounts ( ~ 100 mtDNA copies) and analyzing contrived and biological mixtures with low level variants ( ~ 1%) as well as “complex” mixtures (≥3 contributors). PCR artifact “hybrid” sequences generated by jumping PCR or template switching were observed at a low level (<2%) in the analysis of mixed samples but could be eliminated by reducing the PCR cycle number. Conclusion This study demonstrates the power of NGS technologies targeting the mtDNA HVI/HVII regions for analysis of challenging forensic samples, such as mixtures and specimens with limited DNA

On the Evaluation of Gluon Condensate Effects in the Holographic Approach to QCD

In holographic QCD the effects of gluonic condensate can be encoded in a suitable deformation of the 5D metric. We develop two different methods for the evaluation of first order perturbative corrections to masses and decay constants of vector resonances in 5D Hard-Wall models of QCD due to small deformations of the metric. They are extracted either from a novel compact form for the first order correction to the vector two-point function, or from perturbation theory for vector bound-state eigenfunctions: the equivalence of the two methods is shown. Our procedures are then applied to flat and to AdS 5D Hard-Wall models; we complement results of existing literature evaluating the corrections to vector decay constant and to two-pion-one-vector couplings: this is particularly relevant to satisfy the sum rules. We concentrate our attention on the effects for the Gasser-Leutwyler coefficients; we show that, as in the Chiral Quark model, the addition of the gluonic condensate improves the consistency, the understanding and the agreement with phenomenology of the holographic model.Comment: 23 pages, three figures, sign error in pion wave function fixed, numerical analysis extended, general conclusions unchange

High resolution HLA analysis reveals independent class I haplotypes and amino-acid motifs protective for multiple sclerosis.

We investigated association between HLA class I and class II alleles and haplotypes, and KIR loci and their HLA class I ligands, with multiple sclerosis (MS) in 412 European American MS patients and 419 ethnically matched controls, using next-generation sequencing. The DRB1*15:01~DQB1*06:02 haplotype was highly predisposing (odds ratio (OR) = 3.98; 95% confidence interval (CI) = 3-5.31; p-value (p) = 2.22E-16), as was DRB1*03:01~DQB1*02:01 (OR = 1.63; CI = 1.19-2.24; p = 1.41E-03). Hardy-Weinberg (HW) analysis in MS patients revealed a significant DRB1*03:01~DQB1*02:01 homozyote excess (15 observed; 8.6 expected; p = 0.016). The OR for this genotype (5.27; CI = 1.47-28.52; p = 0.0036) suggests a recessive MS risk model. Controls displayed no HW deviations. The C*03:04~B*40:01 haplotype (OR = 0.27; CI = 0.14-0.51; p = 6.76E-06) was highly protective for MS, especially in haplotypes with A*02:01 (OR = 0.15; CI = 0.04-0.45; p = 6.51E-05). By itself, A*02:01 is moderately protective, (OR = 0.69; CI = 0.54-0.87; p = 1.46E-03), and haplotypes of A*02:01 with the HLA-B Thr80 Bw4 variant (Bw4T) more so (OR = 0.53; CI = 0.35-0.78; p = 7.55E-04). Protective associations with the Bw4 KIR ligand resulted from linkage disequilibrium (LD) with DRB1*15:01, but the Bw4T variant was protective (OR = 0.64; CI = 0.49-0.82; p = 3.37-04) independent of LD with DRB1*15:01. The Bw4I variant was not associated with MS. Overall, we find specific class I HLA polymorphisms to be protective for MS, independent of the strong predisposition conferred by DRB1*15:01

The role of the lateral amygdala in the retrieval and maintenance of fear-memories formed by repeated probabilistic reinforcement

The lateral nucleus of the amygdala (LA) is a key element in the neural circuit subserving Pavlovian fear-conditioning, an animal model of fear and anxiety. Most studies have focused on the role of the LA in fear acquisition and extinction, i.e., how neural plasticity results from changing contingencies between a neutral conditioned stimulus (CS) (e.g., a tone) and an aversive unconditioned stimulus (US) (e.g., a shock). However, outside of the lab, fear-memories are often the result of repeated and unpredictable experiences. Examples include domestic violence, child abuse or combat. To better understand the role of the LA in the expression of fear resulting from repeated and uncertain reinforcement, rats experienced a 30% partial reinforcement (PR) fear-conditioning schedule four days a week for four weeks. Rats reached asymptotic levels of conditioned-fear expression after the first week. We then manipulated LA activity with drug (or vehicle) (VEH) infusions once a week, for the next three weeks, before the training session. LA infusions of muscimol (MUSC), a GABA-A agonist that inhibits neural activity, reduced CS evoked fear-behavior to pre-conditioning levels. LA infusions of pentagastrin (PENT), a cholecystokinin-2 (CCK) agonist that increases neural excitability, resulted in CS-evoked fear-behavior that continued past the offset of the CS. This suggests that neural activity in the LA is required for the retrieval of fear memories that stem from repeated and uncertain reinforcement, and that CCK signaling in the LA plays a role in the recovery from fear after the removal of the fear-evoking stimulus

Tests of Universality of Baryon Form Factors in Holographic QCD

We describe a new exact relation for large $N_c$ QCD for the long-distance behavior of baryon form factors in the chiral limit, satisfied by all 4D semi-classical chiral soliton models. We use this relation to test the consistency of the structure of two different holographic models of baryons.Comment: 4 pages. Talk presented by MN at Light Cone 2009: Relativistic Hadronic and Particle Physics, 8-13 Jul 2009, Sao Jose dos Campos, Brazi

Higher FKBP5, COMT, CHRNA5, and CRHR1 allele burdens are associated with PTSD and interact with trauma exposure: implications for neuropsychiatric research and treatment

Joseph A Boscarino1,2, Porat M Erlich1,3, Stuart N Hoffman4, Xiaopeng Zhang51Center for Health Research, Geisinger Clinic, Danville, PA, 2Department of Psychiatry, 3Department of Medicine, Temple University School of Medicine, Philadelphia, PA, 4Department of Neurology, 5Department of Anesthesiology, Geisinger Clinic, Danville, PA, USAObjective: The study aim was to assess the cumulative burden of polymorphisms located within four genetic loci previously associated with posttraumatic stress disorder (PTSD) among outpatients at risk for PTSD.Methods: Diagnostic interviews were completed and DNA samples collected among 412 pain patients to determine if FKBP5 (rs9470080), COMT (rs4680), CHRNA5 (rs16969968), and CRHR1 (rs110402) single nucleotide polymorphisms were cumulatively associated with increased risk for PTSD.Results: In bivariate analyses, it was found that a count of specific PTSD risk alleles located within FKBP5, COMT, CHRNA5, and CRHR1 genetic loci (allele range = 0&amp;ndash;6, mean count = 2.92, standard deviation = 1.36) was associated with lifetime (t [409] = 3.430, P = 0.001) and early onset PTSD (t [409] = 4.239, P = 0.000028). In logistic regression, controlling for demographic factors, personality traits, and trauma exposures, this risk allele count remained associated with both lifetime (odds ratio = 1.49, P = 0.00158) and early onset PTSD (odds ratio = 2.36, P = 0.000093). Interaction effects were also detected, whereby individuals with higher risk allele counts and higher trauma exposures had an increased risk of lifetime PTSD (allele count &amp;times; high trauma, P = 0.026) and early onset PTSD (allele count &amp;times; high trauma, P = 0.016) in these logistic regressions. Those with no or few risk alleles appeared resilient to PTSD, regardless of exposure history.Conclusion: A cumulative risk allele count involving four single nucleotide polymorphisms located within the FKBP5, COMT, CHRNA5, and CRHR1 genes are associated with PTSD. Level of trauma exposure interacts with risk allele count, such that PTSD is increased in those with higher risk allele counts and higher trauma exposures. Since the single nucleotide polymorphisms studied encompass stress circuitry and addiction biology, these findings may have implications for neuropsychiatric research and treatment.Keywords: posttraumatic stress disorder, genetic association study, single nucleotide polymorphism, risk alleles, trauma exposure, neuroticism, childhood adversit