1,903 research outputs found
Aidnogenesis via Leptogenesis and Dark Sphalerons
We discuss aidnogenesis, the generation of a dark matter asymmetry via new
sphaleron processes associated to an extra non-abelian gauge symmetry common to
both the visible and the dark sectors. Such a theory can naturally produce an
abundance of asymmetric dark matter which is of the same size as the lepton and
baryon asymmetries, as suggested by the similar sizes of the observed baryonic
and dark matter energy content, and provide a definite prediction for the mass
of the dark matter particle. We discuss in detail a minimal realization in
which the Standard Model is only extended by dark matter fermions which form
"dark baryons" through an SU(3) interaction, and a (broken) horizontal symmetry
that induces the new sphalerons. The dark matter mass is predicted to be
approximately 6 GeV, close to the region favored by DAMA and CoGeNT.
Furthermore, a remnant of the horizontal symmetry should be broken at a lower
scale and can also explain the Tevatron dimuon anomaly.Comment: Minor changes, discussion of present constraints expanded. 16 pages,
2 eps figures, REVTeX
Spin Discrimination in Three-Body Decays
The identification of the correct model for physics beyond the Standard Model
requires the determination of the spin of new particles. We investigate to
which extent the spin of a new particle can be identified in scenarios
where it decays dominantly in three-body decays . Here we
assume that is a candidate for dark matter and escapes direct detection at
a high energy collider such as the LHC. We show that in the case that all
intermediate particles are heavy, one can get information on the spins of
and at the LHC by exploiting the invariant mass distribution of the two
standard model fermions. We develop a model-independent strategy to determine
the spins without prior knowledge of the unknown couplings and test it in a
series of Monte Carlo studies.Comment: 31+1 pages, 4 figures, 8 tables, JHEP.cls include
Prediagnostic Serum Concentrations of Organochlorine Compounds and Risk of Testicular Germ Cell Tumors
BACKGROUND: Recent findings suggest that exposure to organochlorine (OC) compounds, chlordanes and p,p′-dichlorodiphenyldichloroethylene (p,p′-DDE) in particular, may increase the risk of developing testicular germ cell tumors (TGCTs). OBJECTIVE: To further investigate this question, we conducted a nested case-control study of TGCTs within the Norwegian Janus Serum Bank cohort. METHODS: The study was conducted among individuals with serum collected between 1972 and 1978. TGCT cases diagnosed through 1999 (n = 49; 27-62 years of age at diagnosis) were identified through linkage to the Norwegian Cancer Registry. Controls (n =51) were matched to cases on region, blood draw year, and age at blood draw. Measurements of 11 OC insecticide compounds and 34 polychlorinated biphenyl (PCB) congeners were performed using gas chromatography/high-resolution mass spectrometry. Case-control comparisons of lipid-adjusted analyte concentrations were performed using the Wilcoxon signed-rank test. Odds ratios (ORs) and 95% confidence intervals (CIs) for tertiles of analyte concentration were calculated using conditional logistic regression. RESULTS: TGCT cases had elevated concentrations of p,p′-DDE (tertile 3 vs. tertile 1 OR (ORT3) 2.2; 95% CI, 0.7-6.5; p Wilcoxon = 0.07), oxychlordane (ORT3 3.2; 95% CI, 0.6-16.8; pWilcoxon = 0.05), trans-nonachlor (ORT3 2.6; 95% CI, 0.7-8.9; pWilcoxon = 0.07), and total chlordanes (OR T3 2.0; 95% CI, 0.6-7.2; pWilcoxon = 0.048) compared with controls, although no ORs were statistically significant. Seminoma cases had significantly lower concentrations of PCB congeners 44, 49, and 52 and significantly higher concentrations of PCBs 99, 138, 153, 167, 183, and 195. CONCLUSIONS: Our study provides additional but qualified evidence supporting an association between exposures to p,p′-DDE and chlordane compounds, and possibly some PCB congeners, and TGCT risk
Validation of graft and standard liver size predictions in right liver living donor liver transplantation
Purpose: To assess the accuracy of a formula derived from 159 living liver donors to estimate the liver size of a normal subject: standard liver weight (g) = 218 + body weight (kg) × 12.3 + 51 (if male). Standard liver volume (SLV) is attained by a conversion factor of 1.19 mL/g. Methods: The total liver volume (TLV) of each of the subsequent consecutive 126 living liver donors was determined using the right liver graft weight (RGW) on the back table, right/left liver volume ratio on computed tomography, and the conversion factor. The estimated right liver graft weight (ERGW) was determined by the right liver volume on computed tomography (CT) and the conversion factor. SLV and ERGW were compared with TLV and RGW, respectively, by paired sample t test. Results: Donor characteristics of both series were similar. SLV and TLV were 1,099.6 ± 139.6 and 1,108.5 ± 175.2 mL, respectively, (R 2 = 0.476) (p = 0.435). The difference between SLV and TLV was only -8.9 ± 128.2 mL (-1.0 ± 11.7%). ERGW and RGW were 601.5 ± 104.1 and 597.1 ± 102.2 g, respectively (R 2 = 0.781) (p = 0.332). The conversion factor from liver weight to volume for this series was 1.20 mL/g. The difference between ERGW and RGW was 4.3 ± 49.8 g (0.3 ± 8.8%). ERGW was smaller than RGW for over 10% (range 0.21-40.66 g) in 18 of the 126 donors. None had the underestimation of RGW by over 20%. Conclusion: SLV and graft weight estimations were accurate using the formula and conversion factor. © 2011 The Author(s).published_or_final_versionSpringer Open Choice, 21 Feb 201
Trans-sialidase Stimulates Eat Me Response from Epithelial Cells
Epithelial cell invasion by the protozoan parasite Trypanosoma cruzi is enhanced by the presence of an enzyme expressed on its cell surface during the trypomastigote life cycle stage. The enzyme, trans-sialidase (TS), is a member of one of the largest gene families expressed by the parasite and the role of its activity in mediating epithelial cell entry has not hitherto been understood. Here we show that the T. cruzi TS generates an eat me signal which is capable of enabling epithelial cell entry. We have utilized purified, recombinant, active (TcTS) and inactive (TcTS2V0) TS coated onto beads to challenge an epithelial cell line. We find that TS activity acts upon G protein coupled receptors present at the epithelial cell synapse with the coated bead, thereby enhancing cell entry. By so doing, we provide evidence that TS proteins bind glycans, mediate the formation of distinct synaptic domains and promote macropinocytotic uptake of microparticles into a perinuclear compartment in a manner which may emulate entosis
Constraining Bosonic Supersymmetry from Higgs results and 8 TeV ATLAS multi-jets plus missing energy data
The collider phenomenology of models with Universal Extra Dimensions (UED) is
surprisingly similar to that of supersymmetric (SUSY) scenarios. For each
level-1 bosonic (fermionic) Kaluza-Klein (KK) state, there is a fermionic
(bosonic) analog in SUSY and thus UED scenarios are often known as bosonic
supersymmetry. The minimal version of UED (mUED) gives rise to a
quasi-degenerate particle spectrum at each KK-level and thus, can not explain
the enhanced Higgs to diphoton decay rate hinted by the ATLAS collaboration of
the Large Hadron Collider (LHC) experiment. However, in the non-minimal version
of the UED (nmUED) model, the enhanced Higgs to diphoton decay rate can be
easily explained via the suitable choice of boundary localized kinetic (BLK)
terms for higher dimensional fermions and gauge bosons. BLK terms remove the
degeneracy in the KK mass spectrum and thus, pair production of level-1 quarks
and gluons at the LHC gives rise to hard jets, leptons and large missing energy
in the final state. These final states are studied in details by the ATLAS and
CMS collaborations in the context of SUSY scenarios. We find that the absence
of any significant deviation of the data from the Standard Model (SM)
prediction puts a lower bound of about 2.1 TeV on equal mass excited quarks and
gluons.Comment: 19 page
Formyl Peptide Receptor as a Novel Therapeutic Target for Anxiety-Related Disorders
Formyl peptide receptors (FPR) belong to a family of sensors of the immune system that detect microbe-associated molecules and inform various cellular and sensorial mechanisms to the presence of pathogens in the host. Here we demonstrate that Fpr2/3-deficient mice show a distinct profile of behaviour characterised by reduced anxiety in the marble burying and light-dark box paradigms, increased exploratory behaviour in an open-field, together with superior performance on a novel object recognition test. Pharmacological blockade with a formyl peptide receptor antagonist, Boc2, in wild type mice reproduced most of the behavioural changes observed in the Fpr2/3(-/-) mice, including a significant improvement in novel object discrimination and reduced anxiety in a light/dark shuttle test. These effects were associated with reduced FPR signalling in the gut as shown by the significant reduction in the levels of p-p38. Collectively, these findings suggest that homeostatic FPR signalling exerts a modulatory effect on anxiety-like behaviours. These findings thus suggest that therapies targeting FPRs may be a novel approach to ameliorate behavioural abnormalities present in neuropsychiatric disorders at the cognitive-emotional interface
Caspase cleavage of the Golgi stacking factor GRASP65 is required for Fas/CD95-mediated apoptosis
GRASP65 (Golgi reassembly and stacking protein of 65 KDa) is a cis-Golgi protein with roles in Golgi structure, membrane trafficking and cell signalling. It is cleaved by caspase-3 early in apoptosis, promoting Golgi fragmentation. We now show that cleavage is needed for Fas-mediated apoptosis: expression of caspase-resistant GRASP65 protects cells, whereas expression of membrane proximal caspase-cleaved GRASP65 fragments dramatically sensitises cells. GRASP65 coordinates passage through the Golgi apparatus of proteins containing C-terminal hydrophobic motifs, via its tandem PDZ type ‘GRASP' domains. Fas/CD95 contains a C-terminal leucine–valine pairing so its trafficking might be coordinated by GRASP65. Mutagenesis of the Fas/CD95 LV motif reduces the number of cells with Golgi-associated Fas/CD95, and generates a receptor that is more effective at inducing apoptosis; however, siRNA-mediated silencing or expression of mutant GRASP65 constructs do not alter the steady state distribution of Fas/CD95. We also find no evidence for a GRASP65–Fas/CD95 interaction at the molecular level. Instead, we find that the C-terminal fragments of GRASP65 produced following caspase cleavage are targeted to mitochondria, and ectopic expression of these sensitises HeLa cells to Fas ligand. Our data suggest that GRASP65 cleavage promotes Fas/CD95-mediated apoptosis via release of C-terminal fragments that act at the mitochondria, and we identify Bcl-XL as a candidate apoptotic binding partner for GRASP65
Persistent anthrax as a major driver of wildlife mortality in a tropical rainforest
Anthrax is a globally important animal disease and zoonosis. Despite this, our current knowledge of anthrax ecology is largely limited to arid ecosystems, where outbreaks are most commonly reported. Here we show that the dynamics of an anthrax-causing agent, Bacillus cereus biovar anthracis, in a tropical rainforest have severe consequences for local wildlife communities. Using data and samples collected over three decades, we show that rainforest anthrax is a persistent and widespread cause of death for a broad range of mammalian hosts. We predict that this pathogen will accelerate the decline and possibly result in the extirpation of local chimpanzee (Pan troglodytes verus) populations. We present the epidemiology of a cryptic pathogen and show that its presence has important implications for conservation
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