389 research outputs found
Probing Colored Particles with Photons, Leptons, and Jets
If pairs of new colored particles are produced at the Large Hadron Collider,
determining their quantum numbers, and even discovering them, can be
non-trivial. We suggest that valuable information can be obtained by measuring
the resonant signals of their near-threshold QCD bound states. If the particles
are charged, the resulting signatures include photons and leptons and are
sufficiently rich for unambiguously determining their various quantum numbers,
including the charge, color representation and spin, and obtaining a precise
mass measurement. These signals provide well-motivated benchmark models for
resonance searches in the dijet, photon+jet, diphoton and dilepton channels.
While these measurements require that the lifetime of the new particles be not
too short, the resulting limits, unlike those from direct searches for pair
production above threshold, do not depend on the particles' decay modes. These
limits may be competitive with more direct searches if the particles decay in
an obscure way.Comment: 39 pages, 9 figures; v2: more recent searches include
Higgs and non-universal gaugino masses: no SUSY signal expected yet?
So far, no supersymmetric particles have been detected at the Large Hadron
Collider (LHC). However, the recent Higgs results have interesting implications
for the SUSY parameter space. In this paper, we study the consequences of an
LHC Higgs signal for a model with non-universal gaugino masses in the context
of SU(5) unification. The gaugino mass ratios associated with the higher
representations produce viable spectra that are largely inaccessible to the
current LHC and direct dark matter detection experiments. Thus, in light of the
Higgs results, the non-observation of SUSY is no surprise.Comment: supplementary file containing plots with log priors in ancillary
files. v2: added some comments on more general settings and references,
accepted for publication in JHE
Cerebral Metabolic Alterations in Rats With Diabetic Ketoacidosis: Effects of Treatment With Insulin and Intravenous Fluids and Effects of Bumetanide
ObjectiveCerebral edema is a life-threatening complication of diabetic ketoacidosis (DKA) in children. Recent data suggest that cerebral hypoperfusion and activation of cerebral ion transporters may be involved, but data describing cerebral metabolic alterations during DKA are lacking.Research design and methodsWe evaluated 50 juvenile rats with DKA and 21 normal control rats using proton and phosphorus magnetic resonance spectroscopy (MRS). MRS measured cerebral intracellular pH and ratios of metabolites including ATP/inorganic phosphate (Pi), phosphocreatine (PCr)/Pi, N-acetyl aspartate (NAA)/creatine (Cr), and lactate/Cr before and during DKA treatment. We determined the effects of treatment with insulin and intravenous saline with or without bumetanide, an inhibitor of Na-K-2Cl cotransport, using ANCOVA with a 2 x 2 factorial study design.ResultsCerebral intracellular pH was decreased during DKA compared with control (mean +/- SE difference -0.13 +/- 0.03; P < 0.001), and lactate/Cr was elevated (0.09 +/- 0.02; P < 0.001). DKA rats had lower ATP/Pi and NAA/Cr (-0.32 +/- 0.10, P = 0.003, and -0.14 +/- 0.04, P < 0.001, respectively) compared with controls, but PCr/Pi was not significantly decreased. During 2-h treatment with insulin/saline, ATP/Pi, PCr/Pi, and NAA/Cr declined significantly despite an increase in intracellular pH. Bumetanide treatment increased ATP/Pi and PCr/Pi and ameliorated the declines in these values with insulin/saline treatment.ConclusionsThese data demonstrate that cerebral metabolism is significantly compromised during DKA and that further deterioration occurs during early DKA treatment--consistent with possible effects of cerebral hypoperfusion and reperfusion injury. Treatment with bumetanide may help diminish the adverse effects of initial treatment with insulin/saline
NLL soft and Coulomb resummation for squark and gluino production at the LHC
We present predictions of the total cross sections for pair production of
squarks and gluinos at the LHC, including the stop-antistop production process.
Our calculation supplements full fixed-order NLO predictions with resummation
of threshold logarithms and Coulomb singularities at next-to-leading
logarithmic (NLL) accuracy, including bound-state effects. The numerical effect
of higher-order Coulomb terms can be as big or larger than that of soft-gluon
corrections. For a selection of benchmark points accessible with data from the
2010-2012 LHC runs, resummation leads to an enhancement of the total inclusive
squark and gluino production cross section in the 15-30 % range. For individual
production processes of gluinos, the corrections can be much larger. The
theoretical uncertainty in the prediction of the hard-scattering cross sections
is typically reduced to the 10 % level.Comment: 45 pages, 16 Figures, LaTex. v2: published version. Grids with
numerical results for the NLL cross sections for squark and gluino production
at the 7/8 TeV LHC are included in the submission and are also available at
http://omnibus.uni-freiburg.de/~cs1010/susy.htm
Genome-wide pleiotropy analysis of neuropathological traits related to Alzheimerâs disease
Background
Simultaneous consideration of two neuropathological traits related to Alzheimerâs disease (AD) has not been attempted in a genome-wide association study.
Methods
We conducted genome-wide pleiotropy analyses using association summary statistics from the Beecham et al. study (PLoS Genet 10:e1004606, 2014) for AD-related neuropathological traits, including neuritic plaque (NP), neurofibrillary tangle (NFT), and cerebral amyloid angiopathy (CAA). Significant findings were further examined by expression quantitative trait locus and differentially expressed gene analyses in AD vs. control brains using gene expression data.
Results
Genome-wide significant pleiotropic associations were observed for the joint model of NP and NFT (NP + NFT) with the single-nucleotide polymorphism (SNP) rs34487851 upstream of C2orf40 (alias ECRG4, P = 2.4 Ă 10â8) and for the joint model of NFT and CAA (NFT + CAA) with the HDAC9 SNP rs79524815 (P = 1.1 Ă 10â8). Gene-based testing revealed study-wide significant associations (P †2.0 Ă 10â6) for the NFT + CAA outcome with adjacent genes TRAPPC12, TRAPPC12-AS1, and ADI1. Risk alleles of proxy SNPs for rs79524815 were associated with significantly lower expression of HDAC9 in the brain (P = 3.0 Ă 10â3), and HDAC9 was significantly downregulated in subjects with AD compared with control subjects in the prefrontal (P = 7.9 Ă 10â3) and visual (P = 5.6 Ă 10â4) cortices.
Conclusions
Our findings suggest that pleiotropy analysis is a useful approach to identifying novel genetic associations with complex diseases and their endophenotypes. Functional studies are needed to determine whether ECRG4 or HDAC9 is plausible as a therapeutic target
Heavy quarkonium: progress, puzzles, and opportunities
A golden age for heavy quarkonium physics dawned a decade ago, initiated by
the confluence of exciting advances in quantum chromodynamics (QCD) and an
explosion of related experimental activity. The early years of this period were
chronicled in the Quarkonium Working Group (QWG) CERN Yellow Report (YR) in
2004, which presented a comprehensive review of the status of the field at that
time and provided specific recommendations for further progress. However, the
broad spectrum of subsequent breakthroughs, surprises, and continuing puzzles
could only be partially anticipated. Since the release of the YR, the BESII
program concluded only to give birth to BESIII; the -factories and CLEO-c
flourished; quarkonium production and polarization measurements at HERA and the
Tevatron matured; and heavy-ion collisions at RHIC have opened a window on the
deconfinement regime. All these experiments leave legacies of quality,
precision, and unsolved mysteries for quarkonium physics, and therefore beg for
continuing investigations. The plethora of newly-found quarkonium-like states
unleashed a flood of theoretical investigations into new forms of matter such
as quark-gluon hybrids, mesonic molecules, and tetraquarks. Measurements of the
spectroscopy, decays, production, and in-medium behavior of c\bar{c}, b\bar{b},
and b\bar{c} bound states have been shown to validate some theoretical
approaches to QCD and highlight lack of quantitative success for others. The
intriguing details of quarkonium suppression in heavy-ion collisions that have
emerged from RHIC have elevated the importance of separating hot- and
cold-nuclear-matter effects in quark-gluon plasma studies. This review
systematically addresses all these matters and concludes by prioritizing
directions for ongoing and future efforts.Comment: 182 pages, 112 figures. Editors: N. Brambilla, S. Eidelman, B. K.
Heltsley, R. Vogt. Section Coordinators: G. T. Bodwin, E. Eichten, A. D.
Frawley, A. B. Meyer, R. E. Mitchell, V. Papadimitriou, P. Petreczky, A. A.
Petrov, P. Robbe, A. Vair
Evaluating the role of pathogenic dementia variants in posterior cortical atrophy
Posterior cortical atrophy (PCA) is an understudied visual impairment syndrome most often due to âposterior Alzheimer's disease (AD)â pathology. Case studies detected mutations in PSEN1, PSEN2, GRN, MAPT, and PRNP in subjects with clinical PCA. To detect the frequency and spectrum of mutations in known dementia genes in PCA, we screened 124 European-American subjects with clinical PCA (n = 67) or posterior AD neuropathology (n = 57) for variants in genes implicated in AD, frontotemporal dementia, and prion disease using NeuroX, a customized exome array. Frequencies in PCA of the variants annotated as pathogenic or potentially pathogenic were compared against âŒ4300 European-American population controls from the NHLBI Exome Sequencing Project. We identified 2 rare variants not previously reported in PCA, TREM2 Arg47His, and PSEN2 Ser130Leu. No other pathogenic or potentially pathogenic variants were detected in the screened dementia genes. In this first systematic variant screen of a PCA cohort, we report 2 rare mutations in TREM2 and PSEN2, validate our previously reported APOE Δ4 association, and demonstrate the utility of NeuroX
Genome-wide association study of corticobasal degeneration identifies risk variants shared with progressive supranuclear palsy
Corticobasal degeneration (CBD) is a neurodegenerative disorder affecting movement and cognition, definitively diagnosed only at autopsy. Here, we conduct a genome-wide association study (GWAS) in CBD cases (n = 152) and 3, 311 controls, and 67 CBD cases and 439 controls in a replication stage. Associations with meta-analysis were 17q21 at MAPT (P = 1.42 x 10(-12)),8p12 at lnc-KIF13B-1, a long non-coding RNA (rs643472;P = 3.41 x 10(-8)),and 2p22 at SOS1 (rs963731;P = 1.76 x 10(-7)). Testing for association of CBD with top progressive supranuclear palsy (PSP) GWAS single-nucleotide polymorphisms (SNPs) identified associations at MOBP (3p22;rs1768208;P = 2.07 x 10(-7)) and MAPT H1c (17q21;rs242557;P = 7.91 x 10(-6)). We previously reported SNP/transcript level associations with rs8070723/MAPT, rs242557/MAPT, and rs1768208/MOBP and herein identified association with rs963731/SOS1. We identify new CBD susceptibility loci and show that CBD and PSP share a genetic risk factor other than MAPT at 3p22 MOBP (myelin-associated oligodendrocyte basic protein)
- âŠ