71 research outputs found

    Measurement of a small atmospheric νμ/νe\nu_\mu/\nu_e ratio

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    From an exposure of 25.5~kiloton-years of the Super-Kamiokande detector, 900 muon-like and 983 electron-like single-ring atmospheric neutrino interactions were detected with momentum pe>100p_e > 100 MeV/cc, pμ>200p_\mu > 200 MeV/cc, and with visible energy less than 1.33 GeV. Using a detailed Monte Carlo simulation, the ratio (μ/e)DATA/(μ/e)MC(\mu/e)_{DATA}/(\mu/e)_{MC} was measured to be 0.61±0.03(stat.)±0.05(sys.)0.61 \pm 0.03(stat.) \pm 0.05(sys.), consistent with previous results from the Kamiokande, IMB and Soudan-2 experiments, and smaller than expected from theoretical models of atmospheric neutrino production.Comment: 14 pages with 5 figure

    Decreased hippocampal translocator protein (18 kDa) expression in alcohol dependence: a [11C]PBR28 PET study

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    Repeated withdrawal from alcohol is clinically associated with progressive cognitive impairment. Microglial activation occurring during pre-clinical models of alcohol withdrawal is associated with learning deficits. We investigated whether there was microglial activation in recently detoxified alcohol-dependent patients (ADP), using [11C]PBR28 positron emission tomography (PET), selective for the 18kDa translocator protein (TSPO) highly expressed in activated microglia and astrocytes. We investigated the relationship between microglial activation and cognitive performance. Twenty healthy control (HC) subjects (45±13; M:F 14:6) and nine ADP (45±6, M:F 9:0) were evaluated. Dynamic PET data were acquired for 90 min following an injection of 331±15 MBq [11C]PBR28. Regional volumes of distribution (VT) for regions of interest (ROIs) identified a priori were estimated using a two-tissue compartmental model with metabolite-corrected arterial plasma input function. ADP had an ~20% lower [11C]PBR28 VT, in the hippocampus (F(1,24) 5.694; P=0.025), but no difference in VT in other ROIs. Hippocampal [11C]PBR28 VT was positively correlated with verbal memory performance in a combined group of HC and ADP (r=0.720, P<0.001), an effect seen in HC alone (r=0.738; P=0.001) but not in ADP. We did not find evidence for increased microglial activation in ADP, as seen pre-clinically. Instead, our findings suggest lower glial density or an altered activation state with lower TSPO expression. The correlation between verbal memory and [11C]PBR28 VT, raises the possibility that abnormalities of glial function may contribute to cognitive impairment in ADP

    Cluster Lenses

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    Clusters of galaxies are the most recently assembled, massive, bound structures in the Universe. As predicted by General Relativity, given their masses, clusters strongly deform space-time in their vicinity. Clusters act as some of the most powerful gravitational lenses in the Universe. Light rays traversing through clusters from distant sources are hence deflected, and the resulting images of these distant objects therefore appear distorted and magnified. Lensing by clusters occurs in two regimes, each with unique observational signatures. The strong lensing regime is characterized by effects readily seen by eye, namely, the production of giant arcs, multiple-images, and arclets. The weak lensing regime is characterized by small deformations in the shapes of background galaxies only detectable statistically. Cluster lenses have been exploited successfully to address several important current questions in cosmology: (i) the study of the lens(es) - understanding cluster mass distributions and issues pertaining to cluster formation and evolution, as well as constraining the nature of dark matter; (ii) the study of the lensed objects - probing the properties of the background lensed galaxy population - which is statistically at higher redshifts and of lower intrinsic luminosity thus enabling the probing of galaxy formation at the earliest times right up to the Dark Ages; and (iii) the study of the geometry of the Universe - as the strength of lensing depends on the ratios of angular diameter distances between the lens, source and observer, lens deflections are sensitive to the value of cosmological parameters and offer a powerful geometric tool to probe Dark Energy. In this review, we present the basics of cluster lensing and provide a current status report of the field.Comment: About 120 pages - Published in Open Access at: http://www.springerlink.com/content/j183018170485723/ . arXiv admin note: text overlap with arXiv:astro-ph/0504478 and arXiv:1003.3674 by other author

    Predictions for Ultra-Deep Radio Counts of Star-Forming Galaxies

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    We have worked out predictions for the radio counts of star-forming galaxies down to nJy levels, along with redshift distributions down to the detection limits of the phase 1 Square Kilometer Array MID telescope (SKA1-MID) and of its precursors. Such predictions were obtained by coupling epoch dependent star formation rate (SFR) functions with relations between SFR and radio (synchrotron and free-free) emission. The SFR functions were derived taking into account both the dust obscured and the unobscured star-formation, by combining far-infrared (FIR), ultra-violet (UV) and H_alpha luminosity functions up to high redshifts. We have also revisited the South Pole Telescope (SPT) counts of dusty galaxies at 95,GHz performing a detailed analysis of the Spectral Energy Distributions (SEDs). Our results show that the deepest SKA1-MID surveys will detect high-z galaxies with SFRs two orders of magnitude lower compared to Herschel surveys. The highest redshift tails of the distributions at the detection limits of planned SKA1-MID surveys comprise a substantial fraction of strongly lensed galaxies. We predict that a survey down to 0.25 microJy at 1.4 GHz will detect about 1200 strongly lensed galaxies per square degree, at redshifts of up to 10. For about 30% of them the SKA1-MID will detect at least 2 images. The SKA1-MID will thus provide a comprehensive view of the star formation history throughout the re-ionization epoch, unaffected by dust extinction. We have also provided specific predictions for the EMU/ASKAP and MIGHTEE/MeerKAT survey

    Pemphigus autoimmunity: Hypotheses and realities

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    The goal of contemporary research in pemphigus vulgaris and pemphigus foliaceus is to achieve and maintain clinical remission without corticosteroids. Recent advances of knowledge on pemphigus autoimmunity scrutinize old dogmas, resolve controversies, and open novel perspectives for treatment. Elucidation of intimate mechanisms of keratinocyte detachment and death in pemphigus has challenged the monopathogenic explanation of disease immunopathology. Over 50 organ-specific and non-organ-specific antigens can be targeted by pemphigus autoimmunity, including desmosomal cadherins and other adhesion molecules, PERP cholinergic and other cell membrane (CM) receptors, and mitochondrial proteins. The initial insult is sustained by the autoantibodies to the cell membrane receptor antigens triggering the intracellular signaling by Src, epidermal growth factor receptor kinase, protein kinases A and C, phospholipase C, mTOR, p38 MAPK, JNK, other tyrosine kinases, and calmodulin that cause basal cell shrinkage and ripping desmosomes off the CM. Autoantibodies synergize with effectors of apoptotic and oncotic pathways, serine proteases, and inflammatory cytokines to overcome the natural resistance and activate the cell death program in keratinocytes. The process of keratinocyte shrinkage/detachment and death via apoptosis/oncosis has been termed apoptolysis to emphasize that it is triggered by the same signal effectors and mediated by the same cell death enzymes. The natural course of pemphigus has improved due to a substantial progress in developing of the steroid-sparing therapies combining the immunosuppressive and direct anti-acantholytic effects. Further elucidation of the molecular mechanisms mediating immune dysregulation and apoptolysis in pemphigus should improve our understanding of disease pathogenesis and facilitate development of steroid-free treatment of patients

    Measurement of dijet photoproduction for events with a leading neutron at HERA

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    Differential cross sections for dijet photoproduction and this process in association with a leading neutron, e+ + p -> e+ + jet + jet + X (+ n), have been measured with the ZEUS detector at HERA using an integrated luminosity of 40 pb-1. The fraction of dijet events with a leading neutron was studied as a function of different jet and event variables. Single- and double-differential cross sections are presented as a function of the longitudinal fraction of the proton momentum carried by the leading neutron, xL, and of its transverse momentum squared, pT^2. The dijet data are compared to inclusive DIS and photoproduction results; they are all consistent with a simple pion-exchange model. The neutron yield as a function of xL was found to depend only on the fraction of the proton beam energy going into the forward region, independent of the hard process. No firm conclusion can be drawn on the presence of rescattering effects.Comment: 40 pages, 18 figure

    Applying polygenic risk scoring for psychiatric disorders to a large family with bipolar disorder and major depressive disorder

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    Psychiatric disorders are thought to have a complex genetic pathology consisting of interplay of common and rare variation. Traditionally, pedigrees are used to shed light on the latter only, while here we discuss the application of polygenic risk scores to also highlight patterns of common genetic risk. We analyze polygenic risk scores for psychiatric disorders in a large pedigree (n similar to 260) in which 30% of family members suffer from major depressive disorder or bipolar disorder. Studying patterns of assortative mating and anticipation, it appears increased polygenic risk is contributed by affected individuals who married into the family, resulting in an increasing genetic risk over generations. This may explain the observation of anticipation in mood disorders, whereby onset is earlier and the severity increases over the generations of a family. Joint analyses of rare and common variation may be a powerful way to understand the familial genetics of psychiatric disorders
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