483 research outputs found

    Interference in Exclusive Vector Meson Production in Heavy Ion Collisions

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    Photons emitted from the electromagnetic fields of relativistic heavy ions can fluctuate into quark anti-quark pairs and scatter from a target nucleus, emerging as vector mesons. These coherent interactions are identifiable by final states consisting of the two nuclei and a vector meson with a small transverse momentum. The emitters and targets can switch roles, and the two possibilities are indistinguishable, so interference may occur. Vector mesons are negative parity so the amplitudes have opposite signs. When the meson transverse wavelength is larger than the impact parameter, the interference is large and destructive. The short-lived vector mesons decay before amplitudes from the two sources can overlap, and so cannot interfere directly. However, the decay products are emitted in an entangled state, and the interference depends on observing the complete final state. The non-local wave function is an example of the Einstein-Podolsky-Rosen paradox.Comment: 13 pages with 3 figures; submitted to Physical Review Letter

    Particle emission following Coulomb excitation in ultrarelativistic heavy-ion collisions

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    We study nuclear reactions induced by virtual photons associated with Lorentz-boosted Coulomb fields of ultrarelativistic heavy ions. Evaporation, fission and multifragmentation mechanisms are included in a new RELDIS code, which describes the deexcitation of residual nuclei formed after single and double photon absorption in peripheral heavy-ion collisions. Partial cross sections for different dissociation channels, including the multiple neutron emission ones, are calculated and compared with data when available. Rapidity and transverse momentum distributions of nucleons, nuclear fragments and pions, produced electromagnetically, are also calculated. These results provide important information for designing large-rapidity detectors and zero-degree calorimeters at RHIC and LHC. The electromagnetic dissociation of nuclei imposes some constrains on the investigation of exotic particle production in gamma-gamma fusion reactions.Comment: 26 LaTeX pages including 8 figures, uses epsf.st

    Developmental axon pruning mediated by BDNF-p75NTR–dependent axon degeneration

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    The mechanisms that regulate the pruning of mammalian axons are just now being elucidated. Here, we describe a mechanism by which, during developmental sympathetic axon competition, winning axons secrete brain-derived neurotrophic factor (BDNF) in an activity-dependent fashion, which binds to the p75 neurotrophin receptor (p75NTR) on losing axons to cause their degeneration and, ultimately, axon pruning. Specifically, we found that pruning of rat and mouse sympathetic axons that project to the eye requires both activity-dependent BDNF and p75NTR. p75NTR and BDNF are also essential for activity-dependent axon pruning in culture, where they mediate pruning by directly causing axon degeneration. p75NTR, which is enriched in losing axons, causes axonal degeneration by suppressing TrkA-mediated signaling that is essential for axonal maintenance. These data provide a mechanism that explains how active axons can eliminate less-active, competing axons during developmental pruning by directly promoting p75NTR-mediated axonal degeneration

    Lymphocyte subsets and the role of Th1/Th2 balance in stressed chronic pain patients

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    Background: The complex regional pain syndrome (CRPS) and fibromyalgia (FM) are chronic pain syndromes occurring in highly stressed individuals. Despite the known connection between the nervous system and immune cells, information on distribution of lymphocyte subsets under stress and pain conditions is limited. Methods: We performed a comparative study in 15 patients with CRPS type I, 22 patients with FM and 37 age- and sex-matched healthy controls and investigated the influence of pain and stress on lymphocyte number, subpopulations and the Th1/Th2 cytokine ratio in T lymphocytes. Results: Lymphocyte numbers did not differ between groups. Quantitative analyses of lymphocyte subpopulations showed a significant reduction of cytotoxic CD8+ lymphocytes in both CRPS (p < 0.01) and FM (p < 0.05) patients as compared with healthy controls. Additionally, CRPS patients were characterized by a lower percentage of IL-2-producing T cell subpopulations reflecting a diminished Th1 response in contrast to no changes in the Th2 cytokine profile. Conclusions: Future studies are warranted to answer whether such immunological changes play a pathogenetic role in CRPS and FM or merely reflect the consequences of a pain-induced neurohumoral stress response, and whether they contribute to immunosuppression in stressed chronic pain patients. Copyright (c) 2008 S. Karger AG, Basel

    Phenotypic and genetic analysis of carcass quality of different breeds’ fatlings

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    Dissection and quantitative-genetic analysis of carcass quality was performed on 318 fatlings of 5 different pig breeds: German, Dutch and Belgian Landrace, Yorkshire and Hampshire. Significant fixed effects (sex and genotype) and regression effects (age and body weight at slaughter) were fitted in the statistical model. Genetic parameters were estimated using the restricted maximum likelihood (REML) procedure based on an animal model with multivariate analyses. Heritability estimates for carcass traits were moderate to high except for back weight and neck weight. Among most of the carcass quality traits, the midrange strong and very strong positive genetic and phenotypic correlations were established. The traits that were analyzed showed sufficient genetic variation, indicating that their improvement is possible through genetic selection. Genetic variability was stable and expressed and justified further genetic changes in the desired direction

    Electronic delocalization in two and three dimensions: differential aggregation in indium ‘metalloid’ clusters

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    Reduction of indium boryl precursors to give two- and three-dimensional M-M bonded networks is influenced by the choice of supporting ligand. While the unprecedented nanoscale cluster [In68(boryl)12]- (with an In12@In44@In12(boryl)12 concentric structure), can be isolated from the potassium reduction of a bis(boryl)indium(III) chloride precursor, analogous reduction of the corresponding (benzamidinate)In^III Br(boryl) system gives a nearplanar (and weakly aromatic) tetranuclear [In4(boryl)4]^2- system

    Progression of liver fibrosis in HIV/HCV genotype 1 co-infected patients is related to the T allele of the rsI2979860 polymorphism of the IL28B gene

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    <p>Abstract</p> <p>Objective</p> <p>HIV/HCV co-infection is characterised by accelerated progression of liver disease. Recently, the rsl2979860 C/T polymorphism in the <it>IL28B </it>gene has been linked to progression towards cirrhosis in HCV mono-infected patients and to treatment response of HCV-infection in HIV/HCV co-infected patients. Our aim was to clarify by non-invasive techniques if this polymorphism affects fibrosis progression in HIV/HCV co-infection.</p> <p>Methods</p> <p>In a cross-sectional design, liver stiffness (transient elastography), surrogate markers of liver fibrosis (APRI and FIB-4 scores) and rsl2979860 genotypes were analysed in 84 HCV/H1V co-infected patients. <it>IL28B </it>genotypes were determined by real-time PCR using a light cycler. In 56 HIV/HCV co-infected patients we also studied progression of fibrosis in relation to rsl2979860 C/T genotypes over two years.</p> <p>Results</p> <p>82% of the patients were on HAART (74% without detectable HI viremia) and 67% were haemophiliacs, respectively. HCV genotype 1 was present in 62%. Cross-sectional median liver stiffness was 7.4 kPa and correlated with APRI and FIB-4 scores (r = 0.6 each, p < 0.001). Frequencies of <it>IL28B </it>genotypes were: CC 50%, CT 43% and TT 7%. In the cross-sectional analysis liver stiffness values were not different between the various <it>IL28B</it>-genotypes. Upon follow-up under HAART carriers of a C allele did not show further progression, while liver stiffness significantly increased in HIV/HCV co-infected patients with the T allele (p = 0.047).</p> <p>Conclusion</p> <p>Although progression of liver fibrosis was low under HAART in our cohort, progression was more pronounced in HIV/HCV genotype 1 co-infected patients with the T allele.</p
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