Global Analysis of Fragmentation Functions for Eta Mesons

Fragmentation functions for eta mesons are extracted at next-to-leading order accuracy of QCD in a global analysis of data taken in electron-positron annihilation and proton-proton scattering experiments. The obtained parametrization is in good agreement with all data sets analyzed and can be utilized, for instance, in future studies of double-spin asymmetries for single-inclusive eta production. The Lagrange multiplier technique is used to estimate the uncertainties of the fragmentation functions and to assess the role of the different data sets in constraining them.Comment: 11 pages, 8 figures, updated reference

potential biomarkers of haemophilic arthropathy correlations with compatible additive magnetic resonance imaging scores

Introduction: Although biomarkers are useful diagnostic tools to assess joint damage in osteoarthritis and rheumatoid arthritis, few data exist for biomarkers of haemophilic arthropathy. Aim: To evaluate the association between biomarkers and compatible additive magnetic resonance imaging (MRI) scores in patients with severe haemophilia A. Methods: Patients aged 12–35 years with no history of factor VIII (FVIII) inhibitors were enrolled in a controlled, cross-sectional, multinational investigation. Patients received primary or secondary prophylaxis or on-demand treatment with FVIII and underwent MRI on four joints (two ankles, two knees). Soluble biomarkers of cartilage and bone degradation, inflammation, and angiogenesis were assessed (serum levels of C-terminal telopeptides of type I collagen [CTX-I], cartilage oligomeric matrix protein [COMP], chondroitin-sulphate aggrecan turnover 846 epitope [CS846], tissue inhibitor of metalloproteinase 1 [TIMP-1]; plasma levels of vascular endothelial growth factor [VEGF], matrix metalloproteinases 3 and 9 [MMP3, MMP9]). Relationships between biomarkers and MRI scores were evaluated using Spearman rank correlation. Results: Biomarkers were assessed in 117 of 118 per-protocol patients. Mean and median CTX-I, COMP, TIMP-1, MMP3, MMP9, and VEGF values were within normal ranges (reference range not available for CS846 in healthy volunteers). No correlations between biomarkers and MRI scores were found, with the exception of CS846, which showed significant correlation in a subgroup of 22 on-demand patients (r = 0.436; P = 0.04). Conclusions: Compatible additive MRI scores showed no clear correlations with any of the potential biomarkers for haemophilic arthropathy in the overall population. CS846 levels were significantly correlated with MRI scores in patients treated on demand. (Less

The target asymmetry in hard vector-meson electroproduction and parton angular momenta

The target asymmetry for electroproduction of vector mesons is investigated within the handbag approach. While the generalized parton distribution (GPD) H is taken from a previous analysis of the elctroproduction cross section, we here construct the GPD E from double distributions and constrain it by the Pauli form factors of the nucleon, positivity bounds and sum rules. Predictions for the target asymmetry are given for various vector mesons and discussed how experimental data on the asymmetry will further constrain E and what we may learn about the angular momenta the partons carry.Comment: 24 pages, 11 figures, late

Fine Mapping Major Histocompatibility Complex Associations in Psoriasis and Its Clinical Subtypes

Psoriasis vulgaris (PsV) risk is strongly associated with variation within the major histocompatibility complex (MHC) region, but its genetic architecture has yet to be fully elucidated. Here, we conducted a large-scale fine-mapping study of PsV risk in the MHC region in 9,247 PsV-affected individuals and 13,589 controls of European descent by imputing class I and II human leukocyte antigen (HLA) genes from SNP genotype data. In addition, we imputed sequence variants for MICA, an MHC HLA-like gene that has been associated with PsV, to evaluate association at that locus as well. We observed that HLA-C*06:02 demonstrated the lowest p value for overall PsV risk (p = 1.7 x 10(-364)). Stepwise analysis revealed multiple HLA-C*06:02-independent risk variants in both class I and class II HLA genes for PsV susceptibility (HLA-C*12:03, HLA-B amino acid positions 67 and 9, HLA-A amino acid position 95, and HLA-DQ alpha 1 amino acid position 53; p \u3c 5.0 x 10(-8)), but no apparent risk conferred by MICA. We further evaluated risk of two major clinical subtypes of PsV, psoriatic arthritis (PsA; n = 3,038) and cutaneous psoriasis (PsC; n = 3,098). We found that risk heterogeneity between PsA and PsC might be driven by HLA-B amino acid position 45 (P-omnibus = 2.2 x 10(-11)), indicating that different genetic factors underlie the overall risk of PsV and the risk of specific PsV subphenotypes. Our study illustrates the value of high-resolution HLA and MICA imputation for fine mapping causal variants in the MHC

The nucleon form-factors of the energy momentum tensor in the Skyrme model

The nucleon form factors of the energy-momentum tensor are studied in the large-Nc limit in the framework of the Skyrme model.Comment: 19 pages, 11 Figures, 2 Tables; correction in footnote 2, extension in App.D, some reformulations, references added, results and conclusions unchange

Pion production in deeply virtual Compton scattering

Using a soft pion theorem based on chiral symmetry and a $\Delta(1232)$ resonance model we propose an estimate for the production cross section of low energy pions in the deeply virtual Compton scattering (DVCS) process. In particular, we express the $e p \to e \gamma \pi N$ processes in terms of generalized parton distributions. We provide estimates of the contamination of the $e p \to e \gamma p$ DVCS observables due to this associated pion production processes when the experimental data are not fully exclusive, for a set of kinematical conditions representative of present or planned experiments at JLab, HERMES and COMPASS.Comment: 50 pages, 22 figure

Improved bone defect healing by a superagonistic GDF5 variant derived from a patient with multiple synostoses syndrome

Multiple synostoses syndrome 2 (SYNS2) is a rare genetic disease characterized by multiple fusions of the joints of the extremities, like phalangeal joints, carpal and tarsal joints or the knee and elbows. SYNS2 is caused by point mutations in the Growth and Differentiation Factor 5 (GDF5), which plays an essential role during skeletal development and regeneration. We selected one of the SYNS2-causing GDF5 mutations, p.N445T, which is known to destabilize the interaction with the Bone Morphogenetic Protein (BMP) antagonist NOGGIN (NOG), in order to generate the superagonistic GDF5 variant GDF5(N445T). In this study, we tested its capacity to support regeneration in a rat critical-sized defect model in vivo. MicroCT and histological analyses indicate that GDF5(N445T)-treated defects show faster and more efficient healing compared to GDF5 wild type (GDF5(wt))-treated defects. Microarray-based gene expression and quantitative PCR analyses from callus tissue point to a specific acceleration of the early phases of bone healing, comprising the inflammation and chondrogenesis phase. These results support the concept that disease-deduced growth factor variants are promising lead structures for novel therapeutics with improved clinical activities