22 research outputs found

    Moments of parton distribution functions for the pion and rho meson from Nf = 2+1 lattice QCD

    Get PDF
    We compute the second Mellin moments of parton distribution functions for the pion and rho meson from Nf=2+1N_f = 2 + 1 lattice QCD using improved Wilson fermions. Our results are presented in terms of singlet and non-singlet flavor combinations and, for the first time, take disconnected contributions fully into account. Besides condensing the common knowledge about spin-1 structure functions and parton distribution functions, we provide a detailed description of the software stack implemented by our group, in order to compute quark-line connected three-point functions using stochastic estimators. The main application is based on the factorization of the entire correlation function into two parts which are evaluated with open spin- (and to some extent flavor-) indices. This allows us to estimate the two contributions of the factorization simultaneously for many different initial and final states and momenta, with little computational overhead. Our numerical analysis yields moments of the structure function F1F_1 (pion and rho) and of the structure function b1b_1, providing additional contributions in the case of spin-1 particles. To this end we use 26 gauge ensembles, mainly generated by the CLS effort, with pion masses ranging from 214 MeV up to 420 MeV and with five different lattice spacings in the range of 0.05 fm to 0.1 fm in our numerical analysis. This choice of gauge configurations enables us to resolve the quark mass dependencies reliably, as well as to extrapolate to the continuum limit. However, due to the resonance character of the rho meson, our final results are possibly contaminated by additional two-pion states, which we also discuss. We present our results in the MS\overline{\text{MS}} scheme at μ=2\mu = 2 GeV We find v2(u+d+s)=0.220(207),v2(u+d2s)=0.344(28),a2(u+d+s)=0.285(295),a2(u+d2s)=0.384(52),d2(u+d+s)=0.226(124),d2(u+d2s)=0.163(39), v_2^{(u+d+s)} = 0.220 (207), v_2^{(u+d-2s)} = 0.344 (28), a_2^{(u+d+s)} = 0.285 (295), a_2^{(u+d-2s)} = 0.384 (52), d_2^{(u+d+s)} = 0.226 (124), d_2^{(u+d-2s)} = 0.163 (39), for the second moment v2v_2 of the pion structure function F1F_1, the second moment a2a_2 of the rho structure function F1F_1, and the second moment d2d_2 of the rho structure function b1b_1 respectively. Based on these values we finally conclude, that the valence quarks in the pion carry about 35% of the total momentum, in the rho the valence quarks carry about 40% of the total momentum, and the non-vanishing values for d2d_2 suggest that the quarks in the rho meson carry a substantial amount of orbital angular momentum

    Mellin moments of spin dependent and independent PDFs of the pion and rho meson

    Get PDF
    We compute the second moments of pion and rho parton distribution functions in lattice QCD with Nf=2+1 flavors of improved Wilson fermions. We determine both singlet and nonsinglet flavor combinations and, for the first time, take disconnected contributions fully into account. In the case of the rho, we also calculate the additional contribution arising from the b1 structure function. The numerical analysis includes 26 ensembles, mainly generated by the CLS effort, with pion masses ranging from 420 down to 214 MeV and with 5 different lattice spacings in the range of 0.1 to 0.05 fm. This enables us to take the continuum limit, as well as to resolve the quark mass dependencies reliably. Additionally we discuss the contaminations of rho correlation functions by two-pion states

    Medical treatment of pulmonary hypertension in adults with congenital heart disease : updated and extended results from the International COMPERA-CHD Registry

    Get PDF
    Funding Information: The authors are indebted to the COMPERA investigators and their staff. We explicitly thank Dr. Claudia S. Copeland for the professional editing of the final draft of the manuscript. Funding: COMPERA is funded by unrestricted grants from Acceleron, Actelion Pharmaceuticals (Janssen), Bayer, OMT and GSK. These companies were not involved in data analysis or the writing of this manuscript. Funding Information: ICMJE uniform disclosure form (available at https:// dx.doi.org/10.21037/cdt-21-351). The series “Current Management Aspects in Adult Congenital Heart Disease (ACHD): Part IV” was commissioned by the editorial office without any funding or sponsorship. Dr. DH reports non-financial support from Actelion, Boehringer-Ingelheim, and Shire, outside the submitted work; Dr. DP reports personal fees from Actelion, Biogen, Aspen, Bayer, Boehringer Ingelheim, Daiichi Sankyo, and Sanofi, outside the submitted work; Dr. MD reports personal fees from Actelion, Bayer, GSK and MSD, outside the submitted work; Dr. HAG reports personal fees from Actelion, Bayer, Gilead, GSK, MSD, Pfizer and United Therapeutics, outside the submitted work; Dr. MG reports personal fees from Actelion, Bayer and GSK, outside the submitted work; Dr. MMH reports personal fees from Acceleron, Actelion, Bayer, MSD and Pfizer, outside the submitted work; Dr. CDV reports personal fees from Actelion, Bayer, GSK, MSD, Pfizer, and United Therapeutics, outside the submitted work; Dr. RE reports personal fees from Actelion, Boehringer Ingelheim, OMT, Bayer, and Berlin Chemie; grants from Actelion and Boehringer Ingelheim, outside the submitted work; Dr. MH reports grants and personal fees from Actelion, personal fees from Bayer, Berlin Chemie, Boehringer Ingelheim, GSK, Janssen, Novartis and MSD, outside the submitted work; Dr. MH reports personal fees from Acceleron, Actelion, AstraZeneca, Bayer, BERLIN CHEMIE, GSK, MSD, Novartis and OMT, outside the submitted work; Dr. HW reports personal fees from Action, Bayer, Biotest, Boehringer, GSK, Pfizer, and Roche, outside the submitted work; Dr. DS reports personal fees from Actelion, Bayer, and GSK, outside the submitted work; Dr. LS reports personal fees from Actelion, Bayer, and MSD, outside the submitted work; Dr. SU reports grants from Swiss National Science Foundation, Zurich Lung, Swiss Lung, and Orpha Swiss, grants and personal fees from Actelion SA/Johnson & Johnson, Switzerland, and MSD Switzerland, outside the submitted work; Dr. TJL reports personal fees from Actelion, Janssen-Cilag, BMS, MSD, and OMT GmbH, outside the submitted work; Dr. LB reports personal fees from Actelion, outside the submitted work; Dr. MC reports personal fees from Boehringer Ingelheim Pharma GmbH, Roche Pharma, and Boehringer Ingelheim, outside the submitted work; Dr. HW reports personal fees from Boehringer Ingelheim, and Roche, outside the submitted work. Dr. EG reports personal fees from Actelion, Janssen, Bayer, MSD, Bial, OrPha Swiss GmbH, OMT and Medscape, outside the submitted work; Dr. SR reports personal fees from Actelion, Bayer, GSK, Pfizer, Novartis, Gilead, MSD, and United Therapeutics, outside the submitted work. The authors have no other conflicts of interest to declare. Publisher Copyright: © Cardiovascular Diagnosis and Therapy. All rights reserved.Background: Pulmonary arterial hypertension (PAH) is common in congenital heart disease (CHD). Because clinical-trial data on PAH associated with CHD (PAH-CHD) remain limited, registry data on the long-term course are essential. This analysis aimed to update information from the COMPERA-CHD registry on management strategies based on real-world data. Methods: The prospective international pulmonary hypertension registry COMPERA has since 2007 enrolled more than 10,000 patients. COMPERA-CHD is a sub-registry for patients with PAH-CHD Results: A total of 769 patients with PAH-CHD from 62 specialized centers in 12 countries were included into COMPERA-CHD from January 2007 through September 2020. At the last follow-up in 09/2020, patients [mean age 45.3±16.8 years; 512 (66%) female] had either post-tricuspid shunts (n=359; 46.7%), pre-tricuspid shunts (n=249; 32.4%), complex CHD (n=132; 17.2%), congenital left heart or aortic valve or aortic disease (n=9; 1.3%), or miscellaneous CHD (n=20; 2.6%). The mean 6-minute walking distance was 369±121 m, and 28.2%, 56.0%, and 3.8% were in WHO functional class I/II, III or IV, respectively (12.0% unknown). Compared with the previously published COMPERA-CHD data, after 21 months of followup, the number of included PAH-CHD patients increased by 91 (13.4%). Within this group the number of Eisenmenger patients rose by 39 (16.3%), the number of “Non-Eisenmenger PAH” patients by 45 (26.9%). Currently, among the 674 patients from the PAH-CHD group with at least one follow-up, 450 (66.8%) received endothelin receptor antagonists (ERA), 416 (61.7%) PDE-5 inhibitors, 85 (12.6%) prostacyclin analogues, and 36 (5.3%) the sGC stimulator riociguat. While at first inclusion in the COMPERA-CHD registry, treatment was predominantly monotherapy (69.3%), this has shifted to favoring combination therapy in the current group (53%). For the first time, the nature, frequency, and treatment of significant comorbidities requiring supportive care and medication are described. Conclusions: Analyzing “real life data” from the international COMPERA-CHD registry, we present a comprehensive overview about current management modalities and treatment concepts in PAH-CHD. There was an trend towards more aggressive treatment strategies and combination therapies. In the future, particular attention must be directed to the “Non-Eisenmenger PAH” group and to patients with complex CHD, including Fontan patients.publishersversionPeer reviewe

    The genomic and transcriptional landscape of primary central nervous system lymphoma

    Get PDF
    Primary lymphomas of the central nervous system (PCNSL) are mainly diffuse large B-cell lymphomas (DLBCLs) confined to the central nervous system (CNS). Molecular drivers of PCNSL have not been fully elucidated. Here, we profile and compare the whole-genome and transcriptome landscape of 51 CNS lymphomas (CNSL) to 39 follicular lymphoma and 36 DLBCL cases outside the CNS. We find recurrent mutations in JAK-STAT, NFkB, and B-cell receptor signaling pathways, including hallmark mutations in MYD88 L265P (67%) and CD79B (63%), and CDKN2A deletions (83%). PCNSLs exhibit significantly more focal deletions of HLA-D (6p21) locus as a potential mechanism of immune evasion. Mutational signatures correlating with DNA replication and mitosis are significantly enriched in PCNSL. TERT gene expression is significantly higher in PCNSL compared to activated B-cell (ABC)-DLBCL. Transcriptome analysis clearly distinguishes PCNSL and systemic DLBCL into distinct molecular subtypes. Epstein-Barr virus (EBV)+ CNSL cases lack recurrent mutational hotspots apart from IG and HLA-DRB loci. We show that PCNSL can be clearly distinguished from DLBCL, having distinct expression profiles, IG expression and translocation patterns, as well as specific combinations of genetic alterations

    Retrospective evaluation of whole exome and genome mutation calls in 746 cancer samples

    No full text
    Funder: NCI U24CA211006Abstract: The Cancer Genome Atlas (TCGA) and International Cancer Genome Consortium (ICGC) curated consensus somatic mutation calls using whole exome sequencing (WES) and whole genome sequencing (WGS), respectively. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2,658 cancers across 38 tumour types, we compare WES and WGS side-by-side from 746 TCGA samples, finding that ~80% of mutations overlap in covered exonic regions. We estimate that low variant allele fraction (VAF < 15%) and clonal heterogeneity contribute up to 68% of private WGS mutations and 71% of private WES mutations. We observe that ~30% of private WGS mutations trace to mutations identified by a single variant caller in WES consensus efforts. WGS captures both ~50% more variation in exonic regions and un-observed mutations in loci with variable GC-content. Together, our analysis highlights technological divergences between two reproducible somatic variant detection efforts

    Baryonic and mesonic 3-point functions with open spin indices

    No full text
    We have implemented a new way of computing three-point correlation functions. It is based on a factorization of the entire correlation function into two parts which are evaluated with open spin-(and to some extent flavor-) indices. This allows us to estimate the two contributions simultaneously for many different initial and final states and momenta, with little computational overhead. We explain this factorization as well as its efficient implementation in a new library which has been written to provide the necessary functionality on modern parallel architectures and on CPUs, including Intel’s Xeon Phi series
    corecore