93 research outputs found

    Obesity is associated with myelin oligodendrocyte glycoprotein antibody-associated disease in acute optic neuritis

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    Optic neuritis (ON) is a frequent presentation at onset of multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). The pathophysiology underlying these diseases, especially MOGAD, is still being elucidated. While obesity has been reported to potentially be a risk factor for MS, this has not been explored in NMOSD or MOGAD. We aimed to investigate a possible association between obesity (body mass index [BMI] > 30 kg/m(2)) in patients with MOGAD, aquaporin 4-IgG positive NMOSD (AQP4-IgG+ NMOSD) or MS. In this multicenter non-interventional retrospective study, data was collected from patients with a first ever demyelinating attack of ON subsequently diagnosed with MOGAD (n = 44), AQP4-IgG+ NMOSD (n = 49) or MS (n = 90) between 2005 and 2020. The following data was collected: age, sex, ethnicity, BMI (documented before corticosteroid treatment), and the ON etiology after diagnostic work-up. A mixed model analysis was performed to assess the potential of obesity or BMI to predict MOGAD-ON, and to distinguish MOGAD-ON from AQP4-IgG+ NMOSD-ON and MS-ON. Main outcome measures included BMI in patients with acute ON and subsequent diagnosis of MOGAD, AQP4-IgG+ NMOSD or MS. A higher BMI was significantly associated with a diagnosis of MOGAD-ON (p < 0.001); in MOGAD patients the mean BMI was 31.6 kg/m(2) (standard deviation (SD) 7.2), while the mean BMI was 24.7 kg/m(2) (SD 5.3) in AQP4-IgG+ NMOSD patients, and 26.9 kg/m(2) (SD 6.2) in MS patients. Mixed-effects multinomial logistic regression, adjusted for age and sex, with obesity as a binary variable, revealed that obesity was associated with a higher odds ratio (OR) of a subsequent MOGAD diagnosis (OR 5.466, 95% CI [2.039, 14.650], p = 0.001) in contradistinction with AQP4-IgG+ NMOSD. This study suggests an association between obesity and MOGAD. Our findings require further exploration, but could have significant pathophysiologic implications if confirmed in larger prospective studies

    Longitudinal retinal changes in MOGAD

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    OBJECTIVE: Patients with myelin oligodendrocyte glycoprotein antibody (MOG-IgG) associated disease (MOGAD) suffer from severe optic neuritis (ON) leading to retinal neuro-axonal loss, which can be quantified by optical coherence tomography (OCT). We assessed whether ON-independent retinal atrophy can be detected in MOGAD. METHODS: Eighty MOGAD patients and 139 healthy controls (HC) were included. OCT data was acquired with 1) Spectralis spectral domain OCT (MOGAD (N=66) and HC (N=103)) and 2) Cirrus HD-OCT (MOGAD (N=14) and HC (N=36)). Macular combined ganglion cell and inner plexiform layer (GCIPL) and peripapillary retinal nerve fibre layer (pRNFL) were quantified. RESULTS: At baseline, GCIPL and pRNFL were lower in MOGAD eyes with a history of ON (MOGAD-ON) compared with MOGAD eyes without a history of ON (MOGAD-NON) and HC (p12 months ago (p<0.001). The overall MOGAD cohort did not exhibit faster GCIPL thinning compared with HC. INTERPRETATION: Our study suggests the absence of attack-independent retinal damage in MOGAD. Yet, ongoing neuroaxonal damage or oedema resolution seems to occur for up to 12 months after ON, which is longer than what has been reported with other ON forms. These findings support that the pathomechanisms underlying optic nerve involvement and the evolution of OCT retinal changes after ON is distinct in MOGAD. This article is protected by copyright. All rights reserved

    Measurement of the mass difference between top quark and antiquark in pp collisions at root s=8 TeV

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    Studies of azimuthal dihadron correlations in ultra-central PbPb collisions at=2.76 TeV

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    Observation of a peaking structure in the J/psi phi mass spectrum from B(+/-) to J/psi phi K(+/-) decays

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    Measurement of the production cross section for a W boson and two b jets in pp collisions at root s=7 TeV

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    The production cross section for a W boson and two b jets is measured using proton&#8211;proton collisions at s=7 TeV in a data sample collected with the CMS experiment at the LHC corresponding to an integrated luminosity of 5.0 fb &#8722;1 . The W+bb¯ events are selected in the W&#8594;&#956;&#957; decay mode by requiring a muon with transverse momentum pT>25 GeV and pseudorapidity |&#951;|25 GeV and |&#951;|<2.4 . The measured W+bb¯ production cross section in the fiducial region, calculated at the level of final-state particles, is &#963;(pp&#8594;W+bb¯)×B(W&#8594;&#956;&#957;)=0.53±0.05(stat.)±0.09(syst.)±0.06(theo.)±0.01(lum.) pb , in agreement with the standard model prediction. In addition, kinematic distributions of the W+bb¯ system are in agreement with the predictions of a simulation using MadGraph and pythia

    Measurements of the t(t)Overbar charge asymmetry using the dilepton decay channel in pp collisions at root s=7 TeV

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    The tt¯ charge asymmetry in proton-proton collisions at s&#8730; = 7 TeV is measured using the dilepton decay channel (ee, e &#956; , or &#956;&#956; ). The data correspond to a total integrated luminosity of 5.0 fb &#8722;1 , collected by the CMS experiment at the LHC. The tt and lepton charge asymmetries, defined as the differences in absolute values of the rapidities between the reconstructed top quarks and antiquarks and of the pseudorapidities between the positive and negative leptons, respectively, are measured to be A C = &#8722;0 . 010 ± 0 . 017 (stat . ) ± 0 . 008 (syst . ) and AlepC = 0 . 009 ± 0 . 010 (stat . ) ± 0 . 006 (syst . ). The lepton charge asymmetry is also measured as a function of the invariant mass, rapidity, and transverse momentum of the tt¯ system. All measurements are consistent with the expectations of the standard model

    Distinct germline genetic susceptibility profiles identified for common non-Hodgkin lymphoma subtypes

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    Lymphoma risk is elevated for relatives with common non-Hodgkin lymphoma (NHL) subtypes, suggesting shared genetic susceptibility across subtypes. To evaluate the extent of mutual heritability among NHL subtypes and discover novel loci shared among subtypes, we analyzed data from eight genome-wide association studies within the InterLymph Consortium, including 10,629 cases and 9505 controls. We utilized Association analysis based on SubSETs (ASSET) to discover loci for subsets of NHL subtypes and evaluated shared heritability across the genome using Genome-wide Complex Trait Analysis (GCTA) and polygenic risk scores. We discovered 17 genome-wide significant loci (P &lt; 5 × 10−8) for subsets of NHL subtypes, including a novel locus at 10q23.33 (HHEX) (P = 3.27 × 10−9). Most subset associations were driven primarily by only one subtype. Genome-wide genetic correlations between pairs of subtypes varied broadly from 0.20 to 0.86, suggesting substantial heterogeneity in the extent of shared heritability among subtypes. Polygenic risk score analyses of established loci for different lymphoid malignancies identified strong associations with some NHL subtypes (P &lt; 5 × 10−8), but weak or null associations with others. Although our analyses suggest partially shared heritability and biological pathways, they reveal substantial heterogeneity among NHL subtypes with each having its own distinct germline genetic architecture

    Searches for light- and heavy-flavour three-jet resonances in pp collisions at root s=8 TeV

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    Measurement of the top-quark mass in all-jets tt events in pp collisions at root = 7 TeV

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    The mass of the top quark is measured using a sample of tt¯ candidate events with at least six jets in the final state. The sample is selected from data collected with the CMS detector in pp collisions at s&#8730;=7 TeV in 2011 and corresponds to an integrated luminosity of 3.54 fb&#8722;1 . The mass is reconstructed for each event employing a kinematic fit of the jets to a tt¯ hypothesis. The top-quark mass is measured to be 173.49±0.69(stat.)±1.21(syst.) GeV. A combination with previously published measurements in other decay modes by CMS yields a mass of 173.54±0.33(stat.)±0.96(syst.) GeV
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