Need satisfaction in intergroup contact:A multinational study of pathways toward social change

none43siFinanziamenti esterni a vari co-autoriWhat role does intergroup contact play in promoting support for social change toward greater social equality? Drawing on the needs-based model of reconciliation, we theorized that when inequality between groups is perceived as illegitimate, disadvantaged group members will experience a need for empowerment and advantaged group members a need for acceptance. When intergroup contact satisfies each group's needs, it should result in more mutual support for social change. Using four sets of survey data collected through the Zurich Intergroup Project in 23 countries, we tested several preregistered predictions, derived from the above reasoning, across a large variety of operationalizations. Two studies of disadvantaged groups (Ns = 689 ethnic minority members in Study 1 and 3,382 sexual/gender minorities in Study 2) support the hypothesis that, after accounting for the effects of intergroup contact and perceived illegitimacy, satisfying the need for empowerment (but not acceptance) during contact is positively related to support for social change. Two studies with advantaged groups (Ns = 2,937 ethnic majority members in Study 3 and 4,203 cis-heterosexual individuals in Study 4) showed that, after accounting for illegitimacy and intergroup contact, satisfying the need for acceptance (but also empowerment) is positively related to support for social change. Overall, findings suggest that intergroup contact is compatible with efforts to promote social change when group-specific needs are met. Thus, to encourage support for social change among both disadvantaged and advantaged group members, it is essential that, besides promoting mutual acceptance, intergroup contact interventions also give voice to and empower members of disadvantaged groups.mixedHässler, Tabea; Ullrich, Johannes; Sebben, Simone; Shnabel, Nurit; Bernardino, Michelle; Valdenegro, Daniel; Van Laar, Colette; González, Roberto; Visintin, Emilio Paolo; Tropp, Linda R; Ditlmann, Ruth K; Abrams, Dominic; Aydin, Anna Lisa; Pereira, Adrienne; Selvanathan, Hema Preya; von Zimmermann, Jorina; Lantos, Nóra Anna; Sainz, Mario; Glenz, Andreas; Kende, Anna; Oberpfalzerová, Hana; Bilewicz, Michal; Branković, Marija; Noor, Masi; Pasek, Michael H; Wright, Stephen C; Žeželj, Iris; Kuzawinska, Olga; Maloku, Edona; Otten, Sabine; Gul, Pelin; Bareket, Orly; Corkalo Biruski, Dinka; Mugnol-Ugarte, Luiza; Osin, Evgeny; Baiocco, Roberto; Cook, Jonathan E; Dawood, Maneeza; Droogendyk, Lisa; Loyo, Angélica Herrera; Jelić, Margareta; Kelmendi, Kaltrina; Pistella, JessicaHässler, Tabea; Ullrich, Johannes; Sebben, Simone; Shnabel, Nurit; Bernardino, Michelle; Valdenegro, Daniel; Van Laar, Colette; González, Roberto; Visintin, Emilio Paolo; Tropp, Linda R; Ditlmann, Ruth K; Abrams, Dominic; Aydin, Anna Lisa; Pereira, Adrienne; Selvanathan, Hema Preya; von Zimmermann, Jorina; Lantos, Nóra Anna; Sainz, Mario; Glenz, Andreas; Kende, Anna; Oberpfalzerová, Hana; Bilewicz, Michal; Branković, Marija; Noor, Masi; Pasek, Michael H; Wright, Stephen C; Žeželj, Iris; Kuzawinska, Olga; Maloku, Edona; Otten, Sabine; Gul, Pelin; Bareket, Orly; Corkalo Biruski, Dinka; Mugnol-Ugarte, Luiza; Osin, Evgeny; Baiocco, Roberto; Cook, Jonathan E; Dawood, Maneeza; Droogendyk, Lisa; Loyo, Angélica Herrera; Jelić, Margareta; Kelmendi, Kaltrina; Pistella, Jessic

A large-scale test of the link between intergroup contact and support for social change

Guided by the early findings of social scientists, practitioners have long advocated for greater contact between groups to reduce prejudice and increase social cohesion. Recent work, however, suggests that intergroup contact can undermine support for social change towards greater equality, especially among disadvantaged group members. Using a large and heterogeneous dataset (12,997 individuals from 69 countries), we demonstrate that intergroup contact and support for social change towards greater equality are positively associated among members of advantaged groups (ethnic majorities and cis-heterosexuals) but negatively associated among disadvantaged groups (ethnic minorities and sexual and gender minorities). Specification-curve analysis revealed important variation in the size—and at times, direction—of correlations, depending on how contact and support for social change were measured. This allowed us to identify one type of support for change—willingness to work in solidarity— that is positively associated with intergroup contact among both advantaged and disadvantaged group members

Quantitative Amyloid Imaging in Autosomal Dominant Alzheimer’s Disease: Results from the DIAN Study Group

Amyloid imaging plays an important role in the research and diagnosis of dementing disorders. Substantial variation in quantitative methods to measure brain amyloid burden exists in the field. The aim of this work is to investigate the impact of methodological variations to the quantification of amyloid burden using data from the Dominantly Inherited Alzheimer’s Network (DIAN), an autosomal dominant Alzheimer’s disease population. Cross-sectional and longitudinal [11C]-Pittsburgh Compound B (PiB) PET imaging data from the DIAN study were analyzed. Four candidate reference regions were investigated for estimation of brain amyloid burden. A regional spread function based technique was also investigated for the correction of partial volume effects. Cerebellar cortex, brain-stem, and white matter regions all had stable tracer retention during the course of disease. Partial volume correction consistently improves sensitivity to group differences and longitudinal changes over time. White matter referencing improved statistical power in the detecting longitudinal changes in relative tracer retention; however, the reason for this improvement is unclear and requires further investigation. Full dynamic acquisition and kinetic modeling improved statistical power although it may add cost and time. Several technical variations to amyloid burden quantification were examined in this study. Partial volume correction emerged as the strategy that most consistently improved statistical power for the detection of both longitudinal changes and across-group differences. For the autosomal dominant Alzheimer’s disease population with PiB imaging, utilizing brainstem as a reference region with partial volume correction may be optimal for current interventional trials. Further investigation of technical issues in quantitative amyloid imaging in different study populations using different amyloid imaging tracers is warranted

Pathways to Injury in Chronic Pancreatitis: Decoding the Role of the High-Risk SPINK1 N34S Haplotype Using Meta-Analysis

Background: The complex interactions between recurrent trypsin-mediated pancreatic injury, alcohol-associated pancreatic injury and SPINK1 polymorphisms in chronic pancreatitis (CP) are undefined. We hypothesize that CP occurs as a result of multiple pathological mechanisms (pathways) that are initiated by different metabolic or environmental factors (etiologies) and may be influenced differentially by downstream genetic risk factors. We tested this hypothesis by evaluating the differences in effect size of the high risk SPINK1 N34S haplotype on CP from multiple etiologies after combining clinical reports of SPINK1 N34S frequency using meta-analysis. Methods and Findings: The Pubmed and the Embase databases were reviewed. We studied 24 reports of SPINK1 N34S in CP (2,421 cases, 4,857 controls) using reported etiological factors as surrogates for pathways and multiple meta-analyses to determine the differential effects of SPINK1 N34S between alcoholic and non-alcoholic etiologies. Using estimates of between-study heterogeneity, we sub-classified our 24 studies into four specific clusters. We found that SPINK1 N34S is strongly associated with CP overall (OR 11.00; 95% CI: 7.59-15.93), but the effect of SPINK1 N34S in alcoholic CP (OR 4.98, 95% CI: 3.16-7.85) was significantly smaller than in idiopathic CP (OR 14.97, 95% C.I. = 9.09-24.67) or tropical CP (OR 19.15, 95% C.I. = 8.83-41.56). Studies analyzing familial CP showed very high heterogeneity suggestive of a complex etiology with an I2 = 80.95%. Conclusion: The small effect of SPINK1 N34S in alcoholic subjects suggests that CP is driven through a different pathway that is largely trypsin-independent. The results also suggest that large effect sizes of SPINK1 N34S in small candidate gene studies in CP may be related to a mixture of multiple etiologic pathways leading to the same clinical endpoint. © 2008 Aoun MD et al

Common genetic variants in the CLDN2 and PRSS1-PRSS2 loci alter risk for alcohol-related and sporadic pancreatitis

Pancreatitis is a complex, progressively destructive inflammatory disorder. Alcohol was long thought to be the primary causative agent, but genetic contributions have been of interest since the discovery that rare PRSS1, CFTR, and SPINK1 variants were associated with pancreatitis risk. We now report two significant genome-wide associations identified and replicated at PRSS1-PRSS2 (1×10-12) and x-linked CLDN2 (p < 1×10-21) through a two-stage genome-wide study (Stage 1, 676 cases and 4507 controls; Stage 2, 910 cases and 4170 controls). The PRSS1 variant affects susceptibility by altering expression of the primary trypsinogen gene. The CLDN2 risk allele is associated with atypical localization of claudin-2 in pancreatic acinar cells. The homozygous (or hemizygous male) CLDN2 genotype confers the greatest risk, and its alleles interact with alcohol consumption to amplify risk. These results could partially explain the high frequency of alcohol-related pancreatitis in men – male hemizygous frequency is 0.26, female homozygote is 0.07

RPC upgrade project for CMS Phase II

The Muon Upgrade Phase II of the Compact Muon Solenoid (CMS) aims to guarantee the optimal conditions of the present system and extend the eta coverage to ensure a reliable system for the High Luminosity Large Hadron Collider (HL-LHC) period. The Resistive Plate Chambers (RPCs) system will upgrade the off-detector electronics (called link system) of the chambers currently installed chambers and place improved RPCs (iRPCs) to cover the high pseudo-rapidity region, a challenging region for muon reconstruction in terms of background and momentum resolution. In order to find the best option for the iRPCs, an R&D program for new detectors was performed and real size prototypes have been tested in the Gamma Irradiation Facility (GIF++) at CERN. The results indicated that the technology suitable for the high background conditions is based on High Pressure Laminate (HPL) double-gap RPC. The RPC Upgrade Phase II program is planned to be ready after the Long Shutdown 3 (LS3)

RPC radiation background simulations for the high luminosity phase in the CMS experiment

The high luminosity expected from the HL-LHC will be a challenge for the CMS detector. The increased rate of particles coming from the collisions and the radioactivity induced in the detector material could cause significant damage and result in a progressive degradation of its performance. Simulation studies are very useful in these scenarios as they allow one to study the radiation environment and the impact on detector performance. Results are presented for CMS RPC stations considering the operating conditions expected at the HL-LHC

The CMS RPC detector performance and stability during LHC RUN-2

The CMS experiment, located at the Large Hadron Collider (LHC) in CERN, has a redundant muon system composed by three different gaseous detector technologies: Cathode Strip Chambers (in the forward regions), Drift Tubes (in the central region), and Resistive Plate Chambers (both its central and forward regions). All three are used for muon reconstruction and triggering. The CMS RPC system confers robustness and redundancy to the muon trigger. The RPC system operation in the challenging background and pileup conditions of the LHC environment is presented. The RPC system provides information to all muon track finders and thus contributing to both muon trigger and reconstruction. The summary of the detector performance results obtained with proton-proton collision at root s = 13 TeV during 2016 and 2017 data taking have been presented. The stability of the system is presented in terms of efficiency and cluster size vs time and increasing instantaneous luminosity. Data-driven predictions about the expected performance during High Luminosity LHC (HL-LHC) stage have been reported

Complement component C4 structural variation and quantitative traits contribute to sex-biased vulnerability in systemic sclerosis

Altres ajuts: Fondo Europeo de Desarrollo Regional (FEDER), "A way of making Europe".Copy number (CN) polymorphisms of complement C4 play distinct roles in many conditions, including immune-mediated diseases. We investigated the association of C4 CN with systemic sclerosis (SSc) risk. Imputed total C4, C4A, C4B, and HERV-K CN were analyzed in 26,633 individuals and validated in an independent cohort. Our results showed that higher C4 CN confers protection to SSc, and deviations from CN parity of C4A and C4B augmented risk. The protection contributed per copy of C4A and C4B differed by sex. Stronger protection was afforded by C4A in men and by C4B in women. C4 CN correlated well with its gene expression and serum protein levels, and less C4 was detected for both in SSc patients. Conditioned analysis suggests that C4 genetics strongly contributes to the SSc association within the major histocompatibility complex locus and highlights classical alleles and amino acid variants of HLA-DRB1 and HLA-DPB1 as C4-independent signals

Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

We identified rare coding variants associated with Alzheimer’s disease (AD) in a 3-stage case-control study of 85,133 subjects. In stage 1, 34,174 samples were genotyped using a whole-exome microarray. In stage 2, we tested associated variants (P<1×10-4) in 35,962 independent samples using de novo genotyping and imputed genotypes. In stage 3, an additional 14,997 samples were used to test the most significant stage 2 associations (P<5×10-8) using imputed genotypes. We observed 3 novel genome-wide significant (GWS) AD associated non-synonymous variants; a protective variant in PLCG2 (rs72824905/p.P522R, P=5.38×10-10, OR=0.68, MAFcases=0.0059, MAFcontrols=0.0093), a risk variant in ABI3 (rs616338/p.S209F, P=4.56×10-10, OR=1.43, MAFcases=0.011, MAFcontrols=0.008), and a novel GWS variant in TREM2 (rs143332484/p.R62H, P=1.55×10-14, OR=1.67, MAFcases=0.0143, MAFcontrols=0.0089), a known AD susceptibility gene. These protein-coding changes are in genes highly expressed in microglia and highlight an immune-related protein-protein interaction network enriched for previously identified AD risk genes. These genetic findings provide additional evidence that the microglia-mediated innate immune response contributes directly to AD development