The Impact of Mergers on the Degree of Competition in the Banking Industry

This paper analyses the relation between competition and concentration in the banking sector. The empirical answer is given by testing a monopolistic competition model of bank branching behaviour on individual bank data at county level (départements and provinces) in France and Italy. We propose a measure of the degree of competiveness in each local market that is function also of market structure indicators. We then use the econometric model to evaluate the impact of horizontal mergers among incumbent banks on competition and discuss when, depending on the pre-merger structure of the market and geographic distribution of branches, the merger is anti-competitive. The paper has implications for competition policy as it suggests an applied tool to evaluate the potential anti-competitive impact of mergers.

The Impact of Mergers on the Degree of Competition in the Banking Industry

This paper analyses the relation between competition and concentration in the banking sector. The empirical answer is given by testing a monopolistic competition model of bank branching behaviour on individual bank data at county level (départements and provinces) in France and Italy. We propose a measure of the degree of competiveness in each local market that is function also of market structure indicators. We then use the econometric model to evaluate the impact of horizontal mergers among incumbent banks on competition and discuss when, depending on the pre-merger structure of the market and geographic distribution of branches, the merger is anti-competitive. The paper has implications for competition policy as it suggests an applied tool to evaluate the potential anti-competitive impact of mergers.Banking Industry, Competition and Market Structure, Merger Policy

Territorial Scenarios for an Integrated Europe: Driving Forces of Change and Quantitative Forecasts

The paper presents the second step of an ambitious research project, which has the aim to provide territorial scenarios of the New Europe in 15 years, developed under different hypotheses on the most important driving forces of change in the fields of economy, demographic, society, technology and institutions. The first step was presented last year at the ERSA conference in Amsterdam. In that occasion, the paper dealt with the econometric model (labelled MASST – Macroeconomic, social, sectoral and territorial model) built for the forecasting activity, presenting its strengths and weaknesses and the main results obtained by the estimates of the model. In this paper the additional work is presented, and the main conceptual and methodological steps forward analysed. In particular, the aims of the paper are the following: - to present the main driving forces that influence the future of Europe and of its territory. These are of different nature: socio-cultural (future migration forces and future birth and death rates), institutional (deepening vs. widening of enlargement), macroeconomic (trend in the euro/$ exchange rate, trend in fiscal morality – i.e. trend in public debts, revision of the Maastricht parameters -, trend in interest rates, trend in inflation rate, geo-political orientation of FDI, rebalancing of external accounts of big emerging countries; increase in energy price), political (reforms of the structural funds and of the Community Agricultural Policy); - to present the different hypotheses under which the scenarios are built. The idea is to build three scenarios, a baseline scenario, a competitive and a cohesive scenario, and to present the differences among them; - to present the results of the simulation. The MASST model is able to provide both regional GDP growth rates and GDP levels, as well as regional population growth rates, and population levels, for the three scenarios. The model is able to provide the simulations for 27 Countries (the old 15 EU members, the new 10 Countries and Bulgaria and Romania) and for their 259 regions.

Territorial Scenarios for an Integrated Europe: Driving Forces of Change and Quantitative Forecasts

The paper presents the second step of an ambitious research project, which has the aim to provide territorial scenarios of the New Europe in 15 years, developed under different hypotheses on the most important driving forces of change in the fields of economy, demographic, society, technology and institutions. The first step was presented last year at the ERSA conference in Amsterdam. In that occasion, the paper dealt with the econometric model (labelled MASST – Macroeconomic, social, sectoral and territorial model) built for the forecasting activity, presenting its strengths and weaknesses and the main results obtained by the estimates of the model. In this paper the additional work is presented, and the main conceptual and methodological steps forward analysed. In particular, the aims of the paper are the following: - to present the main driving forces that influence the future of Europe and of its territory. These are of different nature: socio-cultural (future migration forces and future birth and death rates), institutional (deepening vs. widening of enlargement), macroeconomic (trend in the euro/$ exchange rate, trend in fiscal morality – i.e. trend in public debts, revision of the Maastricht parameters -, trend in interest rates, trend in inflation rate, geo-political orientation of FDI, rebalancing of external accounts of big emerging countries; increase in energy price), political (reforms of the structural funds and of the Community Agricultural Policy); - to present the different hypotheses under which the scenarios are built. The idea is to build three scenarios, a baseline scenario, a competitive and a cohesive scenario, and to present the differences among them; - to present the results of the simulation. The MASST model is able to provide both regional GDP growth rates and GDP levels, as well as regional population growth rates, and population levels, for the three scenarios. The model is able to provide the simulations for 27 Countries (the old 15 EU members, the new 10 Countries and Bulgaria and Romania) and for their 259 regions

Genome-wide whole blood transcriptome profiling in a large European cohort of systemic sclerosis patients

Objectives The analysis of annotated transcripts from genome-wide expression studies may help to understand the pathogenesis of complex diseases, such as systemic sclerosis (SSc). We performed a whole blood (WB) transcriptome analysis on RNA collected in the context of the European PRECISESADS project, aiming at characterising the pathways that differentiate SSc from controls and that are reproducible in geographically diverse populations. Methods Samples from 162 patients and 252 controls were collected in RNA stabilisers. Cases and controls were divided into a discovery (n=79+163; Southern Europe) and validation cohort (n=83+89; Central-Western Europe). RNA sequencing was performed by an Illumina assay. Functional annotations of Reactome pathways were performed with the Functional Analysis of Individual Microarray Expression (FAIME) algorithm. In parallel, immunophenotyping of 28 circulating cell populations was performed. We tested the presence of differentially expressed genes/pathways and the correlation between absolute cell counts and RNA transcripts/FAIME scores in regression models. Results significant in both populations were considered as replicated. Results Overall, 15 224 genes and 1277 functional pathways were available; of these, 99 and 225 were significant in both sets. Among replicated pathways, we found a deregulation in type-I interferon, Toll-like receptor cascade, tumour suppressor p53 protein function, platelet degranulation and activation. RNA transcripts or FAIME scores were jointly correlated with cell subtypes with strong geographical differences; neutrophils were the major determinant of gene expression in SSc-WB samples. Conclusions We discovered a set of differentially expressed genes/pathways validated in two independent sets of patients with SSc, highlighting a number of deregulated processes that have relevance for the pathogenesis of autoimmunity and SSc.EU/EFPIA/Innovative Medicines Initiative Joint Undertaking PRECISESADS 115 56

Integrative epigenomics in Sjögren´s syndrome reveals novel pathways and a strong interaction between the HLA, autoantibodies and the interferon signature

Primary Sjögren's syndrome (SS) is a systemic autoimmune disease characterized by lymphocytic infiltration and damage of exocrine salivary and lacrimal glands. The etiology of SS is complex with environmental triggers and genetic factors involved. By conducting an integrated multi-omics study, we confirmed a vast coordinated hypomethylation and overexpression effects in IFN-related genes, what is known as the IFN signature. Stratified and conditional analyses suggest a strong interaction between SS-associated HLA genetic variation and the presence of Anti-Ro/SSA autoantibodies in driving the IFN epigenetic signature and determining SS. We report a novel epigenetic signature characterized by increased DNA methylation levels in a large number of genes enriched in pathways such as collagen metabolism and extracellular matrix organization. We identified potential new genetic variants associated with SS that might mediate their risk by altering DNA methylation or gene expression patterns, as well as disease-interacting genetic variants that exhibit regulatory function only in the SS population. Our study sheds new light on the interaction between genetics, autoantibody profiles, DNA methylation and gene expression in SS, and contributes to elucidate the genetic architecture of gene regulation in an autoimmune population

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

Racial differences in systemic sclerosis disease presentation: a European Scleroderma Trials and Research group study

Objectives. Racial factors play a significant role in SSc. We evaluated differences in SSc presentations between white patients (WP), Asian patients (AP) and black patients (BP) and analysed the effects of geographical locations.Methods. SSc characteristics of patients from the EUSTAR cohort were cross-sectionally compared across racial groups using survival and multiple logistic regression analyses.Results. The study included 9162 WP, 341 AP and 181 BP. AP developed the first non-RP feature faster than WP but slower than BP. AP were less frequently anti-centromere (ACA; odds ratio (OR) = 0.4, P < 0.001) and more frequently anti-topoisomerase-I autoantibodies (ATA) positive (OR = 1.2, P = 0.068), while BP were less likely to be ACA and ATA positive than were WP [OR(ACA) = 0.3, P < 0.001; OR(ATA) = 0.5, P = 0.020]. AP had less often (OR = 0.7, P = 0.06) and BP more often (OR = 2.7, P < 0.001) diffuse skin involvement than had WP.AP and BP were more likely to have pulmonary hypertension [OR(AP) = 2.6, P < 0.001; OR(BP) = 2.7, P = 0.03 vs WP] and a reduced forced vital capacity [OR(AP) = 2.5, P < 0.001; OR(BP) = 2.4, P < 0.004] than were WP. AP more often had an impaired diffusing capacity of the lung than had BP and WP [OR(AP vs BP) = 1.9, P = 0.038; OR(AP vs WP) = 2.4, P < 0.001]. After RP onset, AP and BP had a higher hazard to die than had WP [hazard ratio (HR) (AP) = 1.6, P = 0.011; HR(BP) = 2.1, P < 0.001].Conclusion. Compared with WP, and mostly independent of geographical location, AP have a faster and earlier disease onset with high prevalences of ATA, pulmonary hypertension and forced vital capacity impairment and higher mortality. BP had the fastest disease onset, a high prevalence of diffuse skin involvement and nominally the highest mortality

Serum profiling identifies CCL8, CXCL13, and IL-1RA as markers of active disease in patients with systemic lupus erythematosus

IntroductionSystemic lupus erythematosus (SLE) is a clinically heterogeneous disease that presents a challenge for clinicians. To identify potential biomarkers for diagnosis and disease activity in SLE, we investigated a selected yet broad panel of cytokines and autoantibodies in patients with SLE, healthy controls (HC), and patients with other autoimmune diseases (AIDs).MethodsSerum samples from 422 SLE patients, 546 HC, and 1223 other AIDs were analysed within the frame of the European PRECISESADS project (NTC02890121). Cytokine levels were determined using Luminex panels, and autoantibodies using different immunoassays.ResultsOf the 83 cytokines analysed, 29 differed significantly between patients with SLE and HC. Specifically, CCL8, CXCL13, and IL-1RA levels were elevated in patients with active, but not inactive, SLE versus HC, as well as in patients with SLE versus other AIDs. The levels of these cytokines also correlated with SLE Disease Activity Index 2000 (SLEDAI-2K) scores, among five other cytokines. Overall, the occurrence of autoantibodies was similar across SLEDAI-2K organ domains, and the correlations between autoantibodies and activity in different organ domains were weak.DiscussionOur findings suggest that, upon validation, CCL8, CXCL13, and IL-1RA could serve as promising serum biomarkers of activity in SLE