Socioeconomic inequalities in suicide mortality in European urban areas before and during the economic recession

Few studies have assessed the impact of the financial crisis on inequalities in suicide mortality in European urban areas. The objective of the study was to analyse the trend in area socioeconomic inequalities in suicide mortality in nine European urban areas before and after the beginning of the financial crisis. This ecological study of trends was based on three periods, two before the economic crisis (2000-2003, 2004-2008) and one during the crisis (2009-2014). The units of analysis were the small areas of nine European cities or metropolitan areas, with a median population ranging from 271 (Turin) to 193 630 (Berlin). For each small area and sex, we analysed smoothed standardized mortality ratios of suicide mortality and their relationship with a socioeconomic deprivation index using a hierarchical Bayesian model. Among men, the relative risk (RR) comparing suicide mortality of the 95th percentile value of socioeconomic deprivation (severe deprivation) to its 5th percentile value (low deprivation) were higher than 1 in Stockholm and Lisbon in the three periods. In Barcelona, the RR was 2.06 (95% credible interval: 1.24-3.21) in the first period, decreasing in the other periods. No significant changes were observed across the periods. Among women, a positive significant association was identified only in Stockholm (RR around 2 in the three periods). There were no significant changes across the periods except in London with a RR of 0.49 (95% CI: 0.35-0.68) in the third period. Area socioeconomic inequalities in suicide mortality did not change significantly after the onset of the crisis in the areas studied

Cell Type–Specific Transcriptome Analysis Reveals a Major Role for Zeb1 and miR-200b in Mouse Inner Ear Morphogenesis

Cellular heterogeneity hinders the extraction of functionally significant results and inference of regulatory networks from wide-scale expression profiles of complex mammalian organs. The mammalian inner ear consists of the auditory and vestibular systems that are each composed of hair cells, supporting cells, neurons, mesenchymal cells, other epithelial cells, and blood vessels. We developed a novel protocol to sort auditory and vestibular tissues of newborn mouse inner ears into their major cellular components. Transcriptome profiling of the sorted cells identified cell type–specific expression clusters. Computational analysis detected transcription factors and microRNAs that play key roles in determining cell identity in the inner ear. Specifically, our analysis revealed the role of the Zeb1/miR-200b pathway in establishing epithelial and mesenchymal identity in the inner ear. Furthermore, we detected a misregulation of the ZEB1 pathway in the inner ear of Twirler mice, which manifest, among other phenotypes, malformations of the auditory and vestibular labyrinth. The association of misregulation of the ZEB1/miR-200b pathway with auditory and vestibular defects in the Twirler mutant mice uncovers a novel mechanism underlying deafness and balance disorders. Our approach can be employed to decipher additional complex regulatory networks underlying other hearing and balance mouse mutants

Introduction—Food Security and Food Waste Reduction: A Social Innovation Approach to Current Social, Environmental, and Political Concerns

This chapter presents the research rationale underpinning the book. It addresses the intertwining challenges of food security and surplus food management, discussing recent data and literature. It also presents how social innovation is conceptualized in the book as the theoretical framework to analyse partnerships between business and non-profit organisations in managing food surplus. The methodology of the research is also detailed, along with the book structure

Loss of function NFKB1 variants are the most common monogenic cause of CVID in Europeans.

BACKGROUND: The genetic etiology of primary immunodeficiency disease (PID) carries prognostic information. OBJECTIVE: We conducted a whole-genome sequencing study assessing a large proportion of the NIHR-BioResource - Rare Disease cohort. METHODS: In the predominantly European study population of principally sporadic unrelated PID cases (n=846), a novel Bayesian method identified NFKB1 as one most strongly associated with PID, and the association was explained by 16 novel heterozygous truncating, missense and gene deletion variants. This accounted for 4% of common variable immunodeficiency (CVID) cases (n=390) in the cohort. Amino-acid substitutions predicted to be pathogenic were assessed by analysis of structural protein data. Immunophenotyping, immunoblotting and ex vivo stimulation of lymphocytes determined the functional effects of these variants. Detailed clinical and pedigree information was collected for genotype-phenotype co-segregation analyses. RESULTS: Both sporadic and familial cases demonstrated evidence of the non-infective complications of CVID, including massive lymphadenopathy (24%), unexplained splenomegaly (48%) and autoimmune disease (48%), features prior studies correlate with worse clinical prognosis. Although partial penetrance of clinical symptoms was noted in certain pedigrees, all carriers have a deficiency in B lymphocyte differentiation. Detailed assessment of B lymphocyte numbers, phenotype and function identifies the presence of a raised CD21lowB cell population: combined with identification of the disease-causing variant, this distinguishes between healthy individuals, asymptomatic carriers and clinically affected cases. CONCLUSION: We show that heterozygous loss-of-function variants in NFKB1 are the most common known monogenic cause of CVID that results in a temporally progressive defect in the formation of immunoglobulin-producing B cells.This study was supported by The National Institute for Health Research England (grant number RG65966), and by the Center of Immunodeficiencies Amsterdam (CIDA). JET is supported by an MRC Clinician Scientist Fellowship (MR/L006197/1). AJT is supported by both the Wellcome Trust (104807/Z/14/Z) and by the National Institute for Health Research Biomedical Research Centre at Great Ormond Street Hospital for Children NHS Foundation Trust and University College London. EO receives personal fees from CSL Behring and MSD

The faunal role in the degradation of the common intertidal salt marsh plant Scirpus maritimus

Abstract The aim of this work was to evaluate the role of different environmental conditions (oxic and anoxic), and the presence of macrofauna and/or meiofauna during the different steps of Scirpus maritimus L. decomposition/mineralization under controlled laboratory conditions. The results showed no significant differences between the anaerobic and the aerobic degradation of plant material, under the presence of bacteria or meiofauna. Nevertheless, under anoxic conditions sediment mineralization was enhanced, with an increase concentration of phosphorus and ammonium in the water phase. Concerning the presence of fauna, results show that, although bacterial activity was responsible for 70% of the S. maritimus leaves degradation, the presence of macrofauna together with meiofauna enhanced the leaves mineralization up to 90%. Moreover, the presence of macrofauna together with meiofauna significantly affected the decomposition of phosphorus and of nitrogen, as well as the leaves lesser labile structural parts, by increasing the mineralization of plant carbon, and raised the nutrient turnover within the system.The present study reinforces the functional link between fauna levels on the nutrient dynamics in salt marshes ecosystems, namely at the vegetation detritus/water column interface