Differential responses of captive southern hairy-nosed wombats (Lasiorhinus latifrons) to the presence of faeces from different species and male and female conspecifics

The southern hairy-nosed wombat (Lasiorhinus latifrons) appears to use scent marking, including defaecation, for social communication in the wild. This premise assumes that the receiver wombat is able to distinguish between faeces from different sources. To examine this theory, four types of faeces (male wombat, female wombat, dingo and a plastic control) were placed into the enclosures of 12 captive wombats. Behaviour, inter-individual distance and enclosure use were recorded during the period of placement, as well as the period before and the period after. When faeces were present, the wombats used concealed locations more often than other periods (mean %: pre-treatment: 71.3, treatment: 75.6, post-treatment: 72.7; P < 0.05). During the same period they also reduced grazing (mean min/period: pre- treatment: 15.8, treatment: 6.9, post- treatment: 13.1; P = 0.0002) and walking 2 activity (mean min/period: pre- treatment: 85.2, treatment: 66.9, post- treatment: 78.2; P = 0.01), indicating an increased perception of risk. Wombats approached the dingo faeces 5.6 times per treatment period, which was greater than for the control (3.0; P = 0.004) or female wombat faeces (3.7; P = 0.049). They also avoided other wombats most when male wombat faeces were present (8.3 retreats/period) compared to the control (4.5; P = 0.02), or female wombat (4.3; P = 0.01). There was a residual effect of increased wombat avoidance the period after presentation of dingo faeces (9.6; P ≤ 0.05). It is concluded that the southern hairy-nosed wombat can differentiate between faeces from different species and sex of conspecifics, and that predator faeces and those from male conspecifics increase wombat avoidance behaviour either during or after presentation

Measurement of the cross-section and charge asymmetry of WW bosons produced in proton-proton collisions at s=8\sqrt{s}=8 TeV with the ATLAS detector

This paper presents measurements of the $W^+ \rightarrow \mu^+\nu$ and $W^- \rightarrow \mu^-\nu$ cross-sections and the associated charge asymmetry as a function of the absolute pseudorapidity of the decay muon. The data were collected in proton--proton collisions at a centre-of-mass energy of 8 TeV with the ATLAS experiment at the LHC and correspond to a total integrated luminosity of 20.2~\mbox{fb^{-1}}. The precision of the cross-section measurements varies between 0.8% to 1.5% as a function of the pseudorapidity, excluding the 1.9% uncertainty on the integrated luminosity. The charge asymmetry is measured with an uncertainty between 0.002 and 0.003. The results are compared with predictions based on next-to-next-to-leading-order calculations with various parton distribution functions and have the sensitivity to discriminate between them.Comment: 38 pages in total, author list starting page 22, 5 figures, 4 tables, submitted to EPJC. All figures including auxiliary figures are available at https://atlas.web.cern.ch/Atlas/GROUPS/PHYSICS/PAPERS/STDM-2017-13

The global, regional, and national burden of inflammatory bowel disease in 195 countries and territories, 1990-2017 : a systematic analysis for the Global Burden of Disease Study 2017

Background The burden of inflammatory bowel disease (IBD) is rising globally, with substantial variation in levels and trends of disease in different countries and regions. Understanding these geographical differences is crucial for formulating effective strategies for preventing and treating IBD. We report the prevalence, mortality, and overall burden of IBD in 195 countries and territories between 1990 and 2017, based on data from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017. Methods We modelled mortality due to IBD using a standard Cause of Death Ensemble model including data mainly from vital registrations. To estimate the non-fatal burden, we used data presented in primary studies, hospital discharges, and claims data, and used DisMod-MR 2.1, a Bayesian meta-regression tool, to ensure consistency between measures. Mortality, prevalence, years of life lost (YLLs) due to premature death, years lived with disability (YLDs), and disability-adjusted life-years (DALYs) were estimated. All of the estimates were reported as numbers and rates per 100 000 population, with 95% uncertainty intervals (UI). Findings In 2017, there were 6.8 million (95% UI 6.4-7.3) cases of IBD globally. The age-standardised prevalence rate increased from 79.5 (75.9-83.5) per 100 000 population in 1990 to 84.3 (79.2-89.9) per 100 000 population in 2017. The age-standardised death rate decreased from 0.61 (0.55-0.69) per 100 000 population in 1990 to 0.51 (0.42-0.54) per 100 000 population in 2017. At the GBD regional level, the highest age-standardised prevalence rate in 2017 occurred in high-income North America (422.0 [398.7-446.1] per 100 000) and the lowest age-standardised prevalence rates were observed in the Caribbean (6.7 [6.3-7.2] per 100 000 population). High Sociodemographic Index (SDI) locations had the highest age-standardised prevalence rate, while low SDI regions had the lowest age-standardised prevalence rate. At the national level, the USA had the highest age-standardised prevalence rate (464.5 [438.6-490.9] per 100 000 population), followed by the UK (449.6 [420.6-481.6] per 100 000). Vanuatu had the highest age-standardised death rate in 2017 (1.8 [0.8-3.2] per 100 000 population) and Singapore had the lowest (0.08 [0.06-0.14] per 100 000 population). The total YLDs attributed to IBD almost doubled over the study period, from 0.56 million (0.39-0.77) in 1990 to 1.02 million (0.71-1.38) in 2017. The age-standardised rate of DALYs decreased from 26.5 (21.0-33.0) per 100 000 population in 1990 to 23.2 (19.1-27.8) per 100 000 population in 2017. Interpretation The prevalence of IBD increased substantially in many regions from 1990 to 2017, which might pose a substantial social and economic burden on governments and health systems in the coming years. Our findings can be useful for policy makers developing strategies to tackle IBD, including the education of specialised personnel to address the burden of this complex disease. Copyright (C) 2019 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license.Peer reviewe

The global, regional, and national burden of inflammatory bowel disease in 195 countries and territories, 1990�2017: a systematic analysis for the Global Burden of Disease Study 2017

Background: The burden of inflammatory bowel disease (IBD) is rising globally, with substantial variation in levels and trends of disease in different countries and regions. Understanding these geographical differences is crucial for formulating effective strategies for preventing and treating IBD. We report the prevalence, mortality, and overall burden of IBD in 195 countries and territories between 1990 and 2017, based on data from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017. Methods: We modelled mortality due to IBD using a standard Cause of Death Ensemble model including data mainly from vital registrations. To estimate the non-fatal burden, we used data presented in primary studies, hospital discharges, and claims data, and used DisMod-MR 2.1, a Bayesian meta-regression tool, to ensure consistency between measures. Mortality, prevalence, years of life lost (YLLs) due to premature death, years lived with disability (YLDs), and disability-adjusted life-years (DALYs) were estimated. All of the estimates were reported as numbers and rates per 100 000 population, with 95 uncertainty intervals (UI). Findings: In 2017, there were 6·8 million (95 UI 6·4�7·3) cases of IBD globally. The age-standardised prevalence rate increased from 79·5 (75·9�83·5) per 100 000 population in 1990 to 84·3 (79·2�89·9) per 100 000 population in 2017. The age-standardised death rate decreased from 0·61 (0·55�0·69) per 100 000 population in 1990 to 0·51 (0·42�0·54) per 100 000 population in 2017. At the GBD regional level, the highest age-standardised prevalence rate in 2017 occurred in high-income North America (422·0 398·7�446·1 per 100 000) and the lowest age-standardised prevalence rates were observed in the Caribbean (6·7 6·3�7·2 per 100 000 population). High Socio-demographic Index (SDI) locations had the highest age-standardised prevalence rate, while low SDI regions had the lowest age-standardised prevalence rate. At the national level, the USA had the highest age-standardised prevalence rate (464·5 438·6�490·9 per 100 000 population), followed by the UK (449·6 420·6�481·6 per 100 000). Vanuatu had the highest age-standardised death rate in 2017 (1·8 0·8�3·2 per 100 000 population) and Singapore had the lowest (0·08 0·06�0·14 per 100 000 population). The total YLDs attributed to IBD almost doubled over the study period, from 0·56 million (0·39�0·77) in 1990 to 1·02 million (0·71�1·38) in 2017. The age-standardised rate of DALYs decreased from 26·5 (21·0�33·0) per 100 000 population in 1990 to 23·2 (19·1�27·8) per 100 000 population in 2017. Interpretation: The prevalence of IBD increased substantially in many regions from 1990 to 2017, which might pose a substantial social and economic burden on governments and health systems in the coming years. Our findings can be useful for policy makers developing strategies to tackle IBD, including the education of specialised personnel to address the burden of this complex disease. Funding: Bill & Melinda Gates Foundation. © 2020 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 licens

Absent B cells, agammaglobulinemia, and hypertrophic cardiomyopathy in folliculin-interacting protein 1 deficiency

Agammaglobulinemia is the most profound primary antibody deficiency that can occur due to an early termination of B-cell development. We here investigated 3 novel patients, including the first known adult, from unrelated families with agammaglobulinemia, recurrent infections, and hypertrophic cardiomyopathy (HCM). Two of them also presented with intermittent or severe chronic neutropenia. We identified homozygous or compound-heterozygous variants in the gene for folliculin interacting protein 1 (FNIP1), leading to loss of the FNIP1 protein. B-cell metabolism, including mitochondria! numbers and activity and phosphatidylinositol 3-kinase/AKT pathway, was impaired. These defects recapitulated the Fnip1(-/-) animal model. Moreover, we identified either uniparental disomy or copy-number variants (CNVs) in 2 patients, expanding the variant spectrum of this novel inborn error of I immunity. The results indicate that FNIP1 deficiency can be caused by complex genetic mechanisms and support the clinical utility of exome sequencing and CNV analysis in patients with broad phenotypes, including agammaglobulinemia and HCM. FNIP1 deficiency is a novel inborn error of immunity characterized by early and severe B-cell development defect, agammaglobulinemia, variable neutropenia, and HCM. Our findings elucidate a functional and relevant role of FNIP1 in B-cell development and metabolism and potentially neutrophil activity.Molecular Technology and Informatics for Personalised Medicine and Healt

Autoantibodies against type I IFNs in patients with life-threatening COVID-19

Interindividual clinical variability in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is vast. We report that at least 101 of 987 patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-w (IFN-w) (13 patients), against the 13 types of IFN-a (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs. The auto-Abs neutralize the ability of the corresponding type I IFNs to block SARS-CoV-2 infection in vitro. These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1227 healthy individuals. Patients with auto-Abs were aged 25 to 87 years and 95 of the 101 were men. A B cell autoimmune phenocopy of inborn errors of type I IFN immunity accounts for life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men