Real bird dataset with imprecise and uncertain values

The theory of belief functions allows the fusion of imperfect data from different sources. Unfortunately, few real, imprecise and uncertain datasets exist to test approaches using belief functions. We have built real birds datasets thanks to the collection of numerous human contributions that we make available to the scientific community. The interest of our datasets is that they are made of human contributions, thus the information is therefore naturally uncertain and imprecise. These imperfections are given directly by the persons. This article presents the data and their collection through crowdsourcing and how to obtain belief functions from the data

Retrospective studies on rabbit haemorrhagic disease outbreaks caused by RHDV GI.2 virus on farms in France from 2013 to 2018

[EN] Rabbit haemorrhagic disease (RHD) is a critical health threat to the rabbit industry in Europe. In 2018, the French rabbit industry adopted a voluntary control plan against this disease. In this context, two epidemiological studies were conducted on RHD outbreaks that occurred between 2013 and 2018 in France. The objectives were to describe the spread of RHD due to the new genotype RHDV GI.2 (rabbit haemorrhagic disease virus GI.2) and to identify rearing factors influencing the occurrence of the disease in order to guide the prevention measures recommended in the control plan. An analysis of cases on 295 farms between 2013 and 2017 showed that 32% of farms were affected at least once; the incidence of the disease increased in 2016-2017 compared to 2013-2015. Farms already affected in 2013-2015 had a higher risk of being infected in 2016-2017 than those that remained unaffected until 2015 (Relative Risk and 95% Confident Interval 1.7 [1.1-2.7]). A case-control study carried out between 2016 and 2018 on 37 outbreaks and 32 control farms revealed variability in biosecurity and decontamination practices between farms. The risk of being infected tends to be linked to these practices, but certain structural factors (e.g. the manure disposal system, transfer of rabbits at weaning) could also influence the risk of virus introduction into farms. In the context of a limited vaccination coverage of the farms (only females are vaccinated), these hypotheses will be studied further, using information from the RHD outbreak monitoring system implemented at the same time as the control plan in 2018.This study was founded by the French Ministry of Agriculture (2017-430 / 170274).Huneau-Salaün, A.; Boucher, S.; Fontaine, J.; Le Normand, B.; Lopez, S.; Maurice, T.; Nouvel, L.... (2021). Retrospective studies on rabbit haemorrhagic disease outbreaks caused by RHDV GI.2 virus on farms in France from 2013 to 2018. World Rabbit Science. 29(2):87-98. https://doi.org/10.4995/wrs.2021.12800OJS8798292Abrantes J., Van der Loo W., Le Pendu J., Esteves P.J. 2012. Rabbit haemorrhagic disease (RHD) and rabbit haemorrhagic disease virus (RHDV): a review. Vet. Res., 43: 12.https://doi.org/10.1186/1297-9716-43-12Capucci L., Cavadini P., Schiavitto M., Lombardi G., Lavazza A. 2017. Increased pathogenicity in rabbit haemorrhagic disease virus type 2 (RHDV2). Vet. Record., 180: 426. https://doi.org/10.1136/vr.104132Carvalho C.L., Leclerc Duarte E., Monteiro J.M., Afonso C., Pacheco J., Carvalho P., Mendonça P., Botelho A., Albuquerque T., Themudo P., Fevereiro M., Henriques A.M., Santos Barros S., Dias Duarte M. 2017. Progression of rabbit haemorrhagic disease virus 2 upon vaccination in anindustrial rabbitry: a laboratorial approach. World Rabbit Sci., 25: 73-85. https://doi.org/10.4995/wrs.2017.5708Cooke B.D., Fenner F. 2002. Rabbit haemorrhagic disease and the biological control of wild rabbits, Oryctolagus Cuniculus, in Australia and New Zealand. Wildlife Res., 29: 689-706. https://doi.org/10.1071/WR02010Dalton K.P., Balseiro A., Juste R.A., Podadera A., Nicieza I., del Llano D., González R., Martin Alonso J.M., Prieto J.M., Parra F., Casais R. 2018. Clinical course and pathogenicity of variant rabbit haemorrhagic disease virus in experimentally infected adult and kit rabbits: Significance towards control and spread. Vet. Microbiol., 220: 24-32. https://doi.org/10.1016/j.vetmic.2018.04.033Dohoo I., Martin W., Stryhn H. 2003. Measures of disease frequency. In: Veterinary Epidemiologic Research, First Edition, AVC Inc., Charlottetown, Canada, 65-84.Hall R.N., Huang N., Roberts J., Strive T. 2019. Carrion flies as sentinels for monitoring lagovirus activity in Australia. Transboundary Emerg. Dis., 66: 2025-2032. https://doi.org/10.1111/tbed.13250Henning J., Meers J., Davies R., Morris R.S. 2005. Survival of rabbit haemorrhagic disease virus (RHDV) in the environment. Epidemiol. Infect., 133: 719-730. https://doi.org/10.1017/S0950268805003766Hurand J. 2016. L'élevage de lapins de chair en France, résultats technico-économiques 2015. Tema, 40.ITAVI. 2019. Situation de la filière cunicole. Novembre 2019. 6 p. Available athttps://www.itavi.asso.fr/content/note-deconjoncture-lapins-7Accessed December 2019.Le Gall-Reculé G., Zwingelstein F., Boucher S., Le Normand B., Plassiart G., Portejoie Y., Decors A., Bertagnoli S., Guérin J.L., Marchandeau S. 2011. Detection of a new variant of rabbit haemorrhagic disease virus in France. Vet. Rec., 168: 137- 138. https://doi.org/10.1136/vr.d697Le Gall-Reculé G., Lavazza A., Marchandeau S., Bertagnoli S., Zwingelstein F., Cavadini P., Martinelli N., Lombardi G., Guérin J.L., Lemaitre E., Decors A., Boucher S., Le Normand B., Capucci L. 2013. Emergence of a new lagovirus related to Rabbit haemorrhagic disease virus. Vet. Res., 44:81. https://doi.org/10.1186/1297-9716-44-81Le Gall-Reculé G., Boucher S. 2017. Connaissances et actualités sur la maladie hémorragique du lapin. In Proc.: 17èmes Journées de la Recherche Cunicole, 21-22 November, 2017. Le Mans, France. 97-109.Le Minor O., Joudou L., Le Moullec T., Beilvert F. 2017. Innocuité et efficacité de la vaccination à 2 et 3 semaines d'âge contre le virus RHDV2 de la maladie hémorragique virale du lapin (VHD). In Proc.:17èmes Journées de la Recherche Cunicole, 21-22 November, 2017. Le Mans, France. 127-130.Le Minor O., Boucher S., Joudou L., Mellet R., Sourice M., Le Moullec T., Nicoler A., Beilvert F., Sigognault-Flochlay A. 2019. Rabbit haemorrhagic disease: experimental study of a recent highly pathogenic GI.2/RJDV2/b strain and evaluation of vaccine efficacy. World Rabbit Sci., 27: 143-156.https://doi.org/10.4995/wrs.2019.11082Le Pendu J., Abrantes J., Bertagnoli S., Guitton J.S., Le Gall-Reculé G., Lopes A.M., Marchandeau S., Alda F., Almeida T., Célio A. C., Barcena J., Burmakina G., Blanco E., Calvete C., Cavadini P., Cooke B., Dalton K., Mateos M.D., Deptula W., Eden J.S., Wang F., Ferreira C.C., Ferreira P., Foronda P., Gonçalves D., Gavier-Widén D., Hall R., Hukowska-Szematowicz B., Kerr P., Kovaliski J., Lavazza A., Mahar J., Malogolovkin A., Marques R.M., Marques S., Martin-Alonso A., Monterroso P., MorenoS., Mutze G., Naimanis A., Niedzwiedzka-Rystwej P., Peacock D., Parra F., Rocchi M., Rouco C., Ruvoën-Clouet N., Silva E., Silvério D., Strive T., Thompson G., Tokarz-Deptula B., Esteves P. 2017. Proposal for a unified classification system and nomenclature of lagoviruses. J. Gen. Virol., 98: 1658-1666. https://doi.org/10.1099/jgv.0.000840Matthaei M., Kerr P.J., Read A.J., Hick P., Haboury S., Wright J.D., Strive T. 2014. Comparative quantitative monitoring of rabbit haemorrhagic disease viruses in rabbit kittens. Virol. J., 11: 109. https://doi.org/10.1186/1743-422X-11-109Mc Coll K.A., Merchant J.C., Hardy J., Cooke B.D., Robinson A., Westbury H.A. 2002. Evidence for insect transmission of rabbit haemorrhagic disease virus. Epidemiol. Infect., 129: 655-663. https://doi.org/10.1017/S0950268802007756Neimanis A.S., Larsson Pettersson U., Huang N., Gavier-Widen D., Strive T. 2018. Elucidation of the pathology and tissue distribution of Lagovirus europaeus GI.2/RHDV2 (rabbit haemorrhagic disease virus 2) in young and adult rabbits (Oryctolagus cuniculus). Vet. Res., 49:46. https://doi.org/10.1186/s13567-018-0540-zRosell J.M., de la Fuente L.F., Parra F., Dalton K.P., Badiola Sáiz J.I., Pérez de Rozas A., Badiola Díez J.J., Fernández de Luco D., Casal J., Majó N., Casas J., Garriga R., Fernández Magariños X.M. 2019. Myxomatosis and Rabbit Haemorrhagic Disease: A 30-Year Study of the Occurrence on Commercial Farms in Spain. Animals, 9: 780. https://doi.org/10.3390/ani9100780Rouco C., Aguayo-Adán J.A., Santoro S., Abrantes J., Delibes-Mateos M. 2019. Worldwide rapid spread of the novel rabbit haemorrhagic disease virus (GI.2/RHDV2/b). Transboundary Emerg. Dis., 66: 1762-1764.https://doi.org/10.1111/tbed.1318

HLA-C and HIV-1: friends or foes?

The major histocompatibility complex class I protein HLA-C plays a crucial role as a molecule capable of sending inhibitory signals to both natural killer (NK) cells and cytotoxic T lymphocytes (CTL) via binding to killer cell Ig-like receptors (KIR). Recently HLA-C has been recognized as a key molecule in the immune control of HIV-1. Expression of HLA-C is modulated by a microRNA binding site. HLA-C alleles that bear substitutions in the microRNA binding site are more expressed at the cell surface and associated with the control of HIV-1 viral load, suggesting a role of HLA-C in the presentation of antigenic peptides to CTLs. This review highlights the role of HLA-C in association with HIV-1 viral load, but also addresses the contradiction of the association between high cell surface expression of an inhibitory molecule and strong cell-mediated immunity. To explore additional mechanisms of control of HIV-1 replication by HLA-C, we address specific features of the molecule, like its tendency to be expressed as open conformer upon cell activation, which endows it with a unique capacity to associate with other cell surface molecules as well as with HIV-1 proteins

Sediment source fingerprinting: benchmarking recent outputs, remaining challenges and emerging themes

Abstract: Purpose: This review of sediment source fingerprinting assesses the current state-of-the-art, remaining challenges and emerging themes. It combines inputs from international scientists either with track records in the approach or with expertise relevant to progressing the science. Methods: Web of Science and Google Scholar were used to review published papers spanning the period 2013–2019, inclusive, to confirm publication trends in quantities of papers by study area country and the types of tracers used. The most recent (2018–2019, inclusive) papers were also benchmarked using a methodological decision-tree published in 2017. Scope: Areas requiring further research and international consensus on methodological detail are reviewed, and these comprise spatial variability in tracers and corresponding sampling implications for end-members, temporal variability in tracers and sampling implications for end-members and target sediment, tracer conservation and knowledge-based pre-selection, the physico-chemical basis for source discrimination and dissemination of fingerprinting results to stakeholders. Emerging themes are also discussed: novel tracers, concentration-dependence for biomarkers, combining sediment fingerprinting and age-dating, applications to sediment-bound pollutants, incorporation of supportive spatial information to augment discrimination and modelling, aeolian sediment source fingerprinting, integration with process-based models and development of open-access software tools for data processing. Conclusions: The popularity of sediment source fingerprinting continues on an upward trend globally, but with this growth comes issues surrounding lack of standardisation and procedural diversity. Nonetheless, the last 2 years have also evidenced growing uptake of critical requirements for robust applications and this review is intended to signpost investigators, both old and new, towards these benchmarks and remaining research challenges for, and emerging options for different applications of, the fingerprinting approach

Human matrix metalloproteinases: An ubiquitarian class of enzymes involved in several pathological processes

Human matrix metalloproteinases (MMPs) belong to the M10 family of the MA clan of endopeptidases. They are ubiquitarian enzymes, structurally characterized by an active site where a Zn(2+) atom, coordinated by three histidines, plays the catalytic role, assisted by a glutamic acid as a general base. Various MMPs display different domain composition, which is very important for macromolecular substrates recognition. Substrate specificity is very different among MMPs, being often associated to their cellular compartmentalization and/or cellular type where they are expressed. An extensive review of the different MMPs structural and functional features is integrated with their pathological role in several types of diseases, spanning from cancer to cardiovascular diseases and to neurodegeneration. It emerges a very complex and crucial role played by these enzymes in many physiological and pathological processes

Mortality from gastrointestinal congenital anomalies at 264 hospitals in 74 low-income, middle-income, and high-income countries: a multicentre, international, prospective cohort study

Background: Congenital anomalies are the fifth leading cause of mortality in children younger than 5 years globally. Many gastrointestinal congenital anomalies are fatal without timely access to neonatal surgical care, but few studies have been done on these conditions in low-income and middle-income countries (LMICs). We compared outcomes of the seven most common gastrointestinal congenital anomalies in low-income, middle-income, and high-income countries globally, and identified factors associated with mortality. // Methods: We did a multicentre, international prospective cohort study of patients younger than 16 years, presenting to hospital for the first time with oesophageal atresia, congenital diaphragmatic hernia, intestinal atresia, gastroschisis, exomphalos, anorectal malformation, and Hirschsprung's disease. Recruitment was of consecutive patients for a minimum of 1 month between October, 2018, and April, 2019. We collected data on patient demographics, clinical status, interventions, and outcomes using the REDCap platform. Patients were followed up for 30 days after primary intervention, or 30 days after admission if they did not receive an intervention. The primary outcome was all-cause, in-hospital mortality for all conditions combined and each condition individually, stratified by country income status. We did a complete case analysis. // Findings: We included 3849 patients with 3975 study conditions (560 with oesophageal atresia, 448 with congenital diaphragmatic hernia, 681 with intestinal atresia, 453 with gastroschisis, 325 with exomphalos, 991 with anorectal malformation, and 517 with Hirschsprung's disease) from 264 hospitals (89 in high-income countries, 166 in middle-income countries, and nine in low-income countries) in 74 countries. Of the 3849 patients, 2231 (58·0%) were male. Median gestational age at birth was 38 weeks (IQR 36–39) and median bodyweight at presentation was 2·8 kg (2·3–3·3). Mortality among all patients was 37 (39·8%) of 93 in low-income countries, 583 (20·4%) of 2860 in middle-income countries, and 50 (5·6%) of 896 in high-income countries (p<0·0001 between all country income groups). Gastroschisis had the greatest difference in mortality between country income strata (nine [90·0%] of ten in low-income countries, 97 [31·9%] of 304 in middle-income countries, and two [1·4%] of 139 in high-income countries; p≤0·0001 between all country income groups). Factors significantly associated with higher mortality for all patients combined included country income status (low-income vs high-income countries, risk ratio 2·78 [95% CI 1·88–4·11], p<0·0001; middle-income vs high-income countries, 2·11 [1·59–2·79], p<0·0001), sepsis at presentation (1·20 [1·04–1·40], p=0·016), higher American Society of Anesthesiologists (ASA) score at primary intervention (ASA 4–5 vs ASA 1–2, 1·82 [1·40–2·35], p<0·0001; ASA 3 vs ASA 1–2, 1·58, [1·30–1·92], p<0·0001]), surgical safety checklist not used (1·39 [1·02–1·90], p=0·035), and ventilation or parenteral nutrition unavailable when needed (ventilation 1·96, [1·41–2·71], p=0·0001; parenteral nutrition 1·35, [1·05–1·74], p=0·018). Administration of parenteral nutrition (0·61, [0·47–0·79], p=0·0002) and use of a peripherally inserted central catheter (0·65 [0·50–0·86], p=0·0024) or percutaneous central line (0·69 [0·48–1·00], p=0·049) were associated with lower mortality. // Interpretation: Unacceptable differences in mortality exist for gastrointestinal congenital anomalies between low-income, middle-income, and high-income countries. Improving access to quality neonatal surgical care in LMICs will be vital to achieve Sustainable Development Goal 3.2 of ending preventable deaths in neonates and children younger than 5 years by 2030

Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980-2015 : a systematic analysis for the Global Burden of Disease Study 2015

Background Improving survival and extending the longevity of life for all populations requires timely, robust evidence on local mortality levels and trends. The Global Burden of Disease 2015 Study (GBD 2015) provides a comprehensive assessment of all-cause and cause-specific mortality for 249 causes in 195 countries and territories from 1980 to 2015. These results informed an in-depth investigation of observed and expected mortality patterns based on sociodemographic measures. Methods We estimated all-cause mortality by age, sex, geography, and year using an improved analytical approach originally developed for GBD 2013 and GBD 2010. Improvements included refinements to the estimation of child and adult mortality and corresponding uncertainty, parameter selection for under-5 mortality synthesis by spatiotemporal Gaussian process regression, and sibling history data processing. We also expanded the database of vital registration, survey, and census data to 14 294 geography-year datapoints. For GBD 2015, eight causes, including Ebola virus disease, were added to the previous GBD cause list for mortality. We used six modelling approaches to assess cause-specific mortality, with the Cause of Death Ensemble Model (CODEm) generating estimates for most causes. We used a series of novel analyses to systematically quantify the drivers of trends in mortality across geographies. First, we assessed observed and expected levels and trends of cause-specific mortality as they relate to the Socio-demographic Index (SDI), a summary indicator derived from measures of income per capita, educational attainment, and fertility. Second, we examined factors affecting total mortality patterns through a series of counterfactual scenarios, testing the magnitude by which population growth, population age structures, and epidemiological changes contributed to shifts in mortality. Finally, we attributed changes in life expectancy to changes in cause of death. We documented each step of the GBD 2015 estimation processes, as well as data sources, in accordance with Guidelines for Accurate and Transparent Health Estimates Reporting (GATHER). Findings Globally, life expectancy from birth increased from 61.7 years (95% uncertainty interval 61.4-61.9) in 1980 to 71.8 years (71.5-72.2) in 2015. Several countries in sub-Saharan Africa had very large gains in life expectancy from 2005 to 2015, rebounding from an era of exceedingly high loss of life due to HIV/AIDS. At the same time, many geographies saw life expectancy stagnate or decline, particularly for men and in countries with rising mortality from war or interpersonal violence. From 2005 to 2015, male life expectancy in Syria dropped by 11.3 years (3.7-17.4), to 62.6 years (56.5-70.2). Total deaths increased by 4.1% (2.6-5.6) from 2005 to 2015, rising to 55.8 million (54.9 million to 56.6 million) in 2015, but age-standardised death rates fell by 17.0% (15.8-18.1) during this time, underscoring changes in population growth and shifts in global age structures. The result was similar for non-communicable diseases (NCDs), with total deaths from these causes increasing by 14.1% (12.6-16.0) to 39.8 million (39.2 million to 40.5 million) in 2015, whereas age-standardised rates decreased by 13.1% (11.9-14.3). Globally, this mortality pattern emerged for several NCDs, including several types of cancer, ischaemic heart disease, cirrhosis, and Alzheimer's disease and other dementias. By contrast, both total deaths and age-standardised death rates due to communicable, maternal, neonatal, and nutritional conditions significantly declined from 2005 to 2015, gains largely attributable to decreases in mortality rates due to HIV/AIDS (42.1%, 39.1-44.6), malaria (43.1%, 34.7-51.8), neonatal preterm birth complications (29.8%, 24.8-34.9), and maternal disorders (29.1%, 19.3-37.1). Progress was slower for several causes, such as lower respiratory infections and nutritional deficiencies, whereas deaths increased for others, including dengue and drug use disorders. Age-standardised death rates due to injuries significantly declined from 2005 to 2015, yet interpersonal violence and war claimed increasingly more lives in some regions, particularly in the Middle East. In 2015, rotaviral enteritis (rotavirus) was the leading cause of under-5 deaths due to diarrhoea (146 000 deaths, 118 000-183 000) and pneumococcal pneumonia was the leading cause of under-5 deaths due to lower respiratory infections (393 000 deaths, 228 000-532 000), although pathogen-specific mortality varied by region. Globally, the effects of population growth, ageing, and changes in age-standardised death rates substantially differed by cause. Our analyses on the expected associations between cause-specific mortality and SDI show the regular shifts in cause of death composition and population age structure with rising SDI. Country patterns of premature mortality (measured as years of life lost [YLLs]) and how they differ from the level expected on the basis of SDI alone revealed distinct but highly heterogeneous patterns by region and country or territory. Ischaemic heart disease, stroke, and diabetes were among the leading causes of YLLs in most regions, but in many cases, intraregional results sharply diverged for ratios of observed and expected YLLs based on SDI. Communicable, maternal, neonatal, and nutritional diseases caused the most YLLs throughout sub-Saharan Africa, with observed YLLs far exceeding expected YLLs for countries in which malaria or HIV/AIDS remained the leading causes of early death. Interpretation At the global scale, age-specific mortality has steadily improved over the past 35 years; this pattern of general progress continued in the past decade. Progress has been faster in most countries than expected on the basis of development measured by the SDI. Against this background of progress, some countries have seen falls in life expectancy, and age-standardised death rates for some causes are increasing. Despite progress in reducing age-standardised death rates, population growth and ageing mean that the number of deaths from most non-communicable causes are increasing in most countries, putting increased demands on health systems. Copyright (C) The Author(s). Published by Elsevier Ltd.Peer reviewe

Mortality from gastrointestinal congenital anomalies at 264 hospitals in 74 low-income, middle-income, and high-income countries: a multicentre, international, prospective cohort study

Summary Background Congenital anomalies are the fifth leading cause of mortality in children younger than 5 years globally. Many gastrointestinal congenital anomalies are fatal without timely access to neonatal surgical care, but few studies have been done on these conditions in low-income and middle-income countries (LMICs). We compared outcomes of the seven most common gastrointestinal congenital anomalies in low-income, middle-income, and high-income countries globally, and identified factors associated with mortality. Methods We did a multicentre, international prospective cohort study of patients younger than 16 years, presenting to hospital for the first time with oesophageal atresia, congenital diaphragmatic hernia, intestinal atresia, gastroschisis, exomphalos, anorectal malformation, and Hirschsprung’s disease. Recruitment was of consecutive patients for a minimum of 1 month between October, 2018, and April, 2019. We collected data on patient demographics, clinical status, interventions, and outcomes using the REDCap platform. Patients were followed up for 30 days after primary intervention, or 30 days after admission if they did not receive an intervention. The primary outcome was all-cause, in-hospital mortality for all conditions combined and each condition individually, stratified by country income status. We did a complete case analysis. Findings We included 3849 patients with 3975 study conditions (560 with oesophageal atresia, 448 with congenital diaphragmatic hernia, 681 with intestinal atresia, 453 with gastroschisis, 325 with exomphalos, 991 with anorectal malformation, and 517 with Hirschsprung’s disease) from 264 hospitals (89 in high-income countries, 166 in middleincome countries, and nine in low-income countries) in 74 countries. Of the 3849 patients, 2231 (58·0%) were male. Median gestational age at birth was 38 weeks (IQR 36–39) and median bodyweight at presentation was 2·8 kg (2·3–3·3). Mortality among all patients was 37 (39·8%) of 93 in low-income countries, 583 (20·4%) of 2860 in middle-income countries, and 50 (5·6%) of 896 in high-income countries (p<0·0001 between all country income groups). Gastroschisis had the greatest difference in mortality between country income strata (nine [90·0%] of ten in lowincome countries, 97 [31·9%] of 304 in middle-income countries, and two [1·4%] of 139 in high-income countries; p≤0·0001 between all country income groups). Factors significantly associated with higher mortality for all patients combined included country income status (low-income vs high-income countries, risk ratio 2·78 [95% CI 1·88–4·11], p<0·0001; middle-income vs high-income countries, 2·11 [1·59–2·79], p<0·0001), sepsis at presentation (1·20 [1·04–1·40], p=0·016), higher American Society of Anesthesiologists (ASA) score at primary intervention (ASA 4–5 vs ASA 1–2, 1·82 [1·40–2·35], p<0·0001; ASA 3 vs ASA 1–2, 1·58, [1·30–1·92], p<0·0001]), surgical safety checklist not used (1·39 [1·02–1·90], p=0·035), and ventilation or parenteral nutrition unavailable when needed (ventilation 1·96, [1·41–2·71], p=0·0001; parenteral nutrition 1·35, [1·05–1·74], p=0·018). Administration of parenteral nutrition (0·61, [0·47–0·79], p=0·0002) and use of a peripherally inserted central catheter (0·65 [0·50–0·86], p=0·0024) or percutaneous central line (0·69 [0·48–1·00], p=0·049) were associated with lower mortality. Interpretation Unacceptable differences in mortality exist for gastrointestinal congenital anomalies between lowincome, middle-income, and high-income countries. Improving access to quality neonatal surgical care in LMICs will be vital to achieve Sustainable Development Goal 3.2 of ending preventable deaths in neonates and children younger than 5 years by 2030

Exploitation conjointe d'un modèle biomécanique patient-spécifique de coeur et vaisseaux et de données mesurées au bloc opératoire pour augmenter le monitorage hémodynamique des patients sous anesthésie générale

Haemodynamic evaluation of anaesthetised patients in operating theatre or in intensive care units can be challenging. Monitoring devices can be inaccurate and/or invasive. Physicians have to evaluate the usefulness of the information given by the monitor, and its potential harms linked to its invasiveness before implementing the technique. Modelling methods may be an interesting alternative to improve the risk/benefit balance for the patients. Biomechanical modelling of heart and vessels, when turned into patient-specific regime using patients' data measured in operating theatre, can allow simulation of cardiovascular physiology, including pressure-volume relationships through the cardiac cycle. In 45 patients undergoing general anaesthesia, we analysed the haemodynamic profile in terms of cardiac bioenergetics or ventricular arterial coupling, and we were able to evaluate the effects of Noradrenaline administered for 16 hypotensive patients, on cardiac efficiency, using pressure-volume loops estimated from a patient-specific biomechanical model. Our approach is original as it is based on a rigorous cardiovascular physiological description and on continuum mechanics theory allowing physical and physiological interpretation of the modelling results. This PhD thesis presents also original methods for model calibration, from limited data availability. We developed a passive constitutive law estimation method which reunites the biomechanical approach, usually difficult to implement in clinical settings, and the phenomenological approach, more efficient but less rigorous. We also explored the potentials of a time-varying elastance model, derived from the full biomechanical model. We demonstrated that for reasonable variation ranges, the time-varying elastance model could be used as a surrogate for the biomechanical model. This approach improves the computational time and resources, allowing to consider the transfer of our approach in real-time monitoring conditions.This PhD thesis is a proof of concept of the coupling between biomechanical modelling of heart and vessels and data measured in operating theatre to augment cardiovascular monitoring in anaesthetised patients. This is also the first step toward transfer of the method from bench to bedside.L'évaluation hémodynamique des patients sous anesthésie générale est une tache complexe pour les médecins anesthésistes et/ou réanimateurs. Puisque les techniques de monitorage sont imprécises et/ou invasives, il est nécessaire de prendre en compte la balance entre leur utilité, et leur invasivité et/ou leur imprécision. Les méthodes numériques peuvent représenter une alternative en améliorant ce rapport bénéfice/risque pour le patient. En particulier, la modélisation biomécanique de coeur et vaisseaux présentée dans cette thèse, une fois calibrée sur les données mesurées au bloc opératoire, peuvent permettre de simuler, entre-autres, un cathétérisme cardiaque gauche. Nous avons pu analyser le profil hémodynamique de 45 patients sous anesthésie générale, et interpréter les effets de la Noradrénaline administrée pour corriger une hypotension artérielle chez 16 patients, en termes de bioénergétique cardiaque, et de couplage ventriculo-aortique, à partir de boucles pression-volume ventriculaires simulées. Notre approche est originale car elle s'intègre dans une démarche rigoureuse basée sur la physiologie cardiovasculaire et la mécanique des milieux continus permettant ainsi de conserver une signification physique et physiologique aux résultats de la modélisation. Cette thèse présente également des méthodes originales, permettant de calibrer le modèle à partir d'une quantité limitée de donnée patient.Nous avons mis au point des méthodes d'estimation des paramètres de la loi passive de comportement du coeur en diastole, réunissant l'approche biomécanique, difficile à mettre en oeuvre en clinique, et l'approche phénoménologique, plus efficace mais moins rigoureuse. Nous avons également exploré les potentialités d'un modèle d'élastance variable, dérivé du modèle biomécanique. Nous avons pu montrer que dans une gamme de variation raisonnable, le modèle d'élastance variable pouvait être utilisé en lieu et place du modèle biomécanique, permettant d'envisager l'utilisation de notre approche dans des conditions de monitorage pour lesquelles l'estimation en temps réel est un enjeu important.Cette thèse représente une preuve de concept de l'exploitation conjointe des données mesurées couramment au bloc opératoire et d'un modèle biomécanique de coeur et vaisseaux pour augmenter le monitorage hémodynamique des patients sous anesthésie générale. Elle représente également la première étape du transfert de la méthode vers la pratique clinique