D’un cheptel conservatoire de races locales à un outil de gestion de la savane : le cas de la chèvre Péï et de la vache Moka à La Réunion

En 2017 une expérimentation de pâturage dirigé a été initiée, avec un troupeau de chèvres Péï, race caprine locale réunionnaise, pour contribuer à la conservation de la savane du cap la Houssaye, protégée par le Conservatoire du littoral sur la commune de Saint-Paul à La Réunion. L’opération est portée par l’Association pour la Promotion du Patrimoine et de l’Ecologie à La Réunion (APPER), qui œuvre depuis plusieurs années à la sauvegarde des races animales locales. Cet article fait état de la mise en œuvre de ce projet expérimental. Nous analysons ainsi l’originalité et la singularité de cette démarche à La Réunion et nous interrogeons les conditions de sa réussite et de sa pérennité.In 2017, an experimental project of pasture was initiated, with a herd of “Péï” goats, a local goat breed from Reunion Island, to contribute to the conservation of savannah areas, protected by Le Conservatoire du littoral in Saint-Paul municipality in Reunion Island. The operation is carried by the Association for the Promotion of Heritage and Ecology in Reunion Island, which has been working for many years to save the local animal breeds in Reunion Island. This article reports on the implementation of this experimental project. We will analyze the originality and the uniqueness of this project in Reunion Island and we will question the conditions for its success and sustainability

Donar: Anonymous VoIP over Tor

International audienceWe present DONAR, a system enabling anonymous VoIP with good quality-of-experience (QoE) over Tor. No individual Tor link can match VoIP networking requirements. DONAR bridges this gap by spreading VoIP traffic over several links. It combines active performance monitoring, dynamic link selection, adaptive traffic scheduling, and redundancy at no extra bandwidth cost. DONAR enables high QoE: latency remains under 360 ms for 99% of VoIP packets during most (86%) 5-minute and 90-minute calls

Streptococcus pyogenes Cas9 ribonucleoprotein delivery for efficient, rapid and marker-free gene editing in Trypanosoma and Leishmania

Kinetoplastids are unicellular eukaryotic flagellated parasites found in a wide range of hosts within the animal and plant kingdoms. They are known to be responsible in humans for African sleeping sickness ( Trypanosoma brucei ), Chagas disease ( Trypanosoma cruzi ), and various forms of leishmaniasis ( Leishmania spp.), as well as several animal diseases with important economic impact (African trypanosomes, including T. congolense ). Understanding the biology of these parasites necessarily implies the ability to manipulate their genomes. In this study, we demonstrate that transfection of a ribonucleoprotein complex, composed of recombinant Streptococcus pyogenes Cas9 ( Sp Cas9) and an in vitro -synthesized guide RNA, results in rapid and efficient genetic modifications of trypanosomatids, in marker-free conditions. This approach was successfully developed to inactivate, delete and mutate candidate genes in various stages of the life cycle of T. brucei and T. congolense , and Leishmania promastigotes. The functionality of Sp Cas9 in these parasites now provides, to the research community working on these parasites, a rapid and efficient method of genome editing, without requiring plasmid construction and selection by antibiotics. Importantly, this approach is adaptable to any wild-type parasite, including field isolates

Autoantibodies neutralizing type I IFNs are present in ~4% of uninfected individuals over 70 years old and account for ~20% of COVID-19 deaths

Publisher Copyright: © 2021 The Authors, some rights reserved.Circulating autoantibodies (auto-Abs) neutralizing high concentrations (10 ng/ml; in plasma diluted 1:10) of IFN-alpha and/or IFN-omega are found in about 10% of patients with critical COVID-19 (coronavirus disease 2019) pneumonia but not in individuals with asymptomatic infections. We detect auto-Abs neutralizing 100-fold lower, more physiological, concentrations of IFN-alpha and/or IFN-omega (100 pg/ml; in 1:10 dilutions of plasma) in 13.6% of 3595 patients with critical COVID-19, including 21% of 374 patients >80 years, and 6.5% of 522 patients with severe COVID-19. These antibodies are also detected in 18% of the 1124 deceased patients (aged 20 days to 99 years; mean: 70 years). Moreover, another 1.3% of patients with critical COVID-19 and 0.9% of the deceased patients have auto-Abs neutralizing high concentrations of IFN-beta. We also show, in a sample of 34,159 uninfected individuals from the general population, that auto-Abs neutralizing high concentrations of IFN-alpha and/or IFN-omega are present in 0.18% of individuals between 18 and 69 years, 1.1% between 70 and 79 years, and 3.4% >80 years. Moreover, the proportion of individuals carrying auto-Abs neutralizing lower concentrations is greater in a subsample of 10,778 uninfected individuals: 1% of individuals 80 years. By contrast, auto-Abs neutralizing IFN-beta do not become more frequent with age. Auto-Abs neutralizing type I IFNs predate SARS-CoV-2 infection and sharply increase in prevalence after the age of 70 years. They account for about 20% of both critical COVID-19 cases in the over 80s and total fatal COVID-19 cases.Peer reviewe

Higher COVID-19 pneumonia risk associated with anti-IFN-α than with anti-IFN-ω auto-Abs in children

We found that 19 (10.4%) of 183 unvaccinated children hospitalized for COVID-19 pneumonia had autoantibodies (auto-Abs) neutralizing type I IFNs (IFN-alpha 2 in 10 patients: IFN-alpha 2 only in three, IFN-alpha 2 plus IFN-omega in five, and IFN-alpha 2, IFN-omega plus IFN-beta in two; IFN-omega only in nine patients). Seven children (3.8%) had Abs neutralizing at least 10 ng/ml of one IFN, whereas the other 12 (6.6%) had Abs neutralizing only 100 pg/ml. The auto-Abs neutralized both unglycosylated and glycosylated IFNs. We also detected auto-Abs neutralizing 100 pg/ml IFN-alpha 2 in 4 of 2,267 uninfected children (0.2%) and auto-Abs neutralizing IFN-omega in 45 children (2%). The odds ratios (ORs) for life-threatening COVID-19 pneumonia were, therefore, higher for auto-Abs neutralizing IFN-alpha 2 only (OR [95% CI] = 67.6 [5.7-9,196.6]) than for auto-Abs neutralizing IFN-. only (OR [95% CI] = 2.6 [1.2-5.3]). ORs were also higher for auto-Abs neutralizing high concentrations (OR [95% CI] = 12.9 [4.6-35.9]) than for those neutralizing low concentrations (OR [95% CI] = 5.5 [3.1-9.6]) of IFN-omega and/or IFN-alpha 2

The risk of COVID-19 death is much greater and age dependent with type I IFN autoantibodies

SignificanceThere is growing evidence that preexisting autoantibodies neutralizing type I interferons (IFNs) are strong determinants of life-threatening COVID-19 pneumonia. It is important to estimate their quantitative impact on COVID-19 mortality upon SARS-CoV-2 infection, by age and sex, as both the prevalence of these autoantibodies and the risk of COVID-19 death increase with age and are higher in men. Using an unvaccinated sample of 1,261 deceased patients and 34,159 individuals from the general population, we found that autoantibodies against type I IFNs strongly increased the SARS-CoV-2 infection fatality rate at all ages, in both men and women. Autoantibodies against type I IFNs are strong and common predictors of life-threatening COVID-19. Testing for these autoantibodies should be considered in the general population

The risk of COVID-19 death is much greater and age dependent with type I IFN autoantibodies

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection fatality rate (IFR) doubles with every 5 y of age from childhood onward. Circulating autoantibodies neutralizing IFN-α, IFN-ω, and/or IFN-β are found in ∼20% of deceased patients across age groups, and in ∼1% of individuals aged 4% of those >70 y old in the general population. With a sample of 1,261 unvaccinated deceased patients and 34,159 individuals of the general population sampled before the pandemic, we estimated both IFR and relative risk of death (RRD) across age groups for individuals carrying autoantibodies neutralizing type I IFNs, relative to noncarriers. The RRD associated with any combination of autoantibodies was higher in subjects under 70 y old. For autoantibodies neutralizing IFN-α2 or IFN-ω, the RRDs were 17.0 (95% CI: 11.7 to 24.7) and 5.8 (4.5 to 7.4) for individuals <70 y and ≥70 y old, respectively, whereas, for autoantibodies neutralizing both molecules, the RRDs were 188.3 (44.8 to 774.4) and 7.2 (5.0 to 10.3), respectively. In contrast, IFRs increased with age, ranging from 0.17% (0.12 to 0.31) for individuals <40 y old to 26.7% (20.3 to 35.2) for those ≥80 y old for autoantibodies neutralizing IFN-α2 or IFN-ω, and from 0.84% (0.31 to 8.28) to 40.5% (27.82 to 61.20) for autoantibodies neutralizing both. Autoantibodies against type I IFNs increase IFRs, and are associated with high RRDs, especially when neutralizing both IFN-α2 and IFN-ω. Remarkably, IFRs increase with age, whereas RRDs decrease with age. Autoimmunity to type I IFNs is a strong and common predictor of COVID-19 death.The Laboratory of Human Genetics of Infectious Diseases is supported by the Howard Hughes Medical Institute; The Rockefeller University; the St. Giles Foundation; the NIH (Grants R01AI088364 and R01AI163029); the National Center for Advancing Translational Sciences; NIH Clinical and Translational Science Awards program (Grant UL1 TR001866); a Fast Grant from Emergent Ventures; Mercatus Center at George Mason University; the Yale Center for Mendelian Genomics and the Genome Sequencing Program Coordinating Center funded by the National Human Genome Research Institute (Grants UM1HG006504 and U24HG008956); the Yale High Performance Computing Center (Grant S10OD018521); the Fisher Center for Alzheimer’s Research Foundation; the Meyer Foundation; the JPB Foundation; the French National Research Agency (ANR) under the “Investments for the Future” program (Grant ANR-10-IAHU-01); the Integrative Biology of Emerging Infectious Diseases Laboratory of Excellence (Grant ANR-10-LABX-62-IBEID); the French Foundation for Medical Research (FRM) (Grant EQU201903007798); the French Agency for Research on AIDS and Viral hepatitis (ANRS) Nord-Sud (Grant ANRS-COV05); the ANR GENVIR (Grant ANR-20-CE93-003), AABIFNCOV (Grant ANR-20-CO11-0001), CNSVIRGEN (Grant ANR-19-CE15-0009-01), and GenMIS-C (Grant ANR-21-COVR-0039) projects; the Square Foundation; Grandir–Fonds de solidarité pour l’Enfance; the Fondation du Souffle; the SCOR Corporate Foundation for Science; The French Ministry of Higher Education, Research, and Innovation (Grant MESRI-COVID-19); Institut National de la Santé et de la Recherche Médicale (INSERM), REACTing-INSERM; and the University Paris Cité. P. Bastard was supported by the FRM (Award EA20170638020). P. Bastard., J.R., and T.L.V. were supported by the MD-PhD program of the Imagine Institute (with the support of Fondation Bettencourt Schueller). Work at the Neurometabolic Disease lab received funding from Centre for Biomedical Research on Rare Diseases (CIBERER) (Grant ACCI20-767) and the European Union's Horizon 2020 research and innovation program under grant agreement 824110 (EASI Genomics). Work in the Laboratory of Virology and Infectious Disease was supported by the NIH (Grants P01AI138398-S1, 2U19AI111825, and R01AI091707-10S1), a George Mason University Fast Grant, and the G. Harold and Leila Y. Mathers Charitable Foundation. The Infanta Leonor University Hospital supported the research of the Department of Internal Medicine and Allergology. The French COVID Cohort study group was sponsored by INSERM and supported by the REACTing consortium and by a grant from the French Ministry of Health (Grant PHRC 20-0424). The Cov-Contact Cohort was supported by the REACTing consortium, the French Ministry of Health, and the European Commission (Grant RECOVER WP 6). This work was also partly supported by the Intramural Research Program of the National Institute of Allergy and Infectious Diseases and the National Institute of Dental and Craniofacial Research, NIH (Grants ZIA AI001270 to L.D.N. and 1ZIAAI001265 to H.C.S.). This program is supported by the Agence Nationale de la Recherche (Grant ANR-10-LABX-69-01). K.K.’s group was supported by the Estonian Research Council, through Grants PRG117 and PRG377. R.H. was supported by an Al Jalila Foundation Seed Grant (Grant AJF202019), Dubai, United Arab Emirates, and a COVID-19 research grant (Grant CoV19-0307) from the University of Sharjah, United Arab Emirates. S.G.T. is supported by Investigator and Program Grants awarded by the National Health and Medical Research Council of Australia and a University of New South Wales COVID Rapid Response Initiative Grant. L.I. reports funding from Regione Lombardia, Italy (project “Risposta immune in pazienti con COVID-19 e co-morbidità”). This research was partially supported by the Instituto de Salud Carlos III (Grant COV20/0968). J.R.H. reports funding from Biomedical Advanced Research and Development Authority (Grant HHSO10201600031C). S.O. reports funding from Research Program on Emerging and Re-emerging Infectious Diseases from Japan Agency for Medical Research and Development (Grant JP20fk0108531). G.G. was supported by the ANR Flash COVID-19 program and SARS-CoV-2 Program of the Faculty of Medicine from Sorbonne University iCOVID programs. The 3C Study was conducted under a partnership agreement between INSERM, Victor Segalen Bordeaux 2 University, and Sanofi-Aventis. The Fondation pour la Recherche Médicale funded the preparation and initiation of the study. The 3C Study was also supported by the Caisse Nationale d’Assurance Maladie des Travailleurs Salariés, Direction générale de la Santé, Mutuelle Générale de l’Education Nationale, Institut de la Longévité, Conseils Régionaux of Aquitaine and Bourgogne, Fondation de France, and Ministry of Research–INSERM Program “Cohortes et collections de données biologiques.” S. Debette was supported by the University of Bordeaux Initiative of Excellence. P.K.G. reports funding from the National Cancer Institute, NIH, under Contract 75N91019D00024, Task Order 75N91021F00001. J.W. is supported by a Research Foundation - Flanders (FWO) Fundamental Clinical Mandate (Grant 1833317N). Sample processing at IrsiCaixa was possible thanks to the crowdfunding initiative YoMeCorono. Work at Vall d’Hebron was also partly supported by research funding from Instituto de Salud Carlos III Grant PI17/00660 cofinanced by the European Regional Development Fund (ERDF/FEDER). C.R.-G. and colleagues from the Canarian Health System Sequencing Hub were supported by the Instituto de Salud Carlos III (Grants COV20_01333 and COV20_01334), the Spanish Ministry for Science and Innovation (RTC-2017-6471-1; AEI/FEDER, European Union), Fundación DISA (Grants OA18/017 and OA20/024), and Cabildo Insular de Tenerife (Grants CGIEU0000219140 and “Apuestas científicas del ITER para colaborar en la lucha contra la COVID-19”). T.H.M. was supported by grants from the Novo Nordisk Foundation (Grants NNF20OC0064890 and NNF21OC0067157). C.M.B. is supported by a Michael Smith Foundation for Health Research Health Professional-Investigator Award. P.Q.H. and L. Hammarström were funded by the European Union’s Horizon 2020 research and innovation program (Antibody Therapy Against Coronavirus consortium, Grant 101003650). Work at Y.-L.L.’s laboratory in the University of Hong Kong (HKU) was supported by the Society for the Relief of Disabled Children. MBBS/PhD study of D.L. in HKU was supported by the Croucher Foundation. J.L.F. was supported in part by the Evaluation-Orientation de la Coopération Scientifique (ECOS) Nord - Coopération Scientifique France-Colombie (ECOS-Nord/Columbian Administrative department of Science, Technology and Innovation [COLCIENCIAS]/Colombian Ministry of National Education [MEN]/Colombian Institute of Educational Credit and Technical Studies Abroad [ICETEX, Grant 806-2018] and Colciencias Contract 713-2016 [Code 111574455633]). A. Klocperk was, in part, supported by Grants NU20-05-00282 and NV18-05-00162 issued by the Czech Health Research Council and Ministry of Health, Czech Republic. L.P. was funded by Program Project COVID-19 OSR-UniSR and Ministero della Salute (Grant COVID-2020-12371617). I.M. is a Senior Clinical Investigator at the Research Foundation–Flanders and is supported by the CSL Behring Chair of Primary Immunodeficiencies (PID); by the Katholieke Universiteit Leuven C1 Grant C16/18/007; by a Flanders Institute for Biotechnology-Grand Challenges - PID grant; by the FWO Grants G0C8517N, G0B5120N, and G0E8420N; and by the Jeffrey Modell Foundation. I.M. has received funding under the European Union’s Horizon 2020 research and innovation program (Grant Agreement 948959). E.A. received funding from the Hellenic Foundation for Research and Innovation (Grant INTERFLU 1574). M. Vidigal received funding from the São Paulo Research Foundation (Grant 2020/09702-1) and JBS SA (Grant 69004). The NH-COVAIR study group consortium was supported by a grant from the Meath Foundation.Peer reviewe

Interactions between the circadian clock and the response to magnesium deficiency in Arabidopsis thaliana: transcriptional, genetic and physiological analysis

Le Magnésium est un élément essentiel pour les plantes. Il est requis en de larges quantités, de l’ordre de 2 mg g-1 de matière sèche, et assure de multiples fonctions. Il constitue notamment l’atome central de la chlorophylle, pigment nécessaire à la photosynthèse, ainsi que le cofacteur ou modulateur allostérique de plus de 300 enzymes. De plus, il est nécessaire au maintien de la structure des ribosomes, influençant par là la traduction, et active l’adénosine-triphosphate, molécule énergétique alimentant de nombreux processus biologiques. La nutrition en magnésium des plantes représente aujourd’hui une réelle problématique pour nos sociétés. Non seulement les teneurs en cet élément ont fortement diminué dans les denrées agricoles depuis la Révolution Verte, mais aussi le magnésium apparaît de plus en en plus clairement comme un facteur limitant des rendements en champ. Les produits d’origine végétale étant la principale source de magnésium dans l’alimentation humaine, cela entraîne une généralisation de carences. Historiquement, le magnésium recevait peu d’attention des agronomes en comparaison à d’autres macroéléments comme l’azote, le phosphore ou le potassium car il était généralement largement abondant. Les problèmes étaient restreints surtout aux arbres fruitiers et aux sols acides, dans des climats fortement pluvieux. Les fertilisations excessives de ces dernières ont cependant rendu beaucoup plus communes les situations où le magnésium ne peut pas être absorbé en suffisance par les plantes cultivées.En 2010, une analyse pionnière de la réponse transcriptomique à une carence en magnésium dans la plante-modèle Arabidopsis thaliana a révélé d’importantes perturbation de l’expression des gènes. La réponse des composants de l’horloge circadienne en particulier a été épinglée. Celle-ci pourrait en effet avoir des répercussions majeures sur la physiologie de la plante. L’horloge circadienne est un oscillateur endogène participant à la modulation de processus biologiques au cours des cycles nycthéméraux et saisonniers. Elle est constituée principalement de facteurs et de cofacteurs de transcription qui sont exprimés successivement au cours du jour et s’autorégulent dans des boucles de rétroaction complexe. Ceux-ci contrôlent l’expression d’approximativement un tiers du transcriptome et jouent un rôle fondamental dans le métabolisme de l’amidon et la photosynthèse, dont l’altération est symptomatique de la carence en magnésium. Dans cette étude, nous avons donc voulu évaluer l’impact réel de la réponse de l’horloge circadienne sur les symptômes de la carence en magnésium. À l’aide d’analyses transcriptionnelles, génétiques et physiologiques, nous avons pu montrer le rôle significatif des facteurs de transcription de l’horloge dans l’orchestration de la réponse transcriptomique de la plante à un apport insuffisant en magnésium. L’action de ces derniers, au niveau transcriptionnel, dépend en grande partie d’interactions avec les voies de signalisation des phytochrome et contribue probablement à la régulation du symptôme d’accumulation de l’amidon. Nous avons obtenu également que la gravité des dérangements de l’activité photosynthétique dus à une carence en magnésium était également connectée aux propriétés de l’horloge mais le détail des mécanismes sous-jacents attend des évaluations plus approfondies.Doctorat en Sciences agronomiques et ingénierie biologiqueinfo:eu-repo/semantics/nonPublishe

CO2 RADIATION IN EXPANDING FLOWS UNDER VIBRATIONAL NON-EQUILIBRIUM CONDITIONS

International audienceABSTRACT. The aim of this paper is to develop a line by line model for CO2 vibrational non- equilibrium radiation and to investigate non-equilibrium effects in the case of an expanding mixture flow in a simple conical nozzle. A vibrational specific collisional relaxation model is developed and is incorporated in a multi-temperature thermodynamic description of the gas mixture, in order to compute vibrational level populations along the expanding flow. The HITEMP-2010 spectroscopic database is employed with a model for level energy splitting to provide line by line absorption and emission total and per-vibrational mode specific spectra. The specific spectra allow us to derive the radiative source terms to be used in the multi-temperature model if a coupled approach is required. It is shown that, for the considered nozzle conditions, the partial freeze of vibrational excitation in the expanding flow increases significantly the radiative intensity escaping from the mixture

Élevage et activités pastorales dans les savanes réunionnaises : pratiques, représentations et enjeux actuels

International audienc