Publications scientifiques de l'EnvA
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Standardized Workflow for Reporting Evidence of Statistical and/or Causal Associations between an Exposure E and an Outcome O
No full textLogigramme permettant de savoir ce qu'il faut écrire dans la partie Résultats et dans la partie Discussion d'un article dont l'objectif est de faire de l'inférence causale en médecine.This workflow applies to associations between a binary exposure (E) and a binary outcome (O), quantified via Odds Ratios (OR) from logistic regression orHazard Ratios (HR) from Cox models, including 95% CIs and p-values. For analyses without use of regression model, select "Univariate" at the initialquestion. Users must adapt the suggested phrasing for qualitative or quantitative exposures and for quantitative outcomesCe logigramme (en anglais) s’applique aux associations entre une exposition binaire (E) et un outcome binaire (O), quantifiées par des Odds Ratios (OR) issus d’une régression logistique ou des Hazard Ratios (HR) issus de modèles de Cox, incluant les intervalles de confiance à 95 % et les valeurs de p. Pour les analyses sans recours à un modèle de régression, sélectionner « Univariate » à la question initiale. Les utilisateurs doivent adapter la formulation proposée selon qu’il s’agit d’expositions qualitatives ou quantitatives, et de critères de jugement quantitatifs
An RTCA-based assay as an innovative approach for thermal inactivation studies of hepatitis A virus
No full textInternational audienceHepatitis A virus (HAV) is responsible for acute viral hepatitis worldwide, mainly transmitted via the fecal-oral route either through direct contact or by consuming contaminated food. Thermal inactivation is widely applied in the food industry to inactivate viruses and ensure the safety of food products. The effectiveness of inactivation treatments depends on the initial viral load and the sensitivity of the method quantifying infectious viruses. This study aimed to assess the real-time cell analysis (RTCA) assay in the framework of heat inactivation studies, compare its suitability to the traditional PFU assay and molecular-based methods (RT-qPCR, integrity-RT-qPCR), and model thermal inactivation kinetics. Our results showed that the RTCA assay is a suitable method for quantifying the decrease in infectious HAV as the time-temperature scale increases. No more infectious virus was detected after treatment at 37°C, 50°C, 65°C, 72°C, and 80°C, lasting 9 days, 24 h, 10 min, 5 min, and 2 min, respectively. The Geeraerd model was identified as the best fit to describe HAV thermal inactivation kinetics. The D values, corresponding to the time required to achieve a 1 log 10 reduction in HAV titer , were comparable between both cell-culture-based methods across all tested temperatures. In contrast, molecular methods yielded significantly higher D values. Kinetic parameters were subsequently validated, confirming that the isothermal-derived parameters can reliably predict viral inactivation under dynamic thermal conditions. This study demonstrates that the RTCA assay provides a powerful tool for modeling HAV thermal inactivation that can offer valuable guidance for implementing effective food safety strategies. IMPORTANCE There has been a significant increase in viral foodborne outbreaks following the consumption of raw or minimally processed foods. Thermal treatments may ensure food safety, with efficacy depending on viral load and method sensitivity. In this study, we present a powerful real-time cell analysis assay that advances our analytical ability to quantify infectious hepatitis A virus. By providing kinetic parameters comparable to those obtained with the traditional infectious titration method, this high-throughput assay overcomes its limitations to conduct viral inactivation studies on a larger scale. In addition, the successful validation of kinetic parameters confirms that isothermal-derived parameters can reliably predict viral inactivation under dynamic thermal conditions. This offers a reliable and essential tool to strengthen food safety measures to be applied in the food industry
Intérêt de l'immunomarquage de la protéine GIRK4 dans la confirmation de l’origine glomérulée des lésions surrénaliennes observées chez des chats atteints d'hyperaldostéronisme primaire
No full textPrimary hyperaldosteronism (PHA) is an increasingly recognized endocrine disorder in ageing cats, characterized by autonomous aldosterone secretion by the adrenal cortex, leading to systemic hypertension and hypokalaemia. Diagnosis relies on a combination of clinical, biochemical, and imaging findings, but characterization of the underlying histological lesions remains challenging, particularly in the absence of formal histological criteria for zona glomerulosa hyperplasia. In this context, the objective of this study was to evaluate the relevance of GIRK4 immunolabeling (a potassium channel encoded by the KCNJ5 gene), physiologically expressed in zona glomerulosa cells, as a marker of glomerulosa cell identity in adrenal lesions associated with PHA. Adrenal tissues from 10 cats with PHA and 7 control cats were analysed using conventional histology combined with immunolabeling for GIRK4 and CYP17 (an enzyme absent from the zona glomerulosa and specific to the zona fasciculata). In control cats, GIRK4 expression was restricted to the zona glomerulosa, confirming its physiological localization. In PHA cats, GIRK4 expression varied according to lesion type: GIRK4- positive and CYP17-negative formations were interpreted as being of glomerulosa origin, whereas four lesions—including three adenocarcinomas—were negative for GIRK4. For three cases, including two adenocarcinomas, an incorrect diagnosis of PHA was excluded. Thus, the absence of GIRK4 labeling raises two main hypotheses: insufficient sensitivity of the antibody, or possible KCNJ5 mutations. The latter warrants investigation through targeted sequencing. Additionally, the use of complementary markers such as DAB2 could improve the detection of glomerulosa-derived cells when GIRK4 expression is weak or absent. We also observed variability in the organization of the zona glomerulosa according to age in healthy cats, suggesting age-related cortical remodeling with potential implications for the diagnosis of bilateral hyperplasia. Finally, although a GIRK4+/CYP17- immunophenotype is suggestive of a glomerulosa origin, it does not constitute formal evidence of aldosterone secretion. A better understanding of the interplay between CYP17 and CYP11B would be required to confirm the endocrine function of the identified lesions.L'hyperaldostéronisme primaire (HAP) est un trouble endocrinien de plus en plus diagnostiqué chez le chat âgé, caractérisé par une sécrétion autonome d'aldostérone par le cortex surrénalien, responsable d'hypertension artérielle systémique et d'hypokaliémie. Le diagnostic repose sur un faisceau convergeant d'arguments biologiques, cliniques et d'imagerie, mais la caractérisation des lésions histologiques causales reste un défi, notamment en l'absence de critères histologiques formels concernant les hyperplasies de la zone glomérulée. Dans ce contexte, ce travail visait à évaluer la pertinence de l'immunomarquage de GIRK4 (canal potassique codé par le gène KCNJ5), physiologiquement exprimé par les cellules de la zone glomérulée, comme marqueur d'identité cellulaire glomérulée des lésions causales d'HAP. Nous avons analysé les tissus surrénaliens de 10 chats atteints d'HAP et de 7 chats témoins, en combinant étude histologique classique et immunomarquages dirigés contre GIRK4 et CYP17 (enzyme absente de la zone glomérulée et spécifique de la zone fasciculée). Chez les témoins, le marquage GIRK4 était restreint à la zone glomérulée, confirmant son expression physiologique dans cette zone. Chez les chats HAP, nous avons observé une expression variable de GIRK4 selon le type de lésion : les formations GIRK4 positives et CYP17 négatives ont été interprétées comme d'origine glomérulée, tandis que quatre lésions, notamment trois adénocarcinomes, étaient négatives pour GIRK4. Pour 3 cas, dont 2 adénocarcinomes, la possibilité d'un diagnostic d'HAP erroné a été exclu. Ainsi, cette absence de marquage soulève principalement deux hypothèses : un défaut de sensibilité de l'anticorps, ou l'existence possible de mutations du gène KCNJ5. Cette dernière hypothèse mériterait d'être explorée par séquençage ciblé. De plus, l'utilisation de marqueurs complémentaires tels que DAB2 pourrait améliorer la détection des cellules glomérulées lorsque l'expression de GIRK4 est faible ou absente. Par ailleurs, nous avons observé une variabilité de l'organisation de la zone glomérulée selon l'âge des chats sains, suggérant une réorganisation corticale liée à l'âge, avec des implications potentielles dans le diagnostic d'hyperplasie bilatérale. Enfin, bien que l'immunomarquage GIRK4+/CYP17- soit évocateur d'une origine glomérulée, il ne constitue pas une preuve formelle de la sécrétion d'aldostérone. Une meilleure compréhension de l'interaction entre CYP17 et CYP11B serait nécessaire pour confirmer la fonction endocrine des lésions identifiées
Maternal preconception and gestational exposure to a mixture of short half-life food chemicals altered fetoplacental development in a rabbit model, based on a French mother-child cohort
No full textInternational audiencePregnant women from the general population are exposed daily to chemicals that can affect offspring's health. The current study aimed to evaluate the effects of a mixture of chemicals on maternal and fetal health in the rabbit model, which was defined based on associations between urinary concentrations of chemicals in pregnant women from the SEPAGES cohort and offspring outcomes. From the SEPAGES cohort data, a mixture including 3 phenols, 1 paraben and four phthalates was established and used in a rabbit model. Female rabbits were exposed orally from preconception to 28 days post-conception (dpc) to this mixture (PPP exposed group, PPP) or excipient (control group, C) daily at the doses, estimated from the maximum urinary concentrations observed in the cohort. Maternal and fetoplacental phenotype were characterized. Maternal glucose concentration decreased significantly in the PPP group, before mating. At 21 dpc, ultrasound monitoring showed that fetal body length and abdominal perimeter were increased in PPP group compared to C group. At 28 dpc, heart to bodyweight ratio was increased in PPP females compared to C females. At this stage, fetal blood biochemistry showed a decrease in insulin levels, while triglycerides and total protein increased, mostly in PPP males compared to controls. Exposure to a PPP mixture defined from a human mother-child cohort impacted rabbit maternal phenotype and affected fetal health in a sex-specific manner, suggesting that this mixture could induce fetal malprogramming with long-term effects
Two types of axonal muscarinic acetylcholine receptors mediate formation of saliva cocktail in the tick Ixodes ricinus
No full textInternational audienceAbstract Hard ticks depend upon an ability to precisely and dynamically regulate their saliva to successfully evade host haemostatic and immune defences during extended blood feeding. Although pilocarpine, an exogenous muscarinic acetylcholine receptor (mAChR) agonist, can stimulate salivation experimentally, the endogenous control of saliva secretion by acetylcholine remains poorly understood. Here, we identify and characterise two pharmacologically distinct mAChRs (type A and B) in the genome of the medically important tick Ixodes ricinus . Molecular dynamics simulations and targeted mutagenesis reveal that type B mAChRs exhibit an atypical muscarinic profile, suggesting unconventional receptor signalling. Combining immunolabelling, in vivo pharmacology, and proteomics, we show that specific central neurons interact with distinct salivary gland regions via mAChR type-specific axons, coordinating fluid and protein secretion through separate acini and likely acting upstream of a neuropeptide-dependent cascade. This previously unrecognised mechanism of neural control offers new insights into how ticks modulate their saliva advancing our understanding of vector-host interactions, with potential implications for disrupting pathogen transmission
The composition of the lactation diet but not the previous rearing feeding level affects the response to an oral drench of propylene glycol in primiparous lactating dairy goats
No full textInternational audienceThe aim of this experiment was to study if different growth trajectories during rearing influence adaptive capacity to metabolic challenges during lactation. Sixteen female Saanen goats were selected at weaning and given either a high growth trajectory diet (High GT, n=8) or a control growth trajectory diet (Control GT, n=8) until parturition. The diets were formulated to produce a weight difference at parturition of 10%. Oestrous cycles were synchronised and the goats were inseminated at 7 months of age. Three weeks after parturition, four metabolic challenges were performed: day 21 (goats were fed the normal lactation diet and given 1 mL PG/kg liveweight, by drenching), day 28 (goats were fed straw for 2 days and then given 1 mL water/kg liveweight, by drenching), day 35 (goats were fed the normal lactation diet and given 1 mL PG/kg liveweight, by drenching) and day 42 (goats were fed straw for 2 days and then given 1 mL PG/kg liveweight, by drenching). The metabolic response to PG (an increase in circulating glucose and insulin) was delayed after the day 42 challenge (straw diet) compared to the day 21 and 35 challenges (lactation diet). Several hypotheses may explain this finding: poor adaptation of rumen microbes for PG fermentation after a straw diet, reduced rumen-emptying in the straw fed goats (therefore slower absorption of PG and its metabolites) or reduced gluconeogenesis in the liver of straw fed goats compared to lactation diet fed goats due to mild steatosis. After the day 28 challenge (straw diet), the High GT goats appeared to be less metabolically versatile than the Control GT goats since the High GT goats had beta-hydroxybutyrate (BHB) concentrations which were close to those defined as indicating sub-clinical ketosis (>1.2 mmol/L) while Control GT goats had low BHB concentrations. Short-term metabolic challenges may be interesting tools in the study of metabolic versatility in farm animal
Transcriptomic plasticity in hybrid schistosomes can contribute to their zoonotic potential
No full textData accessibility: Sequencing data from Schistosoma bovis, hybrids and introgressed worms infecting sheep are available at the NCBISRA under the BioProject accession number PRJNA1199762.International audienceHybrids between Schistosoma haematobium and Schistosoma bovis contribute to human and animal infections, highlighting complex interspecies interactions that facilitate schistosomiasis transmission. Schistosoma bovis infects multiple ruminant hosts, promoting cross-species transmission and increasing zoonotic risk. This study explores transcriptomic plasticity as a mechanism enabling hybrid schistosomes to adapt to different definitive hosts. We analysed two contexts: (1) introgressed S. haematobium × S. bovis hybrids, which exhibited higher virulence in sheep than parental S. bovis; and (2) S. bovis infecting different mammalian hosts. Introgression, the transfer of genetic material between species through hybridization and repeated backcrossing, was associated with 366 differentially expressed genes (4% of coding genes) between introgressed hybrids and S. bovis in sheep. Additionally, S. bovis showed host-dependent transcriptomic changes, with 30% of genes differentially expressed between infections in hamsters and sheep. Enriched biological processes shared across introgression and host adaptation included nuclear mRNA catabolism and inner mitochondrial membrane organization, indicating increased gene expression plasticity and metabolic adaptation to environmental stress. These findings suggest that transcriptomic plasticity enhances the adaptability of S. bovis and hybrid worms, increasing their zoonotic potential. This raises concerns for schistosomiasis control, as such plasticity could expand transmission capacity and complicate intervention strategies.This article is part of the Royal Society Science+ meeting issue ‘Parasite evolution and impact in action: exploring the importance and control of hybrid schistosomes in Africa and beyond’
Distribution of Giardia duodenalis genotypes in diarrheic children from Algiers, Algeria
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Une collaboration gagnant-gagnant entre le médecin Vicq d'Azyr et les vétérinaires, au XVIIIe siècle
No full textInternational audienceA man of the Enlightenment, permanent secretary of the Royal Society of Medicine and member of the Royal Academy of Sciences, Félix Vicq d’Azyr was entrusted by Turgot with managing the cattle plague epidemic in 1774 . On this occasion, he worked with students from the recently created veterinary schools. He also collaborated with local veterinarians who had set up veterinary hospitals. During this time, he perfected his comparative anatomical and functional approach. His uncle, Daubenton, involved him in the restructuring of the education at the Alfort Veterinary School. He was appointed to the chair of comparative anatomy between 1782 and 1787, and students from the school were made available to assist him with his dissections. He worked alongside young scientists, including the chemist and physician Fourcroy, the botanist and physician Broussonet, and the veterinarian Gilbert, who would lay the foundations for emerging sciences, such as agronomy, organic chemistry, comparative anatomy, and, above all, experimental medicine. Thanks to them, the Alfort School became a unique center for research on living organisms, including a center for clinical and agronomic investigations. Vicq d’Az yr had a unified vision of medicine, leading him to suggest integrating veterinary education into medical studies. His premature death in 1794 prevented him from joining the other scholars of Alfort in the first nucleus of the National Institute created by the Directory in 1795. Veterinarians understood what they owed to Daubenton and Vicq d’Azyr: the creation of experimental chairs and the expansion of their field of expertise to everything related to farm animals, enabling them to become fully fledged economic players. At the Alfort School, between 1782 and 1787, the porosity between human and animal medicine fostered an unprecedented circulation of knowledge, foreshadowing the modern concept of “One Medicine” and even, more recently, that of “One Health.”Homme des Lumières, secrétaire perpétuel de la Société royale de médecine et membre de l’Académie royale des sciences, Félix Vicq d’Azyr se voit confier par Turgot la gestion de l’épizootie de peste bovine en 1774. À cette occasion, il travaille avec les élèves des écoles vétérinaires, récemment créées. Il collabore aussi avec les vétérinaires locaux qui ont créé des hôpitaux vétérinaires. À cette occasion, il perfectionne son approche anatomo-fonctionnelle comparative. Grâce à son oncle Daubenton, il participe à la restructuration de l’enseignement de l’École vétérinaire d’Alfort. Il dirige la chaire d’anatomie comparée entre 1782 et 1787 et des élèves de l’école l’aident dans ses dissections. Il travaille aux côtés de jeunes savants, le chimiste et médecin Fourcroy, le botaniste et médecin Broussonet et le vétérinaire Gilbert, qui vont poser les jalons de sciences en devenir : l’agronomie, la chimie organique, l’anatomie comparée et, surtout, la médecine expérimentale. L’École d’Alfort devient un véritable centre de recherche sur le vivant, incluant un centre d’investigation clinique et agronomique. Vicq d’Azyr a u ne vision unitaire de la médecine qui l’incitera à proposer l’intégration de l’enseignement vétérinaire aux études médicales. S’il n’était pas mort prématurément, il aurait participé, avec les savants d’Alfort, au premier noyau de l’Institut national, créé par le Directoire en 1795. Les vétérinaires doivent à Daubenton et à Vicq d’Azyr la création de chaires expérimentales, l’élargissement de leur domaine d’expertise à tout ce qui concerne les animaux d’élevage, leur permettant de devenir des acteurs économiques à part entière. Au sein de l’École d’Alfort, entre 1782 et 1787, la circulation sans précédent des savoirs favorise la porosité entre les médecines humaine et animale. Cette vision unitaire de la santé préfigure le concept moderne de « One Medicine », voire celui, plus récent, de « One Health »
Placental crises: disruptive selection and maternal under‐investment as the foundations of mammalian placental evolution and dysfunction
No full textInternational audienceAmong the vertebrates, mammals are notable for the dominance of live birth and placental nutrition. The structural diversity of the mammalian placenta is remarkable, despite sharing a single common ancestor and conserved physiological functions. Historically, investigations into the evolution of the mammalian placenta have been grounded in 'the efficiency paradigm', i.e. the assumption that certain placental configurations permit easier nutrient exchange, but this paradigm has struggled to explain the diversity of mammalian placentation strategies. Here, we propose a new paradigm to understand mammalian placental evolution. Using multidimensional plotting of recorded placental structures, quantitative metrics for mammalian maternal investment, and illustrative computational modelling of physiological processes, we argue that the ancestral mammalian placenta is not a streamlined 'highly efficient' design, but rather a product of low maternal investment, with fitness costs that manifest as gestational demand increases. Expansion of small mammals into larger-bodied, longer-lived niches induces a 'placental crisis' characterised by maternal under-investment and chronic gestational dysfunction, triggering an arms race through the interaction of disruptive selection and materno-fetal conflict. We propose the acute severity of the placental crisis is the foundation of placental evolution. We go on to argue that some primates are currently in a state of placental crisis and that maternal under-investment and inappropriate placentation are the evolutionary foundations of human gestational dysfunctions such as pre-eclampsia. We conclude that the ancestral mammalian placenta was not an efficiently optimised design that allowed placentation to dominate the clade, but rather an idiosyncrasy of mammal-specific biology, which likely hindered mammalian expansion into larger-bodied niches