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International audience; This report provides the first clinical, radiographic, echocardiographic, and biological description of SARS-CoV-2-associated myocarditis with a 6-month follow-up in a 5-year-old obese male domestic shorthair cat (Cat-1) presented for refractory congestive heart failure, with high cardiac troponin-I level (5.24 ng/ml), and a large lingual ulcer. The animal was SARS-CoV-2 positive on serology. The other cat living in the same household (Cat-2) never showed any clinical sign but was also confirmed SARS-CoV-2 positive on serology. Both cats were SARS-CoV-2 PCR negative. Cat-1 had closer contact than Cat-2 with their owner, who had been in close contact with a coworker tested PCR positive for COVID-19 (Alpha (B.1.1.7) variant) 4 weeks before Cat-1's first episode of congestive heart failure. A focused point-of-care echocardiography at presentation revealed for Cat-1 numerous B-lines, pleural effusion, severe left atrial dilation and dysfunction, and hypertrophic cardiomyopathy phenotype associated with focal pulmonary consolidations. Both myocarditis and pneumonia were suspected, leading to the prescription of cardiac medications and antibiotics. One month later, Cat-1 recovered, with normalization of left atrial size and function, and radiographic and echocardiography disappearance of heart failure signs and pulmonary lesions. An extensive literature review of SARS-CoV-2-related cardiac injury in pets in comparison with human pathology is discussed.

International audience; Air pollution is one of the main causes of damages to human health in Europe with an estimate of about 380 000 premature deaths per year in the EU28, as the result of exposure to fine particulate matter (PM2.5) only. In this work, we focus on one specific region in Europe, the Po basin, a region where chemical regimes are the most complex, showing important non-linear processes, especially those related to interactions between NOx and NH3. We analyse the sensitivity of PM2.5 concentration to NOx and NH3 emissions by means of a set of EMEP model simulations performed with different levels of emission reductions, from 25% up to a total switch-off of those emissions. Both single and combined precursor reduction scenarios are applied to determine the most efficient emission reduction strategies and quantify the interactions between NOx and NH3 emission reductions. The results confirmed the peculiarity of secondary PM2.5 formation in the Po basin, characterised by contrasting chemical regimes within distances of few (hundreds of) kilometres, as well as non-linear responses to emission reductions during wintertime. One of the striking results is the slight increase of the PM2.5 concentration levels when NOx emission reductions are applied in NOx-rich areas, such as the surroundings of Bergamo. The increased oxidative capacity of the atmosphere is the cause of the increase of PM2.5 induced by a reduction in NOx emission. This process can have contributed to the absence of significant PM2.5 concentration decrease during the COVID-19 lockdowns in many European cities. It is important to account for this process when designing air quality plans, since it could well lead to transitionary increases in PM2.5 at some locations in winter as NOx emission reduction measures are gradually implemented. While PM2.5 chemical regimes, determined by the relative importance of the NOx vs. NH3 responses to emission reductions, show large variations seasonally and spatially, they are not very sensitive to moderate (up to 50-60%) emission reductions. Beyond 25% emission reduction strength, responses of PM2.5 concentrations to NOx emission reductions become non-linear in certain areas of the Po basin mainly during wintertime.

In this paper, we consider two-component mixture distributions having one known component. This type of model is of particular interest when a known random phenomenon is contaminated by an unknown random effect. We propose in this setup to compare the unknown random sources involved in two separate samples. For this purpose, we introduce the so-called IBM (Inversion-Best Matching) approach resulting in a relaxed semiparametric Cramér-von Mises type two-sample test requiring very minimal assumptions (shape constraint free) about the unknown distributions. The accomplishment of our work lies in the fact that we establish a functional central limit theorem on the proportion parameters along with the unknown cumulative distribution functions of the model when Patra and Sen [22] prove that the √ n-rate cannot be achieved on these quantities in the basic one-sample case. An intensive numerical study is carried out from a large range of simulation setups to illustrate the asymptotic properties of our test. Finally, our testing procedure is applied to a real-life application through pairwise post-covid mortality effect testing across a panel of European countries. Nous considérons dans cet article des mélanges à deux composantes dont une composante est connue. Ces modèles sont d'un intérêt particulier lorsqu'un phénomène bien connu est affecté par une perturbation inconnue. Nous proposons de comparer les sources de cet impact inconnu entre deux échantillons distincts. Pour ce faire nous introduisons une nouvelle approche, appelée IBM (Inversion-Best Matching), qui permet d'effectuer le test à la manière d'un test de type Cramer-Von Mises sous très peu d'hypothèses concernant les aléas perturbateurs inconnus. Nous établissons un théorème central limite (TCL) fonctionnel sur les estimateurs que sont les proportions de chacun des modèles de contamination, ainsi que la fonction de répartition inconnue, là où Patra et Sen [22] n'obtenait pas de résultat asymptotique de type TCL. Des simulations permettent de valider la performance de la procédure de test et d'en valider ses propriétés asymptotiques. Enfin, nous appliquons notre stratégie de test à un problème concret de comparaison de déformation de la mortalité suite à la pandémie de Covid-19 à travers plusieurs pays européens.

Understanding how SARS-CoV-2 spreads within the respiratory tract is important to define the parameters controlling the severity of COVID-19. Here we examine the functional and structural consequences of SARS-CoV-2 infection in a reconstructed human bronchial epithelium model. SARS-CoV-2 replication causes a transient decrease in epithelial barrier function and disruption of tight junctions, though viral particle crossing remains limited. Rather, SARS-CoV-2 replication leads to a rapid loss of the ciliary layer, characterized at the ultrastructural level by axoneme loss and misorientation of remaining basal bodies. Downregulation of the master regulator of ciliogenesis Foxj1 occurs prior to extensive cilia loss, implicating this transcription factor in the dedifferentiation of ciliated cells. Motile cilia function is compromised by SARS-CoV-2 infection, as measured in a mucociliary clearance assay. Epithelial defense mechanisms, including basal cell mobilization and interferon-lambda induction, ramp up only after the initiation of cilia damage. Analysis of SARS-CoV-2 infection in Syrian hamsters further demonstrates the loss of motile cilia in vivo. This study identifies cilia damage as a pathogenic mechanism that could facilitate SARS-CoV-2 spread to the deeper lung parenchyma. SARS-CoV-2 infection damages the airways. Here the authors show that SARS-CoV-2 infection induces the rapid loss of airway motile cilia, resulting in altered cilia clearance function. Cilia loss is preceded by reduced expression of the ciliogenesis regulator Foxj1.

Seuls les 100 premiers auteurs dont les auteurs INRA ont été entrés dans la notice. La liste complète des auteurs et de leurs affiliations est accessible sur la publication.; International audience; In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes.For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure flux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy.Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation, it is imperative to target by gene knockout or RNA interference more than one autophagy-related protein. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways implying that not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular assays, we hope to encourage technical innovation in the field.