The Complete Genome of Propionibacterium freudenreichii CIRM-BIA1T, a Hardy Actinobacterium with Food and Probiotic Applications

Background: Propionibacterium freudenreichii is essential as a ripening culture in Swiss-type cheeses and is also considered for its probiotic use [1]. This species exhibits slow growth, low nutritional requirements, and hardiness in many habitats. It belongs to the taxonomic group of dairy propionibacteria, in contrast to the cutaneous species P. acnes. The genome of the type strain, P. freudenreichii subsp. shermanii CIRM-BIA1 (CIP 103027T), was sequenced with an 11-fold coverage. Methodology/Principal Findings: The circular chromosome of 2.7 Mb of the CIRM-BIA1 strain has a GC-content of 67% and contains 22 different insertion sequences (3.5% of the genome in base pairs). Using a proteomic approach, 490 of the 2439 predicted proteins were confirmed. The annotation revealed the genetic basis for the hardiness of P. freudenreichii, as the bacterium possesses a complete enzymatic arsenal for de novo biosynthesis of aminoacids and vitamins (except panthotenate and biotin) as well as sequences involved in metabolism of various carbon sources, immunity against phages, duplicated chaperone genes and, interestingly, genes involved in the management of polyphosphate, glycogen and trehalose storage. The complete biosynthesis pathway for a bifidogenic compound is described, as well as a high number of surface proteins involved in interactions with the host and present in other probiotic bacteria. By comparative genomics, no pathogenicity factors found in P. acnes or in other pathogenic microbial species were identified in P. freudenreichii, which is consistent with the Generally Recognized As Safe and Qualified Presumption of Safety status of P. freudenreichii. Various pathways for formation of cheese flavor compounds were identified: the Wood-Werkman cycle for propionic acid formation, amino acid degradation pathways resulting in the formation of volatile branched chain fatty acids, and esterases involved in the formation of free fatty acids and esters. Conclusions/Significance: With the exception of its ability to degrade lactose, P. freudenreichii seems poorly adapted to dairy niches. This genome annotation opens up new prospects for the understanding of the P. freudenreichii probiotic activity

Global burden of 288 causes of death and life expectancy decomposition in 204 countries and territories and 811 subnational locations, 1990–2021: a systematic analysis for the Global Burden of Disease Study 2021

BACKGROUND Regular, detailed reporting on population health by underlying cause of death is fundamental for public health decision making. Cause-specific estimates of mortality and the subsequent effects on life expectancy worldwide are valuable metrics to gauge progress in reducing mortality rates. These estimates are particularly important following large-scale mortality spikes, such as the COVID-19 pandemic. When systematically analysed, mortality rates and life expectancy allow comparisons of the consequences of causes of death globally and over time, providing a nuanced understanding of the effect of these causes on global populations. METHODS The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021 cause-of-death analysis estimated mortality and years of life lost (YLLs) from 288 causes of death by age-sex-location-year in 204 countries and territories and 811 subnational locations for each year from 1990 until 2021. The analysis used 56 604 data sources, including data from vital registration and verbal autopsy as well as surveys, censuses, surveillance systems, and cancer registries, among others. As with previous GBD rounds, cause-specific death rates for most causes were estimated using the Cause of Death Ensemble model-a modelling tool developed for GBD to assess the out-of-sample predictive validity of different statistical models and covariate permutations and combine those results to produce cause-specific mortality estimates-with alternative strategies adapted to model causes with insufficient data, substantial changes in reporting over the study period, or unusual epidemiology. YLLs were computed as the product of the number of deaths for each cause-age-sex-location-year and the standard life expectancy at each age. As part of the modelling process, uncertainty intervals (UIs) were generated using the 2·5th and 97·5th percentiles from a 1000-draw distribution for each metric. We decomposed life expectancy by cause of death, location, and year to show cause-specific effects on life expectancy from 1990 to 2021. We also used the coefficient of variation and the fraction of population affected by 90% of deaths to highlight concentrations of mortality. Findings are reported in counts and age-standardised rates. Methodological improvements for cause-of-death estimates in GBD 2021 include the expansion of under-5-years age group to include four new age groups, enhanced methods to account for stochastic variation of sparse data, and the inclusion of COVID-19 and other pandemic-related mortality-which includes excess mortality associated with the pandemic, excluding COVID-19, lower respiratory infections, measles, malaria, and pertussis. For this analysis, 199 new country-years of vital registration cause-of-death data, 5 country-years of surveillance data, 21 country-years of verbal autopsy data, and 94 country-years of other data types were added to those used in previous GBD rounds. FINDINGS The leading causes of age-standardised deaths globally were the same in 2019 as they were in 1990; in descending order, these were, ischaemic heart disease, stroke, chronic obstructive pulmonary disease, and lower respiratory infections. In 2021, however, COVID-19 replaced stroke as the second-leading age-standardised cause of death, with 94·0 deaths (95% UI 89·2-100·0) per 100 000 population. The COVID-19 pandemic shifted the rankings of the leading five causes, lowering stroke to the third-leading and chronic obstructive pulmonary disease to the fourth-leading position. In 2021, the highest age-standardised death rates from COVID-19 occurred in sub-Saharan Africa (271·0 deaths [250·1-290·7] per 100 000 population) and Latin America and the Caribbean (195·4 deaths [182·1-211·4] per 100 000 population). The lowest age-standardised death rates from COVID-19 were in the high-income super-region (48·1 deaths [47·4-48·8] per 100 000 population) and southeast Asia, east Asia, and Oceania (23·2 deaths [16·3-37·2] per 100 000 population). Globally, life expectancy steadily improved between 1990 and 2019 for 18 of the 22 investigated causes. Decomposition of global and regional life expectancy showed the positive effect that reductions in deaths from enteric infections, lower respiratory infections, stroke, and neonatal deaths, among others have contributed to improved survival over the study period. However, a net reduction of 1·6 years occurred in global life expectancy between 2019 and 2021, primarily due to increased death rates from COVID-19 and other pandemic-related mortality. Life expectancy was highly variable between super-regions over the study period, with southeast Asia, east Asia, and Oceania gaining 8·3 years (6·7-9·9) overall, while having the smallest reduction in life expectancy due to COVID-19 (0·4 years). The largest reduction in life expectancy due to COVID-19 occurred in Latin America and the Caribbean (3·6 years). Additionally, 53 of the 288 causes of death were highly concentrated in locations with less than 50% of the global population as of 2021, and these causes of death became progressively more concentrated since 1990, when only 44 causes showed this pattern. The concentration phenomenon is discussed heuristically with respect to enteric and lower respiratory infections, malaria, HIV/AIDS, neonatal disorders, tuberculosis, and measles. INTERPRETATION Long-standing gains in life expectancy and reductions in many of the leading causes of death have been disrupted by the COVID-19 pandemic, the adverse effects of which were spread unevenly among populations. Despite the pandemic, there has been continued progress in combatting several notable causes of death, leading to improved global life expectancy over the study period. Each of the seven GBD super-regions showed an overall improvement from 1990 and 2021, obscuring the negative effect in the years of the pandemic. Additionally, our findings regarding regional variation in causes of death driving increases in life expectancy hold clear policy utility. Analyses of shifting mortality trends reveal that several causes, once widespread globally, are now increasingly concentrated geographically. These changes in mortality concentration, alongside further investigation of changing risks, interventions, and relevant policy, present an important opportunity to deepen our understanding of mortality-reduction strategies. Examining patterns in mortality concentration might reveal areas where successful public health interventions have been implemented. Translating these successes to locations where certain causes of death remain entrenched can inform policies that work to improve life expectancy for people everywhere. FUNDING Bill & Melinda Gates Foundation

Caractérisation des gènes de biosynthèse de l'albicidine et clonage d'un gène de résistance à l'albicidine produite par Xanthomonas albilineans, agent causal de l'échaudure des feuilles de la canne à sucre

"Xanthomonas albilineans# est un agent pathogène inféodé au xylème, responsable de l'échaudure des feuilles de la canne à sucre. Cette bactérie produit une phytotoxine, l'albicidine, qui inhibe de façon spécifique la réplication des ADN chloroplastiques et bactériens. Trois régions de gènes impliqués dans la biosynthèse de la toxine avaient été identifiées en 1998 chez la souche originaire de Floride Xa23R1 à partir de l'analyse moléculaire de mutants non producteurs d'albicidine obtenus par mutagénèse insertionnelle du transposon #Tn5-GusA# (Rott #et aL#, 1996). Les gènes situés au niveau de ces régions, appelées I, II et III, sont localisés dans des zones respectives de 48, 9 et 3 kb. Ce travail présente la caractérisation de la troisième région de biosynthèse qui, après isolement et clonage chez #E. coli# a permis de restaurer la production de toxine chez deux mutants non producteurs de toxine et non complémentés par les régions I et II. L'analyse de la séquence de la région III et des sites mutés a permis d'identifier cinq ORFs et de proposer une fonction pour quatre d'entre elles (ORF 1, ORF2, ORE 4 et ORF5). Parallèlement, un gène de résistance à l'albicidine, #albE# a récemment été découvert chez une souche australienne de #X. albilineans# (Wall, 1996). Des séquences homologues à ce gène avaient été recherchées en 1998, par PCR dans la souche Xa23R1 au moyen d'amorces définies à partir de la séquence de #alb E#. Au cours de ce travail, plusieurs fragments ont été amplifiés à partir de Xa23R1, mais aucun d'eux ne présentait d'homologie avec la séquence du gène australien. Une séquence homologue au gène australien a donc été recherchée chez une autre souche australienne (Xa126R1) afin d'identifier une sonde pour localiser le gène de résistance dans la souche de Floride Xa23R1. Un fragment PCR d'environ 1 kb présentant une homologie avec #alb E# de 97% sur 767pb a été obtenu. (Résumé d'auteur

Analyse du processus infectieux de Mycosphaerella graminicola, agent responsable de la septoriose du blé

Le champignon Mycosphaerella graminicola est l agent causal d une des septorioses du blé. Malgré des études histologiques préalables, certains aspects, telle la longue phase asymptomatique post-pénétration, demeuraient mal compris. D autre part, très peu de déterminants moléculaires du pouvoir pathogène étaient connus lors de l initiation de ce travail. Nous avons donc cherché à mieux comprendre le cycle de développement de M. graminicola à travers l étude de mutants résultant soit d une stratégie de mutagenèse insertionnelle aléatoire par plasmide soit d une approche gène-candidat . Deux étapes de criblage, selon des tests mis au point au cours de ce travail, ont abouti à l isolement de onze mutants présentant des altérations significatives de leur pathogénie. Des études microbiologique, cytologique et microscopique plus approfondies menées sur sept de ces onze mutants ont mis en évidence trois phases majeures dans le processus infectieux de M. graminicola. L analyse moléculaire, de par la complexité du profil d intégration du plasmide mutagène, n a pu être menée que sur deux mutants, A18 et D22, pour lesquels les régions flanquant l insertion du plasmide ont pu être clonées. Toutefois, la corrélation entre l insertion du plasmide et le phénotype mutant n a été démontrée que pour D22. Une seconde approche de type gène candidat a permis de cloner et de caractériser le gène MgMK1 de M. graminicola orthologue du gène PMK1 de M. grisea codant une MAP kinase impliquée dans la pathogénie. Cette stratégie gène candidat n étant pas envisageable sur la totalité des gènes de M. graminicola, tant pour des raisons techniques que de ressources, s avère complémentaire de la première.Mycosphaerella graminicola is the causal agent of wheat leaf blotch. At the beginning of this work, very few was known about M; graminicola infection cycle, especially at the molecular level. In order to better understand the infection process of this fungus on its host plant, we developed strategies to generate and study pathogenicity mutants. A first approach was random insertional mutagenesis using a plasmid as mutagen. Using two successive screening steps set up during this work, eleven pathogenicity mutants were recovered. More detailed phenotypic analyses of these mutants allowed to identify three major steps in M. graminicola infection cycle : (1) the development of infection hyphae allowing stomatal penetration, (2) the differenciation of invasive hyphae associated with plant tissue colonization and (3) the formation of reproductive hyphae correlated with the diffenciation of pycnidia. Unfortunately, the molecular analysis of these mutants revealed to be laborious as many of them were too complex to be studied. Sequences flanking the insertion were recovered for two mutants, A18 and D22, but the relationship between the plasmid insertion and the mutant phenotype was demonstrated only for the mutant strain D22. A candidate gene approach.was also developed to investigate the role of MgMK1, a PMK1-like orthologous gene, encoding a MAP kinase. Mutant strains were obtained using gene replacement and shown to be non pathogenic, due to a major alteration of stomatal penetration. Altogether, these results show that the two strategies are complementary to identify and study molecular determinants of pathogenicity in a plant pathogenic fungus.ORSAY-PARIS 11-BU Sciences (914712101) / SudocSudocFranceF

Peintres d'ex-voto provençaux

Cousin Bernard, Ramiere de Fortanier Arnaud. Peintres d'ex-voto provençaux. In: Le Monde alpin et rhodanien. Revue régionale d'ethnologie, n°1-4/1979. Artisanat et métiers de tradition. pp. 473-493

Real-time On-Demand Multi-Hop Audio Streaming with Low-Resource Sensor Motes

International audienceThe European EAR-IT project addresses “real-life” experimentations of intelligent acoustic for supporting high societal value applications in a large-scale smart environment. For instance a city emergency center can request on-demand acoustic data samples for surveillance purposes and management of emergencies. In this paper, we will present experimentations on streaming encoded acoustic on the SmartSantander large scale test-bed. We will present the various audio hardware that were developed to meet the constraints of audio capture and transmission with low-resources devices. We will highlight the main sources of delays and will show how multi-hop streaming of acoustic data can be achieved by carefully taking into account these performance limitations with appropriate audio aggregation techniques

Designing responsive foams with an adjustable temperature threshold of destabilization

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Designing responsive foams

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Morphological Transition in Fatty Acid Self-Assemblies: A Process Driven by the Interplay between the Chain-Melting and Surface-Melting Process of the Hydrogen Bonds

International audienceIn surfactant systems, the major role of the nature of the counter-ion on the surfactant behavior is well-known. However, the effect of the molar ratio between the surfactant and its counter-ion is less explored in the literature. We investigated the effect of the molar ratio (R) between 12-hydroxystearic acid (12-HSA) and various alkanolamines as a function of the temperature in aqueous solution from the molecular scale to the mesoscale. By coupling microscopy techniques and small angle neutron scattering, we showed that 12-HSA self-assembled into multilamellar tubes and transitioned into micelles at a precise temperature. This temperature transition depended on both the molar ratio and the alkyl chain length of the counter-ion and could be precisely tuned from 20°C to 75°C. This thermal behaviour was investigated by differential scanning calorimetry and wide angle X-ray scattering. We highlighted that the transition at the supramolecular scale between tubes to micelles came from two different mechanisms at the molecular scale as a function of the molar ratio. At low R, with an excess of counter-ion, the transition came from the chain melting phenomenon. At high R, with an excess of 12-HSA, the transition came from both the chain melting process and the surface melting process of the hydrogen bonds. At the mesoscale, this transition of supramolecular assemblies from tubes to micelles, delimited a regime of high bulk viscosity, with a regime of low viscosity