Synthese directe de chlorures d'acide par carbonylation de derives halogenes aliphatiques

SIGLECNRS T Bordereau / INIST-CNRS - Institut de l'Information Scientifique et TechniqueFRFranc

Etude sanitaire (1987 - 1988) de la côte de Guidel - Ploemeur - Larmor Plage (Morbihan)

Le secteur côtier de Lorient est un littoral rocheux, peu propice à la conchyliculture. La proximité· de l'agglomération Lorientaise y induit une pêche récréative non négligeable en été. avec des risques sanitaires d'autant plus grands que les courants littoraux dévient vers cette côte les apports en mer de la Laïta et de la Rade de Lorient. L'étude bactériologique réalisée par IFREMER en 1987-1988 révèle de fortes contaminations des moules de ce secteur, notamment sur la côte Sud, nettement insalubre de Lomener à Larmor - Plage. II y a en effet une différence de nature fondamentale entre la contamination globale du secteur Sud par les eaux marines de la Rade et les pollutions locales diffuses sur la côte Ouest. On n'observe pas de variations saisonnières très marquées, et la recherche d'une évolution tend à montrer une dégradation sanitaire de la côte Ouest qui risque de devenir franchement insalubre à son tour

Etude sanitaire (1986 - 1987) de la petite mer de Gavres (Morbihan)

La Petite Mer de Gavres est une zone conchylicole, classée salubre, et exploitée en pêche à pied, avec une commercialisation directe difficile à contrôler. A la suite de problèmes de salubrité rencontrés sur les coquillages de cette zone, une étude bactériologique a été réalisée par IFREMER de juin 1986 à septembre 1987, suivie en 1988 d'une comparaison des contaminations des différentes espèces de coquillages. Ces études montrent que l'insalubrité de certains coquillages de la petite Mer de Gavres est particulièrement évidente pour les fouisseurs (coques et palourdes). Malgré la proximité des sources de pollutions de la Rade de Lorient et la petitesse du bassin versant de la Petite Mer, c'est ce dernier qui la contamine, notamment aux abords du bourg de Riantec qui apparaît nettement insalubre. Cette pollution par les eaux douces d'un bassin versant très limité induit évidemment une forte saisonnalité des contaminations qui augmentent significativement en automne-hiver

Quand les cellules iNKT partent au charbon : nouvelles pistes thérapeutiques

International audienc

Targeting the red nucleus for cerebellar tremor

Deep brain stimulation of the thalamus (and especially the ventral intermediate nucleus) does not significantly improve a drug-resistant, disabling cerebellar tremor. The dentato-rubro-olivary tract (Guillain-Mollaret triangle, including the red nucleus) is a subcortical loop that is critically involved in tremor genesis.We report the case of a 48-year-old female patient presenting with generalized cerebellar tremor caused by alcohol-related cerebellar degeneration. Resistance to pharmacological treatment and the severity of the symptoms prompted us to investigate the effects of bilateral deep brain stimulation of the red nucleus. Intra-operative microrecordings of the red nucleus revealed intense, irregular, tonic background activity but no rhythmic components that were synchronous with upper limb tremor. The postural component of the cerebellar tremor disappeared during insertion of the macro-electrodes and for a few minutes after stimulation, with no changes in the intentional (kinetic) component. Stimulation per se did not reduce postural or intentional tremor and was associated with dysautonomic symptoms (the voltage threshold for which was inversed related to the stimulation frequency). Our observations suggest that the red nucleus is (1) an important centre for the genesis of cerebellar tremor and thus (2) a possible target for drug-refractory tremor. Future research must determine how neuromodulation of the red nucleus can best be implemented in patients with cerebellar degeneration. © Springer Science+Business Media 2014.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Plant genetic effects on microbial hubs impact host fitness in repeated field trials

Although complex interactions between hosts and microbial associates are increasingly well documented, we still know little about how and why hosts shape microbial communities in nature. In addition, host genetic effects on microbial communities vary widely depending on the environment, obscuring conclusions about which microbes are impacted and which plant functions are important. We characterized the leaf microbiota of 200 Arabidopsis thaliana genotypes in eight field experiments and detected consistent host effects on specific, broadly distributed microbial species (operational taxonomic unit [OTUs]). Host genetic effects disproportionately influenced central ecological hubs, with heritability of particular OTUs declining with their distance from the nearest hub within the microbial network. These host effects could reflect either OTUs preferentially associating with specific genotypes or differential microbial success within them. Host genetics associated with microbial hubs explained over 10% of the variation in lifetime seed production among host genotypes across sites and years. We successfully cultured one of these microbial hubs and demonstrated its growth-promoting effects on plants in sterile conditions. Finally, genome-wide association mapping identified many putatively causal genes with small effects on the relative abundance of microbial hubs across sites and years, and these genes were enriched for those involved in the synthesis of specialized metabolites, auxins, and the immune system. Using untargeted metabolomics, we corroborate the consistent association between variation in specialized metabolites and microbial hubs across field sites. Together, our results reveal that host genetic variation impacts the microbial communities in consistent ways across environments and that these effects contribute to fitness variation among host genotypes

Plant genetic effects on microbial hubs impact host fitness in repeated field trials

International audienceAlthough complex interactions between hosts and microbial associates are increasingly well documented, we still know little about how and why hosts shape microbial communities in nature. In addition, host genetic effects on microbial communities vary widely depending on the environment, obscuring conclusions about which microbes are impacted and which plant functions are important. We characterized the leaf microbiota of 200 Arabidopsis thaliana genotypes in eight field experiments and detected consistent host effects on specific, broadly distributed microbial species (operational taxonomic unit [OTUs]). Host genetic effects disproportionately influenced central ecological hubs, with heritability of particular OTUs declining with their distance from the nearest hub within the microbial network. These host effects could reflect either OTUs preferentially associating with specific genotypes or differential microbial success within them. Host genetics associated with microbial hubs explained over 10% of the variation in lifetime seed production among host genotypes across sites and years. We successfully cultured one of these microbial hubs and demonstrated its growth-promoting effects on plants in sterile conditions. Finally, genome-wide association mapping identified many putatively causal genes with small effects on the relative abundance of microbial hubs across sites and years, and these genes were enriched for those involved in the synthesis of specialized metabolites, auxins, and the immune system. Using untargeted metabolomics, we corroborate the consistent association between variation in specialized metabolites and microbial hubs across field sites. Together, our results reveal that host genetic variation impacts the microbial communities in consistent ways across environments and that these effects contribute to fitness variation among host genotypes

Neutrophil Elastase Degrades Cystic Fibrosis Transmembrane Conductance Regulator via Calpains and Disables Channel Function In Vitro and In Vivo

Comment in :The yin and yang of cystic fibrosis transmembrane conductance regulator function: implications for chronic lung disease. [Am J Respir Crit Care Med. 2013]International audienceRATIONALE:Cystic fibrosis transmembrane conductance regulator (CFTR) protein is a chloride channel regulating fluid homeostasis at epithelial surfaces. Its loss of function induces hypohydration, mucus accumulation, and bacterial infections in CF and potentially other lung chronic diseases.OBJECTIVES:To test whether neutrophil elastase (NE) and neutrophil-mediated inflammation negatively impact CFTR structure and function, in vitro and in vivo.METHODS:Using an adenovirus-CFTR overexpression approach, we showed that NE degrades wild-type (WT)- and ΔF508-CFTR in vitro and WT-CFTR in mice through a new pathway involving the activation of intracellular calpains.MEASUREMENTS AND MAIN RESULTS:CFTR degradation triggered a loss of function, as measured in vitro by channel patch-clamp and in vivo by nasal potential recording in mice. Importantly, this mechanism was also shown to be operative in a Pseudomonas aeruginosa lung infection murine model, and was NE-dependent, because CFTR integrity was significantly protected in NE(-/-) mice compared with WT mice.CONCLUSIONS:These data provide a new mechanism and show for the first time a link between NE-calpains activation and CFTR loss of function in bacterial lung infections relevant to CF and to other chronic inflammatory lung conditions