Replanting/underplanting strategy for old coconut plantations in Papua New Guinea

Dans la plupart des pays producteurs, la population de cocotiers vieillit et les moyens visant à leur remplacement sont rarement mis en oeuvre pour assurer le maintien de la production et sauvegarde l'avenir de l'industrie et sa rentabilité. La réhabilitation/replantation des cocoteraies et l'adoption de systèmes de cultures associées adaptés est l'un des principaux défis à relever pour l'avenir du cocotier dans la région Asie - Pacifique. L'exemple de la Papouasie-Nouvelle-Guinée (PNG) montre l'un des plus faibles rendements à l'hectare parmi les pays de la zone Asie-Pacifique. On dénombre près de 106 000 ha plantés entre 1910 et 1940, représentant environ 40% de la cocoteraie, et on peut donc envisager la disparition de 80 à 100 000 ha dans les vingt prochaines années. Face à cette prévision, l'Institut de Recherche sur le Cacao et le Cocotier de PNG (CCRI) a entrepris plusieurs actions à partir de la création d'un centre de recherche cocotier sur la Grande Terre de PNG : étude d'une stratégie de replantation des vieilles cocoteraies à partir de matériel végétal hybride, diffusion de matériel végétal amélioré à partir de la création d'un champ semencier et mise au point d'un outil de lutte pour contrôler les populations de ravageurs dans les zones à haut risque. L'expérimentation mise en place sur station vise à optimiser la date d'abattage des vieux arbres en mesurant les effets de compétition avec les hybrides complantés, et à déterminer d'un point de vue économique la meilleure stratégie à appliquer pour la mise en place de programmes de réhabilitation et/ou de replantation des cocoteraies âgées. Les résultats de ces actions sont présentés dans cette communication. (Résumé d'auteur

Laminar Burning Velocities and Markstein Lengths of Jet Fuel Surrogate/Air Mixtures in a Spherical Chamber

International audienceCharacterizing the propagation of jet fuel/air premixed flames during combustion is key to understanding the performances of advanced modes of combustion for turbo-engines. Consequently, a better knowledge of the combustion characteristics is necessary. Particularly, the laminar burning velocity and the Markstein length in laminar adiabatic conditions are both key parameters to improve the efficiency of innovated turbo-engines with technological breakthrough as constant-volume combustion. In the current study, a spherical combustion chamber equipped with various metrology systems is qualified. First, the new experimental setup is validated with methane/air premixed laminar flames at normal temperature and pressure. The laminar burning velocity of four jet fuel surrogates is then characterized. Measurements are performed over a range of equivalence ratios from 0.7 to 1.5, initial temperature of 400 K, and initial pressure of 0.1 MPa. The results are compared with experimental data available in the literature and with calculations using the chemical kinetics code CANTERA (1D model) and existing chemical kinetic mechanisms. A comparison between the different surrogates is then discussed

Complete exon sequencing of all known Usher syndrome genes greatly improves molecular diagnosis

<p>Abstract</p> <p>Background</p> <p>Usher syndrome (USH) combines sensorineural deafness with blindness. It is inherited in an autosomal recessive mode. Early diagnosis is critical for adapted educational and patient management choices, and for genetic counseling. To date, nine causative genes have been identified for the three clinical subtypes (USH1, USH2 and USH3). Current diagnostic strategies make use of a genotyping microarray that is based on the previously reported mutations. The purpose of this study was to design a more accurate molecular diagnosis tool.</p> <p>Methods</p> <p>We sequenced the 366 coding exons and flanking regions of the nine known USH genes, in 54 USH patients (27 USH1, 21 USH2 and 6 USH3).</p> <p>Results</p> <p>Biallelic mutations were detected in 39 patients (72%) and monoallelic mutations in an additional 10 patients (18.5%). In addition to biallelic mutations in one of the USH genes, presumably pathogenic mutations in another USH gene were detected in seven patients (13%), and another patient carried monoallelic mutations in three different USH genes. Notably, none of the USH3 patients carried detectable mutations in the only known USH3 gene, whereas they all carried mutations in USH2 genes. Most importantly, the currently used microarray would have detected only 30 of the 81 different mutations that we found, of which 39 (48%) were novel.</p> <p>Conclusions</p> <p>Based on these results, complete exon sequencing of the currently known USH genes stands as a definite improvement for molecular diagnosis of this disease, which is of utmost importance in the perspective of gene therapy.</p

Meta-analysis of SHANK Mutations in Autism Spectrum Disorders: A Gradient of Severity in Cognitive Impairments.

International audienceSHANK genes code for scaffold proteins located at the post-synaptic density of glutamatergic synapses. In neurons, SHANK2 and SHANK3 have a positive effect on the induction and maturation of dendritic spines, whereas SHANK1 induces the enlargement of spine heads. Mutations in SHANK genes have been associated with autism spectrum disorders (ASD), but their prevalence and clinical relevance remain to be determined. Here, we performed a new screen and a meta-analysis of SHANK copy-number and coding-sequence variants in ASD. Copy-number variants were analyzed in 5,657 patients and 19,163 controls, coding-sequence variants were ascertained in 760 to 2,147 patients and 492 to 1,090 controls (depending on the gene), and, individuals carrying de novo or truncating SHANK mutations underwent an extensive clinical investigation. Copy-number variants and truncating mutations in SHANK genes were present in ∼1% of patients with ASD: mutations in SHANK1 were rare (0.04%) and present in males with normal IQ and autism; mutations in SHANK2 were present in 0.17% of patients with ASD and mild intellectual disability; mutations in SHANK3 were present in 0.69% of patients with ASD and up to 2.12% of the cases with moderate to profound intellectual disability. In summary, mutations of the SHANK genes were detected in the whole spectrum of autism with a gradient of severity in cognitive impairment. Given the rare frequency of SHANK1 and SHANK2 deleterious mutations, the clinical relevance of these genes remains to be ascertained. In contrast, the frequency and the penetrance of SHANK3 mutations in individuals with ASD and intellectual disability-more than 1 in 50-warrant its consideration for mutation screening in clinical practice

Effects of eight neuropsychiatric copy number variants on human brain structure

Many copy number variants (CNVs) confer risk for the same range of neurodevelopmental symptoms and psychiatric conditions including autism and schizophrenia. Yet, to date neuroimaging studies have typically been carried out one mutation at a time, showing that CNVs have large effects on brain anatomy. Here, we aimed to characterize and quantify the distinct brain morphometry effects and latent dimensions across 8 neuropsychiatric CNVs. We analyzed T1-weighted MRI data from clinically and non-clinically ascertained CNV carriers (deletion/duplication) at the 1q21.1 (n = 39/28), 16p11.2 (n = 87/78), 22q11.2 (n = 75/30), and 15q11.2 (n = 72/76) loci as well as 1296 non-carriers (controls). Case-control contrasts of all examined genomic loci demonstrated effects on brain anatomy, with deletions and duplications showing mirror effects at the global and regional levels. Although CNVs mainly showed distinct brain patterns, principal component analysis (PCA) loaded subsets of CNVs on two latent brain dimensions, which explained 32 and 29% of the variance of the 8 Cohen’s d maps. The cingulate gyrus, insula, supplementary motor cortex, and cerebellum were identified by PCA and multi-view pattern learning as top regions contributing to latent dimension shared across subsets of CNVs. The large proportion of distinct CNV effects on brain morphology may explain the small neuroimaging effect sizes reported in polygenic psychiatric conditions. Nevertheless, latent gene brain morphology dimensions will help subgroup the rapidly expanding landscape of neuropsychiatric variants and dissect the heterogeneity of idiopathic conditions

Vaporeformage d'hydrocarbures lourds en presence de composes soufres

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