Nicolas-Edme Rétif de La Bretonne imprimeur (1734-1806)

Mémoire du Master 1 Cultures de l\u27écrit et de l\u27image portant sur Rétif de La Bretonne, imprimeur

éditions françaises et allochtones de l\u27Instruction pour les jardins fruitiers et potagers de Jean-Baptiste de La Quintinie (2) (Les)

Annexes du mémoire du Master 2 Cultures de l\u27écrit et de l\u27image portant sur les éditions françaises et allochtones de l\u27Instruction pour les jardins fruitiers et potagers de Jean-Baptiste de La Quintinie

éditions françaises et allochtones de l\u27Instruction pour les jardins fruitiers et potagers de Jean-Baptiste de La Quintinie (1) (Les)

Mémoire du Master 2 Cultures de l\u27écrit et de l\u27image portant sur les éditions françaises et allochtones de l\u27Instruction pour les jardins fruitiers et potagers de Jean-Baptiste de La Quintinie

On least favorable configurations for step-up-down tests

This paper investigates an open issue related to false discovery rate (FDR) control of step-up-down (SUD) multiple testing procedures. It has been established in earlier literature that for this type of procedure, under some broad conditions, and in an asymptotical sense, the FDR is maximum when the signal strength under the alternative is maximum. In other words, so-called "Dirac uniform configurations" are asymptotically {\em least favorable} in this setting. It is known that this property also holds in a non-asymptotical sense (for any finite number of hypotheses), for the two extreme versions of SUD procedures, namely step-up and step-down (with extra conditions for the step-down case). It is therefore very natural to conjecture that this non-asymptotical {\em least favorable configuration} property could more generally be true for all "intermediate" forms of SUD procedures. We prove that this is, somewhat surprisingly, not the case. The argument is based on the exact calculations proposed earlier by Roquain and Villers (2011), that we extend here by generalizing Steck's recursion to the case of two populations. Secondly, we quantify the magnitude of this phenomenon by providing a nonasymptotic upper-bound and explicit vanishing rates as a function of the total number of hypotheses

Honey bee survival mechanisms against the parasite Varroa destructor: a systematic review of phenotypic and genomic research efforts

The ectoparasitic mite Varroa destructor is the most significant pathological threat to the western honey bee, Apis mellifera, leading to the death of most colonies if left untreated. An alternative approach to chemical treatments is to selectively enhance heritable honey bee traits of resistance or tolerance to the mite through breeding programs, or select for naturally surviving untreated colonies. We conducted a literature review of all studies documenting traits of A. mellifera populations either selectively bred or naturally selected for resistance and tolerance to mite parasitism. This allowed us to conduct an analysis of the diversity, distribution and importance of the traits in different honey bee populations that can survive V. destructor globally. In a second analysis, we investigated the genetic bases of these different phenotypes by comparing 'omics studies (genomics, transcriptomics, and proteomics) of A. mellifera resistance and tolerance to the parasite. Altogether, this review provides a detailed overview of the current state of the research projects and breeding efforts against the most devastating parasite of A. mellifera. By highlighting the most promising traits of Varroa-surviving bees and our current knowledge on their genetic bases, this work will help direct future research efforts and selection programs to control this pest. Additionally, by comparing the diverse populations of honey bees that exhibit those traits, this review highlights the consequences of anthropogenic and natural selection in the interactions between hosts and parasites. (C) 2020 The Authors. Published by Elsevier Ltd on behalf of Australian Society for Parasitology

Progressive Structural Defects in Canine Centronuclear Myopathy Indicate a Role for HACD1 in Maintaining Skeletal Muscle Membrane Systems

Mutations in HACD1/PTPLA cause recessive congenital myopathies in humans and dogs. Hydroxyacyl-coA dehydratases are required for elongation of very long chain fatty acids, and HACD1 has a role in early myogenesis, but the functions of this striated muscle-specific enzyme in more differentiated skeletal muscle remain unknown. Canine HACD1 deficiency is histopathologically classified as a centronuclear myopathy (CNM). We investigated the hypothesis that muscle from HACD1-deficient dogs has membrane abnormalities in common with CNMs with different genetic causes. We found progressive changes in tubuloreticular and sarcolemmal membranes and mislocalized triads and mitochondria in skeletal muscle from animals deficient in HACD1. Furthermore, comparable membranous abnormalities in cultured HACD1-deficient myotubes provide additional evidence that these defects are a primary consequence of altered HACD1 expression. Our novel findings, including T-tubule dilatation and disorganization, associated with defects in this additional CNM-associated gene provide a definitive pathophysiologic link with these disorders, confirm that dogs deficient in HACD1 are relevant models, and strengthen the evidence for a unifying pathogenesis in CNMs via defective membrane trafficking and excitation-contraction coupling in muscle. These results build on previous work by determining further functional roles of HACD1 in muscle and provide new insight into the pathology and pathogenetic mechanisms of HACD1 CNM. Consequently, alterations in membrane properties associated with HACD1 mutations should be investigated in humans with related phenotypes

Archeohandi: protocol for a national disabilities database in archaeology in France

The archaeology of disability is a relatively recent and little-known approach in France. While the study of palaeopathology now goes hand in hand with funerary archaeology and osteoarchaeology, the French study of disabilities and disabling pathologies remains marginal and unevenly treated, depending on location, chronology and researcher’s interest. This paper focuses on highlighting the compatibility between this new research area, the obligations of osteoarchaeology, and the benefits of developing a national, diachronic, and interdisciplinary study. A database is designed within an interpretive, consensual framework, that can be adapted to overcome limitations and promote open-minded research on the care of the disabled in their own communities. A preliminary category selection of disabling pathologies has been made. These are trepanation, completely edentulous and/or compensating denture, neuronal impairment, severe scoliosis, Paget's disease, Diffuse Idiopathic Skeletal Hyperostosis (DISH), rickets, dwarfism, infectious diseases, unreduced fracture, amputation, severe degenerative disease and others. This list has been critically reviewed by experts in the field; it will evolve in a somewhat Darwinian fashion. Our database is hosted on the Huma-Num platform, with a management interface and quick access based on multiple tabs. The data includes information about archaeological operations, subjects, and pathologies; it is complemented by pictorial data stored on the Nakala platform. The development involved creating a prototype using HTML, CSS, JavaScript, SQL, and PHP, with features to display, add, modify, and delete operations and subjects. Enhancements have been made, including search optimization, charts, and the ability to export data in CSV format. The database, whose administrative interface can be accessed at archeohandi.huma-num.fr, contains so far 211 existing operations with a total of 1232 registered subjects spread throughout metropolitan France. These initial data reveal numerous research perspectives in osteoarchaeology that can be combined with other research topics, such as virtual reality

Functioning of the dimeric GABA(B) receptor extracellular domain revealed by glycan wedge scanning

The G-protein-coupled receptor (GPCR) activated by the neurotransmitter GABA is made up of two subunits, GABA(B1) and GABA(B2). GABA(B1) binds agonists, whereas GABA(B2) is required for trafficking GABA(B1) to the cell surface, increasing agonist affinity to GABA(B1), and activating associated G proteins. These subunits each comprise two domains, a Venus flytrap domain (VFT) and a heptahelical transmembrane domain (7TM). How agonist binding to the GABA(B1) VFT leads to GABA(B2) 7TM activation remains unknown. Here, we used a glycan wedge scanning approach to investigate how the GABA(B) VFT dimer controls receptor activity. We first identified the dimerization interface using a bioinformatics approach and then showed that introducing an N-glycan at this interface prevents the association of the two subunits and abolishes all activities of GABA(B2), including agonist activation of the G protein. We also identified a second region in the VFT where insertion of an N-glycan does not prevent dimerization, but blocks agonist activation of the receptor. These data provide new insight into the function of this prototypical GPCR and demonstrate that a change in the dimerization interface is required for receptor activation

Rétif de la Bretonne imprimeur

Intervention de Fanny Blanchard (Enssib) dans le cadre de la journée d\u27étude "Rétif de la Bretonne et le monde du livre"