632 research outputs found
Constructing legitimacy: an ethnography of the struggle for financial capital in two Paris-based private equity funds
No full textThis dissertation uses an original qualitative empirical material (two ethnographic
observations of private equity funds and 44 interviews with managers of these funds) to
investigate how fund managers construct their legitimacy to manage capital. Focusing on the
struggle for capital in the private equity sector, it shows how fund managers use symbols to
assert their legitimacy on different stages and details the symbolic hierarchies of the private
equity sector: it emphasises how this legitimacy struggle is embodied in the body of fund
managers and the geographical organisation of their funds (1); it looks at how fund managers
accumulate local symbols, such as diplomas, experiences in prestigious institutions or ‘track-record’
of past operations (2); it underlines how fund managers turn potential investment
operations into ‘good investment opportunities’ by accumulating symbols of legitimacy
coming from bureaucratic internal and external procedures (such as formal decisions by
internal committees or reports by auditors and consultants) (3). In doing so, this dissertation
shows the cultural dimension of the channels through which capital circulates in the private
equity sector
Exploring accumulation in the New Green Revolution for Africa. Ecological crisis, agrarian development and bio-capitalism
No full textThis chapter interrogates the evolving relations between capital and nature to grasp the transformations of capitalist accumulation in the context of global climate crisis. It addresses these issues by examining the political ecology and labour implications of agrarian development trajectories in the context of the New Green Revolution for Africa understood as a particular field of experimentation for new production paradigms, such as climate-smart agriculture, green economy and bio-economy. The aforementioned paradigms reflect the furthering of nature industrialisation, where new processes of commodification, exploitation and appropriation are at stake, marked by the establishment of a bio-capitalistic mode of production. The chapter argues that these processes bear witness to a broader transformation of global capitalism marked by the reorganisation of the boundaries between productive and reproductive value, the strengthening of the colonial extractivist model and a further casualisation of rural labour driven by financialisation, indebtedness and bio-labour. Following this, in the conclusions, the chapter also proposes some insights for a re-actualisation of Marx’s labour theory of value in the context of the current nature accumulation
Grey-white matter contrast surface files in ABIDE 1&2 datasets
No full textComputed with FreeSurfer.
https://surfer.nmr.mgh.harvard.edu/
ABIDE dataset:
http://fcon_1000.projects.nitrc.org/indi/abide/
Used in:
Fouquet, M., Traut, N., Beggiato, A., Delorme, R., Bourgeron, T., & Toro, R. (2019). Increased contrast of the grey-white matter boundary in the motor, visual and auditory areas in Autism Spectrum Disorders. BioRxiv, 750117. https://doi.org/10.1101/750117
https://github.com/neuroanatomy/GWPC</p
Grey-white matter contrast surface files in ABIDE 1&2 datasets
No full textComputed with FreeSurfer.
https://surfer.nmr.mgh.harvard.edu/
ABIDE dataset:
http://fcon_1000.projects.nitrc.org/indi/abide/
Used in:
Fouquet, M., Traut, N., Beggiato, A., Delorme, R., Bourgeron, T., & Toro, R. (2019). Increased contrast of the grey-white matter boundary in the motor, visual and auditory areas in Autism Spectrum Disorders. BioRxiv, 750117. https://doi.org/10.1101/750117
https://github.com/neuroanatomy/GWP
Publication - La Finance autoritaire, de M. Benquet et T. Bourgeron
No full textLa Finance autoritaire. Vers la fin du néolibéralisme, aux éditions Raisons d'agir. Cet ouvrage étudie les conséquences institutionnelles de la financiarisation à partir du cas britannique. Résumé (4e de couverture) : Donald Trump part mais ses soutiens demeurent et l’on ne peut que s’interroger face à la montée de régimes autoritaires aux États-Unis, au Royaume-Uni de Boris Johnson ou au Brésil de Jair Bolsonaro. À travers le cas du Royaume-Uni, ce livre montre que, loin d’être une insur..
From the genetic architecture to synaptic plasticity in autism spectrum disorder.
No full textInternational audienceGenetics studies of autism spectrum disorder (ASD) have identified several risk genes that are key regulators of synaptic plasticity. Indeed, many of the risk genes that have been linked to these disorders encode synaptic scaffolding proteins, receptors, cell adhesion molecules or proteins that are involved in chromatin remodelling, transcription, protein synthesis or degradation, or actin cytoskeleton dynamics. Changes in any of these proteins can increase or decrease synaptic strength or number and, ultimately, neuronal connectivity in the brain. In addition, when deleterious mutations occur, inefficient genetic buffering and impaired synaptic homeostasis may increase an individual's risk for ASD
Identification de facteurs génétiques impliqués dans les troubles du spectre autistique et de la dyslexie
No full textLes troubles du spectre autistique (TSA) touchent approximativement 1% de la population générale. Ces troubles se caractérisent par un déficit de la communication sociale, ainsi que des comportements stéréotypés et des intérêts restreints. Plusieurs gènes impliqués dans le déterminisme des TSA ont été identifiés, comme par exemple les gènes NLGN3-4X, NRXN1-3 et SHANK1-3. Au cours des années précédentes, les TSA ont été considérés comme un ensemble complexe de troubles monogéniques. Cependant, les études récentes du génome complet suggèrent la présence de gènes modificateurs ( multiple hits model ). La dyslexie est caractérisée par un trouble dans l apprentissage de la lecture et de l écriture qui touche 5- 15% de la population générale. Les facteurs génétiques impliqués restent pour l instant inconnus car seuls des gènes ou loci candidats ont été identifiés. Mon projet de thèse avait pour objectif de poursuivre l identification des facteurs génétiques impliqués dans les TSA et de découvrir un premier facteur génétique pour la dyslexie. Pour cela, deux types de populations ont été étudiés : d une part des patients atteints de TSA (N>600) provenant de France, de Suède et des Iles Faroe, d autre part des patients atteints de dyslexie (N>200) provenant de France, en particulier une famille de 11 personnes atteintes sur 3 générations. J ai utilisé à la fois la technologie des puces à ADN Illumina (600 K et 5M) et le séquençage complet du génome humain pour effectuer des analyses de liaison et d association. Pour les TSA, grâce aux analyses de CNVs, j ai pu identifier des gènes candidats pour l autisme et confirmer l association de plusieurs gènes synaptiques avec l autisme. En particulier, l étude d une population de 30 patients des îles Faroe a pu confirmer l implication des gènes NLGN1 et NRXN1 dans l autisme et identifier un nouveau gène candidat IQSEC3. En parallèle, j ai exploréPRRT2 localisé en 16p11.2. PRRT2 code pour un membre du complexe SNARE synaptique qui permet la libération des vésicules synaptiques. Je n ai pas pu mettre en évidence d association avec les TSA, mais j ai montré que ce gène important pour certaines maladies neurologiques était sous pression de sélection différente selon les populations. Pour la dyslexie, j ai effectué une analyse de liaison (méthode des lod-scores) pour une grande famille de 11 individus atteints sur trois générations. Cette étude a permis d identifier CNTNAP2 comme un gène de vulnérabilité à la dyslexie. Cette découverte est importante car ce même gène est aussi associé aux TSA. Par contre, aucune des 20 variations rares découvertes par le séquençage complet du génome n est localisée dans les parties codantes du gène. Plusieurs variations localisées dans des régions régulatrices sont candidates. En conclusion, les résultats de ma thèse ont permis d identifier des gènes candidats pour les TSA, de confirmer le rôle des gènes synaptiques dans ce trouble, de montrer pour la première fois grâce à une analyse de liaison le rôle de CNTNAP2 dans la dyslexie.Autism spectrum disorders (ASD) affect 1% of the general population. These disorders are characterized by deficits in social communication as well as stereotyped behaviors and restricted interests. Several genes involved in the determination of ASD have been identified, such as NLGN3-4, NRXN1-3 and SHANK1-3. In the previous years, ASD have been considered as a complex set of monogenic disorders. Recent studies on the complete genome nevertheless suggest the presence of modifier genes ("multiple hits model"). Dyslexia is characterized by difficulties in learning to read and write. It affects 5-15 % of the general population. Genetic factors involved remain unknown. Only candidate genes or loci have been identified. My thesis had two main objectives: pursuing the identification of genetic factors involved in ASD, and discovering a first genetic factor for dyslexia. I therefore studied two types of populations: on the one hand a group of patients with ASD (N > 600) from France, Sweden and the Faroe Islands, and on the other hand another group of patients with dyslexia (N > 200) from France, and more specifically a family of 11 people followed over 3 generations. I used both Illumina microarrays technology (600K and 5M) and the complete human genome sequencing to conduct linkage and association analyses. Regarding ASD, CNVs (copy number variants) analyses allowed me to confirm the association of several synaptic genes with autism and to identify new candidate genes. In particular, the study of a population of 30 patients from the Faroe Islands confirmed the involvement of NLGN1 and NRXN1 genes in autism and identified a new candidate gene, IQSEC3. At the same time, I explored PRRT2 located in 16p11.2. PRRT2 encodes a member of the synaptic SNARE complex that allows the release of synaptic vesicles. I have not been able to demonstrate any association with ASD, but I showed that this gene, which is important for some neurological diseases, was under different selection pressures according to the population considered. Regarding dyslexia, I realized a linkage analysis (lod-score method) for a large family of 11 individuals, with three generations affected. This study identified the CNTNAP2 gene as a vulnerability factor for dyslexia. This finding is important because this gene is also associated with ASD. Nevertheless, none of the 20 rare variations discovered by whole genome sequencing is localized in the coding parts of the gene. Only several variations localized in regulatory regions are robust candidates. To conclude, my findings enabled the identification of new candidate genes for ASD, the confirmation of the role of synaptic genes in this disorder, and the highlight for the first time of the role of CNTNAP2 in dyslexia through linkage analysis.PARIS5-Bibliotheque electronique (751069902) / SudocSudocFranceF
Bibliography of Montana vegetation description
No full textListed in alphabetical order by author are 549 references to literature that describes the native vegetation of Montana. This updates the 1965 list of Habeck and Hartley. A keyword subject index is included
- …
