13 research outputs found
Une ethnographie de la relation d'aide : de la ruse Ă la fiction, comment concilier protection et autonomie, rapport de recherche pour la MiRe (DREES):Rapport de recherche pour la MiRe (DREES)
Ce rapport propose une description et une analyse de lâactivitĂ© dâaide Ă domicile. LâenquĂȘte a portĂ© sur le rĂ©seau des proches, aidants et soignants, intervenant auprĂšs de personnes atteintes de troubles psychiques et cognitifs. Les aides visent Ă assurer le bienâĂȘtre des personnes en apportant soins et assistance. Mais ce souci ne suffit pas Ă caractĂ©riser leur activitĂ© : Ă chaque instant, les aides doivent composer entre des aspirations contradictoires, comme la protection et lâautonomie, et assumer des prises de risque. Nous nâopposons pas leur activitĂ© rĂ©elle Ă des principes abstraits, nous faisons au contraire lâhypothĂšse que ce sont les pratiques des aides qui peu Ă peu, Ă partir des situations dâĂ©preuve, donnent un sens concret Ă de telles notions. En trouvant des façons de les composer, elles montrent que leur mise en oeuvre est possible. Selon une mĂ©thode ethnographique, nous avons suivi treize cas, entre six et dix-huit mois, choisis dans trois services dâaide Ă domicile contrastĂ©s, en mettant lâaccent sur les moments dâĂ©preuve, qui montrent en permanence ces compromis obligĂ©s de lâaction en situation : problĂšmes dâhygiĂšne, de mĂ©dicaments, de clĂ©s, risque de chute, dĂ©cision de placement, relation Ă la famille, etc. Le principal rendu de notre recherche est la mise en rĂ©cit de ces treize expĂ©riences collectives. Comment faire faire quelque chose Ă des personnes qui ne lâont pas demandĂ© ou nâen voient pas lâintĂ©rĂȘt ? Ă condition dâen restituer aussi la valeur positive, deux notions ambiguĂ«s, la ruse et la fiction, aident Ă mieux comprendre lâexpĂ©rience du domicile, et les compĂ©tences des personnels et des proches. Lâaide est installation incertaine dâune relation, dâun espace commun. Instaurer cette fiction partagĂ©e fait en partie porter par lâaidant Ă la place de lâaidĂ© son exigence dâautonomie : traiter en ĂȘtre autonome la personne fragilisĂ©e, câest faire persister ce qui nâest plus tout Ă fait lĂ . Curieuse autonomie, par procuration, qui doit ĂȘtre supposĂ©e et supportĂ©e par les autres pour exister. Câest tout lâenjeu Ă©thique, politique et social de la relation dâaide : lâinvention dâune autonomie Ă©largie au collectif
Vivre avec Alzheimer, vivre avec un "Alzheimer". Recueillir l'expérience des aides à domicile
L'article vise à donner une définition en actes de la maladie d'Alzheimer, à partir d'une mise en récit de l'expérience qu'ont les aides à domicile de la vie commune avec une personne atteinte. Travailler dans un espace qui est d'abord celui du soigné leur a appris beaucoup de choses. La méthode consiste, sans pour autant minorer ses contraintes, à traiter de façpn pragmatique la maladie d'Alzheimer non seulement comme un déficit mais , à travers ce qu'elle fait fairen saisi dans la relation d'aide, comme une réalité positive à partir de laquelle se déploie aussi une façon de vivre, provisoire et inédite. Nous cherchons ainsi à ç faire surgir sur la maladie une parole "autre", celle des aides, mais une parole qui a du poids parce qu'elle est durement éprouvée, au deux sens du mot : ressentie et corrigée au quotidien par l'expérienc
Le handicap au quotidien. La personne, les proches, les soignants : sept récits d'expérience à domicile
Rapport dans le cadre d'un contrat de recherche avec la Haute Autorité de la Santé et le CNS
Widespread overexpression from the four DNA hypermethylated HOX clusters in aggressive (IDHwt) glioma is associated with H3K27me3 depletion and alternative promoter usage
International audienc
The Long Non-Coding RNA HOXA-AS2 Promotes Proliferation of Glioma Stem Cells and Modulates Their Inflammation Pathway Mainly through Post-Transcriptional Regulation
International audienceGlioblastomas represent approximatively half of all gliomas and are the most deadly and aggressive form. Their therapeutic resistance and tumor relapse rely on a subpopulation of cells that are called Glioma Stem Cells (GSCs). Here, we investigated the role of the long non-coding RNA HOXA-AS2 in GSC biology using descriptive and functional analyses of glioma samples classified according to their isocitrate dehydrogenase (IDH) gene mutation status, and of GSC lines. We found that HOXA-AS2 is overexpressed only in aggressive (IDHwt) glioma and GSC lines. ShRNA-based depletion of HOXA-AS2 in GSCs decreased cell proliferation and altered the expression of several hundreds of genes. Integrative analysis revealed that these expression changes were not associated with changes in DNA methylation or chromatin signatures at the promoter of the majority of genes deregulated following HOXA-AS2 silencing in GSCs, suggesting a post-transcriptional regulation. In addition, transcription factor binding motif enrichment and correlation analyses indicated that HOXA-AS2 affects, directly or indirectly, the expression of key transcription factors implicated in GCS biology, including E2F8, E2F1, STAT1, and ATF3, thus contributing to GCS aggressiveness by promoting their proliferation and modulating the inflammation pathway
Fontenelle. Digression sur les Anciens et les Modernes : et autres textes philosophiques
International audienc
L1 chimeric transcripts are expressed in healthy brain and their deregulation in glioma follows that of their host locus
International audienceBesides the consequences of retrotransposition, long interspersed element 1 (L1) retrotransposons can affect the host genome through their antisense promoter. In addition to the sense promoter, the evolutionarily recent L1 retrotransposons, which are present in several thousand copies, also possess an anti-sense promoter that can produce L1 chimeric transcripts (LCT) composed of the L1 5âČ UTR followed by the adjacent genomic sequence. The full extent to which LCT expression occurs in a given tissue and whether disruption of the defense mechanisms that normally control L1 retrotransposons affects their expression and function in cancer cells, remain to be established. By using CLIFinder, a dedicated bioinformatics tool, we found that LCT expression was widespread in normal brain and aggressive glioma samples, and that approximately 17% of recent L1 retrotransposons, from the L1PA1 to L1PA7 subfamilies, were involved in their production. Importantly, the transcriptional activities of the L1 antisense promoters and of their host loci were coupled. Accordingly, we detected LCT-producing L1 retrotransposons mainly in transcriptionally active genes and genomic loci. Moreover, changes in the host genomic locus expression level in glioma were associated with a similar change in LCT expression level, regardless of the L1 promoter methylation status. Our findings support a model in which the host genomic locus transcriptional activity is the main driving force of LCT expression. We hypothesize that this model is more applicable when host gene and LCT are transcribed from the same strand
L1 chimeric transcripts are expressed in healthy brain and their deregulation in glioma follows that of their host locus
International audienceBesides the consequences of retrotransposition, long interspersed element 1 (L1) retrotransposons can affect the host genome through their antisense promoter. In addition to the sense promoter, the evolutionarily recent L1 retrotransposons, which are present in several thousand copies, also possess an anti-sense promoter that can produce L1 chimeric transcripts (LCT) composed of the L1 5âČ UTR followed by the adjacent genomic sequence. The full extent to which LCT expression occurs in a given tissue and whether disruption of the defense mechanisms that normally control L1 retrotransposons affects their expression and function in cancer cells, remain to be established. By using CLIFinder, a dedicated bioinformatics tool, we found that LCT expression was widespread in normal brain and aggressive glioma samples, and that approximately 17% of recent L1 retrotransposons, from the L1PA1 to L1PA7 subfamilies, were involved in their production. Importantly, the transcriptional activities of the L1 antisense promoters and of their host loci were coupled. Accordingly, we detected LCT-producing L1 retrotransposons mainly in transcriptionally active genes and genomic loci. Moreover, changes in the host genomic locus expression level in glioma were associated with a similar change in LCT expression level, regardless of the L1 promoter methylation status. Our findings support a model in which the host genomic locus transcriptional activity is the main driving force of LCT expression. We hypothesize that this model is more applicable when host gene and LCT are transcribed from the same strand
GHSI emergency radionuclide bioassay laboratory network: Summary of a recent exercise
The Global Health Security Initiative (GHSI) established a laboratory network within the GHSI community to develop their collective surge capacity for radionuclide bioassay in response to a radiological or nuclear emergency. A recent exercise was conducted to test the participating laboratories for their capabilities in screening and in vitro assay of biological samples, performing internal dose assessment and providing advice on medical intervention, if necessary, using a urine sample spiked with a single radionuclide, 241Am. The laboratories were required to submit their reports according to the exercise schedule and using pre-formatted templates. Generally, the participating laboratories were found to be capable with respect to rapidly screening samples for radionuclide contamination, measuring the radionuclide in the samples, assessing the intake and radiation dose, and providing advice on medical intervention. However, gaps in bioassay measurement and dose assessment have been identified. The network may take steps to ensure that procedures and practices within this network be harmonised and a follow-up exercise be organised on a larger scale, with potential participation of laboratories from the networks coordinated by the International Atomic Energy Agency and theWorld Health Organization. © The Author 2015. Published by Oxford University Press