23 research outputs found

    Supporting stimulation needs in dementia care through wall-sized displays

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    Beside reminiscing, the increasing cognitive decline in dementia can also be addressed through sensory stimulation allowing the immediate, nonverbal engagement with the world through one’s senses. Much HCI work has prioritized cognitive stimulation for reminiscing or personhood often on small screens, while less research has explored sensory stimulation like the one enabled by large displays. We describe a year-long deployment in a residential care home of a wall-sized display, and explored its domestication through 24 contextual interviews. Findings indicate strong engagement and attachment to the display which has inspired four psychosocial interventions using online generic content. We discuss the value of these findings for personhood through residents’ exercise of choices, the tension between generic/personal content and its public/private use, the importance of participatory research approach to domestication, and the infrastructure-based prototype, illustrated by the DementiaWall and its generative quality

    Evaluation du statut oxydatif et inflammatoire (développement analytique et application en biologie clinique)

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    Les lipoprotĂ©ines de haute densitĂ© (HDL) ont des effets bĂ©nĂ©fiques sur le systĂšme cardiovasculaire. Un des mĂ©canismes implique l inhibition de l expression des molĂ©cules d adhĂ©sion cellulaires vasculaires-1 (VCAM-1) par les cellules endothĂ©liales. Nous avons examinĂ© les effets de l apolipoprotĂ©ine A-I, du facteur peptidique anionique (APF) avec ou sans phosphatidylcholines (PCs) et des PCs sur l expression de VCAM-1 par les cellules endothĂ©liales de veines ombilicales humaines (HUVEC). Les HUVEC Ă©taient stimulĂ©es par le tumor necrosis factor-a ou le calcium liĂ© Ă  l hĂ©parine. Les rĂ©sultats indiquent que l APF administrĂ© Ă  dose physiologique seul ou associĂ© aux complexes apolipoprotĂ©ine/PCs apparaĂźt ĂȘtre un facteur pertinent impliquĂ© dans l inhibition de l expression de VCAM-1. Notre Ă©tude apporte la perspective d une stratĂ©gie antiathĂ©rogĂšne Ă  travers l enrichissement des HDL par l APF afin de diminuer le processus inflammatoire. Afin d Ă©valuer le statut oxydatif de patients, nous avons dĂ©veloppĂ© un test ELISA de type sandwich afin de mesurer l albumine modifiĂ©e par HNE, MDA et hexanal et tester diffĂ©rents kits commercialisĂ©s. Des courbes standard reproductibles ont Ă©tĂ© obtenues mais les essais avec les sĂ©rums n ont pas Ă©tĂ© concluants Ă  cause d un effet inhibiteur de la rĂ©action. Nous avons montrĂ© que les dosages sĂ©riques des anticorps anti-LDL oxydĂ©es (oxLDL) et de la matrix Gla protein montrent des rĂ©sultats divergents. Une Ă©tude comparative des kits de dosage des oxLDL est nĂ©cessaire pour dĂ©terminer l Ă©pitope oxydĂ© le plus prĂ©dictif de maladies cardiovasculaires. Les peroxydes, l activitĂ© de la paraoxonase 1 (PON1) et la composition en acide gras des membranes Ă©rythrocytaires apparaissent comme un biomarqueur pertinent du stress oxydant chez les patients. Ce travail aidera Ă  dĂ©terminer le stress oxydatif chez les patients, et les biomarqueurs comme la PON1 et les peroxydes pourraient ĂȘtre intĂ©grĂ©s en routine dans un laboratoire d analyses de biologie mĂ©dicale.High-density lipoproteins (HDLs) have cardiovascular benefits. One of the mechanisms involves the inhibition by HDLs of the vascular cell adhesion molecule-1 (VCAM-1) expression in endothelial cells. We examined the effects of either the apolipoprotein A-I and the anionic peptide factor (APF) in the presence or absence of phosphatidylcholines (PCs), or the free PCs, on the expression of VCAM-1 in human umbilical vein endothelial cells (HUVEC). The HUVEC were stimulated with tumor necrosis factor-a or the calcium bound to heparin. The main result indicates that APF administrated at physiological concentration in the lipid-free form or into apolipoprotein/PCs complexes appears as a relevant factor involved in the inhibition of VCAM-1 expression. Our study provides a perspective of an antiatherogenic strategy, through the expansion of the APF-enriched HDL in order to alleviate the inflammatory process. To evaluate the status of oxidative stress in patients, we aimed to developp a sandwich enzyme-linked immunosorbent assay to measure serum HNE, MDA and Hexanal-modified albumin, and to test different commercial kits. Reproducible standard curves were obtained but assays with serum of patients have not been completed due to an inhibitory effect on the reaction by serum. We show that oxidized low-density lipoproteins (oxLDL) antibodies and matrix Gla protein in clinical cardiovascular disease give diverging results. Comparative studies of the different kit assays of oxLDL are needed to assess which oxidation-specific epitopes are most predictive of cardiovascular disease. Peroxides, paraoxonase 1 activity (PON1) and the fatty acid composition of the erythrocyte plasmic membrane phospholipids appear as a relevant biological markers to evaluate oxidative stress. We believe that this work will be helpful for the assessment of oxidative stress in patients, and that biomarkers like PON1 and peroxides could be integrated into routine clinical laboratory analyses.AIX-MARSEILLE2-BU MĂ©d/Odontol. (130552103) / SudocPARIS-BIUP (751062107) / SudocSudocFranceF

    APPORT DU PARASIGHT*-F DANS LE DIAGNOSTIC DU PALUDISME A PLASMODIUM FALCIPARUM

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    AIX-MARSEILLE2-BU Pharmacie (130552105) / SudocSudocFranceF

    H3K27me3 expression and methylation status in histological variants of malignant peripheral nerve sheath tumours

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    Diagnosing MPNST can be challenging, but genetic alterations recently identified in polycomb repressive complex 2 (PRC2) core component genes, EED and SUZ12, resulting in global loss of the histone 3 lysine 27 trimethylation (H3K27me3) epigenetic mark, represent drivers of malignancy and a valuable diagnostic tool. However, the reported loss of H3K27me3 expression ranges from 35–84%. We show that advances in molecular pathology now allows many MPNST mimics to be classified confidently. We confirm that MPNSTs harbouring mutations in PRC2 core components are associated with loss of H3K27me3 expression; whole genome doubling was detected in 68%, and SSTR2 was amplified in 32% of MPNSTs. We demonstrate that loss of H3K27me3 expression occurs overall in 38% of MPNSTs, but is lost in 76% of histologically classical cases, whereas loss was detected in only 23% cases with heterologous elements and 14% where the diagnosis could not be provided on morphology alone. H3K27me3 loss is rarely seen in other high‐grade sarcomas and was not found to be associated with an inferior outcome in MPNST. We show that DNA methylation profiling distinguish MPNST from its histological mimics, was unrelated to anatomical site and formed two main clusters, MeGroup 4 and 5. MeGroup 4 represents classical MPNSTs lacking H3K27me3 expression in the majority of cases, whereas MeGroup 5 comprise MPNSTs exhibiting non‐classical histology and expressing H3K27me3 and cluster with undifferentiated sarcomas. The two MeGroups are distinguished by differentially methylated PRC2‐associated genes, the majority of which are hypermethylated in the promoter regions in MeGroup 4, indicating that the PRC2 target genes are not expressed in these tumours. The methylation profiles of MPNSTs with retention of H3K27me3 in MeGroup 4 and 5 are independent of mutations in PRC2 core components and the driver(s) in these groups remain to be identified. Our results open new avenues of investigation
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