La restauration au Louvre du retable du Jugement dernier de Roger van der Weyden (1876-1878) : un rare cas de documentation photographique

En France, les restaurations des tableaux des collections publiques ont donné lieu à la production d’un certain nombre de documents écrits dès le xviiie siècle. Ces documents, essentiellement comptables, sont encore nos principales sources pour reconstituer l’histoire matérielle des œuvres tout au long du xixe siècle. Les rapports de restauration n’existent pas encore véritablement, et les témoignages visuels manquent la plupart du temps. Il faudra attendre la fin de la Première Guerre mondiale pour voir se dessiner une véritable évolution vers une documentation visuelle plus systématique des restaurations, avec le recours aux techniques nouvelles d’imagerie, puis les années 1950 pour voir la mise en place progressive de dossiers de restauration et d’une couverture photographique systématique. C’est pourquoi la restauration du retable de Roger van der Weyden, au Louvre à la fin du xixe siècle, qui a donné lieu à une importante documentation écrite et visuelle, représente un cas rare et novateur.In France, since the 18th century, the restoration of paintings belonging to national collections has given rise to the production of a certain number of written documents. Mostly financial in nature, these documents remain our main source of information for piecing together the material history of works throughout the 19th century. Restoration reports did not really exist at this point, and visual records were lacking most of the time. Not until the end of World War I did systematic visual documentation of restoration campaigns begin to emerge, using new imaging techniques. Files on each restoration programme, including systematic photographic documentation, gradually became standard practice in the 1950s. That is why the restoration at the Louvre, in the late 19th century, of Rogier van der Weyden’s altarpiece, which generated extensive written and photographic documentation, represents a rare and innovative case

Maladie d'Alzheimer et Dépression : Quel impact sur la mémoire sémantique ?

Introduction : Les troubles de la mémoire sémantique (MS) constituent un symptôme fréquent de la maladie d'Alzheimer (MA). Par ailleurs, la MA peut également s'accompager de troubles de l'humeur. Il est par ailleurs bien connu que l'état thymique peut impacter la cognition. Cependant, peu d'études se sont intéressées aux liens spécifiques entre MS et dépression dans la MA. L'objectif de cette étude consiste à investiguer l'impact de la dépression des sujets atteints de MA sur leur MS. Méthodologie : Une tâche d'amorçage sémantique et affective a été administrée à 36 participants âgés (un groupe contrôle de personnes âgées sans trouble cognitif (N=20) et un groupe expérimental de patients MA à un stade léger (MMSE>27) (N=16) dont la moitié présente une symptomatologie dépressive (MA-D) et l'autre moitié n'en présentant pas (MA-ND)). Dans ce protocole, un « stimuli amorce » est présenté juste avant un « stimuli cible », sur lequel le sujet doit réaliser un traitement. Les stimuli sont en modalité écrite. La tâche du sujet est de décider si le mot est un mot de la langue française (e.g. «amour») ou non (e.g. «tremon»). Le protocole d'amorçage contient trois conditions sémantiques : 1) Valence Affective (VA) positive (VP+); 2) VA négative (VN-) et 3) VA neutre (Vn). Résultats : Une ANOVA à mesures répétées indique un effet de groupe (F=41.526 ; p=.001) et de condition (F=5.453, p=.008). Un effet d'interaction groupe*condition est également observé (F=3.082 ; p=.025) indiquant un hyperamorçage pour la condition VN- uniquement chez les patients MA-D, tandis que les patients MA-ND et contrôles présentent au contraire des effets d'amorçage plus importants pour la condition VP+. Discussion : Nos résultats montrent un effet d'hyperamorçage spécifique observé pour la condition négative dans le groupe MA-D nous amenant à proposer que l'humeur négative dans la MA entraînerait une modification du traitement sémantique des concepts à valence négative

Impact of depression on semantic processing in alzheimer's disease : results from an affective priming paradigm.

IMPACT OF DEPRESSION ON SEMANTIC PROCESSING IN ALZHEIMER’S DISEASE : RESULTS FROM AN AFFECTIVE PRIMING PARADIGM Isabelle Simoes Loureiro, K. Gerin, A. Rendon de la Cruz, K. Kandana Arachchige, M. Rossignol, L. Lefebvre UMONS - UMONS - MONS PCN - UMONS - Belgium PCN - UMONS - Belgium PCN - UMONS - Belgium PCN - UMONS - Belgium PCN - UMONS - Belgium Target. Alzheimer’s disease (AD) is a neurodegenerative disease characterized by an early breakdown of memory including a semantic memory (SM) impairment. Moreover, AD may be associated to mood disorders that are known to impact memory, such as depression. However, few studies have been conducted to clarify the links between SM and depression in AD. Accordingly, this study aimed to clarify the effect of depression in SM in AD. Material and method. An affective priming paradigm was administered to 36 participants (mean age = 83.4 SD = 6.2): a control group of 20 healthy elderly and an experimental group of 16 mild AD. In the experimental AD group, half of the subjects presented symptoms of depression (D-AD) and half did not (ND-AD). The priming protocol contained 3 different conditions which manipulated the relation between the prime and the target: positive affective valence (V+) (e.g. joke- laugh), negative affective valence (V-) (e.g. army- soldier) and neutral (semantic but not affective relations) (Vn) (e.g. school-student). Results. A repeated-measures ANOVA showed two main effects, of group (F=41.526 ; p=.001) and condition (F=5.453, p=.008). Moreover, a significant group*condition interaction effect (F=3.082 ; p=.025) revealed an hyperpriming effect in the V- condition in D-AD whereas control subjects and ND-AD presented on the contrary a more important priming effect for V+. To sum up, a specific hyperpriming effect was observable for the negative affective valence in AD patients with depression. Discussion and conclusions. These results suggest that mood disorders in AD can negatively impact the processing of semantic knowledge. This highlights the importance of assessing mood disorders in AD as well as to manage these symptoms Topic: Neuropsychology References: Tipo presentazione: POSTE

Multiple Roles for the Non-Coding RNA SRA in Regulation of Adipogenesis and Insulin Sensitivity

Peroxisome proliferator-activated receptor-γ (PPARγ) is a master transcriptional regulator of adipogenesis. Hence, the identification of PPARγ coactivators should help reveal mechanisms controlling gene expression in adipose tissue development and physiology. We show that the non-coding RNA, Steroid receptor RNA Activator (SRA), associates with PPARγ and coactivates PPARγ-dependent reporter gene expression. Overexpression of SRA in ST2 mesenchymal precursor cells promotes their differentiation into adipocytes. Conversely, knockdown of endogenous SRA inhibits 3T3-L1 preadipocyte differentiation. Microarray analysis reveals hundreds of SRA-responsive genes in adipocytes, including genes involved in the cell cycle, and insulin and TNFα signaling pathways. Some functions of SRA may involve mechanisms other than coactivation of PPARγ. SRA in adipocytes increases both glucose uptake and phosphorylation of Akt and FOXO1 in response to insulin. SRA promotes S-phase entry during mitotic clonal expansion, decreases expression of the cyclin-dependent kinase inhibitors p21Cip1 and p27Kip1, and increases phosphorylation of Cdk1/Cdc2. SRA also inhibits the expression of adipocyte-related inflammatory genes and TNFα-induced phosphorylation of c-Jun NH2-terminal kinase. In conclusion, SRA enhances adipogenesis and adipocyte function through multiple pathways

SRA Regulates Adipogenesis by Modulating p38/JNK Phosphorylation and Stimulating Insulin Receptor Gene Expression and Downstream Signaling

The Steroid Receptor RNA Activator (SRA) enhances adipogenesis and increases both glucose uptake and phosphorylation of Akt and FOXO1 in response to insulin. To assess the mechanism, we differentiated ST2 mesenchymal precursor cells that did or did not overexpress SRA into adipocytes using combinations of methylisobutylxanthine, dexamethasone and insulin. These studies showed that SRA overexpression promotes full adipogenesis in part by stimulation of insulin/insulin-like growth factor-1 (IGF-1) signaling. SRA overexpression inhibited phosphorylation of p38 mitogen activated protein kinase (MAPK) and c-Jun NH2-terminal kinase (JNK) in the early differentiation of ST2 cells. Conversely, knockdown of endogenous SRA in 3T3-L1 cells increased phosphorylation of JNK. Knockdown of SRA in mature 3T3-L1 adipocytes reduced insulin receptor (IR) mRNA and protein levels, which led to decreased autophosphorylation of IRβ and decreased phosphorylation of insulin receptor substrate-1 (IRS-1) and Akt. This likely reflects a stimulatory role of SRA on IR transcription, as transfection studies showed that SRA increased expression of an IR promoter-luciferase reporter construct

Clonage de l'ADNc et caractérisation d'un transporteur de glucose-6-phosphate du réticulum endoplasmique

Doctorat en sciences agronomiques et ingénierie biologique (AGRO 3)--UCL, 200

The glucose-6-phosphatase system.

Glucose-6-phosphatase (G6Pase), an enzyme found mainly in the liver and the kidneys, plays the important role of providing glucose during starvation. Unlike most phosphatases acting on water-soluble compounds, it is a membrane-bound enzyme, being associated with the endoplasmic reticulum. In 1975, W. Arion and co-workers proposed a model according to which G6Pase was thought to be a rather unspecific phosphatase, with its catalytic site oriented towards the lumen of the endoplasmic reticulum [Arion, Wallin, Lange and Ballas (1975) Mol. Cell. Biochem. 6, 75--83]. Substrate would be provided to this enzyme by a translocase that is specific for glucose 6-phosphate, thereby accounting for the specificity of the phosphatase for glucose 6-phosphate in intact microsomes. Distinct transporters would allow inorganic phosphate and glucose to leave the vesicles. At variance with this substrate-transport model, other models propose that conformational changes play an important role in the properties of G6Pase. The last 10 years have witnessed important progress in our knowledge of the glucose 6-phosphate hydrolysis system. The genes encoding G6Pase and the glucose 6-phosphate translocase have been cloned and shown to be mutated in glycogen storage disease type Ia and type Ib respectively. The gene encoding a G6Pase-related protein, expressed specifically in pancreatic islets, has also been cloned. Specific potent inhibitors of G6Pase and of the glucose 6-phosphate translocase have been synthesized or isolated from micro-organisms. These as well as other findings support the model initially proposed by Arion. Much progress has also been made with regard to the regulation of the expression of G6Pase by insulin, glucocorticoids, cAMP and glucose

Evidence for glucose-6-phosphate transport in rat liver microsomes

AbstractThe existence of glucose-6-phosphate transport across the liver microsomal membrane is still controversial. In this paper, we show that S3483, a chlorogenic acid derivative known to inhibit glucose-6-phosphatase in intact microsomes, caused the intravesicular accumulation of glucose-6-phosphate when the latter was produced by glucose-6-phosphatase from glucose and carbamoyl-phosphate. S3483 also inhibited the conversion of glucose-6-phosphate to 6-phosphogluconate occurring inside microsomes in the presence of electron acceptors (NADP or metyrapone). These data indicate that liver microsomal membranes contain a reversible glucose-6-phosphate transporter, which furnishes substrate not only to glucose-6-phosphatase, but also to hexose-6-phosphate dehydrogenase