4. Le si@de, un label pour un réseau de coopération entre services de questions-réponses

• Le Si@de http://www.bnf.fr/fr/collections_et_services/poser_une_question_a_bibliothecaire/s.charte_siade.html Le Si@de s’est mis en place au 2e trimestre 2009. Il compte 15 adhérents : le réseau Bibliosésame et 14 établissements dont les services fonctionnent de manière autonome : les bibliothèques nationales suisse et du Québec, des bibliothèques universitaires, municipales, ou spécialisées. On peut citer parmi elles la Bibliothèque municipale de Lyon, l’Enssib, la Cité de la santé. Parm..

Mettre en œuvre un service de questions-réponses en ligne

En quelques années, les bibliothèques françaises ont développé des services de questions-réponses en ligne. Beaucoup d'établissements en sont encore à la phase de réflexion, d'autres démarrent, des réseaux s'élaborent. Dans le contexte actuel du repérage, de la sélection et de la validation de l'information pléthorique disponible sur Internet, les services de questions-réponses en ligne ont un rôle primordial à jouer. En effet, ils valorisent l'offre des bibliothèques dans le contexte du développement des services aux publics et des services à distance. Leur mise en place interroge le professionnel sous de multiples facettes : organisation du travail, politique de services, choix des outils… Ces différents aspects sont abordés, s'appuyant sur des expériences françaises et étrangères, qu'elles soient locales, coopératives et/ou collaboratives. Un éventail d'offres existe aujourd'hui, selon les objectifs, les besoins, les publics, les moyens mis à disposition et les technologies choisies. Le plan s'articule autour de quatre parties pragmatiques et opératoires : construire le projet, développer un savoir-répondre, organiser et travailler au sein d'une équipe et, enfin, adapter le service à l'environnement et à la nature de ses publics. Cet ouvrage collectif, coordonné par Claire Nguyen, se veut un guide utile à tous les professionnels qui veulent créer, maintenir ou faire évoluer un service de questions-réponses à distance

X-linked primary ciliary dyskinesia due to mutations in the cytoplasmic axonemal dynein assembly factor PIH1D3

By moving essential body fluids and molecules, motile cilia and flagella govern respiratory mucociliary clearance, laterality determination and the transport of gametes and cerebrospinal fluid. Primary ciliary dyskinesia (PCD) is an autosomal recessive disorder frequently caused by non-assembly of dynein arm motors into cilia and flagella axonemes. Before their import into cilia and flagella, multi-subunit axonemal dynein arms are thought to be stabilized and pre-assembled in the cytoplasm through a DNAAF2–DNAAF4–HSP90 complex akin to the HSP90 co-chaperone R2TP complex. Here, we demonstrate that large genomic deletions as well as point mutations involving PIH1D3 are responsible for an X-linked form of PCD causing disruption of early axonemal dynein assembly. We propose that PIH1D3, a protein that emerges as a new player of the cytoplasmic pre-assembly pathway, is part of a complementary conserved R2TP-like HSP90 co-chaperone complex, the loss of which affects assembly of a subset of inner arm dyneins

3. Sindbad, les publics et les collections de la bibliothèque nationale de France

• SINDBAD http://www.bnf.fr/fr/collections_et_services/aides_recherche_documentaire.html LA BNF : BIBLIOTHÈQUE DE RECHERCHE ET TOUS PUBLICS Les salles de lecture de la Bibliothèque nationale de France sont fréquentées par des publics différents : tous publics à partir de 16 ans en bibliothèque du Haut-de-jardin, chercheurs en bibliothèque de Recherche. Lors de la mis en place de son service de questions-réponses, la BnF a choisi de refléter cette double vocation : SINDBAD s’adresse au grand..

The mouse Muc5b mucin gene is transcriptionally regulated by thyroid transcription factor-1 (TTF-1) and GATA-6 transcription factors.: Regulation of Muc5b mucin gene by TTF-1 and GATA factors

International audienceMUC5B is one of the major mucin genes expressed in the respiratory tract. Previous studies in our laboratory have demonstrated that MUC5B is expressed in human lung adenocarcinomas and during lung morphogenesis. Moreover, in human lung adenocarcinoma tissues, a converse correlation between MUC5B and thyroid transcription factor-1 (TTF-1) expression, a lung-specific transcription factor, has been established. However, the molecular mechanisms that govern the regulation of MUC5B expression in the lung are largely unknown. In order to better understand the biological role of MUC5B in lung pathophysiology, we report the characterization of the promoter region of the mouse Muc5b mucin gene. The promoter is flanked by a TATA box (TACATAA) identical to that in the human gene. Human and murine promoters share 67.5% similarity over the first 170 nucleotides. By RT-PCR, co-transfection studies and gel-shift assays, we show that Muc5b promoter activity is completely inhibited by TTF-1, whereas factors of the GATA family (GATA-4/GATA-5/GATA-6) are activators. Together, these results demonstrate, for the first time, that Muc5b is a target gene of transcription factors (TTF-1, GATA-6) involved in lung differentiation programs during development and carcinogenesis, and identify TTF-1 as a strong repressor of Muc5b. The characterization of the structural and functional features of the Muc5b mucin gene will provide us with a strong base to develop studies in murine models aimed at the identification of its biological role in lung pathophysiology

Regulation of the human mucin MUC4 by taurodeoxycholic and taurochenodeoxycholic bile acids in oesophageal cancer cells is mediated by hepatocyte nuclear factor 1α

International audienceMUC4 (mucin 4) is a membrane-bound mucin overexpressed in the early steps of oesophageal carcinogenesis and implicated in tumour progression. We previously showed that bile acids, main components of gastro-oesophageal reflux and tumour promoters, up-regulate MUC4 expression [Mariette, Perrais, Leteurtre, Jonckheere, Hemon, Pigny, Batra, Aubert, Triboulet and Van Seuningen (2004) Biochem. J. 377, 701-708]. HNF (hepato-cyte nuclear factor) 1α and HNF4α transcription factors are known to mediate bile acid effects, and we previously identified cis-elements for these factors in MUC4 distal promoter. Our aim was to demonstrate that these two transcription factors were directly involved in MUC4 activation by bile acids. MUC4, HNF1α and HNF4α expressions were evaluated by immunohistochem-istry in human oesophageal tissues. Our results indicate that MUC4, HNF1α and HNF4α were co-expressed in oesophageal metaplastic and adenocarcinomatous tissues. Studies at the mRNA, promoter and protein levels indicated that HNF1α regulates endogenous MUC4 expression by binding to two cognate cis-elements respectively located at − 3332/− 3327 and − 3040/ − 3028 in the distal promoter. We also showed by siRNA (small interfering RNA) approach, co-transfection and site-directed mut-agenesis that HNF1α mediates taurodeoxycholic and taurocheno-deoxycholic bile acid activation of endogenous MUC4 expression and transcription in a dose-dependent manner. In conclusion, these results describe a new mechanism of regulation of MUC4 expression by bile acids, in which HNF1α is a key mediator. These results bring new insights into MUC4 up-regulation in oesophageal carcinoma associated with bile reflux

Chronic corticosterone aggravates behavioral and neuronal symptomatology in a mouse model of alpha-synuclein pathology

Debilitating, yet underinvestigated nonmotor symptoms related to mood/emotion, such as depression, are common in Parkinson's disease. Here, we explore the role of depression and of the amygdala, a brain region robustly linked to mood/emotion, in synucleinopathy. We hypothesized that mood/emotional deficits might accelerate Parkinson's disease-linked symptomatology, including the formation of α-synuclein pathology. We combined elevated corticosterone treatment, modeling chronic stress and depression, with a model of seeded α-synuclein pathology in mouse striatum and assessed behavioral parameters with a focus on mood/emotion, and neuropathology. We report behavioral resilience against α-synuclein proteinopathy in the absence of additional insults, potentially based on hormesis/conditioning mechanisms. Elevated corticosterone, however, reversed α-synuclein pathology-induced behavioral adaptations and was associated with increased dopaminergic cell loss as well as aggravated α-synuclein pathology in specific brain regions, such as the entorhinal cortex. These findings point to elevated glucocorticoids as a risk factor for Parkinson's disease progression and highlight the potential of glucocorticoid level reducing strategies to slow down disease progression in synucleinopathy

Trefoil factor family 3 peptide promotes human airway epithelial ciliated cell differentiation.

Human airway surface epithelium is frequently damaged by inhaled factors (viruses, bacteria, xenobiotic substances) as well as by inflammatory mediators that contribute to the shedding of surface epithelial cells. To regain its protective function, the epithelium must rapidly repair and redifferentiate. The Trefoil Factor Family (TFF) peptides are secretory products of many mucous cells. TFF3, the major TFF in the airways, is able to enhance airway epithelial cell migration, but the role of this protein in differentiation has not been defined. To identify the specific role of TFF3 in the differentiation of the human airway surface epithelium, we analyzed the temporal expression pattern of TFF3, MUC5AC, and MUC5B mucins (goblet cells) and ciliated cell markers beta-tubulin (cilia) and FOXJ1 (ciliogenesis) during human airway epithelial regeneration using in vivo humanized airway xenograft and in vitro air-liquid interface (ALI) culture models. We observed that TFF3, MUC5AC, MUC5B, and ciliated cell markers were expressed in well-differentiated airway epithelium. The addition of exogenous recombinant human TFF3 to epithelial cell cultures before the initiation of differentiation resulted in no change in MUC5AC or cytokeratin 13 (CK13, basal cell marker)-positive cells, but induced an increase in the number of FOXJ1-positive cells and in the number of beta-tubulin-positive ciliated cells (P < 0.05). Furthermore, this effect on ciliated cell differentiation could be reversed by specific epidermal growth factor (EGF) receptor (EGF-R) inhibition. These results indicate that TFF3 is able to induce ciliogenesis and to promote airway epithelial ciliated cell differentiation, in part through an EGF-R-dependent pathway

P02-014 - Consequences of Arginine 92 mutations in TNFR1

International audienc