References of "Thiry, Marc"
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See detailDispositif de suivi personnalisé des étudiants en biologie bloc 1
Rigo, Pierre ULiege; Thiry, Marc ULiege

Conference (2019, May 16)

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See detailHistologie générale - Exercices et méthodes
Thiry, Marc ULiege; Antoine, Nadine ULiege; Caudroy, Stéphanie et al

Book published by DUNOD (2019)

Cet ouvrage propose aux étudiants des premières années d’études supérieures (Licence 2 et 3) une méthode progressive et efficace pour comprendre et appliquer les concepts fondamentaux de l'histologie. Il ... [more ▼]

Cet ouvrage propose aux étudiants des premières années d’études supérieures (Licence 2 et 3) une méthode progressive et efficace pour comprendre et appliquer les concepts fondamentaux de l'histologie. Il traite de l'histologie des tissus sains et adultes chez les mammifères, Homme inclus. À la suite de rappels de cours, sous forme de fiches, chaque chapitre propose des exercices de difficulté croissante pour s’évaluer : QCM, questions Vrai/Faux et exercices de synthèse. Les corrigés détaillés mettent en évidence la méthodologie. Des bonus web avec des exercices d’entraînement supplémentaires, des fiches sur les techniques de préparation des coupes histologiques et des photos de coupes histologiques en couleur complètent l’ouvrage. [less ▲]

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See detailA clinical and histopathological study of malformations observed in fetuses infected by the Zika virus
Beaufrère, A.; Bessières, B.; Bonnière, M. et al

in Brain Pathology (2019), 29(1), 114-125

Background: The recent outbreak of Zika virus (ZIKV) infection and the associated increased prevalence of microcephaly in Brazil underline the impact of viral infections on embryo fetal development. The ... [more ▼]

Background: The recent outbreak of Zika virus (ZIKV) infection and the associated increased prevalence of microcephaly in Brazil underline the impact of viral infections on embryo fetal development. The aim of the present study is to provide a detailed clinical and histopathological study of the fetal disruption caused by the ZIKV, with a special focus on the associated neuropathological findings. Methods: A detailed feto-placental examination, as well as neuropathological and neurobiological studies were performed on three fetuses collected after pregnancy termination between 22 and 25 weeks of gestation (WG), because brain malformations associated with a maternal and fetal ZIKV infection was diagnosed. Results: In all three cases, the maternal infection occurred during the first trimester of pregnancy. A small head was observed on the ultrasound examination of the second trimester of pregnancy and led to the diagnosis of ZIKV fetopathy and pregnancy termination. The fetal histopathological examination was unremarkable on the viscera but showed on the testis an interstitial lymphocytic infiltrate. The placenta contained a Hofbauer cells hyperplasia with signs of inflammation. Neuropathological findings included a meningoencephalitis and an ex vacuo hydrocephalus. Immunohistochemical studies showed the presence of T lymphocytic and histiocytic meningitis associated with an abundant cerebral astroglial and macrophagic reaction. In situ hybridization demonstrated, abundant ZIKV particles within the cerebral parenchyma mainly in the ventricular/subventricular zone and in the cortical plate. In addition massive cells death and endoplasmic reticulum damage were present. Conclusion: The present study reports on the clinical and histopathological findings observed in three fetuses infected by the ZIKV. It emphasizes the severity of brain damages and the minimal visceral and placental changes observed upon ZIKV infection. This confirms the selective neurotropism of ZIKV. Finally, it allows us to describe the cascade of multifactorial developmental defects leading to microcephaly. © 2018 International Society of Neuropathology [less ▲]

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See detailActin-independent trafficking of cochlear connexin 26 to non-lipid raft gap junction plaques.
Defourny, Jean ULiege; Thelen, Nicolas ULiege; Thiry, Marc ULiege

in Hearing Research (2019)

Hereditary hearing loss affects about 1 per 1000 children. Mutations in GJB2, which encodes the connexin 26 protein (Cx26) involved in cochlear homeostasis, are found in about 50% of patients with ... [more ▼]

Hereditary hearing loss affects about 1 per 1000 children. Mutations in GJB2, which encodes the connexin 26 protein (Cx26) involved in cochlear homeostasis, are found in about 50% of patients with autosomal recessive non-syndromic hearing loss. Deciphering the trafficking pathway of cochlear Cx26 in situ should represent an advance in understanding the pathogenic significance of many of these mutations. Connexins trafficking and delivery to lipid raft-associated gap junction plaques usually requires successively microtubule and actin networks. Here we show that cochlear Cx26 exhibits an unusual trafficking pathway. We observed that Cx26 assembly occurs in non-lipid raft membrane domains and that junctional plaques are devoid of actin and associated zonula occludens proteins. Using cytoskeleton-disrupting drugs in organotypic culture, we found that cochlear Cx26 gap junction assembly requires microtubules but not actin filaments. Altogether, our data provide an unexpected insight into Cx26 trafficking pathway and gap junction assembly in the cochlea. [less ▲]

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See detailCochlear connexin 30 homomeric and heteromeric channels exhibit distinct assembly mechanisms.
Defourny, Jean ULiege; Thelen, Nicolas ULiege; Thiry, Marc ULiege

in Mechanisms of Development (2019)

Many of the mutations in GJB2 and GJB6, which encode connexins 26 and 30 (Cx26 and Cx30), impair the formation of membrane channels and cause autosomal syndromic and non-syndromic hearing loss. In ... [more ▼]

Many of the mutations in GJB2 and GJB6, which encode connexins 26 and 30 (Cx26 and Cx30), impair the formation of membrane channels and cause autosomal syndromic and non-syndromic hearing loss. In cochlear non-sensory supporting cells, Cx26 and Cx30 form two types of homomeric and heteromeric gap junctions. The biogenesis processes of these channels occurring in situ remain largely unknown. Here we show that Cx30 homomeric and Cx26/Cx30 heteromeric gap junctions exhibit distinct assembly mechanisms in the cochlea. When expressed as homomeric channels, Cx30 preferentially interacts with beta-actin in the peripheral non-junctional membrane region, called perinexus, and strongly relies on the actin network for gap junction plaque assembly. In contrast, we found that Cx26/Cx30 heteromeric gap junction plaques are devoid of perinexus and associated actin network, and resist to actin-depolymerizating drug. This supports that Cx26/Cx30 oligomers could be directly delivered from the interior of the cell to the junctional plaque. Altogether, our data provide a novel insight in homomeric and heteromeric gap junction plaque assembly in the cochlea. [less ▲]

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See detailStrategies for the study of plant virus-based virus-like particles (VLP) displaying human papillomavirus (HPV) L2 epitope
Yazdani, Razieh; Shams-Bakhsh, Masoud; Thelen, Nicolas ULiege et al

Poster (2018, December 19)

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See detailAides à l’étude en Biologie Cellulaire en première année du bachelier
Thiry, Marc ULiege; Rigo, Pierre ULiege

Scientific conference (2018, November 26)

Marc Thiry & Pierre Rigo (Biologie, ULiège) ont présenté un dispositif d’aide à la réussite mis en place depuis 2011 dans le cours de Biologie cellulaire de première année de la Faculté des Sciences de ... [more ▼]

Marc Thiry & Pierre Rigo (Biologie, ULiège) ont présenté un dispositif d’aide à la réussite mis en place depuis 2011 dans le cours de Biologie cellulaire de première année de la Faculté des Sciences de l’Université de Liège. Ce dispositif vise à amener les étudiants à travailler plus régulièrement la matière. Concrètement, des séances d’aide à l’étude travaillent de façon interactive et en petits groupes la résolution de problèmes au départ de devoirs obligatoires réalisés préalablement. Les étudiants ont à apprendre à se poser des questions sur la matière, à résoudre des problèmes, à intégrer les différents chapitres théoriques et à faire le lien entre théorie et pratique. Les encadrants organisent les interventions des étudiants (en évitant de « simplement donner la bonne réponse »), la co-construction et la validation d’une production finale face au problème posé. Chaque année, ce dispositif est modifié en fonction des résultats issus d’un questionnaire soumis aux étudiants et des suggestions des encadrants ; ce qui a permis une régulation de plus en plus fine et une augmentation du taux de réussite. [less ▲]

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See detailMolecular mechanisms of gap junction assembly in the cochlea
Defourny, Jean ULiege; Thelen, Nicolas ULiege; Thiry, Marc ULiege

Poster (2018, October 19)

Hereditary hearing loss affects about 1 per 1000 children. Mutations in GJB2 and GJB6, which encode connexins 26 and 30 (Cx26 and Cx30) involved in cochlear homeostasis, cause autosomal syndromic and non ... [more ▼]

Hereditary hearing loss affects about 1 per 1000 children. Mutations in GJB2 and GJB6, which encode connexins 26 and 30 (Cx26 and Cx30) involved in cochlear homeostasis, cause autosomal syndromic and non-syndromic hearing loss. In cochlear non-sensory supporting cells, Cx26 and Cx30 form two types of homomeric and heteromeric gap junctions. Deciphering the assembly mechanisms of these channels in situ should represent an advance in understanding the pathogenic significance of many of these mutations. Connexin trafficking and delivery to the gap junction plaque usually occurs from the peripheral non-junctional membrane region, called perinexus, and requires the actin network. Combining immunolabelling and organotypic in vitro assay, we found that Cx30 homomeric and Cx26/Cx30 heteromeric channels exhibit distinct assembly mechanisms in the cochlea. When expressed as homomeric channels, Cx30 preferentially associates with the actin network in the perinexus and strongly relies on it for gap junction plaque assembly. In contrast, we found that Cx26/Cx30 heteromeric gap junction plaques are devoid of perinexus and associated actin network, and resist to actin-depolymerizating drug. This supports that Cx26/Cx30 oligomers could be directly delivered from the interior of the cell to the junctional plaque. Altogether, our data provide a novel insight in homomeric and heteromeric gap junction plaque assembly in the cochlea. [less ▲]

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See detailCombination of analytical approaches for the characterization of plant virus-based VLP displaying HPV L2 epitope
Yazdani, Razieh; Shams-Bakhsh, Masoud; Hassani-Mehraban, Afshin et al

Conference (2018, September 12)

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See detailVaricella Zoster Virus ORF9p binding to cellular adaptor protein complex-1 is important for viral infectivity.
Lebrun, Marielle ULiege; Lambert, Julien ULiege; Riva, Laura et al

in Journal of Virology (2018), 92(15),

ORF9p (homologous to HSV-1 VP22) is a varicella-zoster virus (VZV) tegument protein essential for viral replication. Even though its precise functions are far from being fully described, a role in the ... [more ▼]

ORF9p (homologous to HSV-1 VP22) is a varicella-zoster virus (VZV) tegument protein essential for viral replication. Even though its precise functions are far from being fully described, a role in the secondary envelopment of the virus has long been suggested. We performed a yeast two-hybrid screen to identify cellular proteins interacting with ORF9p that might be important for this function. We found thirty-one ORF9p interaction partners, among which AP1M1, the mu subunit of the adaptor protein complex-1 (AP-1). AP-1 is a heterotetramer involved in intracellular vesicle-mediated transport and regulates the shuttling of cargo proteins between endosomes and the TGN via clathrin-coated vesicles. We confirmed that AP-1 interacts with ORF9p in infected cells and mapped potential interaction motifs within ORF9p. We generated VZV mutants in which each of these motifs is individually impaired and identified leucine 231 in ORF9p as critical to interact with AP-1. Disrupting ORF9p binding to AP-1 by mutating leucine 231 to alanine in ORF9p strongly impaired viral growth, most likely by preventing efficient secondary envelopment of the virus. Leucine 231 is part of a di-leucine motif conserved among alphaherpesviruses and we showed that VP22 of MDV and HSV-2 also interact with AP-1. This indicates that the function of this interaction in the secondary envelopment might be conserved as well.IMPORTANCE Herpesviruses are responsible for infections that, especially in immunocompromised patients, can lead to severe complications, including neurological symptoms and strokes. The constant emergence of viral strains resistant to classical antivirals (mainly acyclovir and its derivatives) pleads for the identification of new targets for future antiviral treatments. Cellular adaptor protein complexes (AP) have been implicated in the correct addressing of herpesvirus glycoproteins in infected cells and the discovery that a major constituent of varicella-zoster virus tegument is interacting with AP-1 reveals a previously unsuspected role of this tegument protein. Unraveling the complex mechanisms leading to virion production will certainly be an important step in the discovery of future therapeutic targets. [less ▲]

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See detailStrategies for the identification and quantitation of intact virus-like particles of human papillomavirus in CE
Bettonville, Virginie ULiege; Nicol, Jérôme; Furst, Tania et al

Conference (2018, July 13)

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See detailMyoferlin controls mitochondrial structure and metabolism in pancreatic ductal adenocarcinoma, and affects tumor aggressiveness.
Rademaker, Gilles ULiege; Hennequière, Vincent; Brohée, Laura et al

Poster (2018, July 01)

Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer, and the third leading cause of cancer related death. Therapeutic options remain very limited and are still based on ... [more ▼]

Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer, and the third leading cause of cancer related death. Therapeutic options remain very limited and are still based on classical chemotherapies. Cell fraction can survive to the chemotherapy and is responsible for tumor relapse. It appears that these cells rely on oxydative phosphorylation (OXPHOS) for survival. Myoferlin, a membrane protein involved in cell fusion was recently shown by our laboratory to be overexpressed in pancreatic cancer. In the present study, we discovered that myoferlin was more expressed in cell lines undergoing (OXPHOS) than in glycolytic cell lines. In the former cell lines, we showed that myoferlin silencing reduced OXPHOS activity and forced cells to switch to glycolysis. The decrease in OXPHOS activity is associated with mitochondrial condensation and network disorganization. An increase of Dynamin-related protein (DRP)-1 phosphorylation in myoferlin-depleted cells led us to suggest mitochondrial fission, reducing cell proliferation, ATP production and inducing autophagy and ROS accumulation. Electron microscopy observation revealed mitophagy, suggesting mitochondrial alterations. To confirm the clinical importance of myoferlin in PDAC, we showed that low myoferlin expression was significantly correlated to high overall survival. Myoferlin staining of PDAC sections was negatively correlated with several 18FDG PET indices indicating that glycolytic lesions had less myoferlin. These observations are fully in accordance with our in vitro data. As the mitochondrial function was associated with cell chemoresistance, the metabolic switch induced by myoferlin silencing could open up a new perspective in the development of therapeutic strategies. Among them, targeting functional domains (C2, Dysf, …) of myoferlin should be a priority. [less ▲]

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See detailPropranolol sensitizes prostate cancer cells to glucose metabolism inhibition and prevents cancer progression.
Brohée, Laura; Peulen, Olivier ULiege; Nusgens, Betty et al

in Scientific Reports (2018), 8(1), 7050

Propranolol, a widely used non-selective beta-adrenergic receptor blocker, was recently shown to display anticancer properties. Its potential to synergize with certain drugs has been also outlined ... [more ▼]

Propranolol, a widely used non-selective beta-adrenergic receptor blocker, was recently shown to display anticancer properties. Its potential to synergize with certain drugs has been also outlined. However, it is necessary to take into account all the properties of propranolol to select a drug that could be efficiently combined with. Propranolol was reported to block the late phase of autophagy. Hence, we hypothesized that in condition enhancing autophagy flux, cancer cells should be especially sensitive to propranolol. 2DG, a glycolysis inhibitor, is an anti-tumor agent having limited effect in monotherapy notably due to induction of pro-survival autophagy. Here, we report that treatment of cancer cells with propranolol in combination with the glycolysis inhibitor 2DG induced a massive accumulation of autophagosome due to autophagy blockade. The propranolol +2DG treatment efficiently prevents prostate cancer cell proliferation, induces cell apoptosis, alters mitochondrial morphology, inhibits mitochondrial bioenergetics and aggravates ER stress in vitro and also suppresses tumor growth in vivo. Our study underlines for the first time the interest to take advantage of the ability of propranolol to inhibit autophagy to design new anti-cancer therapies. [less ▲]

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See detailMyoferlin controls mitochondrial structure and activity in pancreatic ductal adenocarcinoma, and affects tumor aggressiveness
Rademaker, Gilles ULiege; Hennequière, Vincent ULiege; Nokin, Marie-Julie ULiege et al

in Oncogene (2018)

Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer-related death. Therapeutic options remain very limited and are based on classical chemotherapies. Energy metabolism ... [more ▼]

Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer-related death. Therapeutic options remain very limited and are based on classical chemotherapies. Energy metabolism reprogramming appears as an emerging hallmark of cancer and is considered a therapeutic target with considerable potential. Myoferlin, a ferlin family member protein overexpressed in PDAC, is involved in plasma membrane biology and has a tumor-promoting function. In the continuity of our previous studies, we investigated the role of myoferlin in the context of energy metabolism in PDAC. We used selected PDAC tumor samples and PDAC cell lines together with small interfering RNA technology to study the role of myoferlin in energetic metabolism. In PDAC patients, we showed that myoferlin expression is negatively correlated with overall survival and with glycolytic activity evaluated by 18F-deoxyglucose positron emission tomography. We found out that myoferlin is more abundant in lipogenic pancreatic cancer cell lines and is required to maintain a branched mitochondrial structure and a high oxidative phosphorylation activity. The observed mitochondrial fission induced by myoferlin depletion led to a decrease of cell proliferation, ATP production, and autophagy induction, thus indicating an essential role of myoferlin for PDAC cell fitness. The metabolic phenotype switch generated by myoferlin silencing could open up a new perspective in the development of therapeutic strategies, especially in the context of energy metabolism. [less ▲]

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See detailMild mitochondrial uncoupling induces HSL/ATGL-independent lipolysis relying on a form of autophagy in 3T3-L1 adipocytes
Demine, Stéphane; Tejerina, Silvia; Bihin, Benoît et al

in Journal of Cellular Physiology (2018), 233 (2)

Obesity is characterized by an excessive triacylglycerol accumulation in white adipocytes. Various mechanisms allowing the tight regulation of triacylglycerol storage and mobilization by lipid droplet ... [more ▼]

Obesity is characterized by an excessive triacylglycerol accumulation in white adipocytes. Various mechanisms allowing the tight regulation of triacylglycerol storage and mobilization by lipid droplet-associated proteins as well as lipolytic enzymes have been identified. Increasing energy expenditure by inducing a mild uncoupling of mitochondria in adipocytes might represent a putative interesting anti-obesity strategy as it reduces the adipose tissue triacylglycerol content (limiting alterations caused by cell hypertrophy) by stimulating lipolysis through yet unknown mechanisms, limiting the adverse effects of adipocyte hypertrophy. Herein, the molecular mechanisms involved in lipolysis induced by a mild uncoupling of mitochondria in white 3T3-L1 adipocytes were characterized. Mitochondrial uncoupling-induced lipolysis was found to be independent from canonical pathways that involve lipolytic enzymes such as HSL and ATGL. Finally, enhanced lipolysis in response to mitochondrial uncoupling relies on a form of autophagy as lipid droplets are captured by endolysosomal vesicles. This new mechanism of triacylglycerol breakdown in adipocytes exposed to mild uncoupling provides new insights on the biology of adipocytes dealing with mitochondria forced to dissipate energy. [less ▲]

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See detailEvaluation d’un dispositif d’aide à la réussite par les étudiants : le cas du cours de Biologie en premier bachelier de la Faculté des Sciences à l’ULiège
Poffé, Corentin ULiege; Rigo, Pierre ULiege; Thiry, Marc ULiege et al

Conference (2018, January 11)

Depuis l’année académique 2011-2012 et suite à un taux d’échecs à l’examen important (85 % de notes inférieures à 10/20), un dispositif d’aide à la réussite a été mis en place pour les étudiants de la ... [more ▼]

Depuis l’année académique 2011-2012 et suite à un taux d’échecs à l’examen important (85 % de notes inférieures à 10/20), un dispositif d’aide à la réussite a été mis en place pour les étudiants de la Faculté des Sciences à l’Université de Liège pour le cours de Biologie. Ce dispositif à participation obligatoire prend place chaque année, au tout début du cursus universitaire des étudiants inscrits en bachelier scientifique. Brièvement, ce dispositif consiste en différentes séances de travail au cours desquelles les étudiants sont répartis par section en sous-groupes d'une trentaine de personnes et gérées par un encadrant. Préalablement à chaque séance, les étudiants doivent réaliser un devoir qu’ils présentent à l’encadrant afin de se voir ouvrir l’accès à la séance. Durant celle-ci, les étudiants sont amenés à résoudre des exercices d’application en lien avec les autres activités du cours (séances théoriques, laboratoires…). Pour chaque exercice, un étudiant propose aux autres sa résolution et ses condisciples la corrigent, la complètent, etc. Ce n’est qu’en fin de processus que l’encadrant intervient pour valider la résolution à laquelle ont abouti les étudiants. Les exercices à résoudre proposés sont très proches de ceux auxquels les étudiants seront soumis à l’examen du cours de biologie (Poffé, Rigo, Thiry & Hindryckx , 2015 ; Poffé, Rigo, Hindryckx et Thiry, 2017). Au cours des séances, le rôle des encadrants est de vérifier la réalisation du devoir par chacun des étudiants ; d’organiser les interventions des étudiants en respectant le canevas de séance préalablement établi ; de valider la production finale à laquelle les étudiants ont abouti face au problème posé. Durant les phases de travail des étudiants, les encadrants sont également amenés à répondre à leurs questions, tant sur des éléments de savoir que sur des méthodes de résolution de problèmes (comprendre une question complexe, identifier les procédures de résolution à mettre en oeuvre et produire une réponse complète et structurée). À la fin de chacune des séances, les étudiants sont invités à remplir un questionnaire, identique pour toutes les séances. Il comprend une quinzaine de propositions réparties en différentes catégories : la difficulté du devoir et la qualité de la réponse produite par l’étudiant ; l’augmentation des chances de réussite à l’examen (savoirs et/ou méthodes de résolution et/ou implication dans l’étude) ; l’aide apportée par l’encadrant ; la capacité de la séance à apporter des réponses aux questions des étudiants. Pour chaque proposition, les étudiants doivent se positionner sur une échelle à quatre valeurs, allant de « pas du tout d’accord » à « tout à fait d’accord ». Les encadrants sont également amenés à renseigner leur avis par le biais de questionnaires du même type que ceux remplis par les étudiants, mais avec des questions adaptées à leur rôle. Ce questionnaire est également identique d’une séance à l’autre. Cette évaluation par questionnaire veut placer tous les protagonistes dans une posture réflexive par rapport à leur travail : les étudiants par rapport à leur façon de travailler un cours universitaire et les encadrants, dans leur façon de se mettre à disposition de l’apprentissage des étudiants. En fin de quadrimestre, tous les questionnaires sont dépouillés et analysés. Pour chaque séance et pour chaque proposition, la fréquence de chacune des quatre possibilités de réponse est calculée. Ces fréquences sont portées en graphiques. Ces résultats sont comparés entre séances d’une même année et également d’une année à l’autre. Les résultats de cette analyse, accompagnés de différentes données factuelles (taux de réussite aux différentes évaluations, analyse de l’activité des étudiants sur l’espace en ligne dédié au cours, résultats à l’examen…) sont présentés à toute l’équipe d’encadrants. Lors de cette réunion, chaque séance de l’année est discutée. L’ensemble des données permet d’alimenter cette discussion qui porte tant sur les éléments à maintenir pour l’année suivante, que sur les éléments à revoir, compte tenu notamment, de l’avis des étudiants et des encadrants. Ces éléments sont tout autant des éléments de méthodologie que des savoirs scientifiques à faire acquérir. Chaque année, le dispositif d’aide à la réussite et son articulation avec les enseignements sont donc modifiés en fonction des résultats issus de l’analyse des questionnaires et des suggestions des étudiants. On constate que, si, dans un premier temps, la régulation du dispositif s’est opérée essentiellement sur des modifications d’ordre logistique (adéquation des horaires, amélioration de la communication des attentes vers les étudiants, réglage du niveau de difficulté du devoir, par exemple), cette dernière s’est petit à petit affinée. En effet, après quelques années de fonctionnement, l’équipe est parvenue à un dispositif dont l’efficacité était globalement satisfaisante (questionnaires montrant un taux global de satisfaction des étudiants élevé et un taux de réussite à l’examen en évolution positive) et a souhaité s’engager dans des essais de méthodologies d’enseignement plus variées (une séance en classe inversée, une séance en classe puzzle…). À chaque fois, les questionnaires ont permis d’évaluer les impacts de ces méthodologies sur la satisfaction des étudiants par rapport à leurs apprentissages en vue de l’évaluation certificative du cours. La communication tendra à montrer comment la prise en compte systématique des avis de tous les protagonistes (étudiants et encadrants), collectés au travers des questionnaires, a permis une régulation de plus en plus fine du dispositif d’aide à la réussite et une augmentation significative du taux de réussite des étudiants à l’examen du cours de biologie (passage de 15 à 30 % de réussite). [less ▲]

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See detailSpontaneous atopic dermatitis due to immune dysregulation in mice lacking Adamts2 and 14.
Dupont, Laura ULiege; Ehx, Grégory; Chantry, Mathilde et al

in Matrix Biology (2018), 70

Since its first description, ADAMTS14 has been considered as an aminoprocollagen peptidase based on its high similarity with ADAMTS3 and ADAMTS2. As its importance for procollagen processing was never ... [more ▼]

Since its first description, ADAMTS14 has been considered as an aminoprocollagen peptidase based on its high similarity with ADAMTS3 and ADAMTS2. As its importance for procollagen processing was never experimentally demonstrated in vivo, we generated Adamts14-deficient mice. They are healthy, fertile and display normal aminoprocollagen processing. They were further crossed with Adamts2-deficient mice to evaluate potential functional redundancies between these two highly related enzymes. Initial characterizations made on young Adamts2-Adamts14-deficient animals showed the same phenotype as that of Adamts2-deficient mice, with no further reduction of procollagen processing and no significant aggravation of the structural alterations of collagen fibrils. However, when evaluated at older age, Adamts2-Adamts14-deficient mice surprisingly displayed epidermal lesions, appearing in 2 month-old males and later in some females, and then worsening rapidly. Immunohistological evaluations of skin sections around the lesions revealed thickening of the epidermis, hypercellularity in the dermis and extensive infiltration by immune cells. Additional investigations, performed on young mice before the formation of the initial lesions, revealed that the primary cause of the phenotype was not related to alterations of the epidermal barrier but was rather the result of an abnormal activation and differentiation of T lymphocytes towards a Th1 profile. However, the primary molecular defect probably does not reside in the immune system itself since irradiated Adamts2-Adamts14-deficient mice grafted with WT immune cells still developed lesions. While originally created to better characterize the common and specific functions of ADAMTS2 and ADAMTS14 in extracellular matrix and connective tissues homeostasis, the Adamts2-Adamts14-deficient mice revealed an unexpected but significant role of ADAMTS in the regulation of immune system, possibly through a cross-talk involving mesenchymal cells and the TGFβ pathways. [less ▲]

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See detailER-mitochondria cross-talk is regulated by the Ca(2+) sensor NCS1 and is impaired in Wolfram syndrome.
Angebault, Claire; Fauconnier, Jeremy; Patergnani, Simone et al

in Science Signaling (2018), 11(553),

Communication between the endoplasmic reticulum (ER) and mitochondria plays a pivotal role in Ca(2+) signaling, energy metabolism, and cell survival. Dysfunction in this cross-talk leads to metabolic and ... [more ▼]

Communication between the endoplasmic reticulum (ER) and mitochondria plays a pivotal role in Ca(2+) signaling, energy metabolism, and cell survival. Dysfunction in this cross-talk leads to metabolic and neurodegenerative diseases. Wolfram syndrome is a fatal neurodegenerative disease caused by mutations in the ER-resident protein WFS1. Here, we showed that WFS1 formed a complex with neuronal calcium sensor 1 (NCS1) and inositol 1,4,5-trisphosphate receptor (IP3R) to promote Ca(2+) transfer between the ER and mitochondria. In addition, we found that NCS1 abundance was reduced in WFS1-null patient fibroblasts, which showed reduced ER-mitochondria interactions and Ca(2+) exchange. Moreover, in WFS1-deficient cells, NCS1 overexpression not only restored ER-mitochondria interactions and Ca(2+) transfer but also rescued mitochondrial dysfunction. Our results describe a key role of NCS1 in ER-mitochondria cross-talk, uncover a pathogenic mechanism for Wolfram syndrome, and potentially reveal insights into the pathogenesis of other neurodegenerative diseases. [less ▲]

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See detailSputum exosomes: promising biomarkers for idiopathic pulmonary fibrosis.
Njock, Makon-Sébastien ULiege; GUIOT, Julien ULiege; HENKET, Monique ULiege et al

in Thorax (2018)

Idiopathic pulmonary fibrosis (IPF) is a progressive fibrosing interstitial lung disease of unknown aetiology which leads rapidly to death. As diagnosis of IPF is complex, we aimed to characterise ... [more ▼]

Idiopathic pulmonary fibrosis (IPF) is a progressive fibrosing interstitial lung disease of unknown aetiology which leads rapidly to death. As diagnosis of IPF is complex, we aimed to characterise microRNA (miRNA) content of exosomes from sputum of patients with IPF. Using miRNA quantitative PCR array, we found a substantial dysregulation of sputum exosomal miRNA levels between patients with IPF and healthy subjects and identified a unique signature of three miRNAs. Interestingly, we found a negative correlation between miR-142-3p and diffusing capacity of the lungs for carbon monoxide/alveolar volume. This is the first characterisation of miRNA content of sputum-derived exosomes in IPF that identified promising biomarkers for diagnosis and disease severity. [less ▲]

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