Une bibliothèque modèle à l’Université de Liège? : le projet De Laet

Durant les années 1930, la situation des bâtiments occupés par la bibliothèque de l’Université de Liège s’avère particulièrement préoccupante. Devant la menace imminente de l’effondrement d’une partie de la bibliothèque, les autorités universitaires décident la construction d’une nouvelle bibliothèque, plus adaptée aux besoins de l’époque. Le projet est confié à l’architecte Armand De Laet. Celui-ci proposera au cours des années suivantes plusieurs versions d’un bâtiment imposant, en collaboration avec le bibliothécaire en chef de l’époque. Les hostilités du second conflit mondial empêcheront néanmoins à ce projet de voir le jour. Mis de côté au début de la guerre, ce projet sera définitivement abandonné en 1945. L’heure n’est désormais plus tant à l’esthétique et au grandiose qu’au pragmatisme et à la fonctionnalité des lieux. Les documents redécouverts récemment dans les archives de la bibliothèque permettent de retracer la conception et l’évolution de ce projet de grande envergure qui s’inscrit dans la lignée de ceux qui seront réalisés à la bibliothèque de l’Université de Gand et à la Bibliothèque Royale

PDE4 as a target in preterm labour

Cyclic nucleotide phosphodiesterases (PDE) are the enzymes catalyzing the hydrolysis and inactivation of the second messengers, cAMP and cGMP. Eleven PDE families are described to date, and selective inhibitors of some PDEs families are currently used in clinic for treating cardiovascular disorders, erectile dysfunction, and pulmonary hypertension. Isoforms of the PDE4 family are involved in smooth muscle contraction and inflammation. PDE4 selective inhibitors are currently in clinical trials for the treatment of diseases related to inflammatory disorders. Because of their myorelaxant properties, we first examined their expression in human myometrium and uncover an increased expression of one specific isoform, PDE4B2, in the near-term myometrium as compared to myometrium in the nonpregnant state. Using human myometrial cells in culture, we demonstrated that PDE4B2 can be induced by its own substrate, under the control of one of the major utero-contractile agonists, PGE2, itself upregulated by the proinflammatory cytokine IL-1β. Functionally, augmentation of global PDE4 activity decreases the ability of β-adrenergic agonists (the most commonly used tocolytic drugs) to inhibit myometrial contraction at the end of pregnancy and during pathophysiological situations, such as persistent intrauterine inflammation which is a major cause of very preterm delivery. Currently exploring the anti-inflammatory properties of PDE4 inhibitors in gestational tissues, we recently demonstrated the ability of these drugs to block a persistent inflammatory response of the foetal membranes in Humans and to prevent inflammation-driven preterm delivery and foetal demise in mice. These data open up a new therapeutical strategy to prevent inflammation-induced preterm delivery and its sequelae in very preterm infants

Du Pep’s à l’ULg : un fonds de manuscrits médiévaux et renaissants reprend vie à l’écran

Au cours de l’année 2013, 49 manuscrits, parmi les plus précieux des collections du Réseau des Bibliothèques de l’ULg, ont été numérisés. Ces manuscrits médiévaux et renaissants, souvent richement enluminés et décorés, seront rendus accessibles à tous, en ligne, au début du mois de février. Avant de découvrir les résultats en images de cette vaste campagne, cet article propose de plonger dans l’histoire de ces collections et d’en découvrir quelques pièces exceptionnelles

Evidence for a role of phosphodiesterase 4 in lipopolysaccharide-stimulated prostaglandin E2 production and matrix metalloproteinase-9 activity in human amniochorionic membranes.

Chorioamniotic infection is a leading cause of preterm premature rupture of fetal membranes (amnion and chorion). Bacterial infection induces an inflammatory response characterized by elevated production of proinflammatory cytokines; the latter activate the production of both PGs that stimulate uterine contractions, and matrix metalloproteinases (MMPs) that degrade the extracellular matrix of the chorioamniotic membranes. The inflammatory response is under the control of cAMP content, which is partly regulated by phosphodiesterases (PDE). In this study, we investigated the role of the PDE4 family in the inflammatory process triggered by LPS in a model of amniochorionic explants. We found that PDE4 family is the major cAMP-PDE expressed in human fetal membranes and that PDE4 activity is increased by LPS treatment. Selective inhibition of PDE4 activity affected LPS signaling, because PDE4 inhibitors (rolipram and/or cilomilast) reduced the release of the proinflammatory cytokine TNF-alpha and increased the release of the anti-inflammatory cytokine IL-10. PDE4 inhibition reduced cyclooxygenase-2 protein expression and PGE(2) production and also modulated MMP-9, a key mediator of the membrane rupture process, by inhibiting pro-MMP-9 mRNA expression and pro-MMP-9 activity. These results demonstrate that the PDE4 family participates in the regulation of the inflammatory response associated with fetal membrane rupture during infection. The PDE4 family may be an appropriate pharmacological target for the management of infection-induced preterm delivery