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See detailInhibiteurs du cotransporteur du glucose SGLT rénal pour traiter le diabète de type 2
SCHEEN, André ULiege; RADERMECKER, Régis ULiege; ERNEST, Philippe ULiege et al

in Revue Médicale Suisse (2011), 7(306), 1621-1629

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See detailLes inhibiteurs du cotransporteur du glucose SGLT rénal: une nouvelle classe thérapeutique dans le diabète de type 2
Sepulchre, Edith; RADERMECKER, Régis ULiege

in Journal de Cardiologie = Tijdschrift voor Cardiologie (2013), 25(8), 429-434

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See detailInhibiteurs du cotransporteur du glucose SGLT2 renal pour traiter le diabete de type 2.
SCHEEN, André ULiege; Radermecker, Régis ULiege; Ernest, P. et al

in Revue medicale suisse (2011), 7(306), 1621-41626-9

Kidney plays a role in glucose homeostasis, not only by its capacity to produce glucose through local gluconeogenesis, but also, and even more important in presence of diabetes, by its capacity to excrete ... [more ▼]

Kidney plays a role in glucose homeostasis, not only by its capacity to produce glucose through local gluconeogenesis, but also, and even more important in presence of diabetes, by its capacity to excrete glucose in urine when hyperglycaemia exceeds tubular reabsorption threshold. Such reabsorption depends on sodium-glucose cotransporters-2 (SGLT2), which can be blocked by selective inhibitors. These pharmacological agents augment glucosuria and reduce hyperglycaemia independently of insulin. Some have already proven their efficacy to improve glucose control, in monotherapy or in combination, while promoting weight loss and without inducing hypoglycaemia. Dapagliflozin should be the first medication of this new pharmacological class to be commercialized for the management of type 2 diabetes. [less ▲]

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See detailInhibiteurs potentiels de proteases à sérine apparentés aux antibiotiques β-lactamiques
Pirotte, Bernard ULiege; Vilain, A.-C.; Vergely, I. et al

in Regard sur la Biochimie (1991), 6, 91

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See detailInhibiting Effect of Ammonia on Citric Acid-Induced Cough in Pigs: A Possible Involvement of Substance P
Moreaux, B.; Nemmar, A.; Beerens, Dominique ULiege et al

in Pharmacology & Toxicology (2000), 87(6), 279-285

The effect of ammonia on the cough response to citric acid and on substance P release from C-fibers involved in this reflex was assessed. For a period from one to four days, piglets were exposed, in an ... [more ▼]

The effect of ammonia on the cough response to citric acid and on substance P release from C-fibers involved in this reflex was assessed. For a period from one to four days, piglets were exposed, in an inhalation chamber, to ammonia at a concentration of 15 or 30 ppm. During exposure, cough induction tests were done every two days. Recovery of the cough reflex after ammonia exposure was also determined. In a separate group of piglets exposed for 2 days to 30 ppm ammonia, substance P content was determined in bronchial and tracheal lavage fluids and in the tracheal and bronchial mucosa. Ammonia (30 ppm) was found to inhibit coughing significantly (the cough frequency was reduced by 64%) after a two-day exposure. In animals exposed for 4 days to this ammonia concentration, the recovery ranged from 3 to 7 days (mean: 5 days). The same ammonia concentration also caused the substance P content to increase significantly in bronchoalveolar lavage fluid (to 432% of its initial value) and tracheal lavage fluid (to 149%) and to decrease significantly in the tracheal mucosa (-58%), however the content in bronchial mucosa was not significantly affected (-43%). Exposure to 15 ppm ammonia had no effect on the frequency of citric acid-induced coughing. In conclusion, ammonia inhibits citric acid-induced coughing in pigs at concentrations that can be detected in piggeries. This inhibitory effect may be related to substance-P depletion in C-fiber endings [less ▲]

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See detailInhibiting or Antagonizing Glucagon: A Progress in Diabetes Care ?
LEFEBVRE, Pierre ULiege; Paquot, Nicolas ULiege; Scheen, André ULiege

in Diabetes, obesity & metabolism (2015)

Absolute or relative hyperglucagonemia has been recognized for years in all experimental or clinical forms of diabetes. It has been suggested that excess secretion of glucagon by the islet alpha-cells is ... [more ▼]

Absolute or relative hyperglucagonemia has been recognized for years in all experimental or clinical forms of diabetes. It has been suggested that excess secretion of glucagon by the islet alpha-cells is a direct consequence of intra-islet insulin secretory defects. Recent studies have demonstrated that knock-out of the glucagon receptor or administration of a monoclonal specific glucagon receptor antibody make insulin deficient type 1 diabetic rodents thrive without insulin. These observations suggest that glucagon plays an essential role in the pathophysiology of diabetes and that targeting the alpha-cell and glucagon are innovative approaches in the management of diabetes. Despite active research and identification of promising compounds, no one selective glucagon antagonist is presently used in the treatment of diabetes. Interestingly, besides insulin, several drugs used today in the management of diabetes appear to exert their effects in part by inhibiting glucagon secretion (GLP-1 receptor agonists, DPP-4 inhibitors, alpha glucosidase inhibitors and, maybe, sulfonylureas) or glucagon action (metformin). The potential risks associated with total glucagon suppression include alpha-cell hyperplasia, increased mass of the pancreas, increased susceptibility to hepatosteatosis and hepatocellular injury and increased risk of hypoglycaemia and should be considered in the search and development of new compounds reducing glucagon receptor signalling. In conclusion, more than 40 years after its initial description, the hyperglucagonemia of diabetes can no longer be ignored or minimized and its correction represents an attractive way for improving diabetes management. [less ▲]

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See detailL’INHIBITION DE LA MÉTHYLTRANSFÉRASE EZH2 DU COMPLEXE RÉPRESSEUR POLYCOMB FAVORISE LA RÉPONSE ANTI-TUMORALE DES MACROPHAGES M2 DIRIGÉE CONTRE LES CELLULES DU MÉSOTHÉLIOME PLEURAL MALIN
Hamaïdia, Malik ULiege

Doctoral thesis (2017)

Context: Malignant pleural mesothelioma (MPM) is an aggressive neoplasm affecting mesothelial cells from the pleura, pericardium and peritoneum. The disease is closely associated to asbestos exposure ... [more ▼]

Context: Malignant pleural mesothelioma (MPM) is an aggressive neoplasm affecting mesothelial cells from the pleura, pericardium and peritoneum. The disease is closely associated to asbestos exposure. Despite of rules to reduce workplace exposure to asbestos, incidence of mesothelioma is predicted to increase until 2020. Since MPM is resistant to conventional cancer therapies such as surgery, irradiation and chemotherapy, development of new options is urgently needed. In my project, I investigate the ability of immunotherapy to improve patients' outcome. My hypothesis postulates that tumor cells are tightly controlled by the immune system. In fact, clinical evidence indicates that tumor infiltration by tumor associated macrophages (TAMs) correlates with poor prognosis in malignant mesothelioma (MM). By attenuating the immune response, TAMs indeed promote survival of MM cells. TAMs share properties with alternative macrophages (M2) and are activated by anti-inflammatory (e.g. IL-10) or Th2-associated (i.e. IL-4, IL-13) cytokines. In contrast, classical (M1) macrophages are stimulated by interferon (IFN)-γ and microbial components (e.g. LPS). Aim: We hypothesized that macrophage activation is mediated by a transcriptional program tightly regulated by epigenetic modifications. We focused on the Polycomb Repressive Complex 2 (PRC2) EZH2 lysine methyltransferase responsible for trimethylation of histone H3 at lysine 27 (H3K27me3). Results: Our data show that inhibition of EZH2 reduces phagocytic activity by M2-polarised macrophages. Moreover, the cytotoxicity of supernatants conditioned by M2-macrophages is increased in presence of the EZH2 inhibitor. Finally, inhibition of EZH2 enhances the tumoricidal potential of M2 macrophages towards MM cells. We further demonstrate that macrophage killing activity requires superoxide radicals (O2.-) and peroxynitrites (ONOO-) derivatives produced by the NADPH oxidase system. Conclusion: EzH2 inhibition implements the tumoricidal potential of macrophages and may therefore improve the efficacy of immunotherapy of MM patients. [less ▲]

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See detailInhibition de la sclérostine par le romosozumab chez des femmes ménopausées ayant une DMO basse : résultats de l'étude de phase 2
Brown, JP; McClung, MR; Grauer, A et al

in Revue du Rhumatisme (2013), 80(S1), 73

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See detailInhibition des recepteurs CB1 et metabolisme du glucose: rimonabant dans le diabete de type 2.
Scheen, André ULiege; Paquot, Nicolas ULiege; Van Gaal, Luc F

in Revue Médicale Suisse (2008), 4(168), 1812-7

Endocannabinoid system is overactivated in individuals with abdominal obesity. CBI receptors, first individualized in the brain, are also expressed in the adipocyte, the skeletal muscle, the liver, the ... [more ▼]

Endocannabinoid system is overactivated in individuals with abdominal obesity. CBI receptors, first individualized in the brain, are also expressed in the adipocyte, the skeletal muscle, the liver, the gut, and the pancreas. Their blockade improves glucose tolerance and lipid profile, thanks increased insulin sensitivity and adiponectin levels. Rimonabant, a selective antagonist of CBI receptors, improves glucose control in patients with type 2 diabetes, treated with diet alone, metformin, sulfonylurea or insulin, while it also reduces body weight and other risk factors. Ongoing studies aim at further demonstrating the potential of rimonabant in the management of type 2 diabetes, in the prevention of type 2 diabetes and in the protection against cardiovascular complications in (diabetic) patients with abdominal obesity. [less ▲]

Detailed reference viewed: 96 (5 ULiège)
See detailInhibition et lobes frontaux
Le Gall, Didier; Van der Linden, Martial ULiege; Andrès Bénito, Pilar et al

in Boujon, C. (Ed.) L'inhibition au carrefour des neurosciences et des sciences de la cognition : fonctionnements normal et pathologique (2002)

Detailed reference viewed: 61 (7 ULiège)
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See detailInhibition mechanism of serine protease by coumarin derivatives
Pochet; Doucet, C.; Dieu, M. et al

Conference (2001, May)

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See detailInhibition of bovine sperm-zona binding by bovine herpesvirus-1
Tanghe, S.; Vanroose, G.; Van Soom, A. et al

in Reproduction (2005), 130(2), 251-259

The purpose of the present study was to identify a potential interference of bovine herpesvirus-1 (BoHV-1) with sperm-oocyte interactions during bovine in vitro fertilization. An inhibition of almost 70 ... [more ▼]

The purpose of the present study was to identify a potential interference of bovine herpesvirus-1 (BoHV-1) with sperm-oocyte interactions during bovine in vitro fertilization. An inhibition of almost 70% of sperm-zona binding was observed when bovine cumulus-denuded oocytes were inseminated in the presence of 10(7) 50% tissue culture infective dose/ml BoHV-1. The inhibitory effect of BoHV-1 on sperm-zona binding was mediated by an interaction of the virus with spermatozoa, but not with oocytes. Treatment of spermatozoa with BoHV-1, however, did not affect sperm motility and acrosomal status. Antiserum against RoHV-1 prevented the virus-induced inhibition of sperm-zona binding, indicating that BoHV-1 itself affects the fertilization process. In order to investigate which BoHV-1 glycoprotein(s) are responsible for the virus-sperm interaction, BoHV-1 was treated with monoclonal antibodies against the viral glycoproteins gB, gC, gD and gH prior to insemination. Anti-gC completely prevented the inhibitory effect of BoHV-1 on sperm-zona binding, while anti-gD caused a reduction of this inhibition. Further evidence for the involvement of gC and gD in the virus-sperm interaction was provided by the fact that purified gC and gD decreased sperm-zona binding in a dose-dependent way with gC being more effective than gD. These results indicated that BoHV-1 inhibits bovine sperm-zona binding by interacting with spermatozoa. The binding of BoHV-1 to a spermatozoon is mediated by the viral glycoproteins gC and gD, and therefore seems to be comparable with the mechanisms of BoHV-1 attachment to its natural host cell. [less ▲]

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See detailInhibition of cancer cells invasion by coumarin derivatives
Kempen, I.; Pochet, L.; Doucet, C. et al

Poster (2000, January 29)

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See detailInhibition of cellular invasion by 3-chlorophenyl 6-(acetoxymethyl)-2-oxo-2H-1-benzopyran-3-carboxylate
Kempen, I.; Pochet, L.; Papapostulu, D. et al

Poster (2000, September)

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See detailInhibition of cellular invasion by 3-chlorophenyl 6-(acetoxymethyl)-2-oxo-2H-1-benzopyran-3-carboxylate
Kempen, I.; Pochet, L.; Papapostulu, D. et al

in Pflügers Archiv : European Journal of Physiology (2000), 439

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See detailInhibition of ceramide-redox signaling pathway blocks glomerular injury in hyperhomocysteinemic rats.
Yi, F.; Zhang, A. Y.; Li, N. et al

in Kidney International (2006), 70(1), 88-96

Ceramide-activated NAD(P)H oxidase has been reported to participate in homocysteine (Hcys)-induced abnormal metabolism of the extracellular matrix (ECM) in rat glomerular mesangial cells. However, it ... [more ▼]

Ceramide-activated NAD(P)H oxidase has been reported to participate in homocysteine (Hcys)-induced abnormal metabolism of the extracellular matrix (ECM) in rat glomerular mesangial cells. However, it remains unknown whether this ceramide-redox signaling pathway contributes to glomerular injury induced by hyperhomocysteinemia (hHcys) in vivo. The present study was designed to address this question, defining the role of ceramide and activated NAD(P)H oxidase in the development of hHcys-induced glomerular injury. Uninephrectomized Sprague-Dawley rats were fed a folate-free diet for 8 weeks to produce hHcys and the de novo ceramide synthesis inhibitor myriocin or the NAD(P)H oxidase inhibitor apocynin was administrated. Rats with folate-free diet significantly increased plasma Hcys levels, renal ceramide levels, and NAD(P)H oxidase activity accompanied by marked glomerular injury. Treatment of rats with myriocin significantly reduced ceramide levels and improved glomerular injury, as shown by decreased urinary albumin excretion and reduced glomerular damage index. ECM components changed towards to normal levels with decreased tissue inhibitor of metalloproteinase-1 and increased matrix metalloproteinase-1 activity. NAD(P)H oxidase activity and Rac GTPase activity were reduced by 69 and 66%, respectively. In rats treated with apocynin, similar beneficial effects in protecting glomeruli from hHcys-induced injury were observed. These results support the view that de novo ceramide production is involved in Hcys-induced NAD(P)H oxidase activity in the kidney of hHcys rats and indicate the important role of ceramide-mediated redox signaling in hHcys-induced glomerular injury in rats. [less ▲]

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