Browsing
     by title


0-9 A B C D E F G H I J K L M N O P Q R S T U V W X Y Z

or enter first few letters:   
OK
Full Text
Peer Reviewed
See detailOxidative stress in the liver and the brain of rats in fulminant hepatic failure
Detry, Olivier ULg; Gaspar, Yves; Cheramy-Bien, Jean-Paul ULg et al

in Transplantation Proceedings (2005), 37(6, Jul-Aug), 2883-2885

The etiological mechanisms of brain edema in fulminant hepatic failure are incompletely understood. In a surgical model of fulminant hepatic failure in the rat, we tested whether oxidative stress may be ... [more ▼]

The etiological mechanisms of brain edema in fulminant hepatic failure are incompletely understood. In a surgical model of fulminant hepatic failure in the rat, we tested whether oxidative stress may be involved in the early steps of brain edema. Moreover, we took advantage of this model to determine if oxidative stress may be involved in the hepatocyte dysfunction observed in the setting of fulminant hepatic failure. Oxidative stress was evaluated by measurement of tissue ascorbic acid in the brain and liver of rats at 6 hours after induction of fulminant hepatic failure versus in control or partially hepatectomized rats. After 6 hours, the level of ascorbic acid was not different in the brain tissue of the various groups, indicating no oxidative stress. The liver showed a significant decrease in ascorbic acid levels, both in ischemic and nonischemic liver tissue, suggesting that oxidative stress might be involved in the failure of liver regeneration in fulminant hepatic failure. In this rat model no oxidative stress was demonstrated in the brain during the early phase of fulminant liver failure. [less ▲]

Detailed reference viewed: 36 (3 ULg)
Full Text
See detailOxidative stress or not in healthy older subjects?
PINCEMAIL, Joël ULg; CHRISTELBACH, Sophie ULg; RICOUR, Céline ULg et al

in OCC2015 (2015, June)

Detailed reference viewed: 19 (5 ULg)
Full Text
See detailOxidative stress status in top soccer players
Pincemail, Joël ULg; Bonjean, K.; Cayeux, C. et al

in Free Radical Biology & Medicine (2002), 33(Suppl. 1), 249-249

Detailed reference viewed: 8 (2 ULg)
Peer Reviewed
See detailOxidative stress which occurs during chorioamnionitis induces production of prostaglandins by uterus
Temma-Asano, Kumiko; Shimoya, Koichiro; Tskitishvili, Ekaterine ULg et al

Poster (2005)

Detailed reference viewed: 24 (0 ULg)
Full Text
Peer Reviewed
See detailOxidative stress-induced S100B protein from placenta and amnion affects soluble Endoglin release from endothelial cells.
Tskitishvili, Ekaterine ULg; Sharentuya, Namuxila; Temma-Asano, Kumiko et al

in Molecular Human Reproduction (2010), 16(3), 188-99

Oxidative stress with elevated intracellular Ca(2+) concentration as well as endothelial dysfunction is a component of pre-eclampsia. Our aim was to investigate the oxidative stress-dependent expression ... [more ▼]

Oxidative stress with elevated intracellular Ca(2+) concentration as well as endothelial dysfunction is a component of pre-eclampsia. Our aim was to investigate the oxidative stress-dependent expression of Endoglin and Ca(2+)-binding S100B protein from villous and amniotic tissue cultures, and to assess sEng expression from S100B protein-stimulated endothelial cells. We initially examined Endoglin and Hydroxy-nonenal-(HNE)-modified proteins in the placentas and amnion obtained from women with pre-eclampsia (n = 8), and healthy controls (n = 8) by immunohistochemistry. To examine oxidative stress and the S100B protein effect on sEng expression from endothelial cells, normal villous and amniotic tissue cultures were stimulated by 4-HNE, sodium fluoride and xanthine/xanthine oxidase, whereas human umbilical vein endothelial cell cultures were treated with S100B protein in a dose- and time-dependent manner at 37 degrees C in an environment of 95% air and 5% of CO(2). Culture supernatants were assessed using ELISA. Cell viability was determined using MTS assay. The concentrations of sEng and S100B protein were significantly increased in the villous and amniotic tissue culture supernatants under oxidative stress. S100B protein-stimulated endothelial cells released sEng into conditioned media with a significantly higher expression levels at a concentration of 200 pM-20 nM S100B by 2 h, whereas treated with 200 nM of S100B endothelial cells significantly expressed sEng by 12 h and stimulated the cell proliferation by the same period of time. Our findings show that oxidative stress affects sEng and S100B protein expression from villous and amniotic tissues, and picomolar and low nanomolar concentrations of S100B protein significantly up-regulate sEng release from endothelial cells leading to endothelial dysfunction. [less ▲]

Detailed reference viewed: 63 (14 ULg)
Full Text
Peer Reviewed
See detailOxidative stress-mediated iNKT-cell activation is involved in COPD pathogenesis.
Pichavant, M.; Remy, G.; Bekaert, Sandrine ULg et al

in Mucosal Immunology (2013)

Chronic obstructive pulmonary disease (COPD) is a major clinical challenge mostly due to cigarette smoke (CS) exposure. Invariant natural killer T (iNKT) cells are potent immunoregulatory cells that have ... [more ▼]

Chronic obstructive pulmonary disease (COPD) is a major clinical challenge mostly due to cigarette smoke (CS) exposure. Invariant natural killer T (iNKT) cells are potent immunoregulatory cells that have a crucial role in inflammation. In the current study, we investigate the role of iNKT cells in COPD pathogenesis. The frequency of activated NKT cells was found to be increased in peripheral blood of COPD patients relative to controls. In mice chronically exposed to CS, activated iNKT cells accumulated in the lungs and strongly contributed to the pathogenesis. The detrimental role of iNKT cells was confirmed in an acute model of oxidative stress, an effect that depended on interleukin (IL)-17. CS extracts directly activated mouse and human dendritic cells (DC) and airway epithelial cells (AECs) to trigger interferongamma and/or IL-17 production by iNKT cells, an effect ablated by the anti-oxidant N-acetylcystein. In mice, this treatment abrogates iNKT-cell accumulation in the lung and abolished the development of COPD. Together, activation of iNKT cells by oxidative stress in DC and AECs participates in the development of experimental COPD, a finding that might be exploited at a therapeutic level.Mucosal Immunology advance online publication, 30 October 2013; doi:10.1038/mi.2013.75. [less ▲]

Detailed reference viewed: 15 (6 ULg)
Peer Reviewed
See detailOxobenzopyran derivatives as thrombin inhibitors
Bourdel, F.; Lacan, F.; Doucet, C. et al

Poster (2000, September)

Detailed reference viewed: 3 (0 ULg)
Full Text
Peer Reviewed
See detailOxoglutarate translocator of rat-heart mitochondria: regulation by aspartate.
Sluse, Francis ULg; Duyckaerts, Claire ULg; Sluse-Goffart, Claudine et al

in FEBS Letters (1980), 120

Detailed reference viewed: 6 (0 ULg)
Full Text
See detailL'oxydation des poudres: un défi pour l'avenir
Blecker, Christophe ULg

Poster (2014, January 27)

Detailed reference viewed: 7 (1 ULg)
Peer Reviewed
See detailOxydation photochimique de lixiviats de décharge
Deswaef, Sophie; Baidak, Alexandre; Crine, Michel ULg

in Tribune de l'Eau (La) (1997), 590-591

Detailed reference viewed: 42 (4 ULg)
Full Text
Peer Reviewed
See detailOxygen and reactive oxygen species in cartilage degradation: friends or foes?
Henrotin, Yves ULg; Kurz, B.; Aigner, Thomas

in Osteoarthritis and Cartilage (2005), 13(8), 643-54

OBJECTIVES: This review is focused on the influence of oxygen and derived reactive species on chondrocytes aging, metabolic function and chondrogenic phenotype. METHODS: A systematic computer-aided search ... [more ▼]

OBJECTIVES: This review is focused on the influence of oxygen and derived reactive species on chondrocytes aging, metabolic function and chondrogenic phenotype. METHODS: A systematic computer-aided search of the Medline database. RESULTS: Articular cartilage is an avascular tissue, and consequently oxygen supply is reduced. Although the basal metabolic functions of the cells are well adapted to hypoxia, the chondrocyte phenotype seems to be oxygen sensitive. In vitro, hypoxia promotes the expression of the chondrogenic phenotype and cartilage-specific matrix formation, indicating that oxygen tension is probably a key parameter in chondrocyte culture, and particularly in the context of tissue engineering and stem cells transplantation. Besides the influence of oxygen itself, reactive oxygen species (ROS) play a crucial role in the regulation of a number of basic chondrocyte activities such as cell activation, proliferation and matrix remodeling. However, when ROS production exceeds the antioxidant capacities of the cell, an "oxidative stress" occurs leading to structural and functional cartilage damages like cell death and matrix degradation. CONCLUSIONS: This paper is an overview of the in vitro and in vivo studies published on the influence of oxygen and derived reactive species on chondrocyte aging, metabolic function, and the chondrogenic phenotype. It shows, that oxygen and ROS play a crucial role in the control of cartilage homeostasis and that at this time, the exact role of "oxidative stress" in cartilage degradation still remains questionable. [less ▲]

Detailed reference viewed: 9 (0 ULg)
Full Text
Peer Reviewed
See detailOxygen as a critical determinant of bone fracture healing-a multiscale model.
Carlier, Aurelie; Geris, Liesbet ULg; Gastel, Nick Van et al

in Journal of theoretical biology (2015), 365

A timely restoration of the ruptured blood vessel network in order to deliver oxygen and nutrients to the fracture zone is crucial for successful bone healing. Indeed, oxygen plays a key role in the ... [more ▼]

A timely restoration of the ruptured blood vessel network in order to deliver oxygen and nutrients to the fracture zone is crucial for successful bone healing. Indeed, oxygen plays a key role in the aerobic metabolism of cells, in the activity of a myriad of enzymes as well as in the regulation of several (angiogenic) genes. In this paper, a previously developed model of bone fracture healing is further improved with a detailed description of the influence of oxygen on various cellular processes that occur during bone fracture healing. Oxygen ranges of the cell-specific oxygen-dependent processes were established based on the state-of-the art experimental knowledge through a rigorous literature study. The newly developed oxygen model is compared with previously published experimental and in silico results. An extensive sensitivity analysis was also performed on the newly introduced oxygen thresholds, indicating the robustness of the oxygen model. Finally, the oxygen model was applied to the challenging clinical case of a critical sized defect (3mm) where it predicted the formation of a fracture non-union. Further model analyses showed that the harsh hypoxic conditions in the central region of the callus resulted in cell death and disrupted bone healing thereby indicating the importance of a timely vascularization for the successful healing of a large bone defect. In conclusion, this work demonstrates that the oxygen model is a powerful tool to further unravel the complex spatiotemporal interplay of oxygen delivery, diffusion and consumption with the several healing steps, each occurring at distinct, optimal oxygen tensions during the bone repair process. [less ▲]

Detailed reference viewed: 41 (0 ULg)
See detailOxygen budget and associated processes in the regulated Mosel river. Models intercomparison
Garnier, Josette; Billen, Gilles; Schoell, A. et al

in Garnier, Josette; Mouchel, Jean-Marie (Eds.) Man and river systems: the functioning of river systems at the basin scale (2000)

During summer, channelized sectors of the Mosel and Saar rivers undergo severe oxygen depletion episodes that compromise their ecological value. A programme was launched by the International Commission ... [more ▼]

During summer, channelized sectors of the Mosel and Saar rivers undergo severe oxygen depletion episodes that compromise their ecological value. A programme was launched by the International Commission for the Protection of river Mosel and Saar (ICPMS) in order to identify the causes of this situation. All processes involved in the oxygen budget, including photosynthesis, algal, bacterial, zooplanktonic, zoobenthic respiration and nitrification, were investigated, and oxygen budgets for different seasonal situations were established. In close connection with these field investigations, three different mathematical models of the ecological functioning of the river system were implemented: the BfG model of the Saar and Mosel Rivers , the ULg Meuse model, adapted to the river Mosel, and the Mosarel model, resulting from the application to the Mosel-Saar river system of the RIVERSTRAHLER modelling approach We here describe the common features and differences in the conception of these models and present a few examples of their results. [less ▲]

Detailed reference viewed: 11 (3 ULg)
Full Text
See detailOxygen budget and biological processes in the regulated rivers Moselle and Sarre
Everbecq, Etienne ULg; Descy, Jean-Pierre; Gosselain, Véronique

Report (1997)

During summer, channelized sectors of the Mosel and Saar rivers undergo severe oxygen depletion episodes that compromise their ecological value. A programme was launched by the International Commission ... [more ▼]

During summer, channelized sectors of the Mosel and Saar rivers undergo severe oxygen depletion episodes that compromise their ecological value. A programme was launched by the International Commission for the Protection of river Mosel and Saar (ICPMS) in order to identify the causes of this situation. All processes involved in the oxygen budget, including photosynthesis, algal, bacterial, zooplanktonic, zoobenthic respiration and nitrification, were investigated, and oxygen budgets for different seasonal situations were established. In close connection with these field investigations, three different mathematical models of the ecological functioning of the river system were implemented: the BfG model of the Saar and Mosel Rivers , the ULg Meuse model, adapted to the river Mosel, and the Mosarel model, resulting from the application to the Mosel-Saar river system of the RIVERSTRAHLER modelling approach We here describe the ULg Meuse model, and present a few examples of their results. [less ▲]

Detailed reference viewed: 20 (2 ULg)
Full Text
See detailOxygen carriers - Hemoglobin-based solutions
Deby, Ginette ULg; Lamy, Maurice ULg

in Transfusion medicine and alternatives to blood transfusion (2000)

Detailed reference viewed: 14 (0 ULg)
Full Text
Peer Reviewed
See detailOxygen carriers in cardiac surgery
Larbuisson, Robert ULg; Deby, Ginette ULg; Lamy, Maurice ULg

in Transfusion Alternatives in Transfusion Medicine (2005), 7(1), 42-57

Detailed reference viewed: 9 (0 ULg)
Full Text
Peer Reviewed
See detailOxygen consumption and blood oxygen transport in endotoxemic calves
Cambier, Carole ULg; Clerbaux, T.; Detry, B. et al

in Pflügers Archiv : European Journal of Physiology (2004), 447

Detailed reference viewed: 16 (0 ULg)
Full Text
Peer Reviewed
See detailOxygen consumption and electron spin resonance studies of free radical production by alveolar cells exposed to anoxia: inhibiting effects of the antibiotic ceftazidime.
Mouithys-mickalad, A.; Mathy-hartert, M.; Du, G. et al

in Redox Report : Communications in Free Radical Research (2002), 7(2), 85-94

By EPR spectroscopy, we investigated free radical production by cultured human alveolar cells subjected to anoxia/re-oxygenation (A/R), and tested the effects of ceftazidime, an antibiotic previously ... [more ▼]

By EPR spectroscopy, we investigated free radical production by cultured human alveolar cells subjected to anoxia/re-oxygenation (A/R), and tested the effects of ceftazidime, an antibiotic previously demonstrated to possess antioxidant properties. Two A/R models were performed on type II pneumocytes (A549 cell line), either on cells attached to culture dishes (monolayer A/R model; 3.5 h of anoxia, 30 min of re-oxygenation) or after cell detachment (suspension A/R model; 1 h of anoxia, 10 min of re-oxygenation). Ceftazidime and selective inhibitors (SOD, Tiron, L-NMMA) were added before anoxia. Free radical production was assessed by the EPR spin trapping technique. Oxygen consumption was monitored, in parallel with EPR studies, in the suspension A/R model. The production of free radical species was demonstrated by the generation of PBN-radical adducts: (a(N) = 15.2 G) in the monolayer A/R model and a six-line EPR spectrum (a(N) = 15.7 G and a(H) = 2.7 G) in the suspension A/R model. A kinetic study performed by oximetry, in parallel with EPR spectroscopy, demonstrated marked alterations of the cell respiratory function and that the free radical production started during anoxia and increased during re-oxygenation. In the suspension A/R model, the amplitude of EPR spectra were decreased upon the addition of 200 U/ml SOD (37% inhibition), 0.1 mM Tiron (67% inhibition) and 1 mM L-NMMA (43% inhibition). Addition of 1 mM ceftazidime decreased the amplitude of EPR spectra (37% inhibition) in both A/R models. Complementary in vitro EPR studies demonstrated that CAZ scavenged the hydroxyl radical (produced by the Fenton reaction). The protective effect of ceftazidime in the cell model could thus be linked to its ability to scavenge superoxide anions, nitrogen-derived species and hydroxyl radicals. [less ▲]

Detailed reference viewed: 16 (1 ULg)
Full Text
Peer Reviewed
See detailOxygen consumption of equine articular chondrocytes: Influence of applied oxygen tension and glucose concentration during culture.
Schneider, Nicole ULg; Mouithys-Mickalad, Ange ULg; Lejeune, Jean-Philippe ULg et al

in Cell Biology International (2007), 31

We investigated the oxygen (O2) uptake of equine articular chondrocytes to assess their reactions to anoxia/re-oxygenation. They were cultured under 5% or 21% gas phase O2 and at glucose concentrations of ... [more ▼]

We investigated the oxygen (O2) uptake of equine articular chondrocytes to assess their reactions to anoxia/re-oxygenation. They were cultured under 5% or 21% gas phase O2 and at glucose concentrations of 0, 1.0 or 4.5 g/L in the culture medium (n = 3). Afterwards, the O2 consumption rate of the chondrocytes was monitored (oxymetry) before and after an anoxia period of 25 min. The glucose consumption and lactate release were measured at the end of the re-oxygenation period. The chondrocytes showed a minimal O2 consumption rate, which was hardly changed by anoxia. Independently from the O2 tension, glucose uptake by the cells was about 30% of the available culture medium glucose, thus higher for cells at 4.5 g/L glucose (n = 3). Lactate release was also independent from O2 tension, but lower for cells at 4.5 g/L glucose (n = 3). Our observations indicated that O2 consumption by equine chondrocytes was very low despite a functional mitochondrial respiratory chain, and nearly insensitive to anoxia/re-oxygenation. But the chondrocytes metabolism was modified by an excess of O2 and glucose. [less ▲]

Detailed reference viewed: 71 (18 ULg)