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See detailEl niño azul
Bauchau, Henry; Willson, Patricia ULg; García, Hilda H.

Book published by Del Estante (2006)

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See detailLes Niños pendant la guerre civile espagnole, déplacements et placements (Le cas de la Belgique)
Molina Marmol, Maïté ULg

in Témoigner entre Histoire et Mémoire : Revue Pluridisciplinaire de la Fondation Auschwitz (2011), 110

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See detailNIR AND RAMAN SPECTROSCOPY AS PAT TOOLS FOR THE MANUFACTURING OF SILICONE-BASED DRUG RESERVOIRS
Mantanus, Jérôme ULg; Ziemons, Eric ULg; Van Butsele, Kathy et al

Conference (2010, September 24)

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See detailNIR interferometric observations of massive hierarchical triple systems: Tr16-104 and HD150136
Gosset, Eric ULg; Le Bouquin, Jean-Baptiste; Absil, Olivier ULg et al

in de Grijs, Richard (Ed.) Binary Systems: their Evolution and Environments (2014, September)

We report on an observational astrometric study of the orbit of the tertiary stars in two massive hierarchical triple systems. The work is complemented by radial velocity data with the aim of deriving the ... [more ▼]

We report on an observational astrometric study of the orbit of the tertiary stars in two massive hierarchical triple systems. The work is complemented by radial velocity data with the aim of deriving the full 3D orbit and constraints on the orbital planes. This is the first report of the tertiary star's detection for Tr16-104. The work is a natural extension of the search for binaries among massive O-stars. The basic motivation of the study of hierarchical triple systems is the determination of the masses of the individual components and the derivation of the relative orientation of the two orbital planes, with the ultimate aim of understanding the related star formation processes. [less ▲]

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See detailNirad Chaudhuri et V.S. Naipaul: Une identité postcoloniale à la jointure de l'Inde et de l'Angleterre
Munos, Delphine ULg

Master of advanced studies dissertation (2005)

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See detailNIRS for the Determination of Internal Quality of Entire Apples
Sinnaeve, Georges; Pissard, A.; Fernàndez-Pierna, J. A. et al

in NIR-2009 Breaking the Dawn (2009, November)

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See detailNitrated proteins in bronchoalveolar lavage fluid of patients at risk of ventilator-associated bronchopneumonia.
Mathy, Marianne ULg; Damas, Pierre ULg; Nys, Monique ULg et al

in European Respiratory Journal (2000), 16(2), 296-301

The study was designed to identify markers of oxidative injury, related to the nitric oxide derived cascade, in bronchoalveolar lavage (BAL) fluid from intensive care patients suspected of ventilator ... [more ▼]

The study was designed to identify markers of oxidative injury, related to the nitric oxide derived cascade, in bronchoalveolar lavage (BAL) fluid from intensive care patients suspected of ventilator-associated pneumonia (VAP) and/or acute respiratory distress syndrome (ARDS). Thirty-eight patients developing VAP and/or ARDS (VAP/ARDS group) were compared to 20 ventilated patients without VAP/ARDS (control group). Myeloperoxidase (MPO) and elastase, taken as markers of neutrophil activation were measured by enzymatic techniques, and nitrated proteins (NTPs) by an immunological method. The cytotoxicity of the BAL fluid was tested using cultured human epithelial alveolar cells by the release of pre-incorporated 51Cr. Mean NTP concentration and, MPO and elastase activities were different between the VAP/ARDS and control groups (p<0.05 for NTPs; p<0.005 for MPO; p<0.005 for elastase). NTP concentration correlated with MPO and elastase activity and neutrophil number (r=0.93, 0.91 and 0.87, respectively), but not to protein concentration and arterial oxygen tension/inspiratory oxygen fraction. The cytotoxicity of BAL correlated with NTP concentration (r=0.92) and MPO activity (r=0.89). It was concluded that the concentrations of nitrated proteins in bronchoalveolar lavage fluid correlated with the oxidant activity of neutrophils and that, bronchoalveolar lavage fluid cytotoxicity was correlated with the nitrated protein concentration and may be mediated by oxidants. [less ▲]

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See detailNitric oxid (NO) down-regulates cytokines and PGE2 production by human chondrocytes
Henrotin, Yves ULg; Zheng, SX; Deby, G et al

in Revue du Rhumatisme (English ed.) (1998), 11

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See detailNitric oxide "at heart": emerging paradigms after a decade.
Pelat, M.; MASSION, Paul ULg; Balligand, J. L.

in Archives des Maladies du Coeur et des Vaisseaux (2005), 98(3), 242-8

Despite the apparent redundancy of NOS isoforms in the myocardium, subcellular compartmentation dictates specific NO signaling from each isoform to colocalized effectors in response to physical (e.g ... [more ▼]

Despite the apparent redundancy of NOS isoforms in the myocardium, subcellular compartmentation dictates specific NO signaling from each isoform to colocalized effectors in response to physical (e.g. stretch) or receptor-mediated stimuli. Genetic deletion or overexpression experiments helped to characterize each isoform's respective role in the normal or diseased heart. eNOS and nNOS both contribute to sustain normal EC coupling and contribute to the early and late phases of the Frank-Starling mechanism of the heart. They also negatively modulate the beta1-/beta2-adrenergic increase in inotropy and chronotropy, and reinforce the (pre- and post-synaptic) vagal control of cardiac contraction, thereby protecting the heart against excessive stimulation by catecholamines. In the ischemic and failing myocardium, iNOS expression is induced and further contributes to attenuate the inotropic effect of catecholamines, as does eNOS coupled to overexpressed beta3-adrenoceptors. nNOS expression also increases in the aging and ischemic heart, but its role (compensatory or deleterious) remains to be defined. Many drugs currently used for the treatment of ischemic or failing cardiac diseases also activate and/or upregulate eNOS in the myocardium, which supports its proposed protective role, e.g. as "endogenous beta-blocker". Future pharmacologic modulation of the cardiac NOS will have to take into account their specific modulation of the various aspects of cardiac function, if one hopes to deliver more targeted and efficient therapy than currently achieved with exogenous NO donors. [less ▲]

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See detailNitric oxide and cardiac function: ten years after, and continuing.
MASSION, Paul ULg; Feron, O.; Dessy, C. et al

in Circulation Research (2003), 93(5), 388-98

Nitric oxide (NO) is produced from virtually all cell types composing the myocardium and regulates cardiac function through both vascular-dependent and -independent effects. The former include regulation ... [more ▼]

Nitric oxide (NO) is produced from virtually all cell types composing the myocardium and regulates cardiac function through both vascular-dependent and -independent effects. The former include regulation of coronary vessel tone, thrombogenicity, and proliferative and inflammatory properties as well as cellular cross-talk supporting angiogenesis. The latter comprise the direct effects of NO on several aspects of cardiomyocyte contractility, from the fine regulation of excitation-contraction coupling to modulation of (presynaptic and postsynaptic) autonomic signaling and mitochondrial respiration. This multifaceted involvement of NO in cardiac physiology is supported by a tight molecular regulation of the three NO synthases, from cellular spatial confinement to posttranslational allosteric modulation by specific interacting proteins, acting in concert to restrict the influence of NO to a particular intracellular target in a stimulus-specific manner. Loss of this specificity, such as produced on excessive NO delivery from inflammatory cells (or cytokine-stimulated cardiomyocytes themselves), may result in profound cellular disturbances leading to heart failure. Future therapeutic manipulations of cardiac NO synthesis will necessarily draw on additional characterization of the cellular and molecular determinants for the net effect of this versatile radical on the cardiomyocyte biology. [less ▲]

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See detailNitric oxide and the heart: update on new paradigms.
Belge, C.; MASSION, Paul ULg; Pelat, M. et al

in Annals of the New York Academy of Sciences (2005), 1047

The role of nitric oxide (NO) as a regulator of cardiac contraction was suggested in the early nineties, but a consensual view of its main functions in cardiac physiology has only recently emerged with ... [more ▼]

The role of nitric oxide (NO) as a regulator of cardiac contraction was suggested in the early nineties, but a consensual view of its main functions in cardiac physiology has only recently emerged with the help of experiments using genetic deletion or overexpression of the three nitric oxide synthase (NOS) isoforms in cardiomyocytes. Contrary to the effects of exogenous, pharmacologic NO donors, signaling by endogenous NO is restricted to intracellular effectors co-localized with NOS in specific subcellular compartments. This both ensures coordinate signaling by the three NOS isoforms on different aspects of the cardiomyocyte function and helps to reconcile previous apparently contradictory observations based on the use of non-isoform-specific NOS inhibitors. This review will emphasize the role of NOS on excitation-contraction coupling in the normal and diseased heart. Endothelial NOS and neuronal NOS contribute to maintain an adequate balance between adrenergic and vagal input to the myocardium and participate in the early and late phases of the Frank-Starling adaptation of the heart. At the early phases of cardiac diseases, inducible NOS reinforces these effects, which may become maladaptive as disease progresses. [less ▲]

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See detailNitric Oxide Downregulates Interleukin 1β (IL-1β) Stimulated IL-6, IL-8, and Prostaglandin E2 Production by Human Chondrocytes
Henrotin, Yves ULg; Zheng, S. X.; Deby, G. P. et al

in Journal of Rheumatology (1998), 25(8), 1595-601

OBJECTIVE: To investigate the effects of endogenously produced nitric oxide (NO) on interleukin 6 (IL-6), IL-8, prostaglandin E2 (PGE2), and proteoglycan production by human chondrocytes. METHODS: Human ... [more ▼]

OBJECTIVE: To investigate the effects of endogenously produced nitric oxide (NO) on interleukin 6 (IL-6), IL-8, prostaglandin E2 (PGE2), and proteoglycan production by human chondrocytes. METHODS: Human articular chondrocytes were isolated from their extracellular matrix by triple successive enzymatic digestion of the cartilage and cultured 48 h in a well defined culture medium. IL-6 and IL-8 were directly assayed into culture media by specific enzyme amplified sensitivity immunoassays. Proteoglycans and PGE2 were quantified by specific radioimmunoassays. Cell culture media were assayed for NO2 using a spectrophotometric assay based upon the Griess reaction. RESULTS: Unstimulated chondrocytes produced low levels of NO, IL-6, IL-8, and PGE2. Production was significantly stimulated by IL-1beta and lipopolysaccharide (LPS). As well, proteoglycan synthesis was profoundly inhibited by IL-1beta and LPS. Inhibition of NO synthesis with the competitive inhibitor NG-monomethyl-L-arginine (L-NMMA) led to enhancement of IL-6, IL-8, and PGE2 production stimulated by either IL-1beta alone or in combination with LPS, whereas the inhibition of proteoglycan production by IL-1beta was not modified by L-NMMA. CONCLUSION: LPS and IL-1beta stimulated IL-6, IL-8, and PGE2 production are downregulated by endogenously produced NO, which could limit the inflammatory reaction occurring in arthritis. [less ▲]

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See detailNitric oxide-related products and myeloperoxidase in bronchoalveolar lavage fluids from patients with ALI activate NF-kappa B in alveolar cells and monocytes.
Nys, Monique ULg; Preiser, Jean-Charles ULg; Deby, Ginette ULg et al

in Vascular Pharmacology (2005), 43(6), 425-33

An increased production of NO* and peroxynitrite in lungs has been suspected during acute lung injury (ALI) in humans, and recent studies provided evidence for an alveolar production of nitrated compounds ... [more ▼]

An increased production of NO* and peroxynitrite in lungs has been suspected during acute lung injury (ALI) in humans, and recent studies provided evidence for an alveolar production of nitrated compounds. We observed increased concentrations of nitrites/nitrates, nitrated proteins and markers of neutrophil degranulation (myeloperoxidase, elastase and lactoferrine) in the fluids recovered from bronchoalveolar lavage fluids (BALF) of patients with ALI and correlated these changes to the number of neutrophils and the severity of the ALI. We also observed that BALFs stimulated the DNA-binding activity of the nuclear transcription factor kappa B (NF-kappaB) as detected by electrophoretic mobility shift assay in human alveolar cells (A549) and monocytes (THP1). The level of activation of the NF-kappaB-binding activity was correlated to the concentration of nitrated proteins and myeloperoxidase. Furthermore, in vitro studies confirmed that NO*-derived species (peroxynitrite and nitrites) and the neutrophil enzyme myeloperoxidase by themselves increased the activation of NF-kappaB, thereby arguing for an in vivo pathogenetic role of NO*-related products and neutrophil enzymes to human ALI. [less ▲]

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See detailNitric oxide: a new messenger in the brain.
Bruhwyler, J.; Chleide, E.; Liégeois, Jean-François ULg et al

in Neuroscience & Biobehavioral Reviews (1993), 17(4), 373-84

The important role played by nitric oxide (NO) in the central nervous system has largely been emphasized in the recent literature. It can originate at least from four different sources: the endothelium of ... [more ▼]

The important role played by nitric oxide (NO) in the central nervous system has largely been emphasized in the recent literature. It can originate at least from four different sources: the endothelium of cerebral vessels, the immunostimulated microglia and astrocytes, the nonadrenergic noncholinergic nerve, and the glutamate neuron. NO has been implicated in a large number of pathologies (such as neurotoxicity in Alzheimer's disease and Huntington's disease, cerebral ischemia, stroke, and anxiety) and also in normal physiological functions (such as memory and learning, regulation of the cerebrovascular system, modulation of the wakefulness, mediation of nociception, olfaction, food intake and drinking, regulation of noradrenaline, and dopamine release). The aim of this paper is to review and to integrate the most recent advances in our understanding of the roles of NO in the brain. [less ▲]

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See detailNitric oxide: does it play a role in the heart of the critically ill?
MASSION, Paul ULg; Moniotte, S.; Balligand, J. L.

in Current Opinion in Critical Care (2001), 7(5), 323-36

Nitric oxide regulates many aspects of myocardial function, not only in the normal heart but also in ischemic and nonischemic heart failure, septic cardiomyopathy, cardiac allograft rejection, and ... [more ▼]

Nitric oxide regulates many aspects of myocardial function, not only in the normal heart but also in ischemic and nonischemic heart failure, septic cardiomyopathy, cardiac allograft rejection, and myocarditis. Accumulating evidence implicates the endogenous production of nitric oxide in the regulation of myocardial contractility, distensibility, heart rate, coronary vasodilation, myocardial oxygen consumption, mitochondrial respiration, and apoptosis. The effects of nitric oxide promote left ventricular mechanical efficiency, ie, appropriate matching between cardiac work and myocardial oxygen consumption. Most of these beneficial effects are attributed to the low physiologic concentrations generated by the constitutive endothelial or neuronal nitric oxide synthase. By contrast, inducible nitric oxide synthase generates larger concentrations of nitric oxide over longer periods of time, leading to mostly detrimental effects. In addition, the recently identified beta3-adrenoceptor mediates a negative inotropic effect through coupling to endothelial nitric oxide synthase and is overexpressed in heart failure. An imbalance between beta 1 and beta2-adrenoceptor and beta3-adrenoceptor, with a prevailing influence of beta3-adrenoceptor, may play a causal role in the pathogenesis of cardiac diseases such as terminal heart failure. Likewise, changes in the expression of endothelial nitric oxide synthase or inducible nitric oxide synthase within the myocardium may alter the delicate balance between the effects of nitric oxide produced by either of these isoforms. New treatments such as selective inducible nitric oxide synthase blockade, endothelial nitric oxide synthase promoting therapies, and selective beta3-adrenoceptor modulators may offer promising new therapeutic approaches to optimize the care of critically ill patients according to their stage and specific underlying disease process. [less ▲]

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