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See detailDéfi climatique: l'état et le marché
Gautier, Axel ULg

Conference given outside the academic context (2016)

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See detailLe défi de la diversité linguistique des apprenants pour l’apprentissage de la lecture et de l’écriture
Lucchini, Silvia ULg; Flamini, F.; Campolini, L.

in Langues Modernes (2001), (1), 34-41

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See detailLe défi de la santé publique au Rwanda et en République démocratique du Congo.
Porignon, Denis ULg

in Porignon, Denis; et al (Eds.) L’art de la paix : approche transdisciplinaire (2003)

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See detailLE DÉFI DU CONTRÔLE LOCAL DANS LE CANCER PULMONAIRE NON A PETITES CELLULES, LOCALEMENT AVANCE, NON OPERABLE
BARTHELEMY, Nicole ULg; LENNERTS, Evelyne ULg; MEYNS, Mia ULg et al

in Revue Médicale de Liège (2014), 69(Supp 1), 75-80

Le cancer broncho-pulmonaire non à petites cellules (CBNPC) est fréquent. Pour près d’un patient sur cinq, au moment du diagnostic, la maladie est déjà localement avancée et inopérable. A ce stade, le ... [more ▼]

Le cancer broncho-pulmonaire non à petites cellules (CBNPC) est fréquent. Pour près d’un patient sur cinq, au moment du diagnostic, la maladie est déjà localement avancée et inopérable. A ce stade, le pronostic de cette affection est mauvais, caractérisé, entre autres, par un taux élevé de réci - dive locale, malgré la chimiothérapie et la radiothérapie. Le but de cette revue est de décrire l’hétérogénéité de ce groupe de patients, de clarifier les modalités de traitement combinant la chimiothérapie et la radiothérapie et de préciser l’intérêt des techniques modernes de radiothérapie pour améliorer le contrôle local [less ▲]

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See detailLe défi du pluralisme culturel en Europe : le cas de Bruxelles
Martiniello, Marco ULg

Scientific conference (1991, April 05)

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See detailLe défi wallon du FDF
Counet, Maxime ULg; Matagne, Geoffroy ULg; Verjans, Pierre ULg

Learning material (2016)

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See detailDéficience du système glutathion chez le cheval de course
De Moffarts, Brieuc; Kirschvink, N.; Art, Tatiana ULg et al

in 30ème Journée de la Recherche Equine, Les Haras Nationaux (2004)

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See detailLa déficience en hormone de croissance chez l'adulte et son traitement
Beckers, Albert ULg

Scientific conference (1994, February 02)

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See detailLa déficience en hormone de croissance chez l'adulte et son traitement
Moreau, L.; Beckers, Albert ULg

in Médecine et Hygiène (1994), 52(2036), 1660-4

Les adultes déficients en hormone de croissance (GH) décèdent prématurément, principalement à cause de la fréquence élevée des affections cardiovasculaires. Depuis que la GH est produite par les ... [more ▼]

Les adultes déficients en hormone de croissance (GH) décèdent prématurément, principalement à cause de la fréquence élevée des affections cardiovasculaires. Depuis que la GH est produite par les techniques de biologie moléculaire, il est possible de proposer un traitement substitutif. Ce traitement améliore le bilan lipidique, entraîne une redistribution de la graisse d'androïde en gynoïde, une réduction de la masse graisseuse, une augmentation de la masse des tissus maigres et du volume de l'eau extracellulaire. Le poids des patients est légèrement réduit par le traitement substitutif. La masse de muscle strié squelettique est augmentée, ainsi que le contenu osseux (BMC) et la densité osseuse (BMD). La fonction cardiaque et la qualité de vie sont améliorées. [less ▲]

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See detailLa déficience en hormone de croissance chez l'adulte et son traitement
Beckers, Albert ULg

Scientific conference (2001, March 21)

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See detailLa déficience en hormone de croissance chez l'adulte et son traitement
Beckers, Albert ULg

Scientific conference (2001, April 13)

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See detailDéficience sévère en hormone de croissance chez les patients non diabétiques avec un microadénome corticotrope : Effets de la chirurgie hypophysaire et implications thérapeutiques
Valdes Socin, Hernan Gonzalo ULg; Laret, V.; de Fays, C. et al

in XXème Congrès de la Société Française d'Endocrinologie - Abstract book (2002)

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See detailDéficiences hormonales du sujet âgé: faut-il les traiter?
Racaru-Honciuc, Valentina; Betea, Daniela; Scheen, André ULg

in Revue medicale suisse (2014), 10(439), 1555-61558-61

Biological aging is characterized by a progressive loss of the secretion of various hormones, a phenomenon that leads some physicians to propose an anti-aging hormonal therapy. It is mandatory to ... [more ▼]

Biological aging is characterized by a progressive loss of the secretion of various hormones, a phenomenon that leads some physicians to propose an anti-aging hormonal therapy. It is mandatory to differentiate: 1) the physiological functional loss, which is a natural phenomenon without clear deleterious consequences on health and should not be compensated by the administration of hormones only to restore plasma levels similar to those measured in young people and 2) a pathological defect that deserves a replacement therapy to correct the endocrine deficiency and improve the health status of older individuals. This article considers the deficiencies in insulin, thyroid hormones, growth hormone, dehydroepiandrosterone (DHEA) and testosterone. For each hormone, a benefit/risk ratio of a so-called replacement therapy will be analyzed. [less ▲]

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See detailDeficiency in mouse hyaluronidase 2: a new mechanism of chronic thrombotic microangiopathy.
Onclinx, Cecile; Dogne, Sophie; Jadin, Laurence et al

in Haematologica (2015)

Hyaluronan is a major component of the extracellular matrix and glycocalyx. Its main somatic degrading enzymes are the hyaluronidases 1 and 2, none of which is active in the bloodstream. We generated ... [more ▼]

Hyaluronan is a major component of the extracellular matrix and glycocalyx. Its main somatic degrading enzymes are the hyaluronidases 1 and 2, none of which is active in the bloodstream. We generated hyaluronidase 2 deficient mice. They suffer from mild chronic anemia and thrombocytopenia, in parallel with a 10-fold increase in plasma hyaluronan concentration. The current study explores the mechanism of these hematological anomalies. The decreased erythrocyte and platelet counts were assigned to peripheral consumption. The erythrocyte half-life was reduced from 25 to 8 days without signs of premature aging. Hyaluronidase 2 deficient platelets were functional. Major intrinsic defects in erythrocyte membrane or stability, as well as detrimental effects of high hyaluronan levels on erythrocytes, were ruled out in vitro. Normal erythrocytes transfused into hyaluronidase 2 deficient mice were quickly destroyed but neither splenectomy nor anti-C5 administration prevented from chronic hemolysis. Schistocytes were present in hyaluronidase 2 deficient smears at a level of 1 to 6%, while virtually absent in control mice. Hyaluronidase 2 deficient mice had increased markers of endothelial damage and microvascular fibrin deposition, without renal failure, accumulation of ultra-large multimers of von Willebrand factor, deficiency of A Disintegrin And Metalloproteinase with ThromboSpondin type 1 motifs, member 13 (ADAMTS13), or hypertension. There was no sign of structural damage in hepatic or splenic sinusoids, or in any other microvessels. We conclude that hyaluronidase 2 deficiency induces chronic thrombotic microangiopathy with hemolytic anemia in mice. The link between this uncommon condition and hyaluronidase 2 remains to be explored in man. [less ▲]

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See detailDeficiency of Interleukin-1 Receptor-associated Kinase 4 Presenting as Fatal Pseudomonas aeruginosa Bacteremia in Two Siblings.
STERGIOPOULOU, Theodouli ULg; Walsh, Thomas J.; SEGHAYE, Marie-Christine ULg et al

in The Pediatric infectious disease journal (2015), 34(3), 299-300

Interleukin-1 receptor-associated kinase 4 (IRAK-4) deficiency is a primary immunodeficiency of innate immunity. This is the case of a previous healthy toddler and his sibling, who both died of fulminant ... [more ▼]

Interleukin-1 receptor-associated kinase 4 (IRAK-4) deficiency is a primary immunodeficiency of innate immunity. This is the case of a previous healthy toddler and his sibling, who both died of fulminant sepsis due to Pseudomonas aeruginosa. Subsequent genetic analysis demonstrated IRAK-4 deficiency with compound heterozygous splice mutations. Fulminant fatal Pseudomonas aeruginosa sepsis may be the first manifestation of IRAK-4 deficiency. [less ▲]

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See detailDeficiency of tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) impairs nutritionally induced obesity in mice.
Lijnen, Roger; Demeulemeester, Diego; Van Hoef, B. et al

in Thrombosis and Haemostasis (2003), 89(2), 249-255

Tissue inhibitor of matrix metalloproteinase-1 deficient (TIMP-1(-/-)) mice and wild-type (TIMP-1(+/+)) controls were kept on a standard (SFD) or a high fat diet (HFD) for 15 weeks. At the time of ... [more ▼]

Tissue inhibitor of matrix metalloproteinase-1 deficient (TIMP-1(-/-)) mice and wild-type (TIMP-1(+/+)) controls were kept on a standard (SFD) or a high fat diet (HFD) for 15 weeks. At the time of sacrifice, TIMP-1(-/-) mice on HFD had a significantly lower body weight (29 +/- 1.5 versus 41 +/- 1.8 g, p <0.005), and significantly less subcutaneous (0.81 +/- 0.19 versus 1.78 +/- 0.21 g, p <0.05) and gonadal (0.87 +/- 0.17 versus 1.85 +/- 0.18 g, p <0.005) fat mass. These differences were much less pronounced for mice on SFD. On HFD but not on SFD, adipocyte diameters were significantly lower in the adipose tissue of TIMP-1(-/-) mice. Plasma leptin levels in TIMP-1(-/-) mice on HFD were significantly lower as compared to TIMP-1(+/-) mice, and strongly correlated with adipose tissue mass for both genotypes. Staining with an endothelial cell specific lectin revealed a significantly higher blood vessel density, larger stained area and vessel size in adipose tissue of TIMP-1(-/-) mice on HFD. This difference disappeared after normalization to the adipocyte number, suggesting that it does not represent a true enhancement of angiogenesis. Thus, in a murine model of nutritionally induced obesity, TIMP-1 promotes adipose tissue development. [less ▲]

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See detailDeficiency or inhibition of oxygen sensor Phd1 induces hypoxia tolerance by reprogramming basal metabolism.
Aragones, Julian; Schneider, Martin; Van Geyte, Katie et al

in Nature Genetics (2008), 40

HIF prolyl hydroxylases (PHD1-3) are oxygen sensors that regulate the stability of the hypoxia-inducible factors (HIFs) in an oxygen-dependent manner. Here, we show that loss of Phd1 lowers oxygen ... [more ▼]

HIF prolyl hydroxylases (PHD1-3) are oxygen sensors that regulate the stability of the hypoxia-inducible factors (HIFs) in an oxygen-dependent manner. Here, we show that loss of Phd1 lowers oxygen consumption in skeletal muscle by reprogramming glucose metabolism from oxidative to more anaerobic ATP production through activation of a Pparalpha pathway. This metabolic adaptation to oxygen conservation impairs oxidative muscle performance in healthy conditions, but it provides acute protection of myofibers against lethal ischemia. Hypoxia tolerance is not due to HIF-dependent angiogenesis, erythropoiesis or vasodilation, but rather to reduced generation of oxidative stress, which allows Phd1-deficient myofibers to preserve mitochondrial respiration. Hypoxia tolerance relies primarily on Hif-2alpha and was not observed in heterozygous Phd2-deficient or homozygous Phd3-deficient mice. Of medical importance, conditional knockdown of Phd1 also rapidly induces hypoxia tolerance. These findings delineate a new role of Phd1 in hypoxia tolerance and offer new treatment perspectives for disorders characterized by oxidative stress. [less ▲]

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See detailDeficient Habituation of Evoked Cortical Potentials in Migraine: A Link between Brain Biology, Behavior and Trigeminovascular Activation?
Schoenen, Jean ULg

in Biomedicine & Pharmacotherapy (1996), 50(2), 71-8

According to recent evoked potential studies, a fundamental, probably protective, feature of cortical information processing, ie, response habituation during stimulus repetition, is abnormal in migraine ... [more ▼]

According to recent evoked potential studies, a fundamental, probably protective, feature of cortical information processing, ie, response habituation during stimulus repetition, is abnormal in migraine between attacks. The deficient habituation is found for different sensory modalities and experimental paradigms: pattern-reversal visual evoked potentials (same stimulus at a constant intensity), cortical auditory evoked potentials (same stimulus at increasing intensities) and auditory event-related potentials obtained in a passive "oddball" paradigm (novel stimulus). The abnormal information processing is an interictal cortical dysfunction most likely due to inadequate control by the so-called "state-setting, chemically-addressed pathways" originating in the brain stem, in particular by the serotonergic pathway, leading to a low preactivation level of sensory cortices. We suggest that it may play a pivotal role in migraine pathogenesis in conjunction with the reported decrease of brain mitochondrial energy reserve, by favouring a rupture of metabolic homeostasis and biochemical shifts capable of activating the trigeminovascular system and thus capable of producing a migraine attack. We postulate that both the deficient habituation in information processing and the deranged oxygen metabolism may have behavioral correlates. Which of these abnormalities are inherited, acquired or both remains to be determined. [less ▲]

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