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
Peer Reviewed
See detailHypothesis testing identification : A new method for bad data analysis in power system state estimation
Mili, Lamine; Van Cutsem, Thierry ULg; Pavella, Mania

in IEEE Transactions on Power Apparatus and Systems (1984), 103

Detailed reference viewed: 8 (0 ULg)
See detailHypothesis Testing in Escherichia coli using Mathematical Modeling
Sauter, T.; Bullinger, Eric ULg; Allgöwer, F. et al

Poster (2001)

Detailed reference viewed: 5 (0 ULg)
See detailHypothyroïdie frustre : à partir de quand traiter?
Beckers, Albert ULg

Scientific conference (1993, December 11)

Detailed reference viewed: 41 (1 ULg)
Full Text
Peer Reviewed
See detailHypothyroïdie infraclinique non auto-immune et statut iodé : étude prospective d'intervention
VALDES SOCIN, Hernan Gonzalo ULg; Tudorescu, A; Lutteri, L et al

in Annales d'Endocrinologie (2013, October), 74

Detailed reference viewed: 25 (4 ULg)
Full Text
Peer Reviewed
See detailL'hypothyroidie subclinique.
Moreau, L.; Beckers, Albert ULg

in Revue Médicale de Liège (1995), 50(4), 171-4

L'hypothiroïdie subclinique associe, chez des patients asymptomatiques, une élévation de la TSH sérique et une hormonologie thyroïdienne dans les limites de la normale. Le traitement de cette pathologie ... [more ▼]

L'hypothiroïdie subclinique associe, chez des patients asymptomatiques, une élévation de la TSH sérique et une hormonologie thyroïdienne dans les limites de la normale. Le traitement de cette pathologie affectant surtout les personnes âgées est justifié par l'existence de troubles du bilan lipidique, de goitres et de perturbations neuropsychologiques. Celui-ci repose sur l'administration de lévothyroxine à dose minimale pour normaliser la TSH [less ▲]

Detailed reference viewed: 72 (1 ULg)
Full Text
Peer Reviewed
See detailHypothyroidism and Major Depression: A Common Executive Dysfunction?
Constant, Eric; Adam, Stéphane ULg; Seron, Xavier et al

in Journal of Clinical & Experimental Neuropsychology : Official Journal of the International Neuropsychological Society (2006), 28(5), 790-807

Little is known about the possible link between the cognitive disorders associated with hypothyroidism and those encountered in depression. This study examines attentional and executive functions as well ... [more ▼]

Little is known about the possible link between the cognitive disorders associated with hypothyroidism and those encountered in depression. This study examines attentional and executive functions as well as the intensity of anxiety and depressive symptoms in hypothyroidism and major depression and the possible link between these symptoms and cognitive disturbances. This study confirms the existence of psychomotor slowing associated with attentional and executive disturbance in major depression as well as in hypothyroidism. However, while depressed subjects manifested a conscious bias with material of negative emotional valence, no such bias was found in the hypothyroid subjects. While the hypothyroid state is accompanied by anxiety/depressive symptoms, it seems that the latter are too discrete for an attentional bias to be observed with material with a negative emotional valence. [less ▲]

Detailed reference viewed: 36 (2 ULg)
Full Text
Peer Reviewed
See detailHypovitaminose D du patient brûlé : une équation à plusieurs inconnues.
ROUSSEAU, Anne-Françoise ULg; LEDOUX, Didier ULg; DAMAS, Pierre ULg et al

in Revue Médicale de Liège (2013), 68(11), 574-578

Detailed reference viewed: 25 (7 ULg)
Full Text
Peer Reviewed
See detailHypovitaminosis D and osteoporosis in burn patients: are the current practices enough ?
ROUSSEAU, Anne-Françoise ULg; LEDOUX, Didier ULg; DAMAS, Pierre ULg et al

in Osteoporosis International (2013), 24(Suppl 1), 377

Detailed reference viewed: 37 (16 ULg)
See detailHypoxia and hypercapnia during incubation of chicken eggs on development and subsequent performance
Decuypere, E.; Onagbesan, O.; De Smit, L. et al

Conference (2006)

Detailed reference viewed: 12 (0 ULg)
Full Text
Peer Reviewed
See detailHypoxia in the Black Sea northwestern shelf: From eutrophication to climatic stressors.
Capet, Arthur ULg; Beckers, Jean-Marie ULg; Grégoire, Marilaure ULg

in 40th CIESM congress proceedings (2013, October)

Abstract The dynamics of seasonal hypoxia, which affects the Black Sea north-western shelf since the mid 1970's until present days, is investigated by means of a 3D biogeochemical model. Comparison of the ... [more ▼]

Abstract The dynamics of seasonal hypoxia, which affects the Black Sea north-western shelf since the mid 1970's until present days, is investigated by means of a 3D biogeochemical model. Comparison of the model results with in -situ data reveals that the phenomenon may have been underestimated after the mid 1990's due to the distribution of observations. We investigate the mechanism of hypoxia at seasonal scale, and identify the main drivers of its interannual variability. While high nutrients discharge caused severe hypoxia in the 1980's, it was sustained in the 1990's by the pool of organic matter accumulated during the previous years in the sediments layer. With an increasing intensity, climatic stressors intensifies the response of hypoxia to nutrient discharge, and affect the seasonal dynamics of hypoxia by extending its temporal scale. [less ▲]

Detailed reference viewed: 15 (1 ULg)
Full Text
Peer Reviewed
See detailHypoxia induces a phase transition within a kinase signaling network in cancer cells
Wei, Wei; Shia, Qihui; Remacle, Françoise ULg et al

in Proc. Natl. Acad. Sci. USA (2013)

Detailed reference viewed: 9 (0 ULg)
Full Text
Peer Reviewed
See detailHypoxia induces protection against etoposide-induced apoptosis: molecular profiling of changes in gene expression and transcription factor activity
Sermeus, Audrey; Cosse, Jean-Philippe ULg; Crespin, Marianne et al

in Molecular Cancer (2008), 7

Background: it is now well established that hypoxia renders tumor cells resistant to radio- but also chemotherapy. However, few elements are currently available as for the mechanisms underlying this ... [more ▼]

Background: it is now well established that hypoxia renders tumor cells resistant to radio- but also chemotherapy. However, few elements are currently available as for the mechanisms underlying this protection. Results: in this study, physiological hypoxia was shown to inhibit apoptosis induced in HepG2 cells by etoposide. Indeed, hypoxia reduced DNA fragmentation, caspase activation and PARP cleavage. The DNA binding activity of 10 transcription factors was followed while the actual transcriptional activity was measured using specific reporter plasmids. Of note is the inhibition of the etoposideinduced activation of p53 under hypoxia. In parallel, data from low density DNA microarrays indicate that the expression of several pro- and anti-apoptotic genes was modified, among which are Bax and Bak whose expression profile paralleled p53 activity. Cluster analysis of data unravels several possible pathways involved in the hypoxia-induced protection against etoposide-induced apoptosis: one of them could be the inhibition of p53 activity under hypoxia since caspase 3 activity parallels Bax and Bak expression profile. Moreover, specific downregulation of HIF-1α by RNA interference significantly enhanced apoptosis under hypoxia possibly by preventing the hypoxia mediated decrease in Bak expression without altering Bax expression. Conclusion: these results are a clear demonstration that hypoxia has a direct protective effect on apoptotic cell death. Moreover, molecular profiling points to putative pathways responsible for tumor growth in challenging environmental conditions and cancer cell resistance to chemotherapeutic agents. [less ▲]

Detailed reference viewed: 13 (0 ULg)
Full Text
Peer Reviewed
See detailHypoxia is not required for human endometrial breakdown or repair in a xenograft model of menstruation.
Coudyzer, Pauline; Lemoine, Pascale; Jordan, Benedicte F. et al

in FASEB journal : official publication of the Federation of American Societies for Experimental Biology (2013), sous presse

Menstrual endometrial breakdown induced by estradiol and progesterone withdrawal is regularly attributed to vasospasm of spiral arteries causing ischemia and hypoxia. We investigated whether hypoxia ... [more ▼]

Menstrual endometrial breakdown induced by estradiol and progesterone withdrawal is regularly attributed to vasospasm of spiral arteries causing ischemia and hypoxia. We investigated whether hypoxia actually occurred in an in vivo model of menstruation. Three complementary approaches were used to look for signs of hypoxia in fragments of human functionalis xenografted to ovariectomized immunodeficient mice bearing pellets-releasing estradiol and progesterone, and then deprived of ovarian steroids. Hormone withdrawal 21 d after grafting induced menstrual breakdown and MMP expression within 4 d. Local partial oxygen pressure (pO2) was measured by electron paramagnetic resonance using implanted lithium phtalocyanine crystals. In mice with hormone maintenance until sacrifice, pO2 was low one week after grafting (14.8+/-3.4 mmHg) but increased twofold from the second week when tissue was largely revascularized. After 3 wk, pO2 was not modified by hormone withdrawal but was slightly increased on hormone reimpregnation 4 d after removal (34.7+/-6.1 mmHg) by comparison with hormone maintenance (27.1+/-8.6 mmHg). These results were confirmed using fluorescence quenching-based OxyLite measurements. In a further search for signs of hypoxia, we did not find significant HIF1-alpha immunostaining, nor pimonidazole adducts after hormone withdrawal. We conclude that hypoxia is not needed to trigger menstrual-like tissue breakdown or repair in human endometrial xenograft.-Coudyzer, P., Lemoine, P., Jordan, B. F., Gallez, B., Galant, C., Nisolle, M., Courtoy, P. J., Henriet, P., and Marbaix, E. Hypoxia is not required for human endometrial breakdown or repair in a xenograft model of menstruation. [less ▲]

Detailed reference viewed: 27 (3 ULg)
Full Text
Peer Reviewed
See detailHypoxia is responsible for soluble vascular endothelial growth factor receptor-1 (VEGFR-1) but not for soluble endoglin induction in villous trophoblast
Munaut, Carine ULg; Lorquet, Sophie ULg; Pequeux, Christel ULg et al

in Human Reproduction (2008), 23(6), 1407-15

BACKGROUND: Pre-eclampsia is a pregnancy disorder characterized by a maternal endothelial cell dysfunction associated with low levels of circulating placental growth factor (PlGF) and increased levels of ... [more ▼]

BACKGROUND: Pre-eclampsia is a pregnancy disorder characterized by a maternal endothelial cell dysfunction associated with low levels of circulating placental growth factor (PlGF) and increased levels of total vascular endothelial growth factor (VEGF), soluble VEGF receptor-1 (sVEGFR-1), and soluble endoglin, a transforming growth factor b1 and 3 coreceptor. Here, we tested the hypothesis that these altered levels of angiogenic cytokines and of the anti-angiogenic soluble forms of cytokine receptors could be the consequence of hypoxia. METHODS: Normal human umbilical vein endothelial cells, immortalized first trimester extravillous trophoblast cells (HTR8/SVneo) and first trimester placental villi explants (8–14 weeks) were used for culture under normoxia (20% O2) or hypoxia (1% O2). Culture media were collected for the measurement of cytokines by enzyme-linked immunosorbent assay. Total RNA was extracted for RT-PCR analysis. RESULTS: Under hypoxia, villous trophoblast expressed higher levels of VEGF, VEGFR-1, sVEGFR-1 and VEGFR-2 mRNAs (P < 0.001), and secreted more VEGF and sVEGFR-1 proteins (P < 0.05). In contrast, PlGF mRNA and protein were decreased in 1% O2 (P < 0.001), whereas endoglin (Eng) was not modulated. Additionally, sVEGFR-1 directly abolished VEGF/PlGF-induced angiogenesis in the rat aortic ring assay. CONCLUSIONS: Our results support the hypotheses that, in pre-eclampsia, (i) overproduction of VEGF family factors by pre-eclamptic placenta is a consequence of induced hypoxia; (ii) overproduction of sVEGFR-1 by hypoxic villous trophoblast accounts for maternal free VEGF depletion; (iii) low circulating level of free PlGF is not only related to sVEGFR-1 overproduction, but also to hypoxia induced mRNA down-regulation; (iv) Eng is not modulated by hypoxia.. [less ▲]

Detailed reference viewed: 54 (12 ULg)
See detailHypoxia promotes resistance to etoposide by regulating p53 stability and c-jun DNA-binding activity
Cosse, Jean-Philippe ULg; Ronvaux, Marie; Ninane, Noelle et al

Conference (2008)

Detailed reference viewed: 3 (0 ULg)
See detailHypoxia promotes resistance to etoposide by regulating p53 stability and c-jun DNA-binding activity
Cosse, Jean-Philippe ULg; Ronvaux, Marie; Ninane, Noelle et al

Poster (2008)

Detailed reference viewed: 3 (0 ULg)
Full Text
Peer Reviewed
See detailHypoxia protects HepG2 cells against etoposide-induced apoptosis VIA a HIF-1-independent pathway
Piret, Jean-Pascal; Cosse, Jean-Philippe ULg; Ninane, Noelle et al

in Experimental Cell Research (2006), 312

Tumor hypoxia has been described to increase the resistance of cancer cells to radiation therapy and chemotherapy. It also supports the invasiveness and metastatic potential of the tumor. However, few ... [more ▼]

Tumor hypoxia has been described to increase the resistance of cancer cells to radiation therapy and chemotherapy. It also supports the invasiveness and metastatic potential of the tumor. However, few data are available on the transduction pathway set up under hypoxia and leading to this resistance against anti-cancer therapies. HIF-1, the main transcription factor activated by hypoxia, has been recently shown to participate to this process although its role as an anti- or a pro-apoptotic protein is still controversy. In this study, we showed that hypoxia protected HepG2 cells against etoposide-induced apoptosis. The effect of hypoxia on cell death was assayed by measuring different parameters of the apoptotic pathway, like DNA fragmentation, caspase activity and PARP-1 cleavage. The possible implication of HIF-1 in the anti-apoptotic role of hypoxia was investigated using HIF-1α siRNA. Our results indicated that HIF-1 is not involved in the hypoxia-induced antiapoptotic pathway. Another transcription factor, AP-1, was studied for its potential role in the hypoxia-induced protection against apoptosis. Specific inhibition of AP-1 decreased the protection effect of hypoxia against etoposide-induced apoptosis. Together, all these data underline that hypoxia could mediate its anti-apoptotic role via different transcription factors depending on the cellular context and pro-apoptotic stimuli. [less ▲]

Detailed reference viewed: 17 (3 ULg)
Full Text
Peer Reviewed
See detailHypoxia-induced activation of HIF-1: role of HIF-1alpha-Hsp90 interaction.
Minet, E.; Mottet, Denis ULg; Michel, G. et al

in FEBS Letters (1999), 460(2), 251-6

The protein chaperone heat shock protein 90 (Hsp90) is a major regulator of different transcription factors such as MyoD, a basic helix loop helix (bHLH) protein, and the bHLH-Per-aryl hydrocarbon nuclear ... [more ▼]

The protein chaperone heat shock protein 90 (Hsp90) is a major regulator of different transcription factors such as MyoD, a basic helix loop helix (bHLH) protein, and the bHLH-Per-aryl hydrocarbon nuclear translocator (ARNT)-Sim (PAS) factors Sim and aryl hydrocarbon receptor (Ahr). The transcription factor hypoxia-inducible factor-1alpha (HIF-1alpha), involved in the response to hypoxia, also belongs to the bHLH-PAS family. This work was aimed to investigate the putative role of Hsp90 in HIF-1 activation by hypoxia. Using a EGFP-HIF-1alpha fusion protein, co-immunoprecipitation experiments evidenced that the chimeric protein expressed in COS-7 cells interacts with Hsp90 in normoxia but not in hypoxia. We also demonstrated that Hsp90 interacts with the bHLH-PAS domain of HIF-1alpha. Moreover, Hsp90 is not co-translocated with HIF-1alpha into the nucleus. At last, we showed that Hsp90 activity is essential for HIF-1 activation in hypoxia since it is inhibited in the presence of geldanamycin. These results indicate that Hsp90 is a major regulator in HIF-1alpha activation. [less ▲]

Detailed reference viewed: 43 (6 ULg)