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See detailMucociliary function testing in dogs.
Peeters, Dominique ULg; Clercx, Cécile ULg; Mc Entee, Kathleen ULg et al

in Proceedings of the 11th Annual Congress of the ESVIM (2001)

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See detailMucormycose invasive du poumon et du rachis dorsal.
De Pasqual, Aurelie ULg; Deprez, Manuel ULg; Ghaye, Benoît ULg et al

in Revue Médicale de Liège (2008), 63

Nous rapportons le cas d'un patient de 67 ans atteint d'un syndrome myélodysplasique et qui a développé une mucormycose pulmonaire avec extension tout à fait exceptionnelle vers le rachis dorsal ... [more ▼]

Nous rapportons le cas d'un patient de 67 ans atteint d'un syndrome myélodysplasique et qui a développé une mucormycose pulmonaire avec extension tout à fait exceptionnelle vers le rachis dorsal responsable d'un paraplégie aiguë. Après échec d'un traitement probabiliste anti-aspergillaire, c'est finalement l'analyse des prélèvements obtenus lors de la laminectomie décompressive qui a fourni le diagnostic mycologique. En raison d'une altération majeure de l'état général, la lobectomie prévue n'a pu être réalisée et malgré l'adaptation du traitement antifongique (Abelcet, Posaconazole), le patient est décédé. La mucormycose (ou zygomycose) pulmonaire est une infection fongique peu commune qui touche essentiellement les patients immuno-déprimés. Le champignon pathogène fait partie des zygomycètes dont la caractéristique principale est la capacité d'angio-invasion. L'invasion périneurale est une autre voie de propagation récemment mise en évidence. Les difficultés thérapeutiques associées à cette pathologie sont liées au terrain d'immunodépression, aux difficultés d'obtenir rapidement un diagnostic précis ainsi qu'à l'absence de sensibilité du Mucor aux antifongiques récemment introduits (V-Fend, Cancidas). Ceci souligne le risque inhérent à un traitement antifongique empirique par ces agents et la nécessité d'un prélèvement biopsique précoce en cas de non-réponse au traitement. [less ▲]

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See detailMucosal Gene Expression of Antimicrobial Peptides in Inflammatory Bowel Disease Before and After First Infliximab Treatment
Arijs, I.; De Hertogh, G.; Lemaire, K. et al

in PLoS ONE (2009), 4(11), 7984

Background: Antimicrobial peptides (AMPs) protect the host intestinal mucosa against microorganisms. Abnormal expression of defensins was shown in inflammatory bowel disease (IBD), but it is not clear ... [more ▼]

Background: Antimicrobial peptides (AMPs) protect the host intestinal mucosa against microorganisms. Abnormal expression of defensins was shown in inflammatory bowel disease (IBD), but it is not clear whether this is a primary defect. We investigated the impact of anti-inflammatory therapy with infliximab on the mucosal gene expression of AMPs in IBD. Methodology/Principal Findings: Mucosal gene expression of 81 AMPs was assessed in 61 IBD patients before and 4-6 weeks after their first infliximab infusion and in 12 control patients, using Affymetrix arrays. Quantitative real-time reverse-transcription PCR and immunohistochemistry were used to confirm microarray data. The dysregulation of many AMPs in colonic IBD in comparison with control colons was widely restored by infliximab therapy, and only DEFB1 expression remained significantly decreased after therapy in the colonic mucosa of IBD responders to infliximab. In ileal Crohn's disease (CD), expression of two neuropeptides with antimicrobial activity, PYY and CHGB, was significantly decreased before therapy compared to control ileums, and ileal PYY expression remained significantly decreased after therapy in CD responders. Expression of the downregulated AMPs before and after treatment (DEFB1 and PYY) correlated with villin 1 expression, a gut epithelial cell marker, indicating that the decrease is a consequence of epithelial damage. Conclusions/Significance: Our study shows that the dysregulation of AMPs in IBD mucosa is the consequence of inflammation, but may be responsible for perpetuation of inflammation due to ineffective clearance of microorganisms. [less ▲]

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See detailMucosal gene expression of cell adhesion molecules, chemokines, and chemokine receptors in patients with inflammatory bowel disease before and after infliximab treatment.
Arijs, Ingrid; De Hertogh, Gert; Machiels, Kathleen et al

in American Journal of Gastroenterology (2011), 106(4), 748-61

OBJECTIVES: Inflammatory bowel disease (IBD) is characterized by a continuous influx of leukocytes into the gut wall. This migration is regulated by cell adhesion molecules (CAMs), and selective ... [more ▼]

OBJECTIVES: Inflammatory bowel disease (IBD) is characterized by a continuous influx of leukocytes into the gut wall. This migration is regulated by cell adhesion molecules (CAMs), and selective antimigration therapies have been developed. This study investigated the effect of infliximab therapy on the mucosal gene expression of CAMs in IBD. METHODS: Mucosal gene expression of 69 leukocyte/endothelial CAMs and E-cadherin was investigated in 61 IBD patients before and after first infliximab infusion and in 12 normal controls, using Affymetrix gene expression microarrays. Quantitative reverse transcriptase-PCR (qRT-PCR), immunohistochemistry, and western blotting were used to confirm the microarray data. RESULTS: When compared with control colons, the colonic mucosal gene expression of most leukocyte/endothelial adhesion molecules was upregulated and E-cadherin gene expression was downregulated in active colonic IBD (IBDc) before therapy, with no significant colonic gene expression differences between ulcerative colitis and colonic Crohn's disease. Infliximab therapy restored the upregulations of leukocyte CAMs in IBDc responders to infliximab that paralleled the disappearance of the inflammatory cells from the colonic lamina propria. Also, the colonic gene expression of endothelial CAMs and of most chemokines/chemokine receptors returned to normal after therapy in IBDc responders, and only CCL20 and CXCL1-2 expression remained increased after therapy in IBDc responders vs. control colons. When compared with control ileums, the ileal gene expression of MADCAM1, THY1, PECAM1, CCL28, CXCL1, -2, -5, -6, and -11, and IL8 was increased and CD58 expression was decreased in active ileal Crohn's disease (CDi) before therapy, and none of the genes remained dysregulated after therapy in CDi responders vs. control ileums. This microarray study identified a number of interesting targets for antiadhesion therapy including PECAM1, IL8, and CCL20, besides the currently studied alpha4beta7 integrin-MADCAM1 axis. CONCLUSIONS: Our data demonstrate that many leukocyte/endothelial CAMs and chemokines/chemokine receptors are upregulated in inflamed IBD mucosa. Controlling the inflammation with infliximab restores most of these dysregulations in IBD. These results show that at least part of the mechanism of anti-tumor necrosis factor-alpha therapy goes through downregulation of certain adhesion molecules. [less ▲]

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See detailMucosal gene expression profiling differentiates early from late ileal Crohn's disease
Arijs, I; Van Lommel, L; De Hertogh, G et al

in Acta Gastro-Enterologica Belgica (2011)

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See detailMucosal gene expression profiling to predict response to infliximab in patients with ulcerative colitis
Arijs, I.; Van Lommel, L.; Van Steen, Kristel ULg et al

in Gut (2007), 56(Suppl III), 19

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See detailMucosal gene signatures to predict response to infliximab in patients with inflammatory bowel disease
Arijs, I.; Van Lommel, L.; Van Steen, Kristel ULg et al

in Acta Gastro-Enterologica Belgica (2008)

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See detailMucosal gene signatures to predict response to infliximab in patients with inflammatory bowel disease
Arijs, I.; Van Lommel, L.; Van Steen, Kristel ULg et al

in Journal of Crohn’s and Colitis [=JCC] (2008), 2(1), 64

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See detailMucosal gene signatures to predict response to infliximab in patients with inflammatory bowel disease.
Arijs, I.; Van Lommel, L.; Van Steen, Kristel ULg et al

in Gastroenterology (2008), 134

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See detailMucosal gene signatures to predict response to infliximab in patients with ulcerative colitis
Arijs, I.; Li, K.; Toedter, G. et al

in Gut (2009), 58(12), 1612-9

BACKGROUND AND AIMS: Infliximab is an effective treatment for ulcerative colitis with over 60% of patients responding to treatment and up to 30% reaching remission. The mechanism of resistance to anti ... [more ▼]

BACKGROUND AND AIMS: Infliximab is an effective treatment for ulcerative colitis with over 60% of patients responding to treatment and up to 30% reaching remission. The mechanism of resistance to anti-tumour necrosis factor alpha (anti-TNFalpha) is unknown. This study used colonic mucosal gene expression to provide a predictive response signature for infliximab treatment in ulcerative colitis. METHODS: Two cohorts of patients who received their first treatment with infliximab for refractory ulcerative colitis were studied. Response to infliximab was defined as endoscopic and histological healing. Total RNA from pre-treatment colonic mucosal biopsies was analysed with Affymetrix Human Genome U133 Plus 2.0 Arrays. Quantitative RT-PCR was used to confirm microarray data. RESULTS: For predicting response to infliximab treatment, pre-treatment colonic mucosal expression profiles were compared for responders and non-responders. Comparative analysis identified 179 differentially expressed probe sets in cohort A and 361 in cohort B with an overlap of 74 probe sets, representing 53 known genes, between both analyses. Comparative analysis of both cohorts combined, yielded 212 differentially expressed probe sets. The top five differentially expressed genes in a combined analysis of both cohorts were osteoprotegerin, stanniocalcin-1, prostaglandin-endoperoxide synthase 2, interleukin 13 receptor alpha 2 and interleukin 11. All proteins encoded by these genes are involved in the adaptive immune response. These markers separated responders from non-responders with 95% sensitivity and 85% specificity. CONCLUSION: Gene array studies of ulcerative colitis mucosal biopsies identified predictive panels of genes for (non-)response to infliximab. Further study of the pathways involved should allow a better understanding of the mechanisms of resistance to infliximab therapy in ulcerative colitis. ClinicalTrials.gov number, NCT00639821. [less ▲]

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See detailMucosal Healing Predicts Long-term Outcome of Maintenance Therapy with Infliximab in Crohn's Disease
Schnitzler, F.; Fidder, H.; Ferrante, M. et al

in Inflammatory Bowel Diseases (2009), 15(9), 1295-1301

Background: Infliximab (IFX) treatment induces mucosal healing (MH) in patients with Crohn's disease (CD) but the impact of MH oil the long-term outcome of IFX treatment in CID is still debated. Methods ... [more ▼]

Background: Infliximab (IFX) treatment induces mucosal healing (MH) in patients with Crohn's disease (CD) but the impact of MH oil the long-term outcome of IFX treatment in CID is still debated. Methods: We studied MH during long-term treatment with IFX in 214 CID patients. A total of 193 patients (85.5%) responded to induction therapy and 31 patients (14.5%) were primary nonresponders. They underwent lower gastrointestinal (GI) endoscopy within a median of 0.7 months (interquartile range [IQR] 0.1-6.9) prior to first IFX and after a median of 6.7 months (IQR 1.4-24.6) after start of IFX and were further analyzed. The relationship between the outcome of IFX treatment long-term and MH was studied. Results: MH was observed in 67.8% of the 183 initial responders (n = 124), with 83 patients having complete healing (45.4%) and 41 having partial healing (22.4%). Scheduled IFX treatment from the start resulted in MH more frequently (76.9% MH rate) than episodic treatment (61.0% MH rate; P = 0.0222, odds ratio [OR] 2.14, 95% confidence interval [CI] 1.11-4.12). Concomitant treatment with corticosteroids (CS) had a negative impact on MH (37.9% in patients with CS versus 63.2% in patients without CS; P = 0.021, OR 0.36, 95% CI 0.16-0.80). MH was associated with a significantly lower need for major abdominal surgery (MAS) during long-term follow-up (14.1% of patients with MH needed MAS versus 38.4% of patients Without MH: P < 0.0001). Conclusions: MH induced by long-term maintenance IFX treatment is associated with an improved long-term outcome of the I disease especially with a lower need for major abdominal surgeries. [less ▲]

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See detailMucosal junctions: open doors to HPV and HIV infections?
Herfs, Michael ULg; Hubert, Pascale ULg; Moutschen, Michel ULg et al

in Trends in microbiology (2011), 19(3), 114-120

Throughout adult life, new developmental commitment of adult stem cells causes reversible epithelial replacements in various mucosal surfaces, including the uterine cervix and the anal canal. Located at ... [more ▼]

Throughout adult life, new developmental commitment of adult stem cells causes reversible epithelial replacements in various mucosal surfaces, including the uterine cervix and the anal canal. Located at the squamocolumnar junctions, these metaplastic conversions are associated with chronic inflammation and deregulated expression of soluble and cell-membrane factors important for antiviral immune response. In this paper, we propose that these histological and immunological features increase the susceptibility of these metaplastic microenvironments to human papillomavirus and human immunodeficiency virus infections. Identification of the anatomical sites and cell populations within the anogenital tract, which is the site primary infected by these viruses, is crucial for the understanding of the pathogenesis of viral disease and development of antiviral strategies. [less ▲]

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See detailMuddy Mouth : Beckett’s Poetics of Tastelessness
Delville, Michel ULg

in Litteraria Pragensia (2009), 17

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See detail"Muette d'émotion. La Diva recomposée"
Belloi, Livio ULg

Conference (2014, July 04)

Cette communication s'attache à étudier les résurgences de la diva dans le cinéma expérimental contemporain, en particulier dans "Diva Dolorosa" (Peter Delpeut, 1999) et dans "Film ist." (Gustav Deutsch ... [more ▼]

Cette communication s'attache à étudier les résurgences de la diva dans le cinéma expérimental contemporain, en particulier dans "Diva Dolorosa" (Peter Delpeut, 1999) et dans "Film ist." (Gustav Deutsch, 2002). [less ▲]

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