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534 results on '"Kouroumalis, Elias A."'

155. Neuropeptide Urocortin and Its Receptors Are Expressed in Rat Kupffer Cells

Author

Charalampopoulos, Ioannis, primary, Androulidaki, Ariadne, additional, Minas, Vassilis, additional, Chatzaki, Ekaterini, additional, Tsatsanis, Chistos, additional, Notas, George, additional, Xidakis, Costas, additional, Kolios, George, additional, Kouroumalis, Elias, additional, Margioris, Andrew N., additional, and Gravanis, Achille, additional

Published
2006
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191. Hyperhomocysteinemia in greek patients with inflammatory bowel disease

Author

Koutroubakis, Ioannis E., primary, Dilaveraki, Evangelia, additional, Vlachonikolis, Ioannis G., additional, Vardas, Emmanouel M., additional, Vrentzos, Georgios, additional, Ganotakis, Emmanouel, additional, Mouzas, Ioannis A., additional, Gravanis, Achileas, additional, Emmanouel, Dimitrios, additional, and Kouroumalis, Elias A., additional

Published
2000
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198. Proinflammatory cytokines induce crosstalk between colonic epithelial cells and subepithelial myofibroblasts: Implication in intestinal fibrosis.

Author

Drygiannakis, Ioannis, Valatas, Vassilis, Sfakianaki, Ourania, Bourikas, Leonidas, Manousou, Pinelopi, Kambas, Konstantinos, Ritis, Konstantinos, Kolios, George, and Kouroumalis, Elias

Subjects
INFLAMMATORY bowel disease treatment, CYTOKINES, INFLAMMATION, EPITHELIAL cells, MYOFIBROBLASTS, COLLAGEN
Abstract

Abstract: Background and aims: Colonic epithelial cells and adjacent subepithelial myofibroblasts are important counterparts in the pathogenesis of intestinal inflammation and fibrosis. We investigated the possible crosstalk between them, whilst focusing on the mucosal inflammation pathways that potentially trigger intestinal fibrosis. Methods: We studied the effects of proinflammatory cytokines (IL-1α, TNF-α, IFN-γ) on human colonic epithelial cell lines and the effects of epithelial cell-conditioned media on primary human colonic subepithelial myofibroblasts isolated from normal controls or patients with inflammatory Crohn''s disease along with the corresponding 18CO cell line. Readouts included production of TGF-β and TIMP-1, total collagen synthesis, matrix metalloproteinases MMP-2 and MMP-9 and myofibroblast migration/mobility. Results: Proinflammatory cytokines upregulated TGF-β and TIMP-1 in colonic epithelial cells. Conditioned medium from these epithelial cell cultures induced production of MMP-9 and collagen and inhibited the migration/mobility of subepithelial myofibroblasts. MMP-9 production depended on endothelin receptor A signalling on responding myofibroblasts. Collagen up-regulation was independent of TGF-β, CTGF, TF and endothelin. Subepithelial myofibroblasts isolated from Crohn''s disease patients had similar responses to those isolated from normal controls, with the exception of higher basal collagen production. Conclusions: Our study indicates that colonic epithelial cells may respond to an inflammatory milieu by inducing myofibroblast functions similar to those observed during intestinal fibrosis. [Copyright &y& Elsevier]

Published
2013
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199. Increased Fracture Risk Assessed by Fracture Risk Assessment Tool in Greek Patients with Crohn's Disease.

Author

Terzoudis, Sotirios, Zavos, Christos, Damilakis, John, Neratzoulakis, John, Dimitriadi, Daphne, Roussomoustakaki, Maria, Kouroumalis, Elias, and Koutroubakis, Ioannis

Subjects
CROHN'S disease, BONE density, INFLAMMATORY bowel diseases, OSTEOPOROSIS, ULCERATIVE colitis, DUAL-energy X-ray absorptiometry, PATIENTS
Abstract

Background: The World Health Organization has recently developed the Fracture Risk Assessment Tool (FRAX) based on clinical risk factors and bone mineral density (BMD) for evaluation of the 10-year probability of a hip or a major osteoporotic fracture. The aim of this study was to evaluate the use of the FRAX tool in Greek patients with inflammatory bowel disease (IBD). Methods: FRAX scores were applied to 134 IBD patients [68 Crohn's disease (CD); 66 ulcerative colitis (UC)] who underwent dual-energy X-ray absorptiometry scans at the femoral neck and lumbar spine during the period 2007-2012. Calculation of the FRAX scores, with or without BMD, was made through a web-based probability model used to compute individual fracture probabilities according to specific clinical risk factors. Results: The median 10-year probability of a major osteoporotic fracture for IBD patients based on clinical data was 7.1 %, and including the BMD was 6.2 %. A significant overestimation with the first method was found ( P = 0.01). Both scores with and without BMD were significantly higher in CD patients compared with UC patients ( P = 0.02 and P = 0.005, respectively). The median 10-year probability of hip fracture based on clinical data was 0.8 %, and including the BMD was 0.9 %. The score with use of BMD was significantly higher in CD compared with UC patients ( P = 0.04). Conclusions: CD patients have significantly higher FRAX scores and possibly fracture risk compared with UC patients. The clinical FRAX score alone seems to overestimate the risk of osteoporotic fracture in Greek IBD patients. [ABSTRACT FROM AUTHOR]

Published
2013
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200. Increased serum activin-A differentiates alcoholic from cirrhosis of other aetiologies.

Author

Voumvouraki, Argyro, Notas, George, Koulentaki, Mairi, Georgiadou, Maria, Klironomos, Stefanos, and Kouroumalis, Elias

Subjects
FIBROSIS, CELL differentiation, LIVER diseases, ACTIVIN, LIVER cancer
Abstract

Eur J Clin Invest 2012 Abstract Background Activin-A is a molecule of the TGF superfamily, implicated in liver fibrosis, regeneration and stem cell differentiation. However, data on activins in liver diseases are few. We therefore studied serum levels of activin-A in chronic liver diseases. To identify the origin of activin-A, levels in the hepatic vein were also estimated. Materials and methods Nineteen controls and 162 patients participated in the study: 39 with hepatocellular carcinoma (HCC: 19 viral associated and 20 alcohol associated), 18 with chronic hepatitis C (CHC), 47 with primary biliary cirrhosis (26 PBC stage I-II and 21 stage IV), 22 with alcoholic cirrhosis (AC, hepatic vein blood available in 16), 20 with HCV cirrhosis (hepatic vein blood available in 18) and 16 patients with alcoholic fatty liver with mild to moderate fibrosis but no cirrhosis. Results Activin-A levels were significantly increased ( P < 0·001) in serum of patients with AC (median 673 pg/mL, range 449-3279), compared with either controls (149 pg/mL, 91-193) or patients with viral cirrhosis (189 pg/mL, 81-480), CHC (142 pg/mL, 65-559) PBC stage I-II (100 pg/mL, 59-597) and PBC stage IV (104 pg/mL, 81-579). Only patients with AC-associated HCC had significantly increased levels of activin-A (2403 pg/mL, 1561-7220 pg/mL). Activin-A serum levels could accurately discriminate AC from cirrhosis of other aetiologies and noncirrhotic alcoholic fatty liver with fibrosis. Conclusions Increased serum levels of activin-A only in patients with alcohol-related cirrhosis or HCC suggest a possible role of this molecule in the pathophysiology of AC. Further research is warranted to elucidate its role during the profibrotic process and its possible clinical applications. [ABSTRACT FROM AUTHOR]

Published
2012
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