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4. Fatigue is associated with high circulating leptin levels in chronic hepatitis C. (Liver Disease)

Author

Piche, T., Gelsi, E., Schneider, S.M., Hebuterne, X., Giudicelli, J., Ferrua, B., Laffont, C., Benzaken, S., Hastier, P., Montoya, M.L., Longo, F., Rampal, P., and Tran, A.

Subjects
Body composition -- Measurement -- Physiological aspects, Fatigue -- Causes of -- Measurement -- Physiological aspects, Leptin -- Physiological aspects -- Measurement, Hepatitis C -- Physiological aspects -- Measurement, Health
Abstract

Background and aims: Fatigue is a frequent and disabling symptom reported by patients with chronic hepatitis C (CHC). Its mechanism is poorly understood. Recent attention has focused on the role [...]

Published
2002

5. Posters

Author

Török, T., Kardos, A., Rudas, L., Paprika, D., McLuckie, A., Beale, R. J., Bihari, D., Keller, H., Seltzer, N., Weimer, A., Menning, H., Ulrich, P., Staedt, U., Kirschstein, W., Kasai, T., Endo, S., Arakawa, N., Sato, N., Suzuki, T., Taniguchi, S., Inada, K., Hiramori, K., Schmidt, W., Meineke, I., Nottrott, M., Frerichs, I., Müller, S., Hellige, G., De Blasio E., De Sio A., Sibilio G., Papa A., Golia D., Grassia V., Bove G., Zehelgruber, M., Mundigler, G., Christ, G., Merhaut, C., Klaar, U., Kratochwill, C., Hofmann, S., Siostrzonek, P., Suarez, F., Corrales, M., Rábago, R., Gonzalez-Arenas, P., Morales, R., Sanchez J., Fraile, J., Rey, M., Martinell, J., Niederst, P. -N., Mellwig, K. -P., Schmidt, H. K., Gleichmann, U., Körfer, R., Di Bartolomeo, S., Bertolissi, M., Nardi, G., De Monte, A., Janssens, U., Ochs, J. -G., Klues, H. G., Hanrath, P., Sajjanhar, T., Tibby, S. M., Hatherill, M., Anderson, D., Murdoch, I. A., Krivec, B., Voga, G., Žuran, I., Skale, R., Parežnik, R., Podbregar, M., Bonnefoy, E., Chevalier, P., Kirkorian, G., Guidolet, J., Marchand, A., Bouchayer, D., Marcaz, P. Bert, Touboul, P., Welte, T., Molling, J., Jepsen, M. S., Claus, G., Klein, H., Cinnella, G., Dambrosio, M., Brienza, N., Conte, M., Maggiore, S. M., Leone, A. M., Brienza, A., DiVenere, N., Vandewoude, K., Poelaert, J., Vogelaers, D., Garcia, R. Blanca, Buylaert, W., Roosens, C., Colardyn, F., Annane, D., Béllissant, E., Pussard, E., Asmar, R., Lacombe, F., Lanata, E., Madonna, O., Safar, M., Giudicelli, J. F., Raphael, J. C., Gajdos, Ph., Mattys, M., Dumont, L., Annaert, J. F., Mardirosoff, C., Goldstein, J., Verbeet, T., Massaut, J., Haas, N. A., Uhlemann, F., Daehnert, I., Berger, F., Stiller, B., Dittrich, S., Schulze-Neick, I., Eweit, P., Lange, P. E., Langenherp, C. J. M., Pietersen, H., Geskes, G., Wagenmakers, A., Soeters, P., Maggiorini, M., Brimioulle, S., Lejeune, P., Delcroix, M., Vermeulen, F., Stephanazzi, J., Naeije, R., Kunert, M., Stolzenburg, H., Scheuble, L., Emmerich, K., Ulbricht, L. J., Krakau, I., Gülker, H., Broch, M. J., Valentín, V., Murcia, B., Bartual, E., Málaga, A., Miralles, L. L., Valls, F., Wallin, C. J., Sidenö, B., Vaage, J., Leksell, L. G., Stuchlinger, H. G., Seidler, D., Hollenstein, U., Janata, K., Muellner, M., Loeffler, W., Gamper, G., Bur, A., Malzer, R., Laggner, A. N., Hirschl, M. M., Binder, M., Herkner, H., Bur, A., Laggner, A. N., Turani, F., Ceraso, C., Lironcurti, A., Senesi, P., Leonardis, C., Sabato, A. F., Pietersen H. G., Langenberg C. J. M., Geskes G., Wagenmakers A. J. M., de Lange S., Soeters P. B., Royira, A., Oussedik, L., Cambray, C., Glmeno, C., Cerda, M., Sanchez, Ma. A., Lesmes, A., Guerrero, M., Vigil, E., Ortega, F., Lucena, F., Righini, E. R., Alvisi, R., Marangoni, E., Gritti, G., Ordóñez, A., Hernández, A., Pérez-Bernal, J., Hinojosa, R., Borrego, J. M., Franco, A., López-Barneo, J., Pérez-Bernal, J., Gutiérrez, E., Hinojosa, R., Hernández, A., Borrego, J. M., Cerro, J., Rincón, D., Ordóñez, A., Martin, R., Saussine, M., Sany, C. L., Calvet, B., Raison, D., Frapier, J. M., Wallin, C. -J., Olsson, Å., Nordländer, R., Leksell, L. G., Vasilkov, V., Safronov, A., Marinchev, V., Rodrigues, A. C., Moraes, A., Galas, F., Angelim, V., Medeiros, C., Auler, J. O., Bellotti, G., Pilleggi, F., Carmona, M. J., Messias, E. R. R., Joseph, D., Baigorri, F., Artigas, A., Blanch, L., Wagner, F., Dandel, M., Günther, G., Schulze-Neick, I., Weng, Y., Loebe, M., Hetzer, R., Colreavy, F., Balea, M., Cahalan, M., Carpintero, JL., de la Fuente, M. C., Estecha, M. A., Molina, J. M., del Fresno, L. R., Daga, D., Toro, R., Poullet, A., de la Torre, M. V., Garcia, A. J., Michalopoulos, A., Rellos, K., Skambas, D., Liakopoulos, O., and Geroulanos, S.

Published
1996
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13. Surfing the insulin signaling web

Author

Van Obberghen, E., Baron, V., Delahaye, L., Emanuelli, B., Filippa, N., Giorgetti-Peraldi, S., Lebrun, P., Mothe-Satney, I., Peraldi, P., Rocchi, S., Sawka-Verhelle, D., Tartare-Deckert, S., and Giudicelli, J.

Published
2001

20. Induction of apoptosis using sphingolipids activates a chloride current in Xenopus laevis oocytes

Author

SOUKTANI, R., BERDEAUX, A., GHALEH, B., GIUDICELLI, J. F., GUIZE, L., LE HEUZEY, J. Y., and HENRY, P.

Subjects
Cell death -- Physiological aspects, Sphingolipids -- Physiological aspects, Xenopus -- Physiological aspects, Protein kinases -- Physiological aspects, Chloride channels -- Physiological aspects, DNA -- Research, Biological sciences
Abstract

Induction of apoptosis using sphingolipids activates a chloride current in Xenopus laevis oocytes. Am J Physiol Cell Physiol 279: C158-C165, 2000.--The purpose of this study was to investigate whether the cell shrinkage that occurs during apoptosis could be explained by a change of the activity in ion transport pathways. We tested whether sphingolipids, which are potent pro-apoptotic compounds, can activate ionic currents in Xenopus laevis oocytes. Apoptosis was characterized in our model by a decrease in cell volume, a loss of cell viability, and DNA cleavage. Oocytes were studied using voltage-clamp after injection with N,N-dimethyl-D-erythro-sphingosine (DMS) or D-sphingosine (DS). DMS and DS activated a fast-activating, slowly inactivating, outwardly rectifying current, similar to [I.sub.Cl-swell], a swelling-induced chloride current. Lowering the extracellular chloride dramatically reduced the current, and the channel was more selective for thiocyanate and iodide (thiocyanate [is greater than] iodide) than for chloride. The current was blocked by 5-nitro-2-(3-phenyl-propylamino)-benzoic acid (NPPB) and lanthanum but not by niflumic acid. Oocytes injected with a pseudosubstrate inhibitor of protein kinase C (PKC), PKC-(19-31), exhibited the same current. DMS-activated current was abolished by pre-exposure with phorbol myristate acetate. Our results suggest that induction of apoptosis in X. laevis oocytes, using sphingolipids or PKC inhibitors, activates a current similar to swelling-induced chloride current previously described in oocytes. cell shrinkage; swelling-induced chloride channel; protein kinase C; deoxyribonucleic acid fragmentation

Published
2000

34. Cloning and biochemical characterization of a class A beta-lactamase from Prevotella intermedia

Author

Prêcheur, Isabelle, Madinier, I., Fosse, T., Giudicelli, J., Labia, R., Microbiologie Orale, Immunothérapie et Santé (MICORALIS), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA), Microbiologie : Risques Infectieux, Université de Rennes (UR)-CHU Pontchaillou [Rennes]-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )-Université de Rennes - UFR d'Odontologie (UR Odontologie), and Université de Rennes (UR)-Université de Rennes (UR)

Subjects
DNA, Bacterial, [SDV]Life Sciences [q-bio], Molecular Sequence Data, Microbial Sensitivity Tests, Biology, Molecular cloning, Polymerase Chain Reaction, Prevotella intermedia, beta-Lactamases, Mechanisms of Resistance, Bacteroides, Humans, Pharmacology (medical), Amino Acid Sequence, Cloning, Molecular, Gene, Peptide sequence, Letter to the Editor, Antibacterial agent, DNA Primers, Pharmacology, Genetics, Cloning, Sequence Homology, Amino Acid, Structural gene, food and beverages, biology.organism_classification, Molecular biology, Infectious Diseases
Abstract

The gene encoding a β-lactamase of Prevotella intermedia was cloned and sequenced. This gene, called cfxA2 , shared 98% identity with cfxA , the structural gene of a β-lactamase previously described in Bacteroides vulgatus . The deduced protein sequence had a K272E substitution. CfxA2 had the characteristics of class A, group 2e β-lactamases.

Published
2001

36. Rat liver injury following normothermic ischemia is prevented by a phosphinic matrix metalloproteinase inhibitor

Author

Cursio, R Mari, B Louis, K Rostagno, P Saint-Paul, MC and Giudicelli, J Bottero, V Anglard, P Yiotakis, A and Dive, V Gugenheim, J Auberger, P

Abstract

Hepatic ischemia occurs in liver transplantation, hemodynamic or cardiogenic shock, and liver resection associated with trauma or tumor. Ischemia/reperfusion (I/R) injury results in microcirculation failure followed by apoptosis and necrosis. Matrix metalloproteinases (MMPs) are involved in many physiological and pathological processes, but their expression and function during liver I/R remains poorly documented. In this study, we evaluated the expression of nine MMPs and their natural inhibitors, tissue inhibitors of MMPs (TIMPs), in a rat model of liver I/R. Analysis of MMP and TIMP expression show that although most of these genes are not constitutively expressed in the normal liver, they are induced in a specific time-dependent manner following I/R. Stromelysin-1, gelatinase B, and collagenase-3 are induced during the early phase of acute liver injury associated with inflammation and increased necrosis/apoptosis, whereas gelatinase A, membrane type-MMP, stromelysin-3, metalloelastase, TIMP-1, and TIMP-2 are essentially detectable during the recovery phase of liver injury corresponding to hepatocyte regeneration. This observation suggested that MMPs and TIMPs could play both deleterious and beneficial roles following I/R. We thus tested the effect of a specific phosphinic MMP inhibitor on acute liver I/R injury. Inhibition of MMP activity was shown to significantly decrease liver injury in ischemic/reperfused liver tissue as assessed by histological studies and serum hepatic enzyme levels. We therefore propose that MMP inhibitors may be of clinical relevance in liver-associated ischemic diseases or after liver transplantation.

Published
2001

37. Effects of the angiotensin type I receptor antagonist, losartan, on systemic and regional vascular responses to lower body negative pressure in healthy volunteers

Author

Duranteau, J, Pussard, E, Berdeaux, A, and Giudicelli, J F

Subjects
Adult, Lower Body Negative Pressure, Male, Biphenyl Compounds, Hemodynamics, Imidazoles, Tetrazoles, Baroreflex, Losartan, Renal Circulation, Angiotensin Receptor Antagonists, Forearm, Double-Blind Method, Vasoconstriction, Humans, Splanchnic Circulation, Research Article
Abstract

1. The effects of a single oral dose (50 mg) of the angiotensin II AT1-receptor antagonist, losartan, on the systemic and regional vascular responses to simulated orthostatic stress by the lower body negative pressure (LBNP) technique were investigated in nine healthy volunteers, in a double-blind, placebo-controlled crossover study. 2. Arterial blood pressure remained unchanged throughout the study. Three hours after its administration and before LBNP, losartan selectively increased renal blood flow (PAH clearance) by 8.3% (3.5 to 13.1%, 95% CI) from 1.25 +/- 0.08 l min-1 (P < 0.05) and decreased plasma aldosterone levels by 58% (29 to 87%, 95% CI) from 22 +/- 3 ng 100 ml-1 (P < 0.05). 3. LBNP at -10 and -20 mm Hg induced a progressive and significant decrease in central venous pressure and increases in forearm (plethysmography) and splanchnic (indocyanine green clearance) vascular resistances which were similar after losartan and placebo administrations. Losartan blunted the LBNP-induced increase in renal vascular resistance observed at -20 mm Hg after placebo but a similar increase in glomerular filtration rate (inulin clearance) was observed at LBNP -10 and -20 mm Hg after losartan and placebo. Calculated filtration fraction increased after placebo (LBNP -10 mm Hg) and losartan (LBNP -20 mm Hg). Finally, LBNP-induced changes in biological parameters were similar after losartan and placebo at all levels of LBNP. 4. Thus, losartan does not interfere with the adaptive forearm and splanchnic vascular responses and preserves renal haemodynamics during orthostatic stress simulated by LBNP in healthy volunteers.

Published
1995

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