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15 results on '"MESH: Drug Tolerance"'

1. Publisher Correction: Definitions and guidelines for research on antibiotic persistence

Author

Balaban, Nathalie, Helaine, Sophie, Lewis, Kim, Ackermann, Martin, Aldridge, Bree, Andersson, Dan, Brynildsen, Mark, Bumann, Dirk, Camilli, Andrew, Collins, James, Dehio, Christoph, Fortune, Sarah, Ghigo, Jean-Marc, Hardt, Wolf-Dietrich, Harms, Alexander, Heinemann, Matthias, Hung, Deborah, Jenal, Urs, Levin, Bruce, Michiels, Jan, Storz, Gisela, Tan, Man-Wah, Tenson, Tanel, Van Melderen, Laurence, Zinkernagel, Annelies, Racah Institute of Physics, The Hebrew University of Jerusalem (HUJ), Medical Research Council Centre for Molecular Bacteriology and Infection [Londres, Royaume-Uni] (MRC CMBI), Imperial College London, Northeastern University [Boston], Institute of Biogeochemistry and Pollutant Dynamics [ETH Zürich] (IBP), Department of Environmental Systems Science [ETH Zürich] (D-USYS), Eidgenössische Technische Hochschule - Swiss Federal Institute of Technology [Zürich] (ETH Zürich)- Eidgenössische Technische Hochschule - Swiss Federal Institute of Technology [Zürich] (ETH Zürich), Swiss Federal Insitute of Aquatic Science and Technology [Dübendorf] (EAWAG), Tufts University School of Medicine [Boston], Uppsala University, Princeton University, Biozentrum [Basel, Suisse], University of Basel (Unibas), Massachusetts Institute of Technology (MIT), Wyss Institute for Biologically Inspired Engineering [Harvard University], Harvard University, Broad Institute of MIT and Harvard (BROAD INSTITUTE), Harvard Medical School [Boston] (HMS)-Massachusetts Institute of Technology (MIT)-Massachusetts General Hospital [Boston], Harvard T.H. Chan School of Public Health, Génétique des Biofilms, Institut Pasteur [Paris] (IP), Eidgenössische Technische Hochschule - Swiss Federal Institute of Technology [Zürich] (ETH Zürich), Institute of Microbiology [Zurich], Groningen Biomolecular Sciences and Biotechnology Institute (GBB), University of Groningen [Groningen], Emory University [Atlanta, GA], VIB-KU Leuven Center for Microbiology [Leuven, Belgium], Catholic University of Leuven - Katholieke Universiteit Leuven (KU Leuven), Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Genentech, Inc. [San Francisco], Institute of technology, University of Tartu, Université libre de Bruxelles (ULB), University hospital of Zurich [Zurich], B.R.L. is funded by the US National Institutes of Health (NIH, R01GM 091875). N.Q.B. is funded by the European Research Council (ERC, 681619)., The authors thank the Congressi Stefano Franscini, the European Molecular Biology Organization (EMBO), the Federation of European Microbiological Societies (FEMS) and the University of Basel for supporting the EMBO Workshop ‘Bacterial Persistence and Antimicrobial Therapy’ and A.-C. Hiebel for taking a major role in its organization. The authors represent the groups attending the workshop but acknowledge the contributions of many other groups in the antibiotic persistence field., Harvard University [Cambridge], Institut Pasteur [Paris], and VIB-KU Leuven Center for Microbiology [Belgium]

Subjects
MESH: Biomedical Research/standards, MESH: Terminology as Topic, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, MESH: Biomedical Research/methods, Antibiotics, MESH: Anti-Bacterial Agents/pharmacology, Antibacterial drug resistance, MESH: Guidelines as Topic, Antimicrobial resistance, Bacterial physiology, MESH: Bacteria/drug effects, MESH: Drug Tolerance
Abstract

Erratum in : Publisher Correction: Definitions and guidelines for research on antibiotic persistence. [Nat Rev Microbiol. 2019] https://doi.org/10.1038/s41579-019-0207-4; International audience; Increasing concerns about the rising rates of antibiotic therapy failure and advances in single-cell analyses have inspired a surge of research into antibiotic persistence. Bacterial persister cells represent a subpopulation of cells that can survive intensive antibiotic treatment without being resistant. Several approaches have emerged to define and measure persistence, and it is now time to agree on the basic definition of persistence and its relation to the other mechanisms by which bacteria survive exposure to bactericidal antibiotic treatments, such as antibiotic resistance, heteroresistance or tolerance. In this Consensus Statement, we provide definitions of persistence phenomena, distinguish between triggered and spontaneous persistence and provide a guide to measuring persistence. Antibiotic persistence is not only an interesting example of non-genetic single-cell heterogeneity, it may also have a role in the failure of antibiotic treatments. Therefore, it is our hope that the guidelines outlined in this article will pave the way for better characterization of antibiotic persistence and for understanding its relevance to clinical outcomes.

Published
2019

2. Glutamate decarboxylase-dependent acid resistance in Brucella spp.: distribution and contribution to fitness under extremely acidic conditions

Author

Maria Alessandra Damiano, Daniela Bastianelli, Daniela De Biase, Alessandra Occhialini, Axel Cloeckaert, Sascha Al Dahouk, Stephan Köhler, Centre d’études d’Agents Pathogènes et Biotechologies pour la Santé (CPBS), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur, Fondation Cenci Bolognetti - Istituto Pasteur Italia, Fondazione Cenci Bolognetti, Réseau International des Instituts Pasteur (RIIP), Sapienza University [Rome], Bundesinstitut für Risikobewertung - Federal Institute for Risk Assessment (BfR), Institut de Recherche en Infectiologie de Montpellier (IRIM), Infectiologie Santé Publique (ISP-311), Université de Tours-Institut National de la Recherche Agronomique (INRA), This work was supported by grant 1329-485 from the Federal Institute for Risk Assessment, Germany (to A.O. and S.K.), and by funding from Sapienza University of Rome and Fondazione Roma (to D.D.B.). Travels and research stays of A.O., D.D.B., M.A.D., and D.B. were supported by the 2011-2012 Galilée program of Egide (Hubert Curien program), no. 25960UE, from the French and Italian Ministry of Foreign and Europeans Affairs. M.A.D. was a recipient was awarded a postdoctoral fellowship from the foundation Infectiopôle Sud, and A.O. was awarded a Congés pour Recherches ou Conversions Thématiques (CRCT) from Montpellier University, We thank E. Bianchini for her participation in genetic constructions of E. coli strains, B. Saadeh for preliminary GABA tests, C. Göllner for GAD tests, P. Bouhours for preparation of bacterial media, and I. Jacques and D. O'Callaghan for their generous gifts of several marine strains and of B. inopinata BO1 and B. inopinata-like BO2 strains, respectively., Università degli Studi di Roma 'La Sapienza' = Sapienza University [Rome], Infectiologie et Santé Publique (UMR ISP), Institut National de la Recherche Agronomique (INRA)-Université de Tours, and Institut National de la Recherche Agronomique (INRA)-Université de Tours (UT)

Subjects
MESH: Acids/toxicity, Glutamate decarboxylase, MESH: Glutamic Acid/metabolism, Gene Expression, medicine.disease_cause, Applied Microbiology and Biotechnology, MESH: Drug Tolerance, Mice, MESH: Animals, Cloning, Molecular, Brucella inopinata, MESH: Glutamate Decarboxylase/metabolism, MESH: Ochrobactrum/drug effects, 0303 health sciences, Rana catesbeiana, Ecology, biology, Glutamate Decarboxylase, MESH: Brucella/enzymology, Drug Tolerance, Phenotype, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, MESH: Acids/metabolism, Biotechnology, MESH: Gene Expression, Glutamic Acid, Brucella pinnipedialis, MESH: Escherichia coli/genetics, Genetics and Molecular Biology, Brucella, Ochrobactrum, Microbiology, 03 medical and health sciences, medicine, MESH: Brucella/drug effects, Escherichia coli, Animals, Humans, MESH: Cloning, Molecular, extreme acid stress, diagnostic phenotypic trait, glutamate-dependent acid resistance, MESH: Mice, 030304 developmental biology, MESH: Humans, MESH: Ochrobactrum/enzymology, 030306 microbiology, biology.organism_classification, bacterial infections and mycoses, MESH: Rana catesbeiana, Brucella ceti, MESH: Brucella/genetics, MESH: Escherichia coli/metabolism, MESH: Brucella/isolation & purification, Acids, Food Science
Abstract

Brucella is an expanding genus of major zoonotic pathogens, including at least 10 genetically very close species occupying a wide range of niches from soil to wildlife, livestock, and humans. Recently, we have shown that in the new species Brucella microti , the glutamate decarboxylase (Gad)-dependent system (GAD system) contributes to survival at a pH of 2.5 and also to infection in mice by the oral route. In order to study the functionality of the GAD system in the genus Brucella , 47 isolates, representative of all known species and strains of this genus, and 16 strains of the closest neighbor genus, Ochrobactrum , were studied using microbiological, biochemical, and genetic approaches. In agreement with the genome sequences, the GAD system of classical species was not functional, unlike that of most strains of Brucella ceti , Brucella pinnipedialis , and newly described species ( B. microti , Brucella inopinata BO1, B. inopinata -like BO2, and Brucella sp. isolated from bullfrogs). In the presence of glutamate, these species were more acid resistant in vitro than classical terrestrial brucellae. Expression in trans of the gad locus from representative Brucella species in the Escherichia coli MG1655 mutant strain lacking the GAD system restored the acid-resistant phenotype. The highly conserved GAD system of the newly described or atypical Brucella species may play an important role in their adaptation to acidic external and host environments. Furthermore, the GAD phenotype was shown to be a useful diagnostic tool to distinguish these latter Brucella strains from Ochrobactrum and from classical terrestrial pathogenic Brucella species, which are GAD negative.

Published
2014

3. Candida albicans biofilms: building a heterogeneous, drug-tolerant environment

Author

Julie Bonhomme, Christophe d'Enfert, Université de Caen Normandie (UNICAEN), Normandie Université (NU), Biologie et Pathogénicité fongiques (BPF), Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris] (IP), We are grateful to members of the Unite´ Biologie et Pathogénicité Fongiques for lively and fruitful discussions on the topics of this review. CdE is supported by grants of the Agence Nationale de la Recherche (KANJI, ANR-08-MIE-033-01, ERA-Net Pathogenomics CANDICOL ANR-10-01), the French Government’s Investissement d’Avenir program, Laboratoire d’Excellence ‘‘Integrative Biology of Emerging Infectious Diseases’’ (ANR-10-LABX-62-IBEID) and the European Commission (FINSysB, PITN-GA-2008-214004). JB was the recipient of a fellowship of the Fondation pour la Recherche Medicale (DEA20080713005)., ANR-08-MIEN-0033,KANJI,Colonisation et invasion de la muqueuse digestive par le champignon pathogène de l'homme Candida albicans(2008), ANR-10-PATH-0008,CANDICOL(2010), ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), European Project: 214004,PEOPLE,FP7-PEOPLE-2007-1-1-ITN,FINSYSB(2008), Biologie et Pathogénicité fongiques, Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris], KANJI, ANR-08-MIE-033-01,KANJI, ANR-08-MIE-033-01,KANJI, ANR-08-MIE-033-01, Candicol ANR-10-01,Candicol,ANR-10-01, ANR-10-LABX-62-IBEID,IBEID,Laboratoire d'Excellence 'Integrative Biology of Emerging Infectious Diseases'(2010), and Institut Pasteur [Paris]-Institut National de la Recherche Agronomique (INRA)

Subjects
Microbiology (medical), Antifungal, Drug, EFG1 REGULATOR, Antifungal Agents, medicine.drug_class, media_common.quotation_subject, MESH: Drug Tolerance, MESH: Biofilms, Microbiology, 03 medical and health sciences, Molecular level, Candida albicans, medicine, ADAPTATION, [SDV.MP.MYC]Life Sciences [q-bio]/Microbiology and Parasitology/Mycology, 030304 developmental biology, media_common, GENE-EXPRESSION, 0303 health sciences, biology, 030306 microbiology, MESH: Candida albicans, Transcriptional Networks, Biofilm, IN-VITRO, PARAPSILOSIS, Drug Tolerance, biochemical phenomena, metabolism, and nutrition, biology.organism_classification, MESH: Antifungal Agents, Infectious Diseases, INFECTIONS, Biofilms, SURVIVAL, Fungal biofilm, MATRIX, RESISTANCE
Abstract

International audience; Fungi are able to form biofilms on medical implants, causing serious infections. A better understanding of fungal biofilm formation is necessary to develop tools for detection or prevention and to identify new antifungal strategies. This review explores recent advances in the characterization at the molecular level of fungal biofilms, especially those formed by the yeast Candida albicans: the identification of complex transcriptional networks that control their formation; the pivotal role of the extracellular matrix in biofilm antifungal tolerance; and the knowledge gained on the physiology of biofilm cells and heterogeneity within these communities. These findings may help develop new, targeted therapeutic strategies.

Published
2013

4. Active starvation responses mediate antibiotic tolerance in biofilms and nutrient-limited bacteria

Author

Elizabeth Bauerle, Oyebode Olakanmi, James Schafhauser, Yun Wang, Amruta Joshi-Datar, Pradeep K. Singh, Geoffrey McKay, Karlyn D. Beer, Bradley E. Britigan, Richard Siehnel, Dao Nguyen, François Lépine, Departments of Medicine, Microbiology and Immunology, McGill University = Université McGill [Montréal, Canada], Departments of Medicine and Microbiology, University of Washington [Seattle]-School of Medicine, Institut Armand Frappier (INRS-IAF), Institut National de la Recherche Scientifique [Québec] (INRS)-Réseau International des Instituts Pasteur (RIIP), Department of Internal Medicine, Medical Sciences Building-University of Cincinnati (UC), Department of Civil and Environmental Engineering [Evanston], Northwestern University [Evanston], Veterans Administration, Cincinnati Children's Hospital Medical Center, and Funding was provided by the Burroughs Wellcome Fund (D.N. and P.K.S), Cystic Fibrosis Foundation (P.K.S), NIH (P.K.S), and Canadian Institutes for Health Research (D.N.).

Subjects
Ofloxacin, [SDV.BIO]Life Sciences [q-bio]/Biotechnology, Stringent response, Antibiotics, Drug resistance, medicine.disease_cause, Mice, Drug tolerance, Serine, MESH: Animals, [INFO.INFO-BT]Computer Science [cs]/Biotechnology, MESH: Superoxide Dismutase, 0303 health sciences, Multidisciplinary, MESH: Oxidative Stress, MESH: Escherichia coli, MESH: Pseudomonas Infections, Drug Tolerance, MESH: Hydroxyl Radical, Catalase, Anti-Bacterial Agents, Pseudomonas aeruginosa, MESH: Pseudomonas aeruginosa, Hydroxyquinolines, Female, MESH: Mutation, Multidrug tolerance, medicine.drug_class, MESH: Drug Tolerance, MESH: Biofilms, Biology, Article, Microbiology, 03 medical and health sciences, MESH: Mice, Inbred C57BL, MESH: Anti-Bacterial Agents, MESH: Catalase, Drug Resistance, Bacterial, MESH: Drug Resistance, Bacterial, medicine, Escherichia coli, Animals, Pseudomonas Infections, MESH: Serine, MESH: Hydroxyquinolines, MESH: Mice, 030304 developmental biology, 030306 microbiology, Hydroxyl Radical, Superoxide Dismutase, Biofilm, biology.organism_classification, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, Mice, Inbred C57BL, Oxidative Stress, Biofilms, Mutation, MESH: Ofloxacin, MESH: Female, Bacteria
Abstract

International audience; Bacteria become highly tolerant to antibiotics when nutrients are limited. The inactivity of antibiotic targets caused by starvation-induced growth arrest is thought to be a key mechanism producing tolerance. Here we show that the antibiotic tolerance of nutrient-limited and biofilm Pseudomonas aeruginosa is mediated by active responses to starvation, rather than by the passive effects of growth arrest. The protective mechanism is controlled by the starvation-signaling stringent response (SR), and our experiments link SR-mediated tolerance to reduced levels of oxidant stress in bacterial cells. Furthermore, inactivating this protective mechanism sensitized biofilms by several orders of magnitude to four different classes of antibiotics and markedly enhanced the efficacy of antibiotic treatment in experimental infections.

Published
2011

5. Chronic and intermittent morphine treatment differently regulates opioid and dopamine systems: a role in locomotor sensitization

Author

Marie-Claire, Cynthia, Le Marec, Thierry, Marie, Cynthia, Noble, Florence, Marie, Nicolas, Variabilité de réponse aux Psychotropes (VariaPsy - U1144), Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Descartes - Paris 5 (UPD5), Université Paris Descartes - Faculté de Pharmacie de Paris (UPD5 Pharmacie), Alcatel R&D (Alcatel), ALCATEL, Optimisation Thérapeutique en Neuropsychopharmacologie (VariaPsy - U1144), and Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Diderot - Paris 7 (UPD7)

Subjects
Male, Time Factors, Receptors, Opioid, mu, Pharmacology, MESH: Analgesics, Opioid, MESH: Receptors, Dopamine D1, MESH: Corpus Striatum, MESH: Dose-Response Relationship, Drug, Mice, chemistry.chemical_compound, 0302 clinical medicine, MESH: Autoradiography, MESH: Receptors, Dopamine D2, MESH: Behavior, Animal, Medicine, MESH: Animals, Neurotransmitter, Sensitization, 0303 health sciences, Behavior, Animal, Morphine, Drug Tolerance, MESH: Motor Activity, 3. Good health, Analgesics, Opioid, medicine.anatomical_structure, Dopamine receptor, μ-opioid receptor, medicine.drug, MESH: Drug Tolerance, MESH: Receptors, Opioid, mu, Motor Activity, MESH: Drug Administration Schedule, Drug Administration Schedule, 03 medical and health sciences, Dopamine, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Animals, Opioid peptide, MESH: Mice, 030304 developmental biology, Dose-Response Relationship, Drug, Receptors, Dopamine D2, business.industry, Receptors, Dopamine D1, Ventral Tegmental Area, MESH: Time Factors, Corpus Striatum, MESH: Male, MESH: Morphine, chemistry, Opioid, MESH: Ventral Tegmental Area, Autoradiography, business, 030217 neurology & neurosurgery
Abstract

Behavioral sensitization induced by repeated morphine administrations may depend on patterns of administration. However, neurobiological mechanisms involved in this sensitization are largely unknown.We compared the effects of intermittent (20 mg/kg, once daily for 7 days) and chronic (escalating doses from 5 to 40 mg/kg, three times a day for 5 days) morphine treatments in mice on locomotor activity. We also quantified, by autoradiography, mu opioid receptor (MOR) in ventral tegmental area (VTA), dopamine D1 (D1R) and D2 (D2R) receptors in striatum.Whereas the intermittent treatment led to a long-term sensitization to locomotor effects of morphine [until withdrawal day (WD) 14], the chronic treatment induced a tolerance (WD1) followed by a transient sensitization (WD14). Binding studies demonstrated a decrease of MOR in VTA at WD1 for the chronic treatment. In contrast, striatal D1R level was decreased at WD1, and increased at WD14 for the chronic treatment. For the D2R, we observed a decrease from WD1 to WD14 for the intermittent treatment and an increase at WD1 followed by a decrease at WD14 for the chronic treatment.These results demonstrate that chronic and intermittent morphine treatments could induce different behavioral adaptations that could be explained in part by distinct changes occurring in dopamine and opioid systems.

Published
2011

6. Efficacy of icatibant treatment in patients with hereditary angio-oedema type I resistant to treatment with C1 inhibitor concentrate

Author

Bouillet, L., Boccon-Gibod, I., Dumestre-Perard, C., Cesbron, J. Y., Massot, C., Laboratoire Adaptation et pathogénie des micro-organismes [Grenoble] (LAPM), Centre National de la Recherche Scientifique (CNRS)-Université Joseph Fourier - Grenoble 1 (UJF), National Angiodema Reference Centre, Physiopathologie vasculaire : interactions cellulaires, signalisation et vieillissement, Université Joseph Fourier - Grenoble 1 (UJF)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire d'immunohistochimie, CHU Grenoble-Hôpital Michallon, Département de Médecine Interne, CHU Grenoble, and Université Joseph Fourier - Grenoble 1 (UJF)-Centre National de la Recherche Scientifique (CNRS)

Subjects
MESH: Adolescent, MESH: Bradykinin, MESH: Humans, MESH: Complement C1 Inhibitor Protein, MESH: Drug Tolerance, MESH: Drug Resistance, MESH: Hereditary Angioedema Types I and II, MESH: Adult, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH: Female, ComputingMilieux_MISCELLANEOUS, MESH: Receptors, Bradykinin
Abstract

International audience

Published
2011

7. Enhanced T cell recovery in HIV-1-infected adults through IL-7 treatment

Author

Jean-François Delfraissy, Cécile Goujard, François Boué, Thérèse Croughs, Rodolphe Thiébaut, Christine Lacabaratz, Jean-Michel Molina, Yves Levy, Jean-Daniel Lelièvre, Stéphanie Beq, Véronique Avettand-Fenoel, Jean-Paul Viard, Geneviève Chêne, Christine Rouzioux, Laurence Weiss, Michel Morre, Service d'immunologie clinique [Créteil], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Immunologie antivirale systémique et cérébrale, Université Paris-Sud - Paris 11 (UP11)-IFR93-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de médecine interne et maladies infectieuses, Hôpital Bicêtre-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11), Immunologie clinique, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Groupe Henri-Mondor Albert-Chenevier, Hôpital Antoine Béclère, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11), Service de maladies infectieuses et tropicales [Saint-Louis], Université Paris Diderot - Paris 7 (UPD7)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Cythéris, Epidémiologie et Biostatistique [Bordeaux], Université Bordeaux Segalen - Bordeaux 2-Institut de Santé Publique, d'Épidémiologie et de Développement (ISPED)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de Santé Publique, d'Epidémiologie et de Développement (ISPED), Université Bordeaux Segalen - Bordeaux 2, Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Bicêtre, Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 ), Institut Mondor de Recherche Biomédicale ( IMRB ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 ), Hôpital Européen Georges Pompidou [APHP] ( HEGP ), Université Paris-Sud - Paris 11 ( UP11 ) -IFR93-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Université Paris-Sud - Paris 11 ( UP11 ) -Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Bicêtre, Assistance publique - Hôpitaux de Paris (AP-HP)-Groupe Henri-Mondor Albert-Chenevier, Université Paris-Sud - Paris 11 ( UP11 ) -Assistance publique - Hôpitaux de Paris (AP-HP), Assistance publique - Hôpitaux de Paris (AP-HP)-Université Paris Diderot - Paris 7 ( UPD7 ) -Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Université Bordeaux Segalen - Bordeaux 2-Institut de Santé Publique, d'Épidémiologie et de Développement (ISPED)-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut de Santé Publique, d'Epidémiologie et de Développement ( ISPED ), and Guellaen, Georges

Subjects
MESH: CD4 Lymphocyte Count, medicine.medical_treatment, T-Lymphocytes, Cell, MESH : Aged, MESH : Prospective Studies, CD4-CD8 Ratio, HIV Infections, MESH: Cell Cycle, Lymphocyte Activation, MESH: Recombinant Proteins, MESH: HIV-1, 0302 clinical medicine, Prospective Studies, MESH: Aged, 0303 health sciences, MESH: Middle Aged, Cell Cycle, General Medicine, Drug Tolerance, MESH: HIV Infections, MESH : Adult, Cell cycle, Middle Aged, Recombinant Proteins, 3. Good health, medicine.anatomical_structure, MESH: Immunologic Memory, MESH : Lymphopenia, Safety, MESH : HIV-1, Research Article, MESH : Interleukin-7, Adult, MESH : Recombinant Proteins, MESH : Immunologic Memory, T cell, MESH: Drug Tolerance, MESH: Lymphopenia, 03 medical and health sciences, Antigen, Lymphopenia, MESH : Cell Cycle, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH : CD4 Lymphocyte Count, MESH : HIV Infections, medicine, Humans, MESH : Middle Aged, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH : Safety, MESH: Lymphocyte Activation, [ SDV.BBM ] Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH : Lymphocyte Activation, 030304 developmental biology, Aged, MESH : T-Lymphocytes, MESH: Humans, business.industry, Interleukin-7, MESH : Humans, MESH: Safety, MESH: Adult, Immunotherapy, medicine.disease, T cell deficiency, MESH: Interleukin-7, MESH: Prospective Studies, CD4 Lymphocyte Count, MESH: T-Lymphocytes, MESH : CD4-CD8 Ratio, MESH : Drug Tolerance, Immunology, HIV-1, MESH: CD4-CD8 Ratio, business, Immunologic Memory, CD8, 030215 immunology
Abstract

International audience; HIV infection results in CD4+ T cell deficiency, but efficient combination antiretroviral therapy (c-ART) restores T cells and decreases morbidity and mortality. However, immune restoration by c-ART remains variable, and prolonged T cell deficiency remains in a substantial proportion of patients. In a prospective open-label phase I/IIa trial, we evaluated the safety and efficacy of administration of the T cell regulator IL-7. The trial included 13 c-ART-treated HIV-infected patients whose CD4+ cell counts were between 100 and 400 cells/microl and plasma HIV RNA levels were less than 50 copies/ml. Patients received a total of 8 subcutaneous injections of 2 different doses of recombinant human IL-7 (rhIL-7; 3 or 10 microg/kg) 3 times per week over a 16-day period. rhIL-7 was well tolerated and induced a sustained increase of naive and central memory CD4+ and CD8+ T cells. In the highest dose group, 4 patients experienced transient increases in viral replication. However, functional assays showed that the expanded T cells responded to HIV antigen by producing IFN-gamma and/or IL-2. In conclusion, in lymphopenic HIV-infected patients, rhIL-7 therapy induced substantial functional and quantitative changes in T cells for 48 weeks. Therefore, patients may benefit from intermittent therapy with IL-7 in combination with c-ART.

Published
2009

8. Tolerability of enteric-coated mycophenolate sodium to 1 year in combination with cyclosporine and corticosteroids in renal transplant recipients

Author

Georges Mourad, Pierre Merville, Lionel Rostaing, Yvon Lebranchu, Peter Lang, Nassim Kamar, Didier Ducloux, François Bayle, M. Kessler, B. Moulin, Michel Delahousse, Valérie Garrigue, Nicole Lefrançois, Bernard Bourbigot, Claire Pouteil-Noble, C. Legendre, Y. Le Meur, Alexandre Karras, François Berthoux, Bernard Charpentier, Kamel Chaouche-Teyara, Service de Néphrologie - Hypertension Artérielle Dialyse - Transplantation, CHU Toulouse [Toulouse]-Hôpital de Rangueil, CHU Toulouse [Toulouse], Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (RIGHT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté]), Legendre for The French Myriade FR01 Study Group, Saas, Philippe, Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Université de Franche-Comté (UFC), and Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)

Subjects
Male, MESH: Emulsions, MESH: Tissue Donors, 030232 urology & nephrology, 030230 surgery, Mycophenolate, Gastroenterology, MESH: Cyclosporine, MESH: Kidney Transplantation, 0302 clinical medicine, Adrenal Cortex Hormones, Isoantibodies, Leukopenia, MESH: Middle Aged, Histocompatibility Testing, Drug Tolerance, Middle Aged, Tissue Donors, 3. Good health, Tolerability, Cyclosporine, [SDV.IMM]Life Sciences [q-bio]/Immunology, Drug Therapy, Combination, Emulsions, Female, Kidney Diseases, Tablets, Enteric-Coated, medicine.symptom, medicine.drug, Adult, medicine.medical_specialty, [SDV.IMM] Life Sciences [q-bio]/Immunology, Urinary system, MESH: Drug Tolerance, MESH: Tablets, Enteric-Coated, MESH: Histocompatibility Testing, Mycophenolic acid, MESH: Adrenal Cortex Hormones, 03 medical and health sciences, Internal medicine, medicine, Humans, Adverse effect, MESH: Mycophenolic Acid, Transplantation, MESH: Kidney Diseases, MESH: Humans, business.industry, MESH: Adult, Mycophenolic Acid, Ciclosporin, Kidney Transplantation, MESH: Male, MESH: Isoantibodies, Surgery, MESH: Drug Therapy, Combination, business, MESH: Female
Abstract

International audience; Enteric-coated mycophenolate sodium (EC-MPS) is therapeutically equivalent to mycophenolate mofetil, but delays release of mycophenolic acid until it reaches the small intestine. De novo renal transplant patients taking part in a 12-month, multicenter, randomized study received cyclosporine microemulsion (CsA-ME, early or delayed to day 6), EC-MPS, steroids, and interleukin-2 antagonist induction. Tolerability data relating to EC-MPS are reported. Ninety-seven patients were randomized to early CsA-ME and 100 patients to delayed CsA-ME. Median daily dose of EC-MPS was 1440 mg at all time points throughout the 12-month period. The most frequently reported adverse events were constipation, anemia, urinary tract infection, abdominal pain, leukopenia, and cytomegalovirus infection; there were four malignancies. Fifty patients (24.6%) discontinued EC-MPS prematurely by 12 months, including 42 patients (84%) who discontinued owing to adverse events. No patient discontinued treatment because of gastrointestinal adverse events. Two-thirds of patients (137 [67.5%]) maintained full EC-MPS dose throughout the 12-month study and did not require any dose reduction or dose interruption. EC-MPS is well tolerated in de novo renal transplant recipients when administered in combination with CsA-ME and steroids, with low rates of dose reductions or interruptions. Gastrointestinal adverse events were responsible for dose reduction or interruption in only 5% of patients.

Published
2006

9. Mu-opioid receptors are involved in the tolerance to nicotine antinociception

Author

Lola Galeote, Brigitte L. Kieffer, Rafael Maldonado, Fernando Berrendero, Institut de génétique et biologie moléculaire et cellulaire (IGBMC), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Louis Pasteur - Strasbourg I, and Université Louis Pasteur - Strasbourg I-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Time Factors, Receptors, Opioid, mu, MESH: Pain Measurement, MESH: Analgesics, Opioid, Biochemistry, MESH: Mice, Knockout, MESH: Nicotine, MESH: Spinal Cord, Mice, 0302 clinical medicine, MESH: Autoradiography, 030202 anesthesiology, MESH: Behavior, Animal, MESH: Animals, Nicotinic Agonists, Pain Measurement, Mice, Knockout, Behavior, Animal, Brain, Drug Tolerance, 3. Good health, Analgesics, Opioid, Spinal Cord, MESH: Guanosine 5'-O-(3-Thiotriphosphate), MESH: Sulfur Isotopes, Protein Binding, Nicotine, MESH: Drug Tolerance, MESH: Receptors, Opioid, mu, MESH: Enkephalin, Ala(2)-MePhe(4)-Gly(5), MESH: Drug Administration Schedule, In Vitro Techniques, Drug Administration Schedule, 03 medical and health sciences, Cellular and Molecular Neuroscience, MESH: Brain, MESH: Mice, Inbred C57BL, MESH: Analysis of Variance, MESH: Nicotinic Agonists, Sulfur Isotopes, MESH: Protein Binding, Animals, MESH: Mice, Analysis of Variance, MESH: Time Factors, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, Enkephalin, Ala(2)-MePhe(4)-Gly(5), Mice, Inbred C57BL, Guanosine 5'-O-(3-Thiotriphosphate), Autoradiography, 030217 neurology & neurosurgery
Abstract

International audience; Several studies have shown the participation of the endogenous opioid system on the antinociceptive effects and addictive properties of nicotine. The aim of the present study was to explore the involvement of the mu-opioid receptors in the development of tolerance to nicotine antinociception. Chronic treatment of C57BL/6 mice with nicotine (5 mg/kg s.c., three times daily during 12 days) resulted in tolerance to its antinociceptive responses in the tail-immersion test. We investigated the possible existence of adaptive changes in the expression and/or functional activity of mu-opioid receptors in these tolerant mice by using autoradiography of [(3)H]D-Ala(2)-MePhe(4)-Gly-ol(5) enkephalin ([(3)H]DAMGO) binding and DAMGO-stimulated guanosine [(35)S]5'-(gamma-thio)-triphosphate ([(35)S]GTPgammaS) binding. The density of mu-opioid receptors in the spinal cord was not modified in nicotine-tolerant mice, whereas a decrease was found in the caudate-putamen, as well as in the core and the shell of the nucleus accumbens. However, the functional activity of these receptors was significantly increased in the spinal cord as a consequence of nicotine treatment. To further investigate the role of mu-opioid receptors in the tolerance to nicotine-induced antinociception, we evaluated this response in C57BL/6 mu-opioid receptor knockout mice. Chronic nicotine treatment produced tolerance in both wild-type and knockout animals, but tolerance developed faster in mice lacking mu-opioid receptors. These results indicate that mu-opioid receptors play an important role in the development of tolerance to nicotine antinociceptive effects.

Published
2006

10. RF9, a potent and selective neuropeptide FF receptor antagonist, prevents opioid-induced tolerance associated with hyperalgesia

Author

Emilie Laboureyras, Frédéric Simonin, Brigitte L. Kieffer, Jean-Paul Laulin, Marc Parmentier, Audrey Matifas, Jean-Jacques Bourguignon, Catherine Mollereau, David MacTavish, Guy Simonnet, Jack H. Jhamandas, Martine Schmitt, Patrick Laurent, Institut de génétique et biologie moléculaire et cellulaire (IGBMC), Université Louis Pasteur - Strasbourg I-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut Gilbert-Laustriat : Biomolécules, Biotechnologie, Innovation Thérapeutique, and Université Louis Pasteur - Strasbourg I-Centre National de la Recherche Scientifique (CNRS)

Subjects
Receptors, Neuropeptide, Neuropeptide FF receptor, Adamantane, Blood Pressure, Pharmacology, Ligands, MESH: Analgesics, Opioid, 0302 clinical medicine, MESH: Dipeptides, Heart Rate, Drug tolerance, Chlorocebus aethiops, MESH: Ligands, MESH: Animals, Neuropeptide FF, MESH: Heart Rate, Receptor, 0303 health sciences, Multidisciplinary, Molecular Structure, Chemistry, MESH: Receptors, Neuropeptide, Chronic pain, Sciences du Vivant [q-bio]/Biotechnologies, Dipeptides, Drug Tolerance, MESH: Adamantane, MESH: Blood Pressure, Biological Sciences, MESH: Amides, 3. Good health, Analgesics, Opioid, MESH: COS Cells, Hyperalgesia, COS Cells, MESH: Heroin, medicine.symptom, medicine.drug, MESH: Rats, MESH: Drug Tolerance, MESH: Molecular Structure, 03 medical and health sciences, medicine, Animals, Humans, 030304 developmental biology, MESH: Humans, Antagonist, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, medicine.disease, Amides, MESH: Hyperalgesia, MESH: Cercopithecus aethiops, Rats, Heroin, Opioid, 030217 neurology & neurosurgery
Abstract

International audience; Neuropeptide FF (NPFF) has been proposed to play a role in pain modulation, opioid tolerance, and several other physiological processes. However, pharmacological agents that would help define physiological roles for this peptide are still missing. Here we report the discovery of a potent and selective NPFF receptor antagonist, RF9, that can be administered systemically. This compound does not show any effects by itself but can block efficiently the increase in blood pressure and heart rate evoked by NPFF. When chronically coinjected with heroin, RF9 completely blocks the delayed and long-lasting paradoxical opioid-induced hyperalgesia and prevents the development of associated tolerance. Our data indicate that NPFF receptors are part of a bona fide antiopioid system and that selective antagonists of these receptors could represent useful therapeutic agents for improving the efficacy of opioids in chronic pain treatment.

Published
2006

11. Pain, immunity, opiate and opioid compounds and health

Author

George Stefano, Fricchione, G. L., Goumon, Y., Esch, T., Goumon, Yannick, College at Old Westbury [SUNY] (SUNY Old Westbury), State University of New York (SUNY), Massachusetts General Hospital [Boston], Institut des Neurosciences Cellulaires et Intégratives (INCI), Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS), Physiopathologie du système nerveux., Université Louis Pasteur - Strasbourg I-IFR37-Institut National de la Santé et de la Recherche Médicale (INSERM), and Charité - UniversitätsMedizin = Charité - University Hospital [Berlin]

Subjects
Narcotics, MESH: Protein Precursors, MESH: Sequence Homology, Amino Acid, Substance-Related Disorders, MESH: Drug Tolerance, [SDV]Life Sciences [q-bio], Molecular Sequence Data, Pain, MESH: Amino Acid Sequence, Evolution, Molecular, [SCCO]Cognitive science, MESH: Enkephalins, MESH: Opioid Peptides, Animals, Humans, MESH: Animals, Amino Acid Sequence, Protein Precursors, MESH: Evolution, Molecular, MESH: Humans, MESH: Molecular Sequence Data, Morphine, Sequence Homology, Amino Acid, [SCCO] Cognitive science, Drug Tolerance, Enkephalins, MESH: Narcotics, [SDV] Life Sciences [q-bio], MESH: Morphine, Opioid Peptides, MESH: Substance-Related Disorders, MESH: Pain
Abstract

International audience; We surmise that opioid peptides, i.e., methionine enkephalin, first arose during evolution as modulators of cellular immune function given their immune actions and the presence of enkelytin, a potent antibacterial peptide, and its precursor proenkephalin in animals 500 million years divergent in evolution. Pain probably emerged from this perspective because of its association with proinflammatory events. Endogenous morphine appears to exert positive effects on homeostasis by limiting the degree of excitation. Supporting this view is the fact that the mu3 opiate receptor subtype, which is opioid peptide insensitive and morphine selective, is coupled to constitutive nitric oxide release, which also has this down regulating action in neural, immune, vascular and gastrointestinal tissues. Thus, morphine down regulates immune processes in addiction, an action/function that it appears to normally perform when the situation calls for this action and by so doing in this natural setting, sustains life.

Published
2005

12. Chronic ethanol consumption induces tolerance to the spatial memory impairing effects of acute ethanol administration in rats

Author

Martine Daoust, Michel Boulouard, Mickaël Naassila, Véronique Lelong, Centre d'Etudes et de Recherche sur le Médicament de Normandie ( CERMN ), Université de Caen Normandie ( UNICAEN ), Normandie Université ( NU ) -Normandie Université ( NU ), Environnement Toxique Périnatal-Adaptations Physiologiques et Comportementales. Laboratoire de Physiologie-Alcoologie ( ETP-APC ), Université de Picardie Jules Verne ( UPJV ), Centre d'Etudes et de Recherche sur le Médicament de Normandie (CERMN), Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU), Groupe de Recherche sur l'alcool et les pharmacodépendances - UMR INSERM_S 1247 (GRAP), Université de Picardie Jules Verne (UPJV)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Naassila, Mickael

Subjects
Male, Morris water navigation task, MESH: Rats, Sprague-Dawley, Hippocampal formation, MESH : Ethanol, Locomotor activity, Toxicology, Rats, Sprague-Dawley, MESH : Maze Learning, Behavioral Neuroscience, chemistry.chemical_compound, 0302 clinical medicine, Drug tolerance, MESH: Animals, MESH: Memory, 0303 health sciences, MESH : Rats, Acute ethanol, MESH : Memory, Drug Tolerance, MESH: Motor Activity, Ethanol administration, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Psychology, MESH : Space Perception, medicine.medical_specialty, MESH: Ethanol, MESH: Rats, Alcohol Drinking, MESH: Drug Tolerance, MESH : Male, MESH: Space Perception, Motor Activity, 03 medical and health sciences, Memory, Internal medicine, medicine, Animals, [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Maze Learning, 030304 developmental biology, Ethanol, MESH: Maze Learning, MESH : Central Nervous System Depressants, Central Nervous System Depressants, MESH: Male, MESH : Alcoholic Intoxication, MESH : Rats, Sprague-Dawley, Rats, MESH : Alcohol Drinking, Endocrinology, chemistry, MESH: Alcoholic Intoxication, Space Perception, [ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], MESH : Drug Tolerance, Spatial learning, MESH : Animals, MESH: Central Nervous System Depressants, Alcoholic Intoxication, MESH : Motor Activity, 030217 neurology & neurosurgery, MESH: Alcohol Drinking
Abstract

International audience; A large number of studies in rats have investigated the effects of acute and chronic ethanol administration on performance on many spatial learning and memory tasks. However, no study has addressed the problem of whether chronic ethanol consumption induces tolerance to acute ethanol-induced spatial memory deficits. In this study, we analyzed the behavioral effects of acute ethanol administration on spatial memory and locomotor activity in rats chronically intoxicated by ethanol. Male Sprague-Dawley rats were given as their only available liquid source a 10% (v/v) aqueous ethanol solution for 2 weeks before behavioral testing and during the 1-week behavioral testing period. They were treated intraperitoneally with 1.5 g/kg of ethanol 30 min before daily training in the Morris water maze, a spatial memory task sensitive to hippocampal damage. Our results demonstrate that learning and spatial memory of ethanol-consuming animals were not altered compared with control rats. Chronic ethanol consumption had no effect on spatial reference memory in terms of either the distance traveled to find the hidden platform during the acquisition phase of the experiment, or the time spent in the training quadrant during the retention trial. Acute ethanol administration impaired spatial memory in control rats and this impairment was reversed in chronic ethanol-consuming animals, revealing that chronic ethanol consumption did induce tolerance to the spatial memory deficits induced by acute ethanol injection, although plasma ethanol levels did not differ between the two groups. In contrast, chronic ethanol consumption did not induce tolerance to the acute ethanol-induced stimulatory locomotor activity measured in the same animals. Our results, therefore, indicate that chronic ethanol consumption induces tolerance to the cognitive impairing effects, but not to the locomotor stimulatory effects of acute ethanol administration in rats, suggesting that these two behavioral effects of ethanol do not share a common mechanism in the CNS.

Published
2002

13. Low ethanol sensitivity and increased ethanol consumption in mice lacking adenosine A2A receptors

Author

Martine Daoust, Catherine Ledent, Mickaël Naassila, Naassila, Mickael, Groupe de Recherche sur l'alcool et les pharmacodépendances - UMR INSERM_S 1247 (GRAP), Université de Picardie Jules Verne (UPJV)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire (IRIBHM), and Université libre de Bruxelles (ULB)

Subjects
Male, Sucrose, MESH: Body Temperature, MESH: Triazines, Drug Resistance, Adenosine A2A receptor, Administration, Oral, Hypothermia, Choice Behavior, MESH: Mice, Knockout, Body Temperature, MESH: Dose-Response Relationship, Drug, chemistry.chemical_compound, Mice, 0302 clinical medicine, MESH: Hypothermia, MESH: Behavior, Animal, MESH: Animals, Receptor, Mice, Knockout, 0303 health sciences, Quinine, Behavior, Animal, Triazines, General Neuroscience, Drug Tolerance, 3. Good health, Biochemistry, Adenosine a, MESH: Administration, Oral, MESH: Drug Resistance, MESH: Receptor, Adenosine A2A, Female, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], medicine.symptom, Injections, Intraperitoneal, MESH: Injections, Intraperitoneal, medicine.drug, medicine.medical_specialty, MESH: Ethanol, Alcohol Drinking, Receptor, Adenosine A2A, MESH: Quinine, MESH: Reflex, MESH: Drug Tolerance, MESH: Choice Behavior, 03 medical and health sciences, Sex Factors, MESH: Sex Factors, MESH: Purinergic P1 Receptor Antagonists, Internal medicine, Reflex, medicine, Animals, MESH: Receptors, Purinergic P1, [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], ARTICLE, MESH: Mice, 030304 developmental biology, Ethanol, Dose-Response Relationship, Drug, MESH: Sucrose, Antagonist, Receptors, Purinergic P1, Triazoles, MESH: Male, Endocrinology, chemistry, Purinergic P1 Receptor Antagonists, MESH: Triazoles, MESH: Female, 030217 neurology & neurosurgery, MESH: Alcohol Drinking
Abstract

We have shown previously that the severity of handling-induced convulsions during ethanol withdrawal was reduced in A(2A)receptor knock-out (A(2A)R(−/−)) mice. In the present report, we further characterize the role of adenosine A(2A) receptors in ethanol consumption and neurobiological responses to this drug of abuse. Male A(2A)R(−/−) mice showed increased consumption of solutions containing 6 and 20% (v/v) ethanol compared with wild-type (A(2A)R(+/+)) control mice; female A(2A)R(−/−) mice showed increased consumption of solutions containing 6 and 10% ethanol. This slightly higher ethanol consumption was also related to increased ethanol preference. In contrast, A(2A)R(−/−) mice showed normal consumption of solutions containing either sucrose or quinine. Relative to A(2A)R(+/+) mice, A(2A)R(−/−) mice were found to be less sensitive to the sedative effect of 3.0 gm/kg ethanol, as measured by more rapid recovery from ethanol-induced loss of righting reflex, and to the hypothermic effects of 1.5, 3.0, and 4.0 gm/kg ethanol, although plasma ethanol levels did not differ significantly between the two genotypes. The selective adenosine A(2A) receptor antagonist ZM 241385 (4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol) (10–30 mg/kg) significantly attenuated ethanol-induced (4.0 gm/kg) hypothermia in CD1 mice. To assess whether ethanol administration would induce differential tolerance in A(2A)R(−/−) and wild-type mice, we administered ethanol (3.0 gm/kg) over 4 consecutive days and found no difference in the development of tolerance; however, female A(2A)R(−/−) mice showed a lower tolerance-acquisition rate. These data suggest that activating the A(2A) receptors may play a role in suppressing alcohol-drinking behavior and is associated with the sensitivity to the intoxicating effects of acute ethanol administration.

Published
2002

14. [The concept of supersensitivity psychosis. The particular case of clozapine]

Author

Llorca, Pierre-Michel, Penault, F., Lançon, C., Dufumier, E., Vaiva, G., CHU Clermont-Ferrand, Hôpital Sainte-Marguerite [CHU - APHM] (Hôpitaux Sud ), Laboratoire de Neurosciences Fonctionnelles et Pathologies (LNFP), and Université de Lille, Droit et Santé-Centre National de la Recherche Scientifique (CNRS)

Subjects
Adult, Male, MESH: Dissociative Disorders, MESH: Psychoses, Substance-Induced, MESH: Humans, MESH: Drug Tolerance, MESH: Substance Withdrawal Syndrome, Catatonia, MESH: Adult, Dissociative Disorders, Drug Tolerance, Psychoses, Substance-Induced, MESH: Male, Substance Withdrawal Syndrome, MESH: Recurrence, Recurrence, MESH: Catatonia, MESH: Psychomotor Disorders, Humans, MESH: Antipsychotic Agents, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Psychomotor Disorders, MESH: Clozapine, Clozapine, Antipsychotic Agents
Abstract

International audience; Neuroleptics are the main biological treatment for psychotic patients. The brutal withdrawal of a neuroleptic treatment may induce an important aggravation of the psychotic symptoms. A few of those relapses may occur very early after the interruption of treatment; they are often associated with a modification of the symptoms and an unfavorable evolution in the course of the illness. Using those clinical observations a few authors have developed the concept of supersensitivity psychosis to explain those kinds of relapses and to formulate hypothesis about tolerance and resistance to neuroleptics. They focus on the possible correlation between supersensitivity psychosis and tardive dyskinesia. We report three cases of a dramatic aggravation of the psychotic symptomatology following the withdrawal of clozapine in three schizophrenic patients resistant to classical neuroleptic treatment. According to the clinical data and to the physiopathological hypothesis, the concept of supersensitivity psychosis can have implications in the therapeutic management of resistant schizophrenic patients.

Published
1999

15. The long-term effects of the lipid-lowering agent fenofibrate in hyperlipidemic heart transplant recipients

Author

M. De Lorgeril, Serge Renaud, Jean Ninet, P. Boissonnat, Georges Dureau, René Ferrera, J. Guidollet, Patricia Salen, Salen, Patricia, Techniques de l'Ingénierie Médicale et de la Complexité - Informatique, Mathématiques et Applications, Grenoble - UMR 5525 (TIMC-IMAG), VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Institut polytechnique de Grenoble - Grenoble Institute of Technology (Grenoble INP )-Centre National de la Recherche Scientifique (CNRS)-Université Joseph Fourier - Grenoble 1 (UJF), Institut de biologie et chimie des protéines [Lyon] (IBCP), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), Cardioprotection, and Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Adult, medicine.medical_specialty, MESH: Hyperlipidemias, Adolescent, medicine.medical_treatment, MESH: Drug Tolerance, 030232 urology & nephrology, Urology, Lipid-lowering agent, Hyperlipidemias, 030204 cardiovascular system & hematology, 030230 surgery, 03 medical and health sciences, 0302 clinical medicine, Fenofibrate, medicine, Humans, Longitudinal Studies, Prospective Studies, MESH: Longitudinal Studies, ComputingMilieux_MISCELLANEOUS, Aged, MESH: Adolescent, MESH: Aged, Transplantation, Chemotherapy, MESH: Humans, MESH: Middle Aged, business.industry, MESH: Heart Transplantation, MESH: Adult, Drug Tolerance, Middle Aged, Lipids, MESH: Lipids, MESH: Prospective Studies, 3. Good health, Surgery, [SDV.AEN] Life Sciences [q-bio]/Food and Nutrition, Heart Transplantation, MESH: Procetofen, Complication, business, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition, medicine.drug
Abstract

International audience

Published
1994

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