DOCSLIB.ORG

Human Chorionic Gonadotropin Regulates Gastric Emptying in Ovariectomized Rats

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Human Chorionic Gonadotropin Regulates Gastric Emptying in Ovariectomized Rats K-M SEOW, J-L LEE and others hCG and gastric emptying 216:3 307–314 Research Human chorionic gonadotropin regulates gastric emptying in ovariectomized rats Kok-Min Seow1,2,*, Jyun-Lin Lee3,*, Ming-Luen Doong3, Seng-Wong Huang4, Jiann-Loung Hwang1,5, Wei-Ju Huang6, Full-Young Chang7, Low-Tone Ho3,8,9 and Chi-Chang Juan3,9,10 1Department of Obstetrics and Gynecology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan 2Department of Obstetrics and Gynecology, National Yang-Ming University, Linong Street, Taipei 11221, Taiwan 3Institute of Physiology, National Yang-Ming University, No. 155, Section 2, Linong Street, Taipei 11221, Taiwan 4Department of Surgery, National Yang-Ming University, Linong Street, Taipei 11221, Taiwan 5Department of Obstetrics and Gynecology, Taipei Medical University, Taipei, Taiwan 6Department of Nursing, Hsin Sheng College of Medical Care and Management, Taoyuan, Taiwan 7Division of Gastroenterology, Department of Medicine, Taipei Veterans General Hospital, No. 201, Section 2, Shi-Pai Road, Taipei 11217, Taiwan 8Department of Internal Medicine, Taipei Veterans General Hospital, Shi-Pai Road, Taipei 11217, Taiwan Correspondence 9Department of Education and Medical Research, Taipei Veterans General Hospital, Shi-Pai Road, Taipei 11217, should be addressed to Taiwan C-C Juan 10Department of Education and Research, Taipei City Hospital, Taipei, Taiwan Email *(K-M Seow and J-L Lee contributed equally to this work) [email protected] Abstract Prolongation of gastrointestinal transit resulting in nausea and vomiting in pregnancy (NVP) Key Words Journal of Endocrinology is the most common phenomenon during the first trimester of pregnancy. Increased human " human chorionic chorionic gonadotropin (hCG) concentration during the first trimester is the most likely gonadotropin cause of NVP. The aim of this study was to investigate the effect of hCG on gastrointestinal " gastric emptying transit and plasma concentrations of cholecystokinin (CCK) in ovariectomized (Ovx) rats. I.p. " cholecystokinin injection of hCG was used to evaluate the dose effect of hCG on gastrointestinal transit in " ovariectomized rats Ovx rats. The CCK antagonist lorglumide was used to clarify the role of CCK in regulating gastrointestinal transit. Gastrointestinal transit was assessed 15 min after intragastric gavage 51 of a mixture of 10% charcoal and Na2 CrO4 (0.5 mCi/ml). After i.p. administration of hCG, gastric emptying was inhibited in Ovx rats, but intestinal transit was not affected. Plasma CCK concentrations were increased in a dose-dependent manner after hCG treatment, and gastric emptying showed a significant negative correlation with CCK concentrations 2 (PZ0.01, r ZK0.5104). Peripheral administration (i.p.) of lorglumide, a selective CCK1 receptor antagonist, attenuated the hCG-induced inhibition of gastric emptying in Ovx rats, whereas central administration via the i.c.v. route did not. hCG treatment of Ovx rats inhibits gastric emptying in a dose-dependent manner via a peripheral mechanism of CCK hypersecretion and activation of CCK1 receptors. Journal of Endocrinology (2013) 216, 307–314 http://joe.endocrinology-journals.org Ñ 2013 Society for Endocrinology Published by Bioscientifica Ltd. DOI: 10.1530/JOE-12-0421 Printed in Great Britain Downloaded from Bioscientifica.com at 09/27/2021 11:08:42PM via free access Research K-M SEOW, J-L LEE and others hCG and gastric emptying 216:3 308 Introduction Disturbed gastrointestinal transit, leading to a delay in gastric Materials and methods emptying time, is one of the most common phenomenon in Animals pregnant women (Chiloiro et al. 2001), and this effect is probably caused by changes in plasma concentrations of Female Sprague Dawley rats weighing 250–300 g were certain hormones, such as estrogen (Chen et al. 1995) and housed in a temperature-controlled (22G1 8C) and light- progesterone (Sheen-Chen et al. 2001), as concentrations of controlled (0600–2000 h) environment and fed rat chow. these hormones increase throughout pregnancy. Pregnant Tap water was given ad libitum. Animal protocols were womenwithdecreasedgastrointestinal transit suffer from approved by the Institutional Animal Care and Use nausea, vomiting, or abdominal distension during the course Committee of the National Yang-Ming University. All of pregnancy, especially during the first trimester (Jarnfelt- animals received care in compliance with the Principles of Samsioe et al. 1983). The etiology of nausea and vomiting in Laboratory Animal Care and the Guide for the Care and pregnancy (NVP) is still unknown. Human chorionic gonado- Use of Laboratory Animals published by the National tropin (hCG), a hormone secreted by the placental tropho- Science Council, Taiwan. blast, has been proposed as the most likely cause of NVP, as hCG concentrations rise rapidly during the first trimester and Surgery for insertion of i.c.v. cannulas peak at 10–12 weeks of gestation (Soules et al. 1980). Goodwin et al. (1994) reported that serum hCG concentrations are Surgery for insertion of i.c.v. cannulas was performed significantly increased in women with hyperemesis gravi- following the procedure described by Lin et al. (2003) with darum compared with the control subjects of comparable minor modification. Briefly, the rats were anesthetized by gestational age. Furthermore, hCG concentrations correlate i.p. injection of phenobarbital (30 mg/kg) and placed in with the severity of vomiting (Goodwin et al. 1992). These a stereotaxic frame. A stainless steel guide cannula was findings suggest that hCG may play a role in the pathogenesis implanted according to the atlas of Paxinos and Watson, of NVP and gastrointestinal transit. However, there are no data i.e. 0.8 mm posterior to bregma, 1.4 mm lateral to the on the relationship between hCG and gastrointestinal transit. midline, and 3.5 mm ventral to the dura. An AG-4 cannula Cholecystokinin (CCK), a 33 amino acid peptide (Eicom, Kyoto, Japan) was placed 4.5 mm below the scalp extracted from porcine intestine (Jorpes & Mutt 1966), Journal of Endocrinology and secured in place with two anchor screws and dental inhibits gastric emptying in animals (Debas et al. 1975, Wu acrylic (Tempro, GC Corporation, Tokyo, Japan). hCG was et al. 2008) and humans (Konturek et al. 1990) but has also injected through the AG-4 cannula 1 week after insertion in vivo been reported to stimulate colonic transit (Dinoso of the cannula. et al. 1973, Harvey & Read 1973). The biological actions of CCK are mediated by two types of receptors, CCK1 and Materials CCK2 (Noble et al. 1999). CCK1 receptors are present in both the CNS and various peripheral tissues, such as the The chemicals used in the study included recombi- gallbladder, pancreas, stomach, colon, and ileum, while nant hCG (Ovidrel; Merck Serono), EDTA, aprotinin, the CCK receptor is found predominantly in the CNS 2 trifluoroacetic acid (TFA), and lorglumide sodium (all (Silvente-Poirot et al. 1993). from Sigma Chemical Company), acetonitrile (Wako The aim of this study was to investigate the effects of 51 Chemical Industries, Ltd., Osaka, Japan), Na2 CrO4 hCG on gastric emptying and gastrointestinal transit in (DuPont NEN Research Products, Boston, MA, USA), and ovariectomized (Ovx) rats and to clarify the role of CCK CCK EIA kit (Phoenix Pharmaceuticals, Belmont, CA, USA). and its receptors in regulating the effect of hCG on gastrointestinal transit. Furthermore, estrogen is import- ant for maintaining normal uterine weight. Ovariectomy Experimental design of rats without estrogen supplementation caused uterine atrophy. Decreased uterine weight is an important hall- Effect of Ovx on gastric emptying Ten female rats mark of success in ovariectomy surgery. Also, the were randomly divided into two groups of five each, influence of endogenous estrogen on gastrointestinal group 1 as the control group (diestrus rats) and group 2, transit is relatively excluded. Hence, the change of uterine in which rats were bilaterally Ovx under i.p. phenobarbital weight was observed in this study. (30 mg/kg) anesthesia. The rats were fasted overnight and http://joe.endocrinology-journals.org Ñ 2013 Society for Endocrinology Published by Bioscientifica Ltd. DOI: 10.1530/JOE-12-0421 Printed in Great Britain Downloaded from Bioscientifica.com at 09/27/2021 11:08:42PM via free access Research K-M SEOW, J-L LEE and others hCG and gastric emptying 216:3 309 51 were then fed by gavage with a mixture of Na2 CrO4 Measurement of gastric emptying and gastrointestinal (0.5 mCi/ml) and charcoal (10%) at a dose of 3 ml/kg. The transit rats were decapitated 15 min later, the uteri were weighed, Gastric emptying and gastrointestinal transit were and gastrointestinal transit was measured. measured as described by Doong et al. (1998). The rats were fed by gavage via a catheter (PE-205, inner diameter Effect of i.p. injection of hCG on gastric emptying (ID) 1.67 mm, outer diameter (OD) 2.42 mm, Clay-Adam, and intestinal transit Forty female rats were randomly Parsippany, NJ, USA) with physiological saline (3 ml/kg) divided into four groups of ten each and were bilaterally containing Na 51CrO (0.5 mCi/ml) and 10% charcoal, Ovx under light ether anesthesia. Starting 2 weeks later, 2 4 which was stirred continuously before use. Additional air the test rats received a single daily i.p. injection of 50, 100, (0.5 ml) was used to flush the residual charcoal suspension or 200 IU hCG for 2 days, while the control rats were in the catheter into the rat. Fifteen minutes later, the rats injected with normal saline (1 ml/kg). After a 24-h fast, the were decapitated and the stomach and attached small rats received another i.p. injection of hCG (50, 100, or intestine were immediately exposed by laparotomy. After 200 IU) or normal saline, then, 45 min later, underwent 51 ligation of the esophagogastric, gastroduodenal, and gavage with a mixture of Na2 CrO4 (0.5 mCi/ml) and ileocecal junctions, the whole stomach and small intestine charcoal (10%) at a dose of 3 ml/kg, then were decapitated were carefully removed and placed on a wooden board to 15 min later, the uteri were weighed, and gastrointestinal observe the leading edge of the charcoal within the transit was measured.
Load more

Recommended publications
  • 4 Supplementary File
    Supplemental Material for High-throughput screening discovers anti-fibrotic properties of Haloperidol by hindering myofibroblast activation Michael Rehman1, Simone Vodret1, Luca Braga2, Corrado Guarnaccia3, Fulvio Celsi4, Giulia Rossetti5, Valentina Martinelli2, Tiziana Battini1, Carlin Long2, Kristina Vukusic1, Tea Kocijan1, Chiara Collesi2,6, Nadja Ring1, Natasa Skoko3, Mauro Giacca2,6, Giannino Del Sal7,8, Marco Confalonieri6, Marcello Raspa9, Alessandro Marcello10, Michael P. Myers11, Sergio Crovella3, Paolo Carloni5, Serena Zacchigna1,6 1Cardiovascular Biology, 2Molecular Medicine, 3Biotechnology Development, 10Molecular Virology, and 11Protein Networks Laboratories, International Centre for Genetic Engineering and Biotechnology (ICGEB), Padriciano, 34149, Trieste, Italy 4Institute for Maternal and Child Health, IRCCS "Burlo Garofolo", Trieste, Italy 5Computational Biomedicine Section, Institute of Advanced Simulation IAS-5 and Institute of Neuroscience and Medicine INM-9, Forschungszentrum Jülich GmbH, 52425, Jülich, Germany 6Department of Medical, Surgical and Health Sciences, University of Trieste, 34149 Trieste, Italy 7National Laboratory CIB, Area Science Park Padriciano, Trieste, 34149, Italy 8Department of Life Sciences, University of Trieste, Trieste, 34127, Italy 9Consiglio Nazionale delle Ricerche (IBCN), CNR-Campus International Development (EMMA- INFRAFRONTIER-IMPC), Rome, Italy This PDF file includes: Supplementary Methods Supplementary References Supplementary Figures with legends 1 – 18 Supplementary Tables with legends 1 – 5 Supplementary Movie legends 1, 2 Supplementary Methods Cell culture Primary murine fibroblasts were isolated from skin, lung, kidney and hearts of adult CD1, C57BL/6 or aSMA-RFP/COLL-EGFP mice (1) by mechanical and enzymatic tissue digestion. Briefly, tissue was chopped in small chunks that were digested using a mixture of enzymes (Miltenyi Biotec, 130- 098-305) for 1 hour at 37°C with mechanical dissociation followed by filtration through a 70 µm cell strainer and centrifugation.
    [Show full text]
  • 1 to the Stomach Inhibits Gut-Brain Signalling by the Satiety Hormone Cholecystokinin (CCK)
    Targeted Expression of Plasminogen Activator Inhibitor (PAI)-1 to the Stomach Inhibits Gut-Brain Signalling by the Satiety Hormone Cholecystokinin (CCK) Thesis submitted in accordance with the requirements of the University of Liverpool for the degree of Doctor in Philosophy By Joanne Gamble October 2013 I For Lily, you are the sunshine in my life…. II Table of Contents Figures and tables VII Acknowledgements XI Publications XIII Abstract XIV Chapter 1 ................................................................................................................................ 1 1.1 Overview ........................................................................................................................... 2 1.2 The Gastrointestinal Tract and Digestive Function ...................................................... 4 1.2.1 Distribution, Structure and Biology of Enteroendocrine (EEC) Cells ........................ 5 1.2.2 Luminal Sensing ......................................................................................................... 6 1.3 Energy Homeostasis ......................................................................................................... 7 1.3.1 Gut Hormones ........................................................................................................... 10 1.3.1.1 The Gastrin Family ............................................................................................ 11 1.3.2 PP-fold Family .........................................................................................................
    [Show full text]
  • Acute Restraint Stress Induces Cholecystokinin Release Via Enteric
    Neuropeptides 73 (2019) 71–77 Contents lists available at ScienceDirect Neuropeptides journal homepage: www.elsevier.com/locate/npep Acute restraint stress induces cholecystokinin release via enteric apelin T ⁎ Mehmet Bülbüla, , Osman Sinena, Onur Bayramoğlua, Gökhan Akkoyunlub a Department of Physiology, Akdeniz University, Faculty of Medicine, Antalya, Turkey b Department of Histology and Embryology, Akdeniz University, Faculty of Medicine, Antalya, Turkey ARTICLE INFO ABSTRACT Keywords: Stress increases the apelin content in gut, while exogenous peripheral apelin has been shown to induce chole- Apelin cystokinin (CCK) release. The present study was designed to elucidate (i) the effect of acute stress on enteric Restraint stress production of apelin and CCK, (ii) the role of APJ receptors in apelin-induced CCK release depending on the Cholecystokinin nutritional status. CCK levels were assayed in portal vein blood samples obtained from stressed (ARS) and non- APJ receptor stressed (NS) rats previously injected with APJ receptor antagonist F13A or vehicle. Duodenal expressions of Fasting apelin, CCK and APJ receptor were detected by immunohistochemistry. ARS increased the CCK release which was abolished by selective APJ receptor antagonist F13A. The stimulatory effect of ARS on CCK production was only observed in rats fed ad-libitum. Apelin and CCK expressions were upregulated by ARS. In addition to the duodenal I cells, APJ receptor was also detected in CCK-producing myenteric neurons. Enteric apelin appears to regulate the stress-induced changes in GI functions through CCK. Therefore, apelin/APJ receptor systems seem to be a therapeutic target for the treatment of stress-related gastrointestinal disorders. 1. Introduction for APJ in rodents (De Mota et al., 2000; Medhurst et al., 2003).
    [Show full text]
  • G Protein-Coupled Receptors
    S.P.H. Alexander et al. The Concise Guide to PHARMACOLOGY 2015/16: G protein-coupled receptors. British Journal of Pharmacology (2015) 172, 5744–5869 THE CONCISE GUIDE TO PHARMACOLOGY 2015/16: G protein-coupled receptors Stephen PH Alexander1, Anthony P Davenport2, Eamonn Kelly3, Neil Marrion3, John A Peters4, Helen E Benson5, Elena Faccenda5, Adam J Pawson5, Joanna L Sharman5, Christopher Southan5, Jamie A Davies5 and CGTP Collaborators 1School of Biomedical Sciences, University of Nottingham Medical School, Nottingham, NG7 2UH, UK, 2Clinical Pharmacology Unit, University of Cambridge, Cambridge, CB2 0QQ, UK, 3School of Physiology and Pharmacology, University of Bristol, Bristol, BS8 1TD, UK, 4Neuroscience Division, Medical Education Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee, DD1 9SY, UK, 5Centre for Integrative Physiology, University of Edinburgh, Edinburgh, EH8 9XD, UK Abstract The Concise Guide to PHARMACOLOGY 2015/16 provides concise overviews of the key properties of over 1750 human drug targets with their pharmacology, plus links to an open access knowledgebase of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. The full contents can be found at http://onlinelibrary.wiley.com/doi/ 10.1111/bph.13348/full. G protein-coupled receptors are one of the eight major pharmacological targets into which the Guide is divided, with the others being: ligand-gated ion channels, voltage-gated ion channels, other ion channels, nuclear hormone receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading.
    [Show full text]
  • G Protein‐Coupled Receptors
    S.P.H. Alexander et al. The Concise Guide to PHARMACOLOGY 2019/20: G protein-coupled receptors. British Journal of Pharmacology (2019) 176, S21–S141 THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: G protein-coupled receptors Stephen PH Alexander1 , Arthur Christopoulos2 , Anthony P Davenport3 , Eamonn Kelly4, Alistair Mathie5 , John A Peters6 , Emma L Veale5 ,JaneFArmstrong7 , Elena Faccenda7 ,SimonDHarding7 ,AdamJPawson7 , Joanna L Sharman7 , Christopher Southan7 , Jamie A Davies7 and CGTP Collaborators 1School of Life Sciences, University of Nottingham Medical School, Nottingham, NG7 2UH, UK 2Monash Institute of Pharmaceutical Sciences and Department of Pharmacology, Monash University, Parkville, Victoria 3052, Australia 3Clinical Pharmacology Unit, University of Cambridge, Cambridge, CB2 0QQ, UK 4School of Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol, BS8 1TD, UK 5Medway School of Pharmacy, The Universities of Greenwich and Kent at Medway, Anson Building, Central Avenue, Chatham Maritime, Chatham, Kent, ME4 4TB, UK 6Neuroscience Division, Medical Education Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee, DD1 9SY, UK 7Centre for Discovery Brain Sciences, University of Edinburgh, Edinburgh, EH8 9XD, UK Abstract The Concise Guide to PHARMACOLOGY 2019/20 is the fourth in this series of biennial publications. The Concise Guide provides concise overviews of the key properties of nearly 1800 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. Although the Concise Guide represents approximately 400 pages, the material presented is substantially reduced compared to information and links presented on the website.
    [Show full text]
  • GPCR/G Protein
    Inhibitors, Agonists, Screening Libraries www.MedChemExpress.com GPCR/G Protein G Protein Coupled Receptors (GPCRs) perceive many extracellular signals and transduce them to heterotrimeric G proteins, which further transduce these signals intracellular to appropriate downstream effectors and thereby play an important role in various signaling pathways. G proteins are specialized proteins with the ability to bind the nucleotides guanosine triphosphate (GTP) and guanosine diphosphate (GDP). In unstimulated cells, the state of G alpha is defined by its interaction with GDP, G beta-gamma, and a GPCR. Upon receptor stimulation by a ligand, G alpha dissociates from the receptor and G beta-gamma, and GTP is exchanged for the bound GDP, which leads to G alpha activation. G alpha then goes on to activate other molecules in the cell. These effects include activating the MAPK and PI3K pathways, as well as inhibition of the Na+/H+ exchanger in the plasma membrane, and the lowering of intracellular Ca2+ levels. Most human GPCRs can be grouped into five main families named; Glutamate, Rhodopsin, Adhesion, Frizzled/Taste2, and Secretin, forming the GRAFS classification system. A series of studies showed that aberrant GPCR Signaling including those for GPCR-PCa, PSGR2, CaSR, GPR30, and GPR39 are associated with tumorigenesis or metastasis, thus interfering with these receptors and their downstream targets might provide an opportunity for the development of new strategies for cancer diagnosis, prevention and treatment. At present, modulators of GPCRs form a key area for the pharmaceutical industry, representing approximately 27% of all FDA-approved drugs. References: [1] Moreira IS. Biochim Biophys Acta. 2014 Jan;1840(1):16-33.
    [Show full text]
  • Federal Register / Vol. 60, No. 80 / Wednesday, April 26, 1995 / Notices DIX to the HTSUS—Continued
    20558 Federal Register / Vol. 60, No. 80 / Wednesday, April 26, 1995 / Notices DEPARMENT OF THE TREASURY Services, U.S. Customs Service, 1301 TABLE 1.ÐPHARMACEUTICAL APPEN- Constitution Avenue NW, Washington, DIX TO THE HTSUSÐContinued Customs Service D.C. 20229 at (202) 927±1060. CAS No. Pharmaceutical [T.D. 95±33] Dated: April 14, 1995. 52±78±8 ..................... NORETHANDROLONE. A. W. Tennant, 52±86±8 ..................... HALOPERIDOL. Pharmaceutical Tables 1 and 3 of the Director, Office of Laboratories and Scientific 52±88±0 ..................... ATROPINE METHONITRATE. HTSUS 52±90±4 ..................... CYSTEINE. Services. 53±03±2 ..................... PREDNISONE. 53±06±5 ..................... CORTISONE. AGENCY: Customs Service, Department TABLE 1.ÐPHARMACEUTICAL 53±10±1 ..................... HYDROXYDIONE SODIUM SUCCI- of the Treasury. NATE. APPENDIX TO THE HTSUS 53±16±7 ..................... ESTRONE. ACTION: Listing of the products found in 53±18±9 ..................... BIETASERPINE. Table 1 and Table 3 of the CAS No. Pharmaceutical 53±19±0 ..................... MITOTANE. 53±31±6 ..................... MEDIBAZINE. Pharmaceutical Appendix to the N/A ............................. ACTAGARDIN. 53±33±8 ..................... PARAMETHASONE. Harmonized Tariff Schedule of the N/A ............................. ARDACIN. 53±34±9 ..................... FLUPREDNISOLONE. N/A ............................. BICIROMAB. 53±39±4 ..................... OXANDROLONE. United States of America in Chemical N/A ............................. CELUCLORAL. 53±43±0
    [Show full text]
  • (12) United States Patent (10) Patent No.: US 8,158,152 B2 Palepu (45) Date of Patent: Apr
    US008158152B2 (12) United States Patent (10) Patent No.: US 8,158,152 B2 Palepu (45) Date of Patent: Apr. 17, 2012 (54) LYOPHILIZATION PROCESS AND 6,884,422 B1 4/2005 Liu et al. PRODUCTS OBTANED THEREBY 6,900, 184 B2 5/2005 Cohen et al. 2002fOO 10357 A1 1/2002 Stogniew etal. 2002/009 1270 A1 7, 2002 Wu et al. (75) Inventor: Nageswara R. Palepu. Mill Creek, WA 2002/0143038 A1 10/2002 Bandyopadhyay et al. (US) 2002fO155097 A1 10, 2002 Te 2003, OO68416 A1 4/2003 Burgess et al. 2003/0077321 A1 4/2003 Kiel et al. (73) Assignee: SciDose LLC, Amherst, MA (US) 2003, OO82236 A1 5/2003 Mathiowitz et al. 2003/0096378 A1 5/2003 Qiu et al. (*) Notice: Subject to any disclaimer, the term of this 2003/OO96797 A1 5/2003 Stogniew et al. patent is extended or adjusted under 35 2003.01.1331.6 A1 6/2003 Kaisheva et al. U.S.C. 154(b) by 1560 days. 2003. O191157 A1 10, 2003 Doen 2003/0202978 A1 10, 2003 Maa et al. 2003/0211042 A1 11/2003 Evans (21) Appl. No.: 11/282,507 2003/0229027 A1 12/2003 Eissens et al. 2004.0005351 A1 1/2004 Kwon (22) Filed: Nov. 18, 2005 2004/0042971 A1 3/2004 Truong-Le et al. 2004/0042972 A1 3/2004 Truong-Le et al. (65) Prior Publication Data 2004.0043042 A1 3/2004 Johnson et al. 2004/OO57927 A1 3/2004 Warne et al. US 2007/O116729 A1 May 24, 2007 2004, OO63792 A1 4/2004 Khera et al.
    [Show full text]
  • United States Patent (10) Patent No.: US 8,003,794 B2 Boyd Et Al
    USO08003794B2 (12) United States Patent (10) Patent No.: US 8,003,794 B2 Boyd et al. (45) Date of Patent: Aug. 23, 2011 (54) (S)-N-METHYLNALTREXONE 4.385,078 A 5/1983 Onda et al. 4.427,676 A 1, 1984 White et al. (75) Inventors: Thomas A. Boyd, Grandview, NY (US); 4,430,327 A 2, 1984 Frederickson et al. 4,452,775 A 6, 1984 Kent Howard Wagoner, Warwick, NY (US); 4,457.907. A 7/1984 Porter et al. Suketu P. Sanghvi, Kendall Park, NJ 4.462,839 A 7/1984 McGinley et al. (US); Christopher Verbicky, 4,466,968 A 8, 1984 Bernstein Broadalbin, NY (US); Stephen t St. A s 3. Miley al. Andruski, Clifton Park, NY (US) 4,556,552- - - A 12/1985 Porter2 et al.a. 4,606,909 A 8/1986 Bechgaard et al. (73) Assignee: Progenics Pharmaceuticals, Inc., 4,615,885 A 10/1986 Nakagame et al. Tarrytown, NY (US) 4,670.287. A 6/1987 Tsuji et al. 4.675, 189 A 6, 1987 Kent et al. (*) Notice: Subject to any disclaimer, the term of this 4,689,332 A 8/1987 McLaughlin et al. patent is extended or adjusted under 35 2.7868 A SE Se U.S.C. 154(b) by 184 days. 4,765,978 A 8/1988 Abidi et al. 4,806,556 A 2/1989 Portoghese (21) Appl. No.: 12/460,507 4,824,853. A 4, 1989 Walls et al. 4,836,212 A 6, 1989 Schmitt et al. (22) Filed: Jul. 20, 2009 4,837.214 A 6, 1989 Tanaka et al.
    [Show full text]
  • Stembook 2018.Pdf
    The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances FORMER DOCUMENT NUMBER: WHO/PHARM S/NOM 15 WHO/EMP/RHT/TSN/2018.1 © World Health Organization 2018 Some rights reserved. This work is available under the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 IGO licence (CC BY-NC-SA 3.0 IGO; https://creativecommons.org/licenses/by-nc-sa/3.0/igo). Under the terms of this licence, you may copy, redistribute and adapt the work for non-commercial purposes, provided the work is appropriately cited, as indicated below. In any use of this work, there should be no suggestion that WHO endorses any specific organization, products or services. The use of the WHO logo is not permitted. If you adapt the work, then you must license your work under the same or equivalent Creative Commons licence. If you create a translation of this work, you should add the following disclaimer along with the suggested citation: “This translation was not created by the World Health Organization (WHO). WHO is not responsible for the content or accuracy of this translation. The original English edition shall be the binding and authentic edition”. Any mediation relating to disputes arising under the licence shall be conducted in accordance with the mediation rules of the World Intellectual Property Organization. Suggested citation. The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances. Geneva: World Health Organization; 2018 (WHO/EMP/RHT/TSN/2018.1). Licence: CC BY-NC-SA 3.0 IGO. Cataloguing-in-Publication (CIP) data.
    [Show full text]
  • A Abacavir Abacavirum Abakaviiri Abagovomab Abagovomabum
    A abacavir abacavirum abakaviiri abagovomab abagovomabum abagovomabi abamectin abamectinum abamektiini abametapir abametapirum abametapiiri abanoquil abanoquilum abanokiili abaperidone abaperidonum abaperidoni abarelix abarelixum abareliksi abatacept abataceptum abatasepti abciximab abciximabum absiksimabi abecarnil abecarnilum abekarniili abediterol abediterolum abediteroli abetimus abetimusum abetimuusi abexinostat abexinostatum abeksinostaatti abicipar pegol abiciparum pegolum abisipaaripegoli abiraterone abirateronum abirateroni abitesartan abitesartanum abitesartaani ablukast ablukastum ablukasti abrilumab abrilumabum abrilumabi abrineurin abrineurinum abrineuriini abunidazol abunidazolum abunidatsoli acadesine acadesinum akadesiini acamprosate acamprosatum akamprosaatti acarbose acarbosum akarboosi acebrochol acebrocholum asebrokoli aceburic acid acidum aceburicum asebuurihappo acebutolol acebutololum asebutololi acecainide acecainidum asekainidi acecarbromal acecarbromalum asekarbromaali aceclidine aceclidinum aseklidiini aceclofenac aceclofenacum aseklofenaakki acedapsone acedapsonum asedapsoni acediasulfone sodium acediasulfonum natricum asediasulfoninatrium acefluranol acefluranolum asefluranoli acefurtiamine acefurtiaminum asefurtiamiini acefylline clofibrol acefyllinum clofibrolum asefylliiniklofibroli acefylline piperazine acefyllinum piperazinum asefylliinipiperatsiini aceglatone aceglatonum aseglatoni aceglutamide aceglutamidum aseglutamidi acemannan acemannanum asemannaani acemetacin acemetacinum asemetasiini aceneuramic
    [Show full text]
  • Nonpeptide Antagonists of Neuropeptide Receptors: Tools for Research and Therapy
    Nonpeptide antagonists of neuropeptide receptors: tools for research and therapy. Catalina Betancur, Mounia Azzi, William Rostène To cite this version: Catalina Betancur, Mounia Azzi, William Rostène. Nonpeptide antagonists of neuropeptide receptors: tools for research and therapy.. Trends in Pharmacological Sciences, Elsevier, 1997, 18 (10), pp.372-86. inserm-00276481 HAL Id: inserm-00276481 https://www.hal.inserm.fr/inserm-00276481 Submitted on 29 Apr 2008 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. HAL author manuscript Trends in Pharmacological Sciences 1997;18(10):372-86 Nonpeptide antagonists of neuropeptide receptors: Tools for research and therapy HAL author manuscript inserm-00276481, version 1 Catalina Betancur, Mounia Azzi and William Rostène INSERM U339, Hôpital Saint-Antoine, 184 rue du Faubourg Saint-Antoine, 75571 Paris Cedex 12, France Address correspondence to C. Betancur, e-mail: [email protected] Running title: Nonpeptide antagonists of peptide receptors Key words: nonpeptide antagonist, peptide receptor, cholecystokinin, tachykinin, neurotensin, neuropeptide Y, angiotensin, corticotropin releasing factor Summary The recent development of selective and highly potent nonpeptide antagonists for peptide receptors has constituted a major breakthrough in the field of neuropeptide research.
    [Show full text]