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Pharmaceutical Appendix to the Tariff Schedule 2
Harmonized Tariff Schedule of the United States (2007) (Rev. 2) Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE Harmonized Tariff Schedule of the United States (2007) (Rev. 2) Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 2 Table 1. This table enumerates products described by International Non-proprietary Names (INN) which shall be entered free of duty under general note 13 to the tariff schedule. The Chemical Abstracts Service (CAS) registry numbers also set forth in this table are included to assist in the identification of the products concerned. For purposes of the tariff schedule, any references to a product enumerated in this table includes such product by whatever name known. ABACAVIR 136470-78-5 ACIDUM LIDADRONICUM 63132-38-7 ABAFUNGIN 129639-79-8 ACIDUM SALCAPROZICUM 183990-46-7 ABAMECTIN 65195-55-3 ACIDUM SALCLOBUZICUM 387825-03-8 ABANOQUIL 90402-40-7 ACIFRAN 72420-38-3 ABAPERIDONUM 183849-43-6 ACIPIMOX 51037-30-0 ABARELIX 183552-38-7 ACITAZANOLAST 114607-46-4 ABATACEPTUM 332348-12-6 ACITEMATE 101197-99-3 ABCIXIMAB 143653-53-6 ACITRETIN 55079-83-9 ABECARNIL 111841-85-1 ACIVICIN 42228-92-2 ABETIMUSUM 167362-48-3 ACLANTATE 39633-62-0 ABIRATERONE 154229-19-3 ACLARUBICIN 57576-44-0 ABITESARTAN 137882-98-5 ACLATONIUM NAPADISILATE 55077-30-0 ABLUKAST 96566-25-5 ACODAZOLE 79152-85-5 ABRINEURINUM 178535-93-8 ACOLBIFENUM 182167-02-8 ABUNIDAZOLE 91017-58-2 ACONIAZIDE 13410-86-1 ACADESINE 2627-69-2 ACOTIAMIDUM 185106-16-5 ACAMPROSATE 77337-76-9 -
The Influence of Palmatine Isolated from Berberis Sibirica Radix On
cells Article The Influence of Palmatine Isolated from Berberis sibirica Radix on Pentylenetetrazole-Induced Seizures in Zebrafish Kinga Gawel 1,2,* , Wirginia Kukula-Koch 3 , Dorota Nieoczym 4, Katarzyna Stepnik 5 , Wietske van der Ent 1, Nancy Saana Banono 1 , Dominik Tarabasz 3, Waldemar A. Turski 2 and Camila V. Esguerra 1 1 Chemical Neuroscience Group, Faculty of Medicine, Centre for Molecular Medicine Norway, University of Oslo, Gaustadalléen 21, 0349 Oslo, Norway; [email protected] (W.v.d.E.); [email protected] (N.S.B.); [email protected] (C.V.E.) 2 Department of Experimental and Clinical Pharmacology, Medical University of Lublin, Jaczewskiego Str. 8b, 20-090 Lublin, Poland; [email protected] 3 Chair and Department of Pharmacognosy, Medical University of Lublin, 1, Chodzki Str. 1, 20-093 Lublin, Poland; [email protected] (W.K.-K.); [email protected] (D.T.) 4 Department of Animal Physiology and Pharmacology, Institute of Biology and Biochemistry, Faculty of Biology and Biotechnology, Maria Curie-Skłodowska University, Akademicka Str. 19, 20-033 Lublin, Poland; [email protected] 5 Department of Physical Chemistry, Institute of Chemical Sciences, Faculty of Chemistry, Maria Curie-Skłodowska University, Pl. M. Curie-Skłodowskiej 3/243, 20-031 Lublin, Poland; [email protected] * Correspondence: [email protected]; Tel.: +48-81448-6454 Received: 28 April 2020; Accepted: 14 May 2020; Published: 16 May 2020 Abstract: Palmatine (PALM) and berberine (BERB) are widely identified isoquinoline alkaloids among the representatives of the Berberidaceae botanical family. The antiseizure activity of BERB was shown previously in experimental epilepsy models. -
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 -
The Relationship of Alcohol Dependence to Monoamine Oxidase A
The Relationship of Alcohol Dependence to Monoamine Oxidase A by Brittany Matthews A thesis submitted in conformity with the requirements for the degree of Doctor of Philosophy Department of Pharmacology and Toxicology University of Toronto © Copyright by Brittany Matthews 2015 The Relationship of Alcohol Dependence to Monoamine Oxidase A Brittany Matthews Doctor of Philosophy Department of Pharmacology and Toxicology University of Toronto 2015 Abstract Background: Alcohol dependence (AD) is a substance abuse disorder characterized by compulsive alcohol seeking and intake, combined with a negative emotional state during withdrawal. AD is also associated with markers of apoptosis and/or oxidative stress across multiple organs. Monoamine oxidase A (MAO-A) is an important enzyme that participates in the cellular response to oxidative stress, and is elevated during major depressive episodes, somewhat more robustly in the prefrontal cortex (PFC) and anterior cingulate cortex (ACC). It is unknown whether MAO-A levels are abnormal in AD. The current studies examine whether: i) MAO-A level is elevated in the PFC and ACC in AD in humans. ii) Chronic harman exposure, a MAO-A inhibitor found in alcoholic beverages, upregulates MAO-A in the PFC and ACC of rodents. iii) Chronic alcohol exposure upregulates MAO-A in the PFC and ACC of rodents. Methods: i) Sixteen participants with AD underwent [ 11 C]-harmine positron emission tomography to determine MAO-A distribution volume (VT), an index of MAO-A level. ii ii) Rats were treated with harman for 21 days (0, 2, 5, 15 mg/kg/day) via osmotic minipump. MAO-A protein and activity levels, measured with Western blot and a spectrophotometric assay respectively, were assessed immediately and after 8-hour withdrawal. -
Monoamine Oxidase-A in Borderline Personality Disorder and Antisocial Personality Disorder
MONOAMINE OXIDASE-A IN BORDERLINE PERSONALITY DISORDER AND ANTISOCIAL PERSONALITY DISORDER by Nathan J. Kolla A thesis submitted in conformity with the requirements for the degree of Doctor of Philosophy, Institute of Medical Science, University of Toronto © Copyright by Nathan J. Kolla (2015) Nathan J. Kolla Title: Monoamine Oxidase-A in Borderline Personality Disorder and Antisocial Personality Disorder Doctor of Philosophy, Institute of Medical Science, University of Toronto, 2015 ABSTRACT Monoamine oxidase A (MAO-A) is a brain enzyme that serves several physiologic functions, including metabolism of monoamine neurotransmitters and induction of pro-apoptotic signaling pathways. Increased brain MAO-A level is present in clinical disorders characterized by low mood states, whereas decreased brain MAO-A level is associated with higher trait impulsivity and aggression in healthy volunteers. Borderline personality disorder (BPD) and antisocial personality disorder (ASPD) are common psychiatric conditions that exact a high healthcare and societal burden. BPD is associated with acute episodes of severe dysphoria, and ASPD presents high levels of impulsivity and aggression. The overall aim of the thesis was to investigate MAO- A brain level in BPD and ASPD. The first experiment used [11C] harmine positron emission tomography (PET) to assess MAO-A total distribution volume (MAO-A VT), an index of MAO-A density, in females with BPD. Our results showed that MAO-A VT was elevated in the prefrontal cortex (PFC) and anterior cingulate cortex (ACC) of severe BPD compared to control groups. Greater PFC and ACC MAO-A VT was additionally associated with more severe mood symptoms and suicidality in BPD. 11 The second experiment applied [ C] harmine PET to examine MAO-A VT in ii impulsive, violent male offenders with ASPD. -
Agonists of Guanylate Cyclase Useful for the Treatment of Gastrointestinal Disorders, Inflammation, Cancer and Other Disorders
(19) TZZ ¥__T (11) EP 2 998 314 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.: 23.03.2016 Bulletin 2016/12 C07K 7/08 (2006.01) A61K 38/10 (2006.01) A61K 47/48 (2006.01) A61P 1/00 (2006.01) (21) Application number: 15190713.6 (22) Date of filing: 04.06.2008 (84) Designated Contracting States: (72) Inventors: AT BE BG CH CY CZ DE DK EE ES FI FR GB GR • SHAILUBHAI, Kunwar HR HU IE IS IT LI LT LU LV MC MT NL NO PL PT Audubon, PA 19402 (US) RO SE SI SK TR • JACOB, Gary S. New York, NY 10028 (US) (30) Priority: 04.06.2007 US 933194 P (74) Representative: Cooley (UK) LLP (62) Document number(s) of the earlier application(s) in Dashwood accordance with Art. 76 EPC: 69 Old Broad Street 12162903.4 / 2 527 360 London EC2M 1QS (GB) 08770135.5 / 2 170 930 Remarks: (71) Applicant: Synergy Pharmaceuticals Inc. This application was filed on 21-10-2015 as a New York, NY 10170 (US) divisional application to the application mentioned under INID code 62. (54) AGONISTS OF GUANYLATE CYCLASE USEFUL FOR THE TREATMENT OF GASTROINTESTINAL DISORDERS, INFLAMMATION, CANCER AND OTHER DISORDERS (57) The invention provides novel guanylate cycla- esterase. The gastrointestinal disorder may be classified se-C agonist peptides and their use in the treatment of as either irritable bowel syndrome, constipation, or ex- human diseases including gastrointestinal disorders, in- cessive acidity etc. The gastrointestinal disease may be flammation or cancer (e.g., a gastrointestinal cancer). -
Imaging Dopamine
This page intentionally left blank Imaging Dopamine Since its discovery 50 years ago, brain dopamine has been implicated in the control of movement and cognition, and has emerged as a key factor in diverse brain diseases such as Parkinson’s disease, schizophrenia, and drug addiction. This book is an illustrated biography of the dopamine molecule, beginning with an account of its synthesis in brain, and then describing its storage, release and signalling mechanisms, and its ultimate metabolic breakdown. Using color illustrations of positron emission tomography (PET) scans, each chapter presents a specific stage in the biochemical pathway for dopamine. Writing for researchers and graduate students, Paul Cumming presents an overview of all that has been learned about dopamine through molecular imaging, a technology which allows the measurement of formerly invisible processes in the living brain. He reviews current technical controversies in the interpretation of dopamine imaging and presents key results illuminating the roles of brain dopamine in illness and health. Paul Cumming is Professor in the Department of Nuclear Medicine at Ludwig- Maximilian University in Munich, Germany. He currently serves on the editorial boards of the journals Synapse, Journal of Cerebral Blood Flow and Metabolism, and NeuroImage. Imaging Dopamine PAUL CUMMING Ludwig-Maximilian University, Munich, Germany CAMBRIDGE UNIVERSITY PRESS Cambridge, New York, Melbourne, Madrid, Cape Town, Singapore, São Paulo Cambridge University Press The Edinburgh Building, Cambridge CB2 8RU, UK Published in the United States of America by Cambridge University Press, New York www.cambridge.org Information on this title: www.cambridge.org/9780521790024 © P. Cumming 2009 This publication is in copyright. -