Back Matter (PDF)
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Seizure Disorders and Commercial Motor Vehicle Driver Safety (Comprehensive Review)
Evidence Report: Seizure Disorders and Commercial Motor Vehicle Driver Safety (Comprehensive Review) Presented to Federal Motor Carrier Safety Administration November 30, 2007 Prepared for Prepared by MANILA Consulting Group, Inc. ECRI 1420 Beverly Road, Suite 220 5200 Butler Pike McLean, VA 22101 Plymouth Meeting, PA 19462 This report is comprised of research conducted to analyze the impact of Seizure Disorders on Commercial Motor Vehicle Driver Safety. Federal Motor Carrier Safety Administration considers evidence, expert recommendations, and other data, however, all proposed changes to current standards and guidance (guidelines) will be subject to public-notice-and-comment and regulatory processes. FMCSA Evidence Report: Seizure Disorders and Commercial Motor Vehicle Driver Safety 11/30/2007 Policy Statement This evidence report was prepared by ECRI under subcontract to MANILA Consulting Group, Inc., which holds prime Contract No: GS-10F-0177N/DTMC75-06-F-00039 with the Department of Transportation’s Federal Motor Carrier Safety Administration. ECRI is an independent, nonprofit health services research agency and a Collaborating Center for Health Technology Assessment of the World Health Organization. ECRI has been designated an Evidence-based Practice Center (EPC) by the United States Agency for Healthcare Research and Quality. ECRI’s mission is to provide information and technical assistance to the healthcare community worldwide to support safe and cost-effective patient care. The results of ECRI’s research and experience are available through its publications, information systems, databases, technical assistance programs, laboratory services, seminars, and fellowships. The purpose of this evidence report is to provide information regarding the current state of knowledge on this topic. -
Both N-Methyl-D-Aspartate and Non-N-Methyl- D-Aspartate Glutamate Receptors in the Bed
JOP0010.1177/0269881117691468Journal of PsychopharmacologyAdami et al. 691468research-article2017 Original Paper Both N-methyl-D-aspartate and non-N-methyl- D-aspartate glutamate receptors in the bed nucleus of the stria terminalis modulate the Journal of Psychopharmacology 2017, Vol. 31(6) 674 –681 cardiovascular responses to acute restraint © The Author(s) 2017 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav stress in rats DOI:https://doi.org/10.1177/0269881117691468 10.1177/0269881117691468 journals.sagepub.com/home/jop Mariane B Adami1*, Lucas Barretto-de-Souza1,2*, Josiane O Duarte1, Jeferson Almeida1,2 and Carlos C Crestani1,2 Abstract The bed nucleus of the stria terminalis (BNST) is a forebrain structure that has been implicated on cardiovascular responses evoked by emotional stress. However, the local neurochemical mechanisms mediating the BNST control of stress responses are not fully described. In our study we investigated the involvement of glutamatergic neurotransmission within the BNST in cardiovascular changes evoked by acute restraint stress in rats. For this study, we investigated the effects of bilateral microinjections of selective antagonists of either N-methyl-D-aspartate (NMDA) or non-NMDA glutamate receptors into the BNST on the arterial pressure and heart rate increase and the decrease in tail skin temperature induced by acute restraint stress. Microinjection of the selective NMDA glutamate receptor antagonist LY235959 (1 nmol/100 nL) into the BNST decreased the tachycardiac response to restraint stress, without affecting the arterial pressure increase and the drop in skin temperature. Bilateral BNST treatment with the selective non-NMDA glutamate receptor NBQX (1 nmol/100 nL) decreased the heart rate increase and the fall in tail skin temperature, without affecting the blood pressure increase. -
(12) Patent Application Publication (10) Pub. No.: US 2013/0165511 A1 Lederman Et Al
US 2013 O165511A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2013/0165511 A1 Lederman et al. (43) Pub. Date: Jun. 27, 2013 (54) TREATMENT FOR COCANE ADDICTION Publication Classification (75) Inventors: Seth Lederman, NEW York, NY (US); (51) Int. Cl. Herbert Harris, Chapel Hill, NC (US) A63/37 (2006.01) A63/6 (2006.01) (73) Assignee: TONIX Pharmaceuticals Holding (52) U.S. Cl. Corp, New York, NY (US) CPC ............... A61K 31/137 (2013.01); A61K3I/I6 (2013.01) (21) Appl. No.: 13/820,338 USPC ........................................... 514/491; 514/654 (22) PCT Fled: Aug. 31, 2011 (57) ABSTRACT (86) PCT NO.: PCT/US11/O1529 A novel pharmaceutical composition is provided for the con S371 (c)(1), trol of stimulant effects, in particular treatment of cocaine (2), (4) Date: Mar. 1, 2013 addiction, or further to treatment of both cocaine and alcohol dependency, including simultaneous therapeutic dose appli Related U.S. Application Data cation or a single dose of a combined therapeutically effective (60) Provisional application No. 61/379,095, filed on Sep. composition of disulfiram and selegiline compounds or phar 1, 2010. maceutically acceptable non-toxic salt thereof. US 2013/01655 11 A1 Jun. 27, 2013 TREATMENT FOR COCANE ADDCTION the United States in 2005. In the sense of this invention the term “addiction' may be defined as a compulsive drug taking CROSS-REFERENCE TO RELATED or abuse condition related to “reward’ system of the afflicted APPLICATIONS: patient. The treatment of cocaine addiction or dependency 0001. The present application which claims priority from has targeted a lowering of dopaminergic tone to help decrease U.S. -
Thyroid Hormones Modulate GABAA Receptor-Mediated Currents in Hippocampal Neurons
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Archivio istituzionale della ricerca - Università di Modena e Reggio Emilia Neuropharmacology 60 (2011) 1254e1261 Contents lists available at ScienceDirect Neuropharmacology journal homepage: www.elsevier.com/locate/neuropharm Thyroid hormones modulate GABAA receptor-mediated currents in hippocampal neurons G. Puia*, G. Losi 1 Department of Biomedical Science, Pharmacology Section, University of Modena and Reggio Emilia, via Campi 287, 41100 Modena, Italy article info abstract Article history: Thyroid hormones (THs) play a crucial role in the maturation and functioning of mammalian central 0 Received 4 August 2010 nervous system. Thyroxine (T4) and 3, 3 ,5-L-triiodothyronine (T3) are well known for their genomic Received in revised form effects, but recently attention has been focused on their non genomic actions as modulators of neuronal 28 October 2010 activity. In the present study we report that T4 and T3 reduce, in a non competitive manner, GABA- Accepted 15 December 2010 evoked currents in rat hippocampal cultures with IC50sof13Æ 4 mM and 12 Æ 3 mM, respectively. The genomically inactive compound rev-T3 was also able to inhibit the currents elicited by GABA. Blocking Keywords: PKC or PKA activity, chelating intracellular calcium, or antagonizing the integrin receptor aVb3 with Thryoid hormones GABAergic neurotransmission TETRAC did not affect THs modulation of GABA-evoked currents. THs affect also synaptic activity in Neuronal cultures hippocampal and cortical cultured neurons. sIPSCs T3 and T4 reduced to approximately 50% the amplitude and frequency of spontaneous inhibitory Tonic currents synaptic currents (sIPSCs), without altering their decay kinetic. -
Neuroenhancement in Healthy Adults, Part I: Pharmaceutical
l Rese ca arc ni h li & C f B o i o l e Journal of a t h n Fond et al., J Clinic Res Bioeth 2015, 6:2 r i c u s o J DOI: 10.4172/2155-9627.1000213 ISSN: 2155-9627 Clinical Research & Bioethics Review Article Open Access Neuroenhancement in Healthy Adults, Part I: Pharmaceutical Cognitive Enhancement: A Systematic Review Fond G1,2*, Micoulaud-Franchi JA3, Macgregor A2, Richieri R3,4, Miot S5,6, Lopez R2, Abbar M7, Lancon C3 and Repantis D8 1Université Paris Est-Créteil, Psychiatry and Addiction Pole University Hospitals Henri Mondor, Inserm U955, Eq 15 Psychiatric Genetics, DHU Pe-psy, FondaMental Foundation, Scientific Cooperation Foundation Mental Health, National Network of Schizophrenia Expert Centers, F-94000, France 2Inserm 1061, University Psychiatry Service, University of Montpellier 1, CHU Montpellier F-34000, France 3POLE Academic Psychiatry, CHU Sainte-Marguerite, F-13274 Marseille, Cedex 09, France 4 Public Health Laboratory, Faculty of Medicine, EA 3279, F-13385 Marseille, Cedex 05, France 5Inserm U1061, Idiopathic Hypersomnia Narcolepsy National Reference Centre, Unit of sleep disorders, University of Montpellier 1, CHU Montpellier F-34000, Paris, France 6Inserm U952, CNRS UMR 7224, Pierre and Marie Curie University, F-75000, Paris, France 7CHU Carémeau, University of Nîmes, Nîmes, F-31000, France 8Department of Psychiatry, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Eschenallee 3, 14050 Berlin, Germany *Corresponding author: Dr. Guillaume Fond, Pole de Psychiatrie, Hôpital A. Chenevier, 40 rue de Mesly, Créteil F-94010, France, Tel: (33)178682372; Fax: (33)178682381; E-mail: [email protected] Received date: January 06, 2015, Accepted date: February 23, 2015, Published date: February 28, 2015 Copyright: © 2015 Fond G, et al. -
NBQX Attenuates Excitotoxic Injury in Developing White Matter
The Journal of Neuroscience, December 15, 2000, 20(24):9235–9241 NBQX Attenuates Excitotoxic Injury in Developing White Matter Pamela L. Follett, Paul A. Rosenberg, Joseph J. Volpe, and Frances E. Jensen Department of Neurology and Program in Neuroscience, Children’s Hospital and Harvard Medical School, Boston, Massachusetts 02115 The excitatory neurotransmitter glutamate is released from axons hr) resulted in selective, subcortical white matter injury with a and glia under hypoxic/ischemic conditions. In vitro, oligoden- marked ipsilateral decrease in immature and myelin basic drocytes (OLs) express non-NMDA glutamate receptors (GluRs) protein-expressing OLs that was also significantly attenuated by and are susceptible to GluR-mediated excitotoxicity. We evalu- 6-nitro-7-sulfamoylbenzo(f)quinoxaline-2,3-dione (NBQX). Intra- ated the role of GluR-mediated OL excitotoxicity in hypoxic/ cerebral AMPA demonstrated greater susceptibility to OL injury ischemic white matter injury in the developing brain. Hypoxic/ at P7 than in younger or older pups, and this was attenuated by ischemic white matter injury is thought to mediate periventricular systemic pretreatment with the AMPA antagonist NBQX. These leukomalacia, an age-dependent white matter lesion seen in results indicate a parallel, maturation-dependent susceptibility of preterm infants and a common antecedent to cerebral palsy. immature OLs to AMPA and hypoxia/ischemia. The protective Hypoxia/ischemia in rat pups at postnatal day 7 (P7) produced efficacy of NBQX suggests a role for glutamate receptor- selective white matter lesions and OL death. Furthermore, OLs in mediated excitotoxic OL injury in immature white matter in vivo. pericallosal white matter express non-NMDA GluRs at P7. -
By Michael J. Marmura, MD and Stephen Silberstein, MD
By Michael J. Marmura, MD and Stephen Silberstein, MD igraine is a common chronic and often disabling OTCs without substantial relief.2 Providers treating migraine neurological disorder characterized by attacks of must be familiar with different acute treatments, be comfortable moderate to severe headache. Migraineurs usually with individualizing treatment, and be able to combine treat- experience nausea and light and sound sensitivity ment modalities. Mduring their attacks, and many have aura. Most Acute attack medications include specific medications, such patients experience reduced ability to function with attacks and as triptans, ergots and dihydroergotamine (DHE), and non-spe- many are bed-bound. Migraines can have multiple triggers such cific medications used for other pain disorders. In selecting acute as food, sleep changes, or hormonal factors.1 Often migraineurs migraine medication, patients need a treatment plan tailored to elect to treat their headaches without physician consultation their headache type. Mild or moderate intensity attacks often using rest or over-the-counter (OTC) medications. Patients who respond to treatment with non-steroidal anti-inflammatory present for evaluation with migraine have usually tried some medications (NSAIDs) or combination medications, while more 12 Practical Neurology February 2009 severe attacks may respond better to specific medications. If the or combination medications more than 10 days a month for initial treatments fail, rescue medication is needed. This review more than three months.11 Frequent opioid and barbiturate use discusses acute evidence-based and practical treatments for are risk factors for the development of CDH,12 and stopping migraine, and specifically focuses on the treatment of intractable these medications can result in increased headache and with- headaches such as status migrainosus. -
NIH Public Access Author Manuscript Addict Biol
NIH Public Access Author Manuscript Addict Biol. Author manuscript; available in PMC 2014 January 01. Published in final edited form as: Addict Biol. 2013 January ; 18(1): 54–65. doi:10.1111/adb.12000. Enhanced AMPA Receptor Activity Increases Operant Alcohol Self-administration and Cue-Induced Reinstatement $watermark-text $watermark-text $watermark-text Reginald Cannadya,b, Kristen R. Fishera, Brandon Duranta, Joyce Besheera,b,c, and Clyde W. Hodgea,b,c,d aBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 bCurriculum in Neurobiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 cDepartment of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 dDepartment of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 Abstract Long-term alcohol exposure produces neuroadaptations that contribute to the progression of alcohol abuse disorders. Chronic alcohol consumption results in strengthened excitatory neurotransmission and increased AMPA receptor signaling in animal models. However, the mechanistic role of enhanced AMPA receptor activity in alcohol reinforcement and alcohol- seeking behavior remains unclear. This study examined the role of enhanced AMPA receptor function using the selective positive allosteric modulator, aniracetam, in modulating operant alcohol self-administration and cue-induced reinstatement. Male alcohol-preferring (P-) rats, trained to self-administer alcohol (15%, v/v) versus water were pretreated with aniracetam to assess effects on maintenance of alcohol self-administration. To determine reinforcer specificity, P-rats were trained to self-administer sucrose (0.8%, w/v) versus water, and effects of aniracetam were tested. -
Homomeric Q/R Edited AMPA Receptors Conduct When Desensitized Ian D
bioRxiv preprint doi: https://doi.org/10.1101/595009; this version posted April 1, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Homomeric Q/R edited AMPA receptors conduct when desensitized Ian D. Coombs1, David Soto1, 2, Thomas P. McGee1, Matthew G. Gold1, Mark Farrant*1, and Stuart G. Cull-Candy*1 1Department of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK; 2Present Address – Department of Biomedicine, Neurophysiology Laboratory, Medical School, Institute of Neurosciences, University of Barcelona, Casanova 143, 08036 Barcelona, Spain. Correspondence to [email protected] or [email protected] Desensitization is a canonical property of ligand-gated ion channels, causing progressive current decline in the continued presence of agonist. AMPA-type glutamate receptors, which mediate fast excitatory sig- naling throughout the brain, exhibit profound desensitization. Recent cryo-EM studies of AMPAR assem- blies show their ion channels to be closed in the desensitized state. Here we report the surprising finding that homomeric Q/R edited AMPARs still allow ions to flow when the receptors are desensitized. GluA2(R) expressed alone, or with auxiliary subunits (γ-2, γ-8 or GSG1L), generates large steady-state currents and anomalous current-variance relationships. Using fluctuation analysis, single-channel recording, and kinetic modeling we demonstrate that the steady-state current is mediated predominantly by ‘conducting desensitized’ receptors. -
Structure-Based Discovery of Prescription Drugs That Interact with the Norepinephrine Transporter, NET
Structure-based discovery of prescription drugs that interact with the norepinephrine transporter, NET Avner Schlessingera,b,c,1, Ethan Geiera, Hao Fana,b,c, John J. Irwinb,c, Brian K. Shoichetb,c, Kathleen M. Giacominia, and Andrej Salia,b,c,1 aDepartment of Bioengineering and Therapeutic Sciences, bDepartment of Pharmaceutical Chemistry, and cCalifornia Institute for Quantitative Biosciences, University of California, San Francisco, CA 94158 Edited by Barry Honig, Columbia University, Howard Hughes Medical Institute, New York, NY, and approved July 20, 2011 (received for review April 15, 2011) The norepinephrine transporter (NET) transports norepinephrine transporter (SERT, SLC6A4) (4). Because of the lack of high- from the synapse into presynaptic neurons, where norepinephrine resolution structural information, most drug discovery efforts regulates signaling pathways associated with cardiovascular targeting NET and other SLC6 transporters, including SERT and effects and behavioral traits via binding to various receptors dopamine transporter (DAT,SLC6A3), have relied on quantitative (e.g., β2-adrenergic receptor). NET is a known target for a variety structure-activity relationship (QSAR) approaches and pharmaco- of prescription drugs, including antidepressants and psychosti- phore modeling (5). mulants, and may mediate off-target effects of other prescription As for other SLC6 family members, NET is predicted to have drugs. Here, we identify prescription drugs that bind NET, using one domain containing 12 transmembrane helices (2). No struc- virtual ligand screening followed by experimental validation of tures of human SLC6 members have been determined at atomic predicted ligands. We began by constructing a comparative struc- resolution; however, the leucine transporter LeuT from the bac- tural model of NET based on its alignment to the atomic structure terium Aquifex aeolicus has been determined by X-ray crystallo- of a prokaryotic NET homolog, the leucine transporter LeuT. -
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 -
Identification of Novel Monoamine Oxidase B Inhibitors from Ligand Based Virtual Screening
Identification of novel monoamine oxidase B inhibitors from ligand based virtual screening A thesis submitted to Kent State University in partial Fulfillment of the requirements for the Degree of Master of Science By Mohammed Alaasam August, 2014 Thesis written by Mohammed Alaasam B.S., University of Baghdad, 2007 M.S., Kent State University, 2014 Approved by Werner Geldenhuys , Chair, Master’s Thesis Committee Richard Carroll , Member, Master’s Thesis Committee Prabodh Sadana , Member, Master’s Thesis Committee Eric Mintz , Director, School of Biomedical Sciences James Blank , Dean, College of Arts and Sciences ii Table of Contents List of figure ...................................................................................................................... vi List of tables ..................................................................................................................... xiii Acknowledgments............................................................................................................ xiv Chapter one: Introduction ............................................................................................... 1 1.1.Parkinson's disease ....................................................................................................... 1 1.2.Monoamine oxidase enzymes ....................................................................................... 7 1.3.Structures of MAO enzymes ....................................................................................... 12 1.4.Three dimentiona