Guaiana, G., Barbui, C., Caldwell, DM, Davies, SJC, Furukawa, TA
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Strategies for Managing Sexual Dysfunction Induced by Antidepressant Medication
King’s Research Portal DOI: 10.1002/14651858.CD003382.pub3 Document Version Publisher's PDF, also known as Version of record Link to publication record in King's Research Portal Citation for published version (APA): Taylor, M. J., Rudkin, L., Bullemor-Day, P., Lubin, J., Chukwujekwu, C., & Hawton, K. (2013). Strategies for managing sexual dysfunction induced by antidepressant medication. Cochrane Database of Systematic Reviews, (5). https://doi.org/10.1002/14651858.CD003382.pub3 Citing this paper Please note that where the full-text provided on King's Research Portal is the Author Accepted Manuscript or Post-Print version this may differ from the final Published version. If citing, it is advised that you check and use the publisher's definitive version for pagination, volume/issue, and date of publication details. And where the final published version is provided on the Research Portal, if citing you are again advised to check the publisher's website for any subsequent corrections. General rights Copyright and moral rights for the publications made accessible in the Research Portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognize and abide by the legal requirements associated with these rights. •Users may download and print one copy of any publication from the Research Portal for the purpose of private study or research. •You may not further distribute the material or use it for any profit-making activity or commercial gain •You may freely distribute the URL identifying the publication in the Research Portal Take down policy If you believe that this document breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. -
Test Update Immediate Action Notification
Effective Date: Monday, April 27, 2020 Test Updates Immediate Action In our continuing effort to provide you with the highest quality toxicology laboratory services available, we have compiled important changes regarding a number of tests we perform. Listed below are the types of changes that may be included in this notification, effective Monday, April 27, 2020 Test Changes - Tests that have had changes to the method/ CPT code, units of measurement, scope of analysis, reference comments, or specimen requirements. Discontinued Tests - Tests being discontinued with alternate testing suggestions. Please use this information to update your computer systems/records. These changes are important to ensure standardization of our mutual laboratory databases. If you have any questions about the information contained in this notification, please call our Client Support Department at (866) 522-2206. Thank you for your continued support of NMS Labs and your assistance in implementing these changes. The CPT Codes provided in this document are based on AMA guidelines and are for informational purposes only. NMS Labs does not assume responsibility for billing errors due to reliance on the CPT Codes listed in this document. NMS Labs 200 Welsh Rd. Horsham, PA 19044-2208 [email protected] Page 1 of 6 Effective Date: Monday, April 27, 2020 Test Updates Test Test Name Test Method / Specimen Stability Scope Units Reference Discontinue Code Name CPT Code Req. Comments Designer Benzodiazepines (Qualitative), 0570U • Urine (Forensic) Designer Benzodiazepines Confirmation 52487U • (Qualitative), Urine Designer Benzodiazepines Confirmation, 52487B • Blood Designer Benzodiazepines Confirmation, 52487SP • Serum/Plasma Designer Benzodiazepines, Blood 0570B • (Forensic) Designer Benzodiazepines, 0570SP • Serum/Plasma (Forensic) NMS Labs 200 Welsh Rd. -
GABA Receptors
D Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews Review No.7 / 1-2011 GABA receptors Wolfgang Froestl , CNS & Chemistry Expert, AC Immune SA, PSE Building B - EPFL, CH-1015 Lausanne, Phone: +41 21 693 91 43, FAX: +41 21 693 91 20, E-mail: [email protected] GABA Activation of the GABA A receptor leads to an influx of chloride GABA ( -aminobutyric acid; Figure 1) is the most important and ions and to a hyperpolarization of the membrane. 16 subunits with γ most abundant inhibitory neurotransmitter in the mammalian molecular weights between 50 and 65 kD have been identified brain 1,2 , where it was first discovered in 1950 3-5 . It is a small achiral so far, 6 subunits, 3 subunits, 3 subunits, and the , , α β γ δ ε θ molecule with molecular weight of 103 g/mol and high water solu - and subunits 8,9 . π bility. At 25°C one gram of water can dissolve 1.3 grams of GABA. 2 Such a hydrophilic molecule (log P = -2.13, PSA = 63.3 Å ) cannot In the meantime all GABA A receptor binding sites have been eluci - cross the blood brain barrier. It is produced in the brain by decarb- dated in great detail. The GABA site is located at the interface oxylation of L-glutamic acid by the enzyme glutamic acid decarb- between and subunits. Benzodiazepines interact with subunit α β oxylase (GAD, EC 4.1.1.15). It is a neutral amino acid with pK = combinations ( ) ( ) , which is the most abundant combi - 1 α1 2 β2 2 γ2 4.23 and pK = 10.43. -
Neurobiological and Neurobehavioral Mechanisms of Chronic Alcohol Drinking
Neurobiological and Neurobehavioral Mechanisms of Chronic Alcohol Drinking Neurobiological and Neurobehavioral Mechanisms of Chronic Alcohol Drinking Alcoholism comprises a set of complex behaviors seeking behaviors, have been developed. These in which an individual becomes increasingly models, which remain an integral part of the preoccupied with obtaining alcohol. These study of alcoholism, include animals that pref- behaviors ultimately lead to a loss of control over erentially drink solutions containing alcohol, consumption of the drug and to the development animals that self-administer alcohol during of tolerance, dependence, and impaired social and withdrawal, animals with a history of dependence occupational functioning. that self-administer alcohol, and animals that self- administer alcohol after a period of abstinence Although valuable information regarding toler- from the drug. Genetic models for alcoholism ance and dependence has been, and continues to also exist and include animals that have been bred be, gathered through human studies, much of the selectively for high alcohol consumption. Studies detailed understanding of the impact of exposure using such models are uncovering the systemic, to alcohol on behavior and on the biological cellular, and molecular neurobiological mech- mechanisms underlying those behaviors has been anisms that appear to contribute to chronic obtained through the use of animal models for alcohol consumption. The challenge of current alcoholism and a variety of in vitro, or cellular, and future studies is to understand which specific systems. Through the use of cellular systems and cellular and subcellular systems undergo mole- animal models, researchers can control the genetic cular changes to influence tolerance and depen- background and experimental conditions under dence in motivational systems that lead to which a specific alcohol-related behavior or chronic drinking. -
Alprazolam Dependence Prevented by Substituting with the ß-Carboline
Proc. Natl. Acad. Sci. USA Vol. 94, pp. 2719–2723, March 1997 Pharmacology Alprazolam dependence prevented by substituting with the b-carboline abecarnil (benzodiazepinesywithdrawalytoleranceyreplacement therapy) GRAZIANO PINNA*, RUGGERO GALICI*, HERBERT H. SCHNEIDER,DAVID N. STEPHENS†, AND LECHOSLAW TURSKI‡ Research Laboratories of Schering AG, Mu¨llerstrasse 178, D-13342 Berlin, Germany Communicated by Jan Bures, Czech Academy of Sciences, Prague, Czech Republic, December 26, 1996 (received for review December 2, 1996) ABSTRACT Abrupt termination of the treatment of hu- although this view is not adequately supported by controlled mans with benzodiazepines (BDZs) leads to a rapid onset of human data (5). There are also no adequately controlled discontinuation syndrome characterized by anxiety, muscle animal experimental data that allow comparison of the risk of spasms, and occasionally convulsions. For this reason, it is producing dependence between BDZs with short and long recommended in clinical practice to reduce the dose of the half-lives (7). Similarly, there is scanty experimental data BDZs gradually at the end of treatment. Nevertheless, many demonstrating how to discontinue safely treatment with BDZs clinicians report signs of dependence even during gradual with short half-lives. reduction of doses (tapering) of the BDZs in a large propor- To address this issue we have employed newly developed tion of patients. Thus, there is considerable interest in dis- methods for electroencephalographic (EEG) monitoring of covering means of weaning patients away from BDZs without seizures, for electromyographic (EMG) monitoring of muscle the risk of discontinuation syndrome. In the present study, tone, and for detecting anxiety-like behavioral changes after mice withdrawn from chronic treatment with alprazolam discontinuation of long-term treatment with sedative drugs in showed anxiety, muscle rigidity, and seizures between days 1 mice (8) for controlled and standardized assessment of de- and 28 after termination of the treatment. -
Smoking Modulates Neuroendocrine Responses to Ipsapirone in Patients with Panic Disorder A
Smoking Modulates Neuroendocrine Responses to Ipsapirone in Patients with Panic Disorder A. Broocks, M.D., Ph.D., B. Bandelow, M.D., Ph.D., K. Koch, U. Bartmann, J. Kinkelbur, M.D., U. Schweiger, M.D., Ph.D., F. Hohagen, M.D., Ph.D., and G. Hajak, M.D., Ph.D. Reduced 5-HT1A-receptor responsiveness has been reported temperature. In comparison to placebo, administration of in patients with panic disorder(PD) and/or agoraphobia ipsapirone was associated with significant increases of (PDA). Although many of these patients are regular various psychological symptoms and plasma cortisol smokers, it has not been examined whether psychological or concentrations. The subgroup of PD patients who were neurobiological effects induced by the selective 5-HT1A- smokers showed significantly higher cortisol responses to receptor agonist, ipsapirone, are affected by the smoking ipsapirone than non-smokers. status of the patients. In conclusion, smoking status has to be taken into In order to clarify this question neuroendocrine account when assessing the responsiveness of 5-HT1A challenges with oral doses of ipsapirone (0.3 mg/kg) and receptors in patients with psychiatric disorders. The placebo were performed in 39 patients with PDA, and prevention of smoking during challenge sessions might not results were compared between patients who smoked (Ͼ10 be the ideal approach in heavy smokers, since sudden cigarettes per day, n ϭ 17) and patients who had been non- abstinence from smoking is likely to affect neurobiological smokers for at least two years (n ϭ 22). and possibly psychological responses to ipsapirone. Patients who were smokers (but did not smoke during [Neuropsychopharmacology 27:270–278, 2002] the challenge procedure) had significantly reduced baseline © 2002 American College of Neuropsychopharmacology. -
(12) United States Patent (10) Patent No.: US 8.598,119 B2 Mates Et Al
US008598119B2 (12) United States Patent (10) Patent No.: US 8.598,119 B2 Mates et al. (45) Date of Patent: Dec. 3, 2013 (54) METHODS AND COMPOSITIONS FOR AOIN 43/00 (2006.01) SLEEP DSORDERS AND OTHER AOIN 43/46 (2006.01) DSORDERS AOIN 43/62 (2006.01) AOIN 43/58 (2006.01) (75) Inventors: Sharon Mates, New York, NY (US); AOIN 43/60 (2006.01) Allen Fienberg, New York, NY (US); (52) U.S. Cl. Lawrence Wennogle, New York, NY USPC .......... 514/114: 514/171; 514/217: 514/220; (US) 514/229.5: 514/250 (58) Field of Classification Search (73) Assignee: Intra-Cellular Therapies, Inc. NY (US) None See application file for complete search history. (*) Notice: Subject to any disclaimer, the term of this patent is extended or adjusted under 35 (56) References Cited U.S.C. 154(b) by 215 days. U.S. PATENT DOCUMENTS (21) Appl. No.: 12/994,560 6,552,017 B1 4/2003 Robichaud et al. 2007/0203120 A1 8, 2007 McDevitt et al. (22) PCT Filed: May 27, 2009 FOREIGN PATENT DOCUMENTS (86). PCT No.: PCT/US2O09/OO3261 S371 (c)(1), WO WOOOf77OO2 * 6, 2000 (2), (4) Date: Nov. 24, 2010 OTHER PUBLICATIONS (87) PCT Pub. No.: WO2009/145900 Rye (Sleep Disorders and Parkinson's Disease, 2000, accessed online http://www.waparkinsons.org/edu research/articles/Sleep PCT Pub. Date: Dec. 3, 2009 Disorders.html), 2 pages.* Alvir et al. Clozapine-Induced Agranulocytosis. The New England (65) Prior Publication Data Journal of Medicine, 1993, vol. 329, No. 3, pp. 162-167.* US 2011/0071080 A1 Mar. -
)&F1y3x PHARMACEUTICAL APPENDIX to THE
)&f1y3X PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE )&f1y3X PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 3 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. Product CAS No. Product CAS No. ABAMECTIN 65195-55-3 ACTODIGIN 36983-69-4 ABANOQUIL 90402-40-7 ADAFENOXATE 82168-26-1 ABCIXIMAB 143653-53-6 ADAMEXINE 54785-02-3 ABECARNIL 111841-85-1 ADAPALENE 106685-40-9 ABITESARTAN 137882-98-5 ADAPROLOL 101479-70-3 ABLUKAST 96566-25-5 ADATANSERIN 127266-56-2 ABUNIDAZOLE 91017-58-2 ADEFOVIR 106941-25-7 ACADESINE 2627-69-2 ADELMIDROL 1675-66-7 ACAMPROSATE 77337-76-9 ADEMETIONINE 17176-17-9 ACAPRAZINE 55485-20-6 ADENOSINE PHOSPHATE 61-19-8 ACARBOSE 56180-94-0 ADIBENDAN 100510-33-6 ACEBROCHOL 514-50-1 ADICILLIN 525-94-0 ACEBURIC ACID 26976-72-7 ADIMOLOL 78459-19-5 ACEBUTOLOL 37517-30-9 ADINAZOLAM 37115-32-5 ACECAINIDE 32795-44-1 ADIPHENINE 64-95-9 ACECARBROMAL 77-66-7 ADIPIODONE 606-17-7 ACECLIDINE 827-61-2 ADITEREN 56066-19-4 ACECLOFENAC 89796-99-6 ADITOPRIM 56066-63-8 ACEDAPSONE 77-46-3 ADOSOPINE 88124-26-9 ACEDIASULFONE SODIUM 127-60-6 ADOZELESIN 110314-48-2 ACEDOBEN 556-08-1 ADRAFINIL 63547-13-7 ACEFLURANOL 80595-73-9 ADRENALONE -
Cochrane Central Register of Controlled Trials (CENTRAL) to 28 September 2018
Zurich Open Repository and Archive University of Zurich Main Library Strickhofstrasse 39 CH-8057 Zurich www.zora.uzh.ch Year: 2019 Comparative effectiveness of continuation and maintenance treatments for persistent depressive disorder in adults Machmutow, Katja ; Meister, R ; Jansen, A ; Kriston, L ; Watzke, Birgit ; Härter, M ; Liebherz, Sarah Abstract: Background: Persistent depressive disorder (PDD) is defined as a depressive disorder witha minimum illness duration of two years, including four diagnostic subgroups (dysthymia, chronic major depression, recurrent major depression with incomplete remission between episodes, and double depres- sion). Persistent forms of depression represent a substantial proportion of depressive disorders, with a lifetime prevalence ranging from 3% to 6% in the Western world. Growing evidence indicates that PDD responds well to several acute interventions, such as combined psychological and pharmacological treatments. Yet, given the high rates of relapse and recurrences of depression following response to acute treatment, long-term continuation and maintenance therapy are of great importance. To date, there has been no evidence synthesis available on continuation and maintenance treatments of PDDs. Objec- tives: To assess the effects of pharmacological and psychological (either alone or combined) continuation and maintenance treatments for persistent depressive disorder, in comparison with each other, placebo (drug/attention placebo/non-specific treatment control), and treatment as usual (TAU). Continuation treatments are defined as treatments given to currently remitted people (remission is defined asdepres- sive symptoms dropping below case level) or to people who previously responded to an antidepressant treatment. Maintenance therapy is given during recovery (which is defined as remission lasting longer than six months). Search methods: We searched Ovid MEDLINE (1950- ), Embase (1974- ), PsycINFO (1967- ) and the Cochrane Central Register of Controlled Trials (CENTRAL) to 28 September 2018. -
Serotonergic Modulation of Suicidal Behaviour: Integrating Preclinical Data with Clinical Practice and Psychotherapy
Serotonergic modulation of suicidal behaviour: integrating preclinical data with clinical practice and psychotherapy Vasileios Boulougouris, Ioannis Malogiannis, George Lockwood, Iannis Zervas & Giuseppe Di Giovanni Experimental Brain Research ISSN 0014-4819 Exp Brain Res DOI 10.1007/s00221-013-3669-z 1 23 Your article is protected by copyright and all rights are held exclusively by Springer- Verlag Berlin Heidelberg. This e-offprint is for personal use only and shall not be self- archived in electronic repositories. If you wish to self-archive your article, please use the accepted manuscript version for posting on your own website. You may further deposit the accepted manuscript version in any repository, provided it is only made publicly available 12 months after official publication or later and provided acknowledgement is given to the original source of publication and a link is inserted to the published article on Springer's website. The link must be accompanied by the following text: "The final publication is available at link.springer.com”. 1 23 Author's personal copy Exp Brain Res DOI 10.1007/s00221-013-3669-z SeroTONIN Serotonergic modulation of suicidal behaviour: integrating preclinical data with clinical practice and psychotherapy Vasileios Boulougouris · Ioannis Malogiannis · George Lockwood · Iannis Zervas · Giuseppe Di Giovanni Received: 6 May 2013 / Accepted: 30 July 2013 © Springer-Verlag Berlin Heidelberg 2013 Abstract Many studies have provided important infor- with personality disorders), aiming to invite the reader to mation regarding the anatomy, development and func- integrate some aspects of the neurobiology of human sui- tional organization of the 5-HT system and the alterations cidal behaviour into a model of suicide that can be used in in this system that are present within the brain of the sui- a clinical encounter. -
Chemsex and Drug Use Among MSM in Kyiv: New Challenges", 2017
ANALYTICAL REPORT based on the results of the study "Chemsex and drug use among MSM in Kyiv: new challenges", 2017. Public organization "ALLIANCE. GLOBAL" in cooperation with the Center of Social Expertises of the Institute of Sociology of the National Academy of Sciences of Ukraine and with the financial support of AFEW International Authors: Olesya Trofymenko Volodymyr Kosenko Inna Schwab Maria Shevchuk Natalia Dmitruk Andrii Chernyshev Svyatoslav Sheremet Andrii Radetsky Kyiv, 2018 1 [Disclaimer:] The analytical report was prepared in the framework of the study "Chemsex and Drug Use among MSM in Kyiv: New Challenges", which was implemented by the public organization "ALLIANCE. GLOBAL" in cooperation with the Center of Social Expertises of the Institute of Sociology of the National Academy of Sciences of Ukraine, with the financial support of AFEW International and is part of the program Strengthening the capacity of civil society organizations in EECA region in conduction of the studies involving community representatives within the framework of the AIDS2018 Project, funded by the Ministry of Foreign Affairs of the Netherlands. Expert assistance in preparing the report was provided by the Expert Group on Health and Rights of Gay and Other MSM in Ukraine within the framework of the program of technical assistance to the entities of the Ukrainian MSM- service and LGBT movement, supported by the Eurasian Coalition on Male Health (ECOM) within the framework of the regional program "Right to health" and administered by the NGO “Association LGBT "LIGA". 2 CONTENTS GLOSSARY OF TERMS AND ABBREVIATIONS .................................................................................................. 4 METHODOLOGY .............................................................................................................................................. 9 Section 1. Social Portrait of MSM, who has Chemsex experience. -
Effect of Diazepam and Fosazepam (A Soluble Derivative of Diazepam) on Sleep in Man A.N
Br. J. clin. Pharmac. (1976), 3, 533-541 EFFECT OF DIAZEPAM AND FOSAZEPAM (A SOLUBLE DERIVATIVE OF DIAZEPAM) ON SLEEP IN MAN A.N. NICHOLSON, BARBARA M. STONE & CORAL H. CLARKE Royal Air Force Institute of Aviation Medicine, Farnborough, Hampshire 1 The effect of diazepam (5 mg and 10 mg), and fosazepam (60 mg and 80 mg), a soluble derivative of diazepam, on sleep was studied in six healthy adult males using electroencephalography for sleep measures, and analogue scales for subjective assessments of well-being and sleep quality. The effect of diazepam was limited to the night of ingestion, but the effect of fosazepam was carried over to the next night and so modified sleep for about 30 h after ingestion. 2 Effects on total sleep time were limited to the night of ingestion. There were increases with diazepam (10 mg) (P = 0.05), and with fosazepam (60 mg and 80 mg) (P = 0.001). For the night of ingestion sleep onset latencies were shortened, and awakenings were reduced by both drugs. The latency to stage 3 was shortened by fosazepam (60 mg and 80 mg) (P = 0.05). 3 The low and high dose of each drug reduced the duration (min) of stage 0 sleep (P = 0.01), but fosazepam also reduced the duration (min) of stage 1 sleep (P = 0.001), and there was an increase in stage 2 sleep (P = 0.01). With fosazepam there were carry over effects to the next night with reduction of stage 1 sleep (P = 0.05). There were no effects on the duration of stage 3, but there was evidence that stage 4 activity was reduced during the recovery night after ingestion of fosazepam (80 mg).