Drugs That Can Cause Sz
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The National Drugs List
^ ^ ^ ^ ^[ ^ The National Drugs List Of Syrian Arab Republic Sexth Edition 2006 ! " # "$ % &'() " # * +$, -. / & 0 /+12 3 4" 5 "$ . "$ 67"5,) 0 " /! !2 4? @ % 88 9 3: " # "$ ;+<=2 – G# H H2 I) – 6( – 65 : A B C "5 : , D )* . J!* HK"3 H"$ T ) 4 B K<) +$ LMA N O 3 4P<B &Q / RS ) H< C4VH /430 / 1988 V W* < C A GQ ") 4V / 1000 / C4VH /820 / 2001 V XX K<# C ,V /500 / 1992 V "!X V /946 / 2004 V Z < C V /914 / 2003 V ) < ] +$, [2 / ,) @# @ S%Q2 J"= [ &<\ @ +$ LMA 1 O \ . S X '( ^ & M_ `AB @ &' 3 4" + @ V= 4 )\ " : N " # "$ 6 ) G" 3Q + a C G /<"B d3: C K7 e , fM 4 Q b"$ " < $\ c"7: 5) G . HHH3Q J # Hg ' V"h 6< G* H5 !" # $%" & $' ,* ( )* + 2 ا اوا ادو +% 5 j 2 i1 6 B J' 6<X " 6"[ i2 "$ "< * i3 10 6 i4 11 6! ^ i5 13 6<X "!# * i6 15 7 G!, 6 - k 24"$d dl ?K V *4V h 63[46 ' i8 19 Adl 20 "( 2 i9 20 G Q) 6 i10 20 a 6 m[, 6 i11 21 ?K V $n i12 21 "% * i13 23 b+ 6 i14 23 oe C * i15 24 !, 2 6\ i16 25 C V pq * i17 26 ( S 6) 1, ++ &"r i19 3 +% 27 G 6 ""% i19 28 ^ Ks 2 i20 31 % Ks 2 i21 32 s * i22 35 " " * i23 37 "$ * i24 38 6" i25 39 V t h Gu* v!* 2 i26 39 ( 2 i27 40 B w< Ks 2 i28 40 d C &"r i29 42 "' 6 i30 42 " * i31 42 ":< * i32 5 ./ 0" -33 4 : ANAESTHETICS $ 1 2 -1 :GENERAL ANAESTHETICS AND OXYGEN 4 $1 2 2- ATRACURIUM BESYLATE DROPERIDOL ETHER FENTANYL HALOTHANE ISOFLURANE KETAMINE HCL NITROUS OXIDE OXYGEN PROPOFOL REMIFENTANIL SEVOFLURANE SUFENTANIL THIOPENTAL :LOCAL ANAESTHETICS !67$1 2 -5 AMYLEINE HCL=AMYLOCAINE ARTICAINE BENZOCAINE BUPIVACAINE CINCHOCAINE LIDOCAINE MEPIVACAINE OXETHAZAINE PRAMOXINE PRILOCAINE PREOPERATIVE MEDICATION & SEDATION FOR 9*: ;< " 2 -8 : : SHORT -TERM PROCEDURES ATROPINE DIAZEPAM INJ. -
Could Mycolactone Inspire New Potent Analgesics? Perspectives and Pitfalls
toxins Review Could Mycolactone Inspire New Potent Analgesics? Perspectives and Pitfalls 1 2 3, 4, , Marie-Line Reynaert , Denis Dupoiron , Edouard Yeramian y, Laurent Marsollier * y and 1, , Priscille Brodin * y 1 France Univ. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019-UMR8204-CIIL-Center for Infection and Immunity of Lille, F-59000 Lille, France 2 Institut de Cancérologie de l’Ouest Paul Papin, 15 rue André Boquel-49055 Angers, France 3 Unité de Microbiologie Structurale, Institut Pasteur, CNRS, Univ. Paris, F-75015 Paris, France 4 Equipe ATIP AVENIR, CRCINA, INSERM, Univ. Nantes, Univ. Angers, 4 rue Larrey, F-49933 Angers, France * Correspondence: [email protected] (L.M.); [email protected] (P.B.) These three authors contribute equally to this work. y Received: 29 June 2019; Accepted: 3 September 2019; Published: 4 September 2019 Abstract: Pain currently represents the most common symptom for which medical attention is sought by patients. The available treatments have limited effectiveness and significant side-effects. In addition, most often, the duration of analgesia is short. Today, the handling of pain remains a major challenge. One promising alternative for the discovery of novel potent analgesics is to take inspiration from Mother Nature; in this context, the detailed investigation of the intriguing analgesia implemented in Buruli ulcer, an infectious disease caused by the bacterium Mycobacterium ulcerans and characterized by painless ulcerative lesions, seems particularly promising. More precisely, in this disease, the painless skin ulcers are caused by mycolactone, a polyketide lactone exotoxin. In fact, mycolactone exerts a wide range of effects on the host, besides being responsible for analgesia, as it has been shown notably to modulate the immune response or to provoke apoptosis. -
Management of Chronic Problems
MANAGEMENT OF CHRONIC PROBLEMS INTERACTIONS BETWEEN ALCOHOL AND DRUGS A. Leary,* T. MacDonald† SUMMARY concerned. Alcohol may alter the effects of the drug; drug In western society alcohol consumption is common as is may change the effects of alcohol; or both may occur. the use of therapeutic drugs. It is not surprising therefore The interaction between alcohol and drug may be that concomitant use of these should occur frequently. The pharmacokinetic, with altered absorption, metabolism or consequences of this combination vary with the dose of elimination of the drug, alcohol or both.2 Alcohol may drug, the amount of alcohol taken, the mode of affect drug pharmacokinetics by altering gastric emptying administration and the pharmacological effects of the drug or liver metabolism. Drugs may affect alcohol kinetics by concerned. Interactions may be pharmacokinetic or altering gastric emptying or inhibiting gastric alcohol pharmacodynamic, and while coincidental use of alcohol dehydrogenase (ADH).3 This may lead to altered tissue may affect the metabolism or action of a drug, a drug may concentrations of one or both agents, with resultant toxicity. equally affect the metabolism or action of alcohol. Alcohol- The results of concomitant use may also be principally drug interactions may differ with acute and chronic alcohol pharmacodynamic, with combined alcohol and drug effects ingestion, particularly where toxicity is due to a metabolite occurring at the receptor level without important changes rather than the parent drug. There is both inter- and intra- in plasma concentration of either. Some interactions have individual variation in the response to concomitant drug both kinetic and dynamic components and, where this is and alcohol use. -
Understanding Benzodiazephine Use, Abuse, and Detection
Siemens Healthcare Diagnostics, the leading clinical diagnostics company, is committed to providing clinicians with the vital information they need for the accurate diagnosis, treatment and monitoring of patients. Our comprehensive portfolio of performance-driven systems, unmatched menu offering and IT solutions, in conjunction with highly responsive service, is designed to streamline workflow, enhance operational efficiency and support improved patient care. Syva, EMIT, EMIT II, EMIT d.a.u., and all associated marks are trademarks of General Siemens Healthcare Diagnostics Inc. All Drugs other trademarks and brands are the Global Division property of their respective owners. of Abuse Siemens Healthcare Product availability may vary from Diagnostics Inc. country to country and is subject 1717 Deerfield Road to varying regulatory requirements. Deerfield, IL 60015-0778 Please contact your local USA representative for availability. www.siemens.com/diagnostics Siemens Global Headquarters Global Siemens Healthcare Headquarters Siemens AG Understanding Wittelsbacherplatz 2 Siemens AG 80333 Muenchen Healthcare Sector Germany Henkestrasse 127 Benzodiazephine Use, 91052 Erlangen Germany Abuse, and Detection Telephone: +49 9131 84 - 0 www.siemens.com/healthcare www.usa.siemens.com/diagnostics Answers for life. Order No. A91DX-0701526-UC1-4A00 | Printed in USA | © 2009 Siemens Healthcare Diagnostics Inc. Syva has been R1 R2 a leading developer N and manufacturer of AB R3 X N drugs-of-abuse tests R4 for more than 30 years. R2 C Now part of Siemens Healthcare ® Diagnostics, Syva boasts a long and Benzodiazepines have as their basic chemical structure successful track record in drugs-of-abuse a benzene ring fused to a seven-membered diazepine ring. testing, and leads the industry in the All important benzodiazepines contain a 5-aryl substituent ring (ring C) and a 1,4–diazepine ring. -
Outcome of Different Therapeutic Interventions in Mild COVID-19 Patients in a Single OPD Clinic of West Bengal: a Retrospective Study
medRxiv preprint doi: https://doi.org/10.1101/2021.03.08.21252883; this version posted March 12, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-ND 4.0 International license . Title page Outcome of Different Therapeutic Interventions in Mild COVID-19 Patients in a Single OPD Clinic of West Bengal: A Retrospective study Running Title: Mild COVID-19 and the Buffet of Treatments: A case series Sayak Roy1, Shambo Samrat Samajdar2, Santanu K Tripathi3, Shatavisa Mukherjee4, Kingshuk Bhattacharjee5 1. Consultant Physician, Dept. of Internal Medicine, Medica Superspeciality Hospital, Kolkata; ORCID ID: https://orcid.org/0000-0002-6185-9375 2. Senior Resident, Dept of Clinical & Experimental Pharmacology, School of Tropical Medicine, Kolkata. 3. Dean (Academics) and Head, Dept of Pharmacology, Netaji Subhash Medical College & Hospital, Bihta, Patna 4. PhD Research Scholar, Dept of Clinical & Experimental Pharmacology, School of Tropical Medicine, Kolkata. ORCID ID: https://orcid.org/0000-0001-9524-1525 5. Independent Biostatistician, Kolkata Corresponding Author: Dr. Sayak Roy 609, G.T.Road, Battala, Serampore, Hooghly, WB, India; PIN – 712201 Email: [email protected] Words: 1906 Tables: 2 References: 20 Informed Consent and Institutional ethical clearance: Taken Conflicts of interest: None Funding: None Acknowledgement: None Data availability: Available on request with the corresponding author NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. 1 medRxiv preprint doi: https://doi.org/10.1101/2021.03.08.21252883; this version posted March 12, 2021. -
Exploring the Activity of an Inhibitory Neurosteroid at GABAA Receptors
1 Exploring the activity of an inhibitory neurosteroid at GABAA receptors Sandra Seljeset A thesis submitted to University College London for the Degree of Doctor of Philosophy November 2016 Department of Neuroscience, Physiology and Pharmacology University College London Gower Street WC1E 6BT 2 Declaration I, Sandra Seljeset, confirm that the work presented in this thesis is my own. Where information has been derived from other sources, I can confirm that this has been indicated in the thesis. 3 Abstract The GABAA receptor is the main mediator of inhibitory neurotransmission in the central nervous system. Its activity is regulated by various endogenous molecules that act either by directly modulating the receptor or by affecting the presynaptic release of GABA. Neurosteroids are an important class of endogenous modulators, and can either potentiate or inhibit GABAA receptor function. Whereas the binding site and physiological roles of the potentiating neurosteroids are well characterised, less is known about the role of inhibitory neurosteroids in modulating GABAA receptors. Using hippocampal cultures and recombinant GABAA receptors expressed in HEK cells, the binding and functional profile of the inhibitory neurosteroid pregnenolone sulphate (PS) were studied using whole-cell patch-clamp recordings. In HEK cells, PS inhibited steady-state GABA currents more than peak currents. Receptor subtype selectivity was minimal, except that the ρ1 receptor was largely insensitive. PS showed state-dependence but little voltage-sensitivity and did not compete with the open-channel blocker picrotoxinin for binding, suggesting that the channel pore is an unlikely binding site. By using ρ1-α1/β2/γ2L receptor chimeras and point mutations, the binding site for PS was probed. -
268 Part 522—Implantation Or Injectable Dosage Form
§ 520.2645 21 CFR Ch. I (4–1–18 Edition) (ii) Indications for use. For the control 522.82 Aminopropazine. of American foulbrood (Paenibacillus 522.84 Beta-aminopropionitrile. larvae). 522.88 Amoxicillin. 522.90 Ampicillin injectable dosage forms. (iii) Limitations. The drug should be 522.90a Ampicillin trihydrate suspension. fed early in the spring or fall and con- 522.90b Ampicillin trihydrate powder for in- sumed by the bees before the main jection. honey flow begins, to avoid contamina- 522.90c Ampicillin sodium. tion of production honey. Complete 522.144 Arsenamide. treatments at least 4 weeks before 522.147 Atipamezole. main honey flow. 522.150 Azaperone. 522.161 Betamethasone. [40 FR 13838, Mar. 27, 1975, as amended at 50 522.163 Betamethasone dipropionate and FR 49841, Dec. 5, 1985; 59 FR 14365, Mar. 28, betamethasone sodium phosphate aque- 1994; 62 FR 39443, July 23, 1997; 68 FR 24879, ous suspension. May 9, 2003; 70 FR 69439, Nov. 16, 2005; 73 FR 522.167 Betamethasone sodium phosphate 76946, Dec. 18, 2008; 75 FR 76259, Dec. 8, 2010; and betamethasone acetate. 76 FR 59024, Sept. 23, 2011; 77 FR 29217, May 522.204 Boldenone. 17, 2012; 79 FR 37620, July 2, 2014; 79 FR 53136, 522.224 Bupivacaine. Sept. 8, 2014; 79 FR 64116, Oct. 28, 2014; 80 FR 522.230 Buprenorphine. 34278, June 16, 2015; 81 FR 48702, July 26, 2016] 522.234 Butamisole. 522.246 Butorphanol. § 520.2645 Tylvalosin. 522.275 N-Butylscopolammonium. 522.300 Carfentanil. (a) Specifications. Granules containing 522.304 Carprofen. 62.5 percent tylvalosin (w/w) as 522.311 Cefovecin. -
Ketamine: an Update for Its Use in Complex Regional Pain Syndrome
xperim & E en l ta a l ic P in h Bentley et al., Clin Exp Pharmacol 2015, 5:2 l a C r m f Journal of DOI: 10.4172/2161-1459.1000169 o a l c a o n l o r g u y o J ISSN: 2161-1459 Clinical and Experimental Pharmacology Commentry Open Access Ketamine: An Update for Its Use in Complex Regional Pain Syndrome and Major Depressive Disorder William E Bentley*, Michael Sabia, Michael E Goldberg and Irving W Wainer Cooper University Hospital, Camden, New Jersey, United States of America Abstract In recent years, there has been significant research in regard to the efficacy of ketamine in regards to treating Complex Regional Pain Syndrome (CRPS) and Major Depressive Disorder (MDD). Many patients have had substantial symptomatic relief; however, not all patients have had positive results. This has prompted current research with evidence to suggest certain biomarkers exist that would infer which patients will/will not respond to ketamine treatment. Current biomarkers of interest include D-Serine (D-Ser) and magnesium, which will be discussed. Whether or not D-Ser and/or magnesium levels should be checked and possibly dictate therapy is an area of future research. It is also possible that downstream metabolites of ketamine are the key to successful therapy. Keywords: Complex regional pain syndrome; Major Depressive thoughts; and slowing of speech and action. These changes must last a Disorder(MDD); Ketamine minimum of 2 weeks and interfere considerably with work and family relations” [6]. Treatment options include antidepressant medications, Complex Regional Pain Syndrome (CRPS) and Major Depressive cognitive behavioral therapy, and interpersonal therapy. -
Investigating the Inhibition Mechanism of L,D-Transpeptidase 5 from Mycobacterium Tuberculosis Using Computational Methods
INVESTIGATING THE INHIBITION MECHANISM OF L,D-TRANSPEPTIDASE 5 FROM MYCOBACTERIUM TUBERCULOSIS USING COMPUTATIONAL METHODS BY: GIDEON FEMI TOLUFASHE 216076453 Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy in Pharmaceutical Chemistry School of Health Sciences, College of Health Sciences, University of KwaZulu-Natal, Durban, South Africa. 2018 PREFACE The work described in this thesis was conducted at the Catalysis and Peptide Research Unit, Westville Campus, University of KwaZulu-Natal, Durban, South Africa, under the supervision of Dr Bahareh Honarparvar, Prof. H.G. Kruger and Dr G.E.M. Maguire. This work has not been submitted in any form for any degree or diploma to any institution, where use has been made of the work of others, it is duly acknowledged in the text. Supervisors: Dr B. Honarparvar Date 30/10/2018 Prof. H. G. Kruger________________ Date ___________ Dr. G.E.M Maguire_______________ Date ___________ As candidate’s supervisor I agree to the submission of this thesis. i DECLARATION DECLARATION I- PLAGIARISM I, Gideon Femi Tolufashe declare that (i). The research reports in this thesis, except where otherwise indicated, is my original work. (ii). This thesis has not been submitted for any degree or examination at any other university. (iii). This thesis does not contain other person’s data, pictures, graphs or other information, unless specifically acknowledged as being sourced from other persons. (iv). This thesis does not contain other person’s writing, unless specifically acknowledged as being sourced from other researchers. Where other written sources have been quoted, then: a. Their words have been re-written, but the general information attributed to them has been referenced. -
Tufts Health Unify 202 0 List of Covered Drugs (Formulary)
Tufts Health Unify 202 0 List of Covered Drugs (Formulary) Effective: 12/01/2020 Tufts Health Plan P.O. Box 9194 Watertown, MA 02471-9194 Phone: 855.393.3154 Seven days a week, from 8 a.m. to 8 p.m. TuftsHealthUnify.org Formulary ID: 20533 Version: 20 H7419_6507B Approved DISCRIMINATION IS AGAINST THE LAW Tufts Health Plan complies with applicable Federal civil rights laws and does not discriminate on the basis of race, color, national origin, age, disability, or sex. Tufts Health Plan does not exclude people or treat them differently because of race, color, national origin, age, disability, or sex. Tufts Health Plan: . Provides free aids and services to people with disabilities to communicate effectively with us, such as: — Written information in other formats (large print, audio, accessible electronic formats, other formats) . Provides free language services to people whose primary language is not English, such as: — Qualified interpreters — Information written in other languages If you need these services, contact Tufts Health Plan Member Services at 855.393.3154. If you believe that Tufts Health Plan has failed to provide these services or discriminated in another way on the basis of race, color, national origin, age, disability, or sex, you can file a grievance with: Tufts Health Plan Attention: Civil Rights Coordinator, Legal Dept. 705 Mount Auburn St. Watertown, MA 02472 Phone: 888.880.8699 ext. 48000, [TTY number— 711 or 800.439.2370] Fax: 617.972.9048 Email: [email protected] You can file a grievance in person or by mail, fax, or email. If you need help filing a grievance, the Tufts Health Plan Civil Rights Coordinator is available to help you. -
Drugs to Avoid in Patients with Dementia
Detail-Document #240510 -This Detail-Document accompanies the related article published in- PHARMACIST’S LETTER / PRESCRIBER’S LETTER May 2008 ~ Volume 24 ~ Number 240510 Drugs To Avoid in Patients with Dementia Elderly people with dementia often tolerate drugs less favorably than healthy older adults. Reasons include increased sensitivity to certain side effects, difficulty with adhering to drug regimens, and decreased ability to recognize and report adverse events. Elderly adults with dementia are also more prone than healthy older persons to develop drug-induced cognitive impairment.1 Medications with strong anticholinergic (AC) side effects, such as sedating antihistamines, are well- known for causing acute cognitive impairment in people with dementia.1-3 Anticholinergic-like effects, such as urinary retention and dry mouth, have also been identified in drugs not typically associated with major AC side effects (e.g., narcotics, benzodiazepines).3 These drugs are also important causes of acute confusional states. Factors that may determine whether a patient will develop cognitive impairment when exposed to ACs include: 1) total AC load (determined by number of AC drugs and dose of agents utilized), 2) baseline cognitive function, and 3) individual patient pharmacodynamic and pharmacokinetic features (e.g., renal/hepatic function).1 Evidence suggests that impairment of cholinergic transmission plays a key role in the development of Alzheimer’s dementia. Thus, the development of the cholinesterase inhibitors (CIs). When used appropriately, the CIs (donepezil [Aricept], rivastigmine [Exelon], and galantamine [Razadyne, Reminyl in Canada]) may slow the decline of cognitive and functional impairment in people with dementia. In order to achieve maximum therapeutic effect, they ideally should not be used in combination with ACs, agents known to have an opposing mechanism of action.1,2 Roe et al studied AC use in 836 elderly patients.1 Use of ACs was found to be greater in patients with probable dementia than healthy older adults (33% vs. -
Euthanasia of Experimental Animals
EUTHANASIA OF EXPERIMENTAL ANIMALS • *• • • • • • • *•* EUROPEAN 1COMMISSIO N This document has been prepared for use within the Commission. It does not necessarily represent the Commission's official position. A great deal of additional information on the European Union is available on the Internet. It can be accessed through the Europa server (http://europa.eu.int) Cataloguing data can be found at the end of this publication Luxembourg: Office for Official Publications of the European Communities, 1997 ISBN 92-827-9694-9 © European Communities, 1997 Reproduction is authorized, except for commercial purposes, provided the source is acknowledged Printed in Belgium European Commission EUTHANASIA OF EXPERIMENTAL ANIMALS Document EUTHANASIA OF EXPERIMENTAL ANIMALS Report prepared for the European Commission by Mrs Bryony Close Dr Keith Banister Dr Vera Baumans Dr Eva-Maria Bernoth Dr Niall Bromage Dr John Bunyan Professor Dr Wolff Erhardt Professor Paul Flecknell Dr Neville Gregory Professor Dr Hansjoachim Hackbarth Professor David Morton Mr Clifford Warwick EUTHANASIA OF EXPERIMENTAL ANIMALS CONTENTS Page Preface 1 Acknowledgements 2 1. Introduction 3 1.1 Objectives of euthanasia 3 1.2 Definition of terms 3 1.3 Signs of pain and distress 4 1.4 Recognition and confirmation of death 5 1.5 Personnel and training 5 1.6 Handling and restraint 6 1.7 Equipment 6 1.8 Carcass and waste disposal 6 2. General comments on methods of euthanasia 7 2.1 Acceptable methods of euthanasia 7 2.2 Methods acceptable for unconscious animals 15 2.3 Methods that are not acceptable for euthanasia 16 3. Methods of euthanasia for each species group 21 3.1 Fish 21 3.2 Amphibians 27 3.3 Reptiles 31 3.4 Birds 35 3.5 Rodents 41 3.6 Rabbits 47 3.7 Carnivores - dogs, cats, ferrets 53 3.8 Large mammals - pigs, sheep, goats, cattle, horses 57 3.9 Non-human primates 61 3.10 Other animals not commonly used for experiments 62 4.