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Classification of Medicinal Drugs and Driving: Co-Ordination and Synthesis Report
Project No. TREN-05-FP6TR-S07.61320-518404-DRUID DRUID Driving under the Influence of Drugs, Alcohol and Medicines Integrated Project 1.6. Sustainable Development, Global Change and Ecosystem 1.6.2: Sustainable Surface Transport 6th Framework Programme Deliverable 4.4.1 Classification of medicinal drugs and driving: Co-ordination and synthesis report. Due date of deliverable: 21.07.2011 Actual submission date: 21.07.2011 Revision date: 21.07.2011 Start date of project: 15.10.2006 Duration: 48 months Organisation name of lead contractor for this deliverable: UVA Revision 0.0 Project co-funded by the European Commission within the Sixth Framework Programme (2002-2006) Dissemination Level PU Public PP Restricted to other programme participants (including the Commission x Services) RE Restricted to a group specified by the consortium (including the Commission Services) CO Confidential, only for members of the consortium (including the Commission Services) DRUID 6th Framework Programme Deliverable D.4.4.1 Classification of medicinal drugs and driving: Co-ordination and synthesis report. Page 1 of 243 Classification of medicinal drugs and driving: Co-ordination and synthesis report. Authors Trinidad Gómez-Talegón, Inmaculada Fierro, M. Carmen Del Río, F. Javier Álvarez (UVa, University of Valladolid, Spain) Partners - Silvia Ravera, Susana Monteiro, Han de Gier (RUGPha, University of Groningen, the Netherlands) - Gertrude Van der Linden, Sara-Ann Legrand, Kristof Pil, Alain Verstraete (UGent, Ghent University, Belgium) - Michel Mallaret, Charles Mercier-Guyon, Isabelle Mercier-Guyon (UGren, University of Grenoble, Centre Regional de Pharmacovigilance, France) - Katerina Touliou (CERT-HIT, Centre for Research and Technology Hellas, Greece) - Michael Hei βing (BASt, Bundesanstalt für Straßenwesen, Germany). -
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. -
Clinical Significance of Small Molecule Metabolites in the Blood of Patients
www.nature.com/scientificreports OPEN Clinical signifcance of small molecule metabolites in the blood of patients with diferent types of liver injury Hui Li1,2,5, Yan Wang1,5, Shizhao Ma1,3, Chaoqun Zhang1,4, Hua Liu2 & Dianxing Sun1,4* To understand the characteristic of changes of serum metabolites between healthy people and patients with hepatitis B virus (HBV) infection at diferent stages of disease, and to provide reference metabolomics information for clinical diagnosis of liver disease patients. 255 patients with diferent stages of HBV infection were selected. 3 mL blood was collected from each patient in the morning to detect diferences in serum lysophosphatidylcholine, acetyl-l-carnitine, oleic acid amide, and glycocholic acid concentrations by UFLC-IT-TOF/MS. The diagnostic values of four metabolic substances were evaluated by receiver operating characteristic (ROC) curve. The results showed that the optimal cut-of value of oleic acid amide concentration of the liver cirrhosis and HCC groups was 23.6 mg/L, with a diagnostic sensitivity of 88.9% and specifcity of 70.6%. The diagnostic efcacies of the three substances were similar in the hepatitis and HCC groups, with an optimal cut-of value of 2.04 mg/L, and a diagnostic sensitivity and specifcity of 100% and 47.2%, respectively. The optimal cut-of value of lecithin of the HBV-carrier and HCC groups was 132.85 mg/L, with a diagnostic sensitivity and specifcity of 88.9% and 66.7%, respectively. The optimal cut-of value of oleic acid amide of the healthy and HCC groups was 129.03 mg/L, with a diagnostic sensitivity and specifcity of 88.4% and 83.3%, respectively. -
Sample Chapter
LCMS_Chap09 (JB-D) 8/5/06 3:14 pm Page 193 9 LC-MS in doping control Detlef Thieme Introduction adjacent fields with similar analytical prospects, like veterinary residue control (predominantly dealing with identification of growth promoters Definition of doping in various matrices), forensic sciences (the major- ity of doping-relevant substances are scheduled Doping analysis comprises a diversity of sub- as controlled substances in most countries), stance classes with different pharmaceutical and environmental analysis (e.g. steroids in waste chemical properties. Therefore, the discussion of water) or clinical chemistry (e.g. due to the the suitability of liquid chromatography-mass increasing relevance of steroid hormone replace- spectrometry (LC-MS) in doping analysis needs ment therapy). to distinguish various categories. This chapter describes the key fields of appli- According to its formal definition, a doping cation of LC-MS in routine doping control (i.e. violation in sports can be caused by various screening analysis, confirmation and quantifica- events, e.g.: tion of positive results) extra to particular • the detection of a prohibited substance or research activities. The latter are focused on the metabolites or markers of that substance (as intended technical improvements (e.g. extension defined by the recent document [1] of the of detection time windows, reduction of turn- World Anti-Doping Agency [WADA]) in the around times and costs) of conventional analyti- athlete’s specimen cal procedures and, in particular, on the detection • the use of prohibited substances or methods of prohibited substances that cannot be ade- • possession or trafficking prohibited substances quately identified so far (e.g. -
DIURETICS Diuretics Are Drugs That Promote the Output of Urine Excreted by the Kidneys
DIURETICS Diuretics are drugs that promote the output of urine excreted by the Kidneys. The primary action of most diuretics is the direct inhibition of Na+ transport at one or more of the four major anatomical sites along the nephron, where Na+ reabsorption takes place. The increased excretion of water and electrolytes by the kidneys is dependent on three different processes viz., glomerular filtration, tubular reabsorption (active and passive) and tubular secretion. Diuretics are very effective in the treatment of Cardiac oedema, specifically the one related with congestive heart failure. They are employed extensively in various types of disorders, for example, nephritic syndrome, diabetes insipidus, nutritional oedema, cirrhosis of the liver, hypertension, oedema of pregnancy and also to lower intraocular and cerebrospinal fluid pressure. Therapeutic Uses of Diuretics i) Congestive Heart Failure: The choice of the diuretic would depend on the severity of the disorder. In an emergency like acute pulmonary oedema, intravenous Furosemide or Sodium ethacrynate may be given. In less severe cases. Hydrochlorothiazide or Chlorthalidone may be used. Potassium-sparing diuretics like Spironolactone or Triamterene may be added to thiazide therapy. ii) Essential hypertension: The thiazides usually sever as primary antihypertensive agents. They may be used as sole agents in patients with mild hypertension or combined with other antihypertensives in more severe cases. iii) Hepatic cirrhosis: Potassium-sparing diuretics like Spironolactone may be employed. If Spironolactone alone fails, then a thiazide diuretic can be added cautiously. Furosemide or Ethacrymnic acid may have to be used if the oedema is regractory, together with spironolactone to lessen potassium loss. Serum potassium levels should be monitored periodically. -
Uniform Classification Guidelines for Foreign Substances and Recommended Penalties Model Rule
DRUG TESTING STANDARDS AND PRACTICES PROGRAM. Uniform Classification Guidelines for Foreign Substances And Recommended Penalties Model Rule. January, 2018 (V.13.4) Ó ASSOCIATION OF RACING COMMISSIONERS INTERNATIONAL – 2018. Association of Racing Commissioners International 1510 Newtown Pike, Lexington, Kentucky, United States www.arci.com Page 1 of 61 Preamble to the Uniform Classification Guidelines of Foreign Substances The Preamble to the Uniform Classification Guidelines was approved by the RCI Drug Testing and Quality Assurance Program Committee (now the Drug Testing Standards and Practices Program Committee) on August 26, 1991. Minor revisions to the Preamble were made by the Drug Classification subcommittee (now the Veterinary Pharmacologists Subcommittee) on September 3, 1991. "The Uniform Classification Guidelines printed on the following pages are intended to assist stewards, hearing officers and racing commissioners in evaluating the seriousness of alleged violations of medication and prohibited substance rules in racing jurisdictions. Practicing equine veterinarians, state veterinarians, and equine pharmacologists are available and should be consulted to explain the pharmacological effects of the drugs listed in each class prior to any decisions with respect to penalities to be imposed. The ranking of drugs is based on their pharmacology, their ability to influence the outcome of a race, whether or not they have legitimate therapeutic uses in the racing horse, or other evidence that they may be used improperly. These classes of drugs are intended only as guidelines and should be employed only to assist persons adjudicating facts and opinions in understanding the seriousness of the alleged offenses. The facts of each case are always different and there may be mitigating circumstances which should always be considered. -
An Integrated Meta-Analysis of Peripheral Blood Metabolites and Biological Functions in Major Depressive Disorder
Molecular Psychiatry https://doi.org/10.1038/s41380-020-0645-4 ARTICLE An integrated meta-analysis of peripheral blood metabolites and biological functions in major depressive disorder 1,2,3 1,2,3 1,2,3 1,3 1,3 4,5 1,3 1,3 Juncai Pu ● Yiyun Liu ● Hanping Zhang ● Lu Tian ● Siwen Gui ● Yue Yu ● Xiang Chen ● Yue Chen ● 1,2,3 1,3 1,3 1,3 1,3 1,2,3 Lining Yang ● Yanqin Ran ● Xiaogang Zhong ● Shaohua Xu ● Xuemian Song ● Lanxiang Liu ● 1,2,3 1,3 1,2,3 Peng Zheng ● Haiyang Wang ● Peng Xie Received: 3 June 2019 / Revised: 24 December 2019 / Accepted: 10 January 2020 © The Author(s) 2020. This article is published with open access Abstract Major depressive disorder (MDD) is a serious mental illness, characterized by high morbidity, which has increased in recent decades. However, the molecular mechanisms underlying MDD remain unclear. Previous studies have identified altered metabolic profiles in peripheral tissues associated with MDD. Using curated metabolic characterization data from a large sample of MDD patients, we meta-analyzed the results of metabolites in peripheral blood. Pathway and network analyses were then performed to elucidate the biological themes within these altered metabolites. We identified 23 differentially 1234567890();,: 1234567890();,: expressed metabolites between MDD patients and controls from 46 studies. MDD patients were characterized by higher levels of asymmetric dimethylarginine, tyramine, 2-hydroxybutyric acid, phosphatidylcholine (32:1), and taurochenode- soxycholic acid and lower levels of L-acetylcarnitine, creatinine, L-asparagine, L-glutamine, linoleic acid, pyruvic acid, palmitoleic acid, L-serine, oleic acid, myo-inositol, dodecanoic acid, L-methionine, hypoxanthine, palmitic acid, L-tryptophan, kynurenic acid, taurine, and 25-hydroxyvitamin D compared with controls. -
RAC-GWVI: Research Alerts—Pubmed Citations for August 21 to 28, 2018 1
RAC-GWVI: Research Alerts—PubMed Citations for August 21 to 28, 2018 1 GULF WAR ILLNESS Neurotoxicity in acute and repeated organophosphate exposure. Naughton SX1, Terry AV Jr2. Toxicology. 2018 Aug 22. pii: S0300-483X(18)30264-6. doi: 10.1016/j.tox.2018.08.011. PMID: 30144465. [Epub ahead of print] The term organophosphate (OP) refers to a diverse group of chemicals that are found in hundreds of products worldwide. As pesticides, their most common use, OPs are clearly beneficial for agricultural productivity and the control of deadly vector-borne illnesses. However, as a consequence of their widespread use, OPs are now among the most common synthetic chemicals detected in the environment as well as in animal and human tissues. This is an increasing environmental concern because many OPs are highly toxic and both accidental and intentional exposures to OPs resulting in deleterious health effects have been documented for decades. Some of these deleterious health effects include a variety of long-term neurological and psychiatric disturbances including impairments in attention, memory, and other domains of cognition. Moreover, some chronic illnesses that manifest these symptoms such as Gulf War Illness and Aerotoxic Syndrome have (at least in part) been attributed to OP exposure. In addition to acute acetylcholinesterase inhibition, OPs may affect a number of additional targets that lead to oxidative stress, axonal transport deficits, neuroinflammation, and autoimmunity. Some of these targets could be exploited for therapeutic purposes. The purpose of this review is thus to: 1) describe the important uses of organophosphate (OP)-based compounds worldwide, 2) provide an overview of the various risks and toxicology associated with OP exposure, particularly long-term neurologic and psychiatric symptoms, 3) discuss mechanisms of OP toxicity beyond cholinesterase inhibition, 4) review potential therapeutic strategies to reverse the acute toxicity and long term deleterious effects of OPs. -
Mechanisms of Sevoflurane-Induced Myocardial Preconditioning In
Anesthesiology 2003; 99:27–33 © 2003 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc. Mechanisms of Sevoflurane-induced Myocardial Preconditioning in Isolated Human Right Atria In Vitro Alexandra Yvon, B.Sc.,* Jean-Luc Hanouz, M.D, Ph.D.,† Benoît Haelewyn, B.Sc.,* Xavier Terrien, B.Sc.,* Massimo Massetti, M.D.,‡ Gérard Babatasi, M.D., Ph.D.,‡ André Khayat, M.D.,§ Pierre Ducouret, Ph.D., Henri Bricard, M.D.,# Jean-Louis Gérard, M.D., Ph.D.** Background: The authors examined the role of adenosine postischemic contractile function,5–7 and metabolic triphosphate–sensitive potassium channels and adenosine A 7 1 function. Although the mechanisms involved in anes- receptors in sevoflurane-induced preconditioning on isolated thetic preconditioning remain incompletely understood, human myocardium. Methods: The authors recorded isometric contraction of hu- protein kinase C, adenosine triphosphate–sensitive po- man right atrial trabeculae suspended in oxygenated Tyrode’s tassium (KATP) channels, and adenosine A1 receptors Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/99/1/27/408853/0000542-200307000-00008.pdf by guest on 02 October 2021 solution (34°C; stimulation frequency, 1 Hz). In all groups, a seem to play a key role.1,2,5,6 However, recent studies 30-min hypoxic period was followed by 60 min of reoxygenation. suggest that volatile anesthetic–induced myocardial pre- Seven minutes before hypoxia reoxygenation, muscles were ex- posed to 4 min of hypoxia and 7 min of reoxygenation or 15 min conditioning may be dependent on species and experi- 5,8 of sevoflurane at concentrations of 1, 2, and 3%. In separate mental models. -
FAST FACTS and CONCEPTS #20 OPIOID DOSE ESCALATION in END-OF-LIFE CARE David E Weissman MD, Andrew Kamell MD Background a Comm
FAST FACTS AND CONCEPTS #20 OPIOID DOSE ESCALATION IN END-OF-LIFE CARE David E Weissman MD, Andrew Kamell MD Background A common question from trainees is “How fast, and by how much, can opioids be safely dose escalated in terminally ill patients?” Consider the analogy of furosemide (Lasix) when discussing this topic. An increase in Lasix from 10 mg to 11 mg is unheard of, yet that is precisely what often happens with opioids, especially parenteral infusions. For example, increasing a morphine infusion from 1 to 2 mg/hr is a 100% does increase; while going from 5 to 6 mg/hr is only a 20% increase. Yet, many orders are written, “increase drip by 1 mg/hr, titrate to comfort.” Some hospitals and nursing units even have this as a standing order or nursing policy. Such titration orders are unlikely to lead to be effective. Key clinical considerations for appropriate opioid escalation: 1. Is an opioid dose escalation appropriate? To answer that question, clinicians need to consider: a. Is the patient tolerating opioids well with little adverse effects? b. Is the pain or dyspnea expected to continue at a similar or progressive pattern (particularly relevant for scheduled medications or infusions) or might it be temporary? c. Is the source of discomfort opioid responsive? d. Is there evidence of hyperalgesia or neurotoxicity from opioids? See Fast Facts #57,58, and 142. e. Is the pain related to a chronic, non-malignant source in which the patient has an extended prognosis? If so, then aggressive opioid titrations may not be the best long-term solution. -
Drug and Medication Classification Schedule
KENTUCKY HORSE RACING COMMISSION UNIFORM DRUG, MEDICATION, AND SUBSTANCE CLASSIFICATION SCHEDULE KHRC 8-020-1 (11/2018) Class A drugs, medications, and substances are those (1) that have the highest potential to influence performance in the equine athlete, regardless of their approval by the United States Food and Drug Administration, or (2) that lack approval by the United States Food and Drug Administration but have pharmacologic effects similar to certain Class B drugs, medications, or substances that are approved by the United States Food and Drug Administration. Acecarbromal Bolasterone Cimaterol Divalproex Fluanisone Acetophenazine Boldione Citalopram Dixyrazine Fludiazepam Adinazolam Brimondine Cllibucaine Donepezil Flunitrazepam Alcuronium Bromazepam Clobazam Dopamine Fluopromazine Alfentanil Bromfenac Clocapramine Doxacurium Fluoresone Almotriptan Bromisovalum Clomethiazole Doxapram Fluoxetine Alphaprodine Bromocriptine Clomipramine Doxazosin Flupenthixol Alpidem Bromperidol Clonazepam Doxefazepam Flupirtine Alprazolam Brotizolam Clorazepate Doxepin Flurazepam Alprenolol Bufexamac Clormecaine Droperidol Fluspirilene Althesin Bupivacaine Clostebol Duloxetine Flutoprazepam Aminorex Buprenorphine Clothiapine Eletriptan Fluvoxamine Amisulpride Buspirone Clotiazepam Enalapril Formebolone Amitriptyline Bupropion Cloxazolam Enciprazine Fosinopril Amobarbital Butabartital Clozapine Endorphins Furzabol Amoxapine Butacaine Cobratoxin Enkephalins Galantamine Amperozide Butalbital Cocaine Ephedrine Gallamine Amphetamine Butanilicaine Codeine