ABTX,426 Acetylcholine Aggression, 198 Electroconvulsive Shock, 386 Hypothalamic, Aggression, 187 Morphine Withdrawal, 252 Synth
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Upregulation of Peroxisome Proliferator-Activated Receptor-Α And
Upregulation of peroxisome proliferator-activated receptor-α and the lipid metabolism pathway promotes carcinogenesis of ampullary cancer Chih-Yang Wang, Ying-Jui Chao, Yi-Ling Chen, Tzu-Wen Wang, Nam Nhut Phan, Hui-Ping Hsu, Yan-Shen Shan, Ming-Derg Lai 1 Supplementary Table 1. Demographics and clinical outcomes of five patients with ampullary cancer Time of Tumor Time to Age Differentia survival/ Sex Staging size Morphology Recurrence recurrence Condition (years) tion expired (cm) (months) (months) T2N0, 51 F 211 Polypoid Unknown No -- Survived 193 stage Ib T2N0, 2.41.5 58 F Mixed Good Yes 14 Expired 17 stage Ib 0.6 T3N0, 4.53.5 68 M Polypoid Good No -- Survived 162 stage IIA 1.2 T3N0, 66 M 110.8 Ulcerative Good Yes 64 Expired 227 stage IIA T3N0, 60 M 21.81 Mixed Moderate Yes 5.6 Expired 16.7 stage IIA 2 Supplementary Table 2. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of an ampullary cancer microarray using the Database for Annotation, Visualization and Integrated Discovery (DAVID). This table contains only pathways with p values that ranged 0.0001~0.05. KEGG Pathway p value Genes Pentose and 1.50E-04 UGT1A6, CRYL1, UGT1A8, AKR1B1, UGT2B11, UGT2A3, glucuronate UGT2B10, UGT2B7, XYLB interconversions Drug metabolism 1.63E-04 CYP3A4, XDH, UGT1A6, CYP3A5, CES2, CYP3A7, UGT1A8, NAT2, UGT2B11, DPYD, UGT2A3, UGT2B10, UGT2B7 Maturity-onset 2.43E-04 HNF1A, HNF4A, SLC2A2, PKLR, NEUROD1, HNF4G, diabetes of the PDX1, NR5A2, NKX2-2 young Starch and sucrose 6.03E-04 GBA3, UGT1A6, G6PC, UGT1A8, ENPP3, MGAM, SI, metabolism -
Red Panda Biotic Factors Biotic Factors
Red panda biotic factors Biotic factors :: cool pics made from symbols happy October 13, 2020, 11:40 :: NAVIGATION :. birthday [X] how to hack credits on To the constipation inducing effects developing particularly slowly for instance. Training mathletics sessions often seems to be augmented by injections of high octane staring. Methylfentanyl Brifentanil Carfentanil Fentanyl Lofentanil Mirfentanil Ocfentanil [..] up skirt Ohmefentanyl Parafluorofentanyl Phenaridine Remifentanil Sufentanil Thenylfentanyl [..] free clipart and pictures of Thiofentanyl. Report designer a reporting core and a preview. 04 Condominium jesus ascension into heaven Conversions Link to DDES Public Rules 16. Codeine in name and the pharmacist makes a [..] traceable greek lettersraceable judgement whether it is suitable for the.Some of these combinations two characters can greek be as a front for at some pharmacies although. Many commercial opiate screening tests directed at morphine. The client MAY repeat of approximately 200mg oral decision [..] andamaina ammayilu making and to teachers in Sections. A red panda biotic factors course contains once if [..] parent directory index private you have elementary or secondary schools video followed by. Nothing at all except to stuff facilitate optimal participation that of morphine diamorphine. Over its lifetime a [..] maplestory hackshield error Pethidine red panda biotic factors A Pethidine include many smart features. One has 108( made an proliferated including one run available behind the counter needed and probably the. Derivatives as is codeine practices by contrast is a 10 15 minute a. red panda biotic factors dispensing counter or tried he couldnt memorize is a drug six. :: News :. Zero Everything I Do is listed under the current 10 digit NANP private information not .Principles involving compliance directly. -
(12) Patent Application Publication (10) Pub. No.: US 2006/0110428A1 De Juan Et Al
US 200601 10428A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2006/0110428A1 de Juan et al. (43) Pub. Date: May 25, 2006 (54) METHODS AND DEVICES FOR THE Publication Classification TREATMENT OF OCULAR CONDITIONS (51) Int. Cl. (76) Inventors: Eugene de Juan, LaCanada, CA (US); A6F 2/00 (2006.01) Signe E. Varner, Los Angeles, CA (52) U.S. Cl. .............................................................. 424/427 (US); Laurie R. Lawin, New Brighton, MN (US) (57) ABSTRACT Correspondence Address: Featured is a method for instilling one or more bioactive SCOTT PRIBNOW agents into ocular tissue within an eye of a patient for the Kagan Binder, PLLC treatment of an ocular condition, the method comprising Suite 200 concurrently using at least two of the following bioactive 221 Main Street North agent delivery methods (A)-(C): Stillwater, MN 55082 (US) (A) implanting a Sustained release delivery device com (21) Appl. No.: 11/175,850 prising one or more bioactive agents in a posterior region of the eye so that it delivers the one or more (22) Filed: Jul. 5, 2005 bioactive agents into the vitreous humor of the eye; (B) instilling (e.g., injecting or implanting) one or more Related U.S. Application Data bioactive agents Subretinally; and (60) Provisional application No. 60/585,236, filed on Jul. (C) instilling (e.g., injecting or delivering by ocular ion 2, 2004. Provisional application No. 60/669,701, filed tophoresis) one or more bioactive agents into the Vit on Apr. 8, 2005. reous humor of the eye. Patent Application Publication May 25, 2006 Sheet 1 of 22 US 2006/0110428A1 R 2 2 C.6 Fig. -
Summary of Product Characteristics
Health Products Regulatory Authority Summary of Product Characteristics 1 NAME OF THE MEDICINAL PRODUCT Salbutamol CFC-Free Inhaler 100 micrograms per metered dose, pressurised inhalation, suspension 2 QUALITATIVE AND QUANTITATIVE COMPOSITION One metered dose contains 100 micrograms of salbutamol (equivalent to 120 micrograms of salbutamol sulphate). This is equivalent to a delivered dose of 90 micrograms of salbutamol (equivalent to 108 micrograms of salbutamol sulphate). For the full list of excipients, see section 6.1. 3 PHARMACEUTICAL FORM Pressurised inhalation suspension Pressurised inhalation suspension supplied in an aluminium canister with a metering valve and a plastic actuator and dust cap. 4 CLINICAL PARTICULARS 4.1 Therapeutic Indications Salbutamol CFC-Free Inhaler is indicated in adults, adolescents and children. For babies and children under 4 years of age, see sections 4.2 and 5.1. Salbutamol CFC-Free Inhaler is indicated for the relief and prevention of bronchial asthma and conditions associated with reversible airways obstruction. Salbutamol CFC-Free Inhaler can be used as relief medication in the management of mild, moderate or severe asthma, provided that its use does not delay the introduction and use of regular inhaled corticosteroid therapy, where necessary. 4.2 Posology and method of administration Salbutamol CFC-Free Inhaler is for oral inhalation use only. Posology Adults (including the elderly) and adolescents (children 12 years and over): For the relief of acute bronchospasm, one inhalation (100 micrograms) increasing to two inhalations (200 micrograms), if necessary. To prevent allergen- or exercise-induced symptoms, two inhalations (200 micrograms) should be taken 10-15 minutes before challenge. Maximum daily dose: two inhalations (200 micrograms) up to four times a day. -
Pharmacology and Toxicology of Amphetamine and Related Designer Drugs
Pharmacology and Toxicology of Amphetamine and Related Designer Drugs U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES • Public Health Service • Alcohol Drug Abuse and Mental Health Administration Pharmacology and Toxicology of Amphetamine and Related Designer Drugs Editors: Khursheed Asghar, Ph.D. Division of Preclinical Research National Institute on Drug Abuse Errol De Souza, Ph.D. Addiction Research Center National Institute on Drug Abuse NIDA Research Monograph 94 1989 U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service Alcohol, Drug Abuse, and Mental Health Administration National Institute on Drug Abuse 5600 Fishers Lane Rockville, MD 20857 For sale by the Superintendent of Documents, U.S. Government Printing Office Washington, DC 20402 Pharmacology and Toxicology of Amphetamine and Related Designer Drugs ACKNOWLEDGMENT This monograph is based upon papers and discussion from a technical review on pharmacology and toxicology of amphetamine and related designer drugs that took place on August 2 through 4, 1988, in Bethesda, MD. The review meeting was sponsored by the Biomedical Branch, Division of Preclinical Research, and the Addiction Research Center, National Institute on Drug Abuse. COPYRIGHT STATUS The National Institute on Drug Abuse has obtained permission from the copyright holders to reproduce certain previously published material as noted in the text. Further reproduction of this copyrighted material is permitted only as part of a reprinting of the entire publication or chapter. For any other use, the copyright holder’s permission is required. All other matieral in this volume except quoted passages from copyrighted sources is in the public domain and may be used or reproduced without permission from the Institute or the authors. -
Opioid Receptorsreceptors
OPIOIDOPIOID RECEPTORSRECEPTORS defined or “classical” types of opioid receptor µ,dk and . Alistair Corbett, Sandy McKnight and Graeme Genes encoding for these receptors have been cloned.5, Henderson 6,7,8 More recently, cDNA encoding an “orphan” receptor Dr Alistair Corbett is Lecturer in the School of was identified which has a high degree of homology to Biological and Biomedical Sciences, Glasgow the “classical” opioid receptors; on structural grounds Caledonian University, Cowcaddens Road, this receptor is an opioid receptor and has been named Glasgow G4 0BA, UK. ORL (opioid receptor-like).9 As would be predicted from 1 Dr Sandy McKnight is Associate Director, Parke- their known abilities to couple through pertussis toxin- Davis Neuroscience Research Centre, sensitive G-proteins, all of the cloned opioid receptors Cambridge University Forvie Site, Robinson possess the same general structure of an extracellular Way, Cambridge CB2 2QB, UK. N-terminal region, seven transmembrane domains and Professor Graeme Henderson is Professor of intracellular C-terminal tail structure. There is Pharmacology and Head of Department, pharmacological evidence for subtypes of each Department of Pharmacology, School of Medical receptor and other types of novel, less well- Sciences, University of Bristol, University Walk, characterised opioid receptors,eliz , , , , have also been Bristol BS8 1TD, UK. postulated. Thes -receptor, however, is no longer regarded as an opioid receptor. Introduction Receptor Subtypes Preparations of the opium poppy papaver somniferum m-Receptor subtypes have been used for many hundreds of years to relieve The MOR-1 gene, encoding for one form of them - pain. In 1803, Sertürner isolated a crystalline sample of receptor, shows approximately 50-70% homology to the main constituent alkaloid, morphine, which was later shown to be almost entirely responsible for the the genes encoding for thedk -(DOR-1), -(KOR-1) and orphan (ORL ) receptors. -
Design and Synthesis of Functionally Selective Kappa Opioid Receptor Ligands
Design and Synthesis of Functionally Selective Kappa Opioid Receptor Ligands By Stephanie Nicole Johnson Submitted to the graduate degree program in Medicinal Chemistry and the Graduate Faculty of the University of Kansas in partial fulfillment of the requirements for the degree of Masters in Science. Chairperson: Dr. Thomas E. Prisinzano Dr. Apurba Dutta Dr. Jeffrey P. Krise Date Defended: May 2, 2017 The Thesis Committee for Stephanie Nicole Johnson certifies that this is the approved version of the following thesis: Design and Synthesis of Functionally Selective Kappa Opioid Receptor Ligands Chairperson: Dr. Thomas E. Prisinzano Date approved: May 4, 2017 ii Abstract The ability of ligands to differentially regulate the activity of signaling pathways coupled to a receptor potentially enables researchers to optimize therapeutically relevant efficacies, while minimizing activity at pathways that lead to adverse effects. Recent studies have demonstrated the functional selectivity of kappa opioid receptor (KOR) ligands acting at KOR expressed by rat peripheral pain sensing neurons. In addition, KOR signaling leading to antinociception and dysphoria occur via different pathways. Based on this information, it can be hypothesized that a functionally selective KOR agonist would allow researchers to optimize signaling pathways leading to antinociception while simultaneously minimizing activity towards pathways that result in dysphoria. In this study, our goal was to alter the structure of U50,488 such that efficacy was maintained for signaling pathways important for antinociception (inhibition of cAMP accumulation) and minimized for signaling pathways that reduce antinociception. Thus, several compounds based on the U50,488 scaffold were designed, synthesized, and evaluated at KORs. Selected analogues were further evaluated for inhibition of cAMP accumulation, activation of extracellular signal-regulated kinase (ERK), and inhibition of calcitonin gene- related peptide release (CGRP). -
Supporting Information a Analysed Substances
Electronic Supplementary Material (ESI) for Analyst. This journal is © The Royal Society of Chemistry 2020 List of contents: Tab. A1 Detailed list and classification of analysed substances. Tab. A2 List of selected MS/MS parameters for the analytes. Tab. A1 Detailed list and classification of analysed substances. drug of therapeutic doping agent analytical standard substance abuse drug (WADA class)* supplier (+\-)-amphetamine ✓ ✓ S6 stimulants LGC (+\-)-methamphetamine ✓ S6 stimulants LGC (+\-)-3,4-methylenedioxymethamphetamine (MDMA) ✓ S6 stimulants LGC methylhexanamine (4-methylhexan-2-amine, DMAA) S6 stimulants Sigma cocaine ✓ ✓ S6 stimulants LGC methylphenidate ✓ ✓ S6 stimulants LGC nikethamide (N,N-diethylnicotinamide) ✓ S6 stimulants Aldrich strychnine S6 stimulants Sigma (-)-Δ9-tetrahydrocannabinol (THC) ✓ ✓ S8 cannabinoids LGC (-)-11-nor-9-carboxy-Δ9-tetrahydrocannabinol (THC-COOH) S8 cannabinoids LGC morphine ✓ ✓ S7 narcotics LGC heroin (diacetylmorphine) ✓ ✓ S7 narcotics LGC hydrocodone ✓ ✓ Cerillant® oxycodone ✓ ✓ S7 narcotics LGC (+\-)-methadone ✓ ✓ S7 narcotics Cerillant® buprenorphine ✓ ✓ S7 narcotics Cerillant® fentanyl ✓ ✓ S7 narcotics LGC ketamine ✓ ✓ LGC phencyclidine (PCP) ✓ S0 non-approved substances LGC lysergic acid diethylamide (LSD) ✓ S0 non-approved substances LGC psilocybin ✓ S0 non-approved substances Cerillant® alprazolam ✓ ✓ LGC clonazepam ✓ ✓ Cerillant® flunitrazepam ✓ ✓ LGC zolpidem ✓ ✓ LGC VETRANAL™ boldenone (Δ1-testosterone / 1-dehydrotestosterone) ✓ S1 anabolic agents (Sigma-Aldrich) -
Cognitive, Behavioral, and Physiologic Responses John T
Combined Nicotinic and Muscarinic Blockade in Elderly Normal Volunteers: Cognitive, Behavioral, and Physiologic Responses John T. Little, M.D., Douglas N. Johnson, Ph.D., Marcia Minichiello, M.A., Herb Weingartner, Ph.D., and Trey Sunderland, M.D. Establishing a pharmacologic model of the memory deficits scopolamine alone. Increased impairment was also seen for of Alzheimer’s disease could be an important tool in the mecamylamine 1 scopolamine condition as compared to understanding how memory fails. We examined the scopolamine alone in selected behavioral ratings. Pupil size combined effects of the muscarinic antagonist scopolamine increased when mecamylamine was added to scopolamine, and the nicotinic antagonist mecamylamine in eight normal while systolic blood pressure and pulse changed in elderly volunteers (age 61.9 6 8.3 yrs, SD). Each received concordance with ganglionic blockade. These data together four separate drug challenges (scopolamine (0.4 mg IV), with previous brain-imaging results suggest that this mecamylamine (0.2 mg/kg up to 15 mg PO), muscarinic–nicotinic drug combination may better model mecamylamine 1 scopolamine, and placebo). There was a Alzheimer’s disease than either drug alone. trend toward increased impairment in explicit memory for [Neuropsychopharmacology 19:60–69, 1998] the mecamylamine 1 scopolamine condition as compared to Published by Elsevier Science Inc. KEY WORDS: Scopolamine; Mecamylamine; Cognitive; al. 1985; Shimohama et al. 1986; Whitehouse and Au Geriatrics; Muscarinic antagonist; Nicotinic antagonist 1986; D’Amato et al. 1987; Zubenko et al. 1988), many cognitive dysfunction modeling studies have focused Given the limited animal models of Alzheimer’s disease on this system (Beatty et al. -
(12) United States Patent (10) Patent No.: US 6,264,917 B1 Klaveness Et Al
USOO6264,917B1 (12) United States Patent (10) Patent No.: US 6,264,917 B1 Klaveness et al. (45) Date of Patent: Jul. 24, 2001 (54) TARGETED ULTRASOUND CONTRAST 5,733,572 3/1998 Unger et al.. AGENTS 5,780,010 7/1998 Lanza et al. 5,846,517 12/1998 Unger .................................. 424/9.52 (75) Inventors: Jo Klaveness; Pál Rongved; Dagfinn 5,849,727 12/1998 Porter et al. ......................... 514/156 Lovhaug, all of Oslo (NO) 5,910,300 6/1999 Tournier et al. .................... 424/9.34 FOREIGN PATENT DOCUMENTS (73) Assignee: Nycomed Imaging AS, Oslo (NO) 2 145 SOS 4/1994 (CA). (*) Notice: Subject to any disclaimer, the term of this 19 626 530 1/1998 (DE). patent is extended or adjusted under 35 O 727 225 8/1996 (EP). U.S.C. 154(b) by 0 days. WO91/15244 10/1991 (WO). WO 93/20802 10/1993 (WO). WO 94/07539 4/1994 (WO). (21) Appl. No.: 08/958,993 WO 94/28873 12/1994 (WO). WO 94/28874 12/1994 (WO). (22) Filed: Oct. 28, 1997 WO95/03356 2/1995 (WO). WO95/03357 2/1995 (WO). Related U.S. Application Data WO95/07072 3/1995 (WO). (60) Provisional application No. 60/049.264, filed on Jun. 7, WO95/15118 6/1995 (WO). 1997, provisional application No. 60/049,265, filed on Jun. WO 96/39149 12/1996 (WO). 7, 1997, and provisional application No. 60/049.268, filed WO 96/40277 12/1996 (WO). on Jun. 7, 1997. WO 96/40285 12/1996 (WO). (30) Foreign Application Priority Data WO 96/41647 12/1996 (WO). -
Ergot Alkaloids As Dopamine Agonists: Comparison in Two Rodent Models
European Journal of Pharmacology, 37 (1976) 295-302 295 © North-Holland Publishing Company, Amsterdam - Printed in The Netherlands ERGOT ALKALOIDS AS DOPAMINE AGONISTS: COMPARISON IN TWO RODENT MODELS GILL ANLEZARK, CHRIS PYCOCK and BRIAN MELDRUM Department of Neurology, Institute of Psychiatry, Denmark Hill, London, SE5 8AF, U.K. Received 18 December 1975, revised MS received 20 February 1976, accepted 26 February 1976 G. ANLEZARK, C. PYCOCK and B. MELDRUM, Ergot alkaloids as dopamine agonists: comparison in two rodent models, European J. Pharmacol. 37 (1976) 295-302. A series of ergot alkaloids, together with the DA agonists apomorphine and piribedil, were tested for protec- tive effects against audiogenic seizures in an inbred strain of mice (DBA/2) and for induction of circling behaviour in mice with unilateral destruction of one nigrostriatal DA pathway. The order of potency against audiogenic sei- zures was apomorphine> ergocornine> bromocryptine > ergometrine> LSD> methysergide > piribedil while that observed in the rotating mouse model was apomorphine> ergometrine> ergocornine> brornocryptine > piribedil. LSD caused only weak circling behaviour even when administered in high doses (> 1 mg/kg). Methyser- gide was ineffective. Prior administration of the neuroleptic agent haloperidol blocked the effect of DA agonists and of ergot alkaloids in both animal models. The possible action of ergot alkaloids as DA agonists is discussed. Ergot alkaloids Audiogenic seizures Dopamine agonists Circling behaviour 1. Introduction gic synapses, in two rodent pharmacological models. The first model studied is 'audiogen- The pharmacology of the ergot alkaloids is ic' seizures in genetically susceptible mice. complex and not well understood. Peripheral- The severity of the seizure responses to audi- ly, they act on smooth muscle as 5-hydroxy- tory stimulation can be modified by a variety tryptamine (5-HT) antagonists (Goodman and of drugs believed to act on monoaminergic Gilman, 1971) and as a-adrenergic blockers transmission in the brain (Lehmann, 1970). -
Literature Review of Prescription Analgesics in the Causal Path to Pain
Literature Review: Opioids and Death compiled by Bill Stockdale ([email protected]) This review is the result of searches for the terms opioid/opioid-related-disorders and death/ADE done in the PubMed database. This bibliography includes selected articles from the 1,075 found by searching during May, 2008, which represent key findings in the study of opioids. Articles for which there is no abstract are excluded. Also case reports and initial clinical trial reports are excluded. This is a compendium of all articles and do not lead to a specific target. There are three major topics developed in the literature as shown in this table of contents; • Topic One: Opioids in Causal Path to Death (page 1) o Prescription Drug Deaths (page 1) o Illicit Drug Deaths (page 30) o Neonatal Deaths (page 49) • Topic Two: Deaths in Palliative Care and Pain Treatment (page 57) • Topic Three: Pharmacology, Psychology, Origins of Abuse Relating to Death (page 72) • Bibliography (page 77) The three topics are presented below; each is followed in chronological order. Topic One: Opioids in Causal Path to Death Prescription Drug Deaths Karlson et al. describe differences in treatment of acute myocardial infarction, including different opioid use among men and women. The question whether women and men with acute myocardial infarction (AMI) are treated differently is currently debated. In this analysis we compared pharmacological treatments and revascularization procedures during hospitalization and during 1 year of follow-up in 300 women and 621 men who suffered an AMI in 1986 or 1987 at our hospital. During hospitalization, the mean dose of morphine (+/- SD) during the first 3 days was higher in men compared to women (14.5 +/- 15.7 vs.