World of Cognitive Enhancers
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European Review for Medical and Pharmacological Sciences 2019; 23: 3-15 Use of cognitive enhancers: methylphenidate and analogs J. CARLIER1, R. GIORGETTI2, M.R. VARÌ3, F. PIRANI2, G. RICCI4, F.P. BUSARDÒ2 1Unit of Forensic Toxicology, Sapienza University of Rome, Rome, Italy 2Section of Legal Medicine, Universita Politecnica delle Marche, Ancona, Italy 3National Centre on Addiction and Doping, Istituto Superiore di Sanità, Rome, Italy 4School of Law, University of Camerino, Camerino, Italy Abstract. – OBJECTIVE: In the last decades, phenidate analogs should be undertaken to re- several cognitive-enhancing drugs have been duce the uprising threat, and education efforts sold onto the drug market. Methylphenidate and should be made among high-risk populations. analogs represent a sub-class of these new psy- choactive substances (NPS). We aimed to re- Key Words: view the use and misuse of methylphenidate and Cognitive enhancers, Methylphenidate, Ritalin, Eth- analogs, and the risk associated. Moreover, we ylphenidate, Methylphenidate analogs, New psycho- exhaustively reviewed the scientific data on the active substances. most recent methylphenidate analogs (methyl- phenidate and ethylphenidate excluded). MATERIALS AND METHODS: Literature Introduction search was performed on methylphenidate and analogs, using specialized search engines ac- cessing scientific databases. Additional reports Consumption of various pharmaceutical drugs were retrieved from international agencies, in- by healthy individuals in an attempt to improve stitutional websites, and drug user forums. cognitive faculties is on the rise, whether for aca- RESULTS: Methylphenidate/Ritalin has been demic or recreational purposes1. These substances used for decades to treat attention deficit disor- are stimulants that preferentially target the cate- ders and narcolepsy. More recently, it has been used as a cognitive enhancer and a recreation- cholamines of the prefrontal cortex of the brain to al drug. -
Lifestyle Drugs” for Men and Women
Development of “Lifestyle Drugs” for Men and Women Armin Schultz CRS - Clinical Research Services Mannheim GmbH AGAH Annual Meeting 2012, Leipzig, March 01 - 02 Lifestyle drugs Smart drugs, Quality-of-life drugs, Vanity drugs etc. Lifestyle? Lifestyle-Drugs? Active development? Discovery by chance? AGAH Annual Meeting 2012, Leipzig, March 01 - 02 Lifestyle A lifestyle is a characteristic bundle of behaviors that makes sense to both others and oneself in a given time and place, including social relations, consumption, entertainment, and dress. The behaviors and practices within lifestyles are a mixture of habits, conventional ways of doing things, and reasoned actions „Ein Lebensstil ist [...] der regelmäßig wiederkehrende Gesamtzusammenhang der Verhaltensweisen, Interaktionen, Meinungen, Wissensbestände und bewertenden Einstellungen eines Menschen“ (Hradil 2005: 46) Different definitions in social sciences, philosophy, psychology or medicine AGAH Annual Meeting 2012, Leipzig, March 01 - 02 Lifestyle Many “subdivisions” LOHAS: “Lifestyles of Health and Sustainability“ LOVOS: “Lifestyles of Voluntary Simplicity“ SLOHAS: “Slow Lifestyles of Happiness and Sustainability” PARKOS: “Partizipative Konsumenten“ ……. ……. ……. AGAH Annual Meeting 2012, Leipzig, March 01 - 02 Lifestyle drugs Lifestyle drug is an imprecise term commonly applied to medications which treat non-life threatening and non-painful conditions such as baldness, impotence, wrinkles, or acne, without any medical relevance at all or only minor medical relevance relative to others. Desire for increase of personal well-being and quality of life It is sometimes intended as a pejorative, bearing the implication that the scarce medical research resources allocated to develop such drugs were spent frivolously when they could have been better spent researching cures for more serious medical conditions. -
The 2006 Prohibited List International Standard
The World Anti-Doping Code THE 2006 PROHIBITED LIST INTERNATIONAL STANDARD The official text of the Prohibited List shall be maintained by WADA and shall be published in English and French. In the event of any conflict between the English and French versions, the English version shall prevail. This List shall come into effect on 1 January 2006. THE 2006 PROHIBITED LIST WORLD ANTI-DOPING CODE Valid 1 January 2006 The use of any drug should be limited to medically justified indications SUBSTANCES AND METHODS PROHIBITED AT ALL TIMES (IN- AND OUT-OF-COMPETITION) PROHIBITED SUBSTANCES S1. ANABOLIC AGENTS Anabolic agents are prohibited. 1. Anabolic Androgenic Steroids (AAS) a. Exogenous* AAS, including: 1-androstendiol (5α-androst-1-ene-3β,17β-diol ); 1-androstendione (5α- androst-1-ene-3,17-dione); bolandiol (19-norandrostenediol); bolasterone; boldenone; boldione (androsta-1,4-diene-3,17-dione); calusterone; clostebol; danazol (17α-ethynyl-17β-hydroxyandrost-4-eno[2,3-d]isoxazole); dehydrochlormethyltestosterone (4-chloro-17β-hydroxy-17α-methylandrosta- 1,4-dien-3-one); desoxymethyltestosterone (17α-methyl-5α-androst-2-en- 17β-ol); drostanolone; ethylestrenol (19-nor-17α-pregn-4-en-17-ol); fluoxymesterone; formebolone; furazabol (17β-hydroxy-17α-methyl-5α- androstano[2,3-c]-furazan); gestrinone; 4-hydroxytestosterone (4,17β-dihydroxyandrost-4-en-3-one); mestanolone; mesterolone; metenolone; methandienone (17β-hydroxy-17α- methylandrosta-1,4-dien-3-one); methandriol; methasterone (2α, 17α- dimethyl-5α-androstane-3-one-17β-ol); methyldienolone -
Horsemen's Information 2016和文TGP 1 薬物修正後 E
[Conditions] 1 Date December 29 (Tue), 2020 2020 Oi Racetrack, Race 10 2 Location TCK, Oi Racetrack 3 Race The 66th Running of Tokyo Daishoten (GI) 4 Eligibility Thoroughbreds, 3 years old & up 5 Full Gate 16 horses 6 Foreign Runners Selected by the selection committee from among the pre-entered horses. 7 Distance 2,000m, 1 1/4 mile (Right-handed, dirt course) 8 Weight 3 years old: 121.5 lbs,4 years old & up: 125.5 lbs, Female: 4.4 lbs less For 3 year-old-horses from the southern hemisphere, reduce 4.4 lbs from the above weight. 9 Purse Unit: 1,000 JPY Prize Purse & Bonus money Running Record 1st place 6th place allowances prize *1 prize *2 1st place 2nd place 3rd place 4th place 5th place or lower Owner 80,000 28,000 16,000 8,000 4,000 300 300 50 1,600 Trainer 880 70 60 50 40 30 30 80 Jockey 120 110 100 80 70 60 30 80 Groom 80 70 60 50 40 30 30 80 Rider 30 30 80 *1 Paid for the runner who broke the previous record and also set the best record during the race. *2 Prize equivalent to the amount listed in the table above is presented. *3 1 USD= 105.88 JPY (As of August,2020) 10 Handling of Late Scratch No allowance is paid in the case of a late scratch (including cancelation of race due to standstill in a starting gate) approved by TCK, Stewards, and Starter. However, if the chairman of the race meeting operation committee deems that the horse is involved in an accident not caused by the horse, the owner is given an running allowance. -
Seven Fatalities Associated with Ethylphenidate
University of Huddersfield Repository Maskell, Peter D., Smith, Paul, Cole, Richard, Hikin, Laura and Morley, Stephen Seven fatalities associated with ethylphenidate Original Citation Maskell, Peter D., Smith, Paul, Cole, Richard, Hikin, Laura and Morley, Stephen (2016) Seven fatalities associated with ethylphenidate. Forensic Science International, 265. pp. 70-74. ISSN 03790738 This version is available at http://eprints.hud.ac.uk/id/eprint/27267/ The University Repository is a digital collection of the research output of the University, available on Open Access. Copyright and Moral Rights for the items on this site are retained by the individual author and/or other copyright owners. Users may access full items free of charge; copies of full text items generally can be reproduced, displayed or performed and given to third parties in any format or medium for personal research or study, educational or not-for-profit purposes without prior permission or charge, provided: • The authors, title and full bibliographic details is credited in any copy; • A hyperlink and/or URL is included for the original metadata page; and • The content is not changed in any way. For more information, including our policy and submission procedure, please contact the Repository Team at: [email protected]. http://eprints.hud.ac.uk/ Seven fatalities associated with ethylphenidate a* b b b b P.D. Maskell P.R. Smith , R. Cole , L. Hikin , S.R. Morley , aDepartment of Chemical and Forensic Sciences, School of Applied Sciences. University of Huddersfield. Huddersfield. HD1 3DH bForensic Toxicology Unit, Department of Clinical Chemistry and Metabolic Medicine, University Hospitals of Leicester, Leicester Royal Infirmary, Leicester, LE1 5WW, UK. -
Neuroprotection in Alzheimer's Disease
Chapter 8 Neuroprotection in Alzheimer’s Disease Introduction Alzheimer’s disease (AD) is a progressive degenerative disorder of the brain that begins with memory impairment and eventually progresses to dementia, physical impairment, and death. Patients develop various psychiatric and neurological signs during the course of the disease. The prevalence rates of dementia vary significantly in different countries, but range from 2.1 to 10.5%. AD is the most common type of dementia, accounting for 50–60% of all cases, and is described in detail in a special report on AD (Jain 2010). Several other types of dementias are considered in the differential diagnosis of AD and sometimes all the dementias are lumped together if the type is not known. Other well-known types of dementias are vascular dementia, dementia of aging, and dementia associated with HIV infection. The focus of this section is on AD and some other dementias will be described in Chap. 11. Pathomechanism of Alzheimer’s Disease Several factors that play a role in the etiology and pathogenesis of AD include the following: • Aging • Genetic risk factors • Amyloid precursor protein (APP) and beta-amyloid (Ab) accumulation with neural and vascular sequelae • Tau hyperphosphorylation • Membrane disturbances, phospholipid metabolism, and disruption of signal transduction • Inflammatory reactions and immunological disturbances • Environmental toxins: trace metals • Neurotransmitter defects and imbalances K.K. Jain, The Handbook of Neuroprotection, DOI 10.1007/978-1-61779-049-2_8, 337 © Springer Science+Business Media, LLC 2011 338 8 Neuroprotection in Alzheimer’s Disease • Neuroendocrine disturbances • Oxidative injury and free radicals • Disturbances in regulation and receptors of neurotrophic factors (NTFs) Such a large number of factors in the etiology of AD are responsible for the plethora of theories of cause of AD. -
(19) United States (12) Patent Application Publication (10) Pub
US 20130289061A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2013/0289061 A1 Bhide et al. (43) Pub. Date: Oct. 31, 2013 (54) METHODS AND COMPOSITIONS TO Publication Classi?cation PREVENT ADDICTION (51) Int. Cl. (71) Applicant: The General Hospital Corporation, A61K 31/485 (2006-01) Boston’ MA (Us) A61K 31/4458 (2006.01) (52) U.S. Cl. (72) Inventors: Pradeep G. Bhide; Peabody, MA (US); CPC """"" " A61K31/485 (201301); ‘4161223011? Jmm‘“ Zhu’ Ansm’ MA. (Us); USPC ......... .. 514/282; 514/317; 514/654; 514/618; Thomas J. Spencer; Carhsle; MA (US); 514/279 Joseph Biederman; Brookline; MA (Us) (57) ABSTRACT Disclosed herein is a method of reducing or preventing the development of aversion to a CNS stimulant in a subject (21) App1_ NO_; 13/924,815 comprising; administering a therapeutic amount of the neu rological stimulant and administering an antagonist of the kappa opioid receptor; to thereby reduce or prevent the devel - . opment of aversion to the CNS stimulant in the subject. Also (22) Flled' Jun‘ 24’ 2013 disclosed is a method of reducing or preventing the develop ment of addiction to a CNS stimulant in a subj ect; comprising; _ _ administering the CNS stimulant and administering a mu Related U‘s‘ Apphcatlon Data opioid receptor antagonist to thereby reduce or prevent the (63) Continuation of application NO 13/389,959, ?led on development of addiction to the CNS stimulant in the subject. Apt 27’ 2012’ ?led as application NO_ PCT/US2010/ Also disclosed are pharmaceutical compositions comprising 045486 on Aug' 13 2010' a central nervous system stimulant and an opioid receptor ’ antagonist. -
Modafinil and Modafinil Analogues: Free Radical Mechanism of the Eugeroic and Cognitive Enhancment Effect Clifford Fong
Modafinil and modafinil analogues: free radical mechanism of the eugeroic and cognitive enhancment effect Clifford Fong To cite this version: Clifford Fong. Modafinil and modafinil analogues: free radical mechanism of the eugeroic and cognitive enhancment effect. [Research Report] Eigenenergy. 2018. hal-01933737 HAL Id: hal-01933737 https://hal.archives-ouvertes.fr/hal-01933737 Submitted on 24 Nov 2018 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Modafinil and modafinil analogues: free radical mechanism of the eugeroic and cognitive enhancment effect Clifford W. Fong Eigenenergy, Adelaide, South Australia. Keywords: Modafinil, modafinil-like analogues, eugeroic effect, cognitive enhancement, free radicals, quantum mechanics Abbreviations Dopamine DA, dopamine transporter DAT, Dissociative electron transfer or attachment DET, Linear free energy relationship LFER, free energy of water desolvation ΔG desolv,CDS , lipophilicity free energy ΔG lipo,CDS, cavity dispersion solvent structure of the first solvation shell CDS, highest occupied molecular orbital HOMO, lowest unoccupied molecular orbital LUMO, multiple correlation coefficient R 2, the F test of significance, standards errors for the estimate (SEE) and standard errors of the variables SE(ΔG desolCDS ), SE(ΔG lipoCDS ), SE(Dipole Moment), SE (Molecular Volume), transition state TS, reactive oxygen species ROS. -
Patterns Of, and Motivations for Illicit Drug Use Among Long Haul
Fatigue and beyond: Patterns of, and motivations for illicit drug use among long haul truck drivers Naomi Richards BPsych (Hons) This thesis is submitted for the degree of Masters of Applied Science (Research) within the Centre for Accident Research and Road Safety-Queensland (CARRS-Q), School of Psychology and Counselling, Queensland University of Technology 2004 Key words Drug use Drug use career Illicit drug use Road safety Truck drivers Abstract Long distance truck drivers are considered a special interest group in terms of drug driving research and policy due to high rates of use, involvement of drugs in truck accidents and the link between drug use and work related fatigue. Qualitative interview data was collected from 35 long haul truck drivers in South East Queensland and analysed using NVivo 2.0. High rates of licit and illicit drug use (particularly amphetamines) were reported. However, unlike previous studies which focus on fatigue, this research found overlapping and changing motivations for drug use during individual lifetimes. Using Becker’s model of a drug use ‘career’ it was revealed that some drivers begin illicit drug use before they begin truck driving. As well as fatigue, powerful motives such as peer pressure, wanting to fit the trucking ‘image’, socialisation, relaxation and addiction were reported. These may need to be considered along side fatigue in the development of effective drug prevention or cessation policies for truck drivers. Contents Page 1. Introduction 1 2. Literature Review 5 2.1. Drugs of concern to road safety 5 2.1.1. Cannabis 6 2.1.1.1. Effects of cannabis on driving performance 7 2.1.2. -
42711 IPEG Programmaboekje
19 th Biennial Conference 19th Biennial Conference October 26th – 30th 2016 October 26 Nijmegen, the Netherlands th – 30 th 2016 Nijmegen, the Netherlands 2016 Nijmegen, 42711 IPEG programmaboekje omslag.indd 1 06-10-16 17:52 The “International Pharmaco-EEG Society, Association for Electrophysiological Brain Research in Preclinical and Clinical Pharmacology and Related Fields” (IPEG) is a non-profit organization, established in 1980 and composed of scientists and researchers actively involved in electrophysiological brain research in preclinical and clinical pharmacology, neurotoxicology and related areas of interest. my.thesis nl for the design of your Thesis & to show your Thesis 42711 IPEG programmaboekje omslag.indd 2 06-10-16 17:52 IPEG 2016 in Nijmegen | 1 Welcome to Nijmegen, dear attendants of the 19th IPEG meeting. Nijmegen, a 2000 year old city; Nijmegen, a Roman and a medieval city; Nijmegen, the home town of the first catholic university funded by the Faithfull to improve education of a suppressed part of the Netherlands; Nijmegen, the city that heavily suffered in WWII; Nijmegen, the home town of the Donders Institute. Nijmegen, as we hope and trust, your home town for the upcoming IPEG meeting. As you all know, electrophysiological brain research has a long tradition going back as far as 1875 when the first report on the animal electroencephalogram (EEG) was published by Caton. The often forgotten Polish physiologist Adolf Beck was also a EEG pioneer many years before Hans Berger’s initial reports. Beck recorded electrical potentials in several brain areas evoked by peripheral sensory stimuli. Using this technique, Beck localised various centres in the brain of several animal species and described desynchronization in electrical brain potentials. -
19Th Biennial IPEG Meeting Nijmegen, the Netherlands
Neuropsychiatric Electrophysiology 2016, 2(Suppl 1):8 DOI 10.1186/s40810-016-0021-4 MEETINGABSTRACTS Open Access 19th biennial IPEG Meeting Nijmegen, The Netherlands. 26-30 October 2016 Published: 29 November 2016 Training course measures. This will be illustrated by means of pertinent examples. These include elucidating the mechanisms of stimulant action re- A1 mediating deficient impulse control and the role of the cannabinoid Thalamocortical sleep oscillations system in human working memory, as well as drug effects on Igor Timofeev1,2 sensory gating and specific aspects of visual-spatial attention. Other 1Department of Psychiatry and Neuroscience, Université Laval, Québec, examples concern the added sensitivity of EEG and ERP measures, Canada; 2Centre de recherche de l’Institut universitaire en santé mentale relative to that of performance measures, in detecting effects of alco- de Québec (CRIUSMQ), Université Laval, Québec, Canada hol, and more generally in monitoring and predicting vigilance and Neuropsychiatric Electrophysiology 2016, 2(Suppl 1):A1 the ability to detect external signals in the immediate future. Rela- tions between brain signals and cognitive competences are revealed In waking and sleeping states, thalamocortical system generates a by either comparing different individuals, or moment-to-moment variety of oscillations ranging from 0.1 Hz to hundreds of Hz. Most of fluctuations within individuals, or differences in state (e.g., drug- them are present during NREM sleep, but slower activities prevail in induced) within individuals. this state of vigilance. Thalamocortical network is organized in a loop in which thalamocortical cells excite reticular thalamic and neocor- tical cells, reticular thalamic cells inhibit thalamocortical cells and A3 corticothalamic cells excite thalamocortical and reticular thalamic EEG and ERP as key techniques for functional brain alterations cells. -
Enhanced Reporting
Drug Profile, Targeted with Interpretation by Tandem Mass Spectrometry and Enzyme Immunoassay, Urine Patient: PAIN HYB 2, 2009288 | Date of Birth: | Gender: M | Physician: DR T. TEST Patient Identifiers: | Visit Number (FIN): Drug Analyte Result Cutoff Notes Meperidine metabolite Not Detected 50 ng/mL normeperidine Tapentadol Not Detected 100 ng/mL --Tapentadol-o-sulfate Not Detected 200 ng/mL tapentadol metabolite AMPHETAMINE-LIKE, MASS SPEC Amphetamine Present 50 ng/mL eg, Vyvanse; also a metabolite of methamphetamine Methamphetamine Present 200 ng/mL d- and l- isomers are not distinguished by this test; may reflect Vicks inhaler, Desoxyn, Selegiline, or illicit source MDMA - Ecstasy Not Detected 200 ng/mL MDA Not Detected 200 ng/mL also a metabolite of MDMA and MDEA MDEA - Eve Not Detected 200 ng/mL Phentermine Not Detected 100 ng/mL Methylphenidate Not Detected 100 ng/mL eg, Ritalin, Dexmethylphenidate, Focalin, Concerta BENZODIAZEPINE-LIKE, MASS SPEC Alprazolam Not Detected 40 ng/mL eg, Xanax --Alpha-hydroxyalprazolam Not Detected 20 ng/mL alprazolam metabolite Clonazepam Not Detected 20 ng/mL eg, Klonopin --7-aminoclonazepam Not Detected 40 ng/mL clonazepam metabolite Diazepam Not Detected 50 ng/mL eg, Valium Nordiazepam Not Detected 50 ng/mL metabolite of chlordiazepoxide (Librium), clorazepate (Tranxene), diazepam, halazepam (Alapryl), prazepam (Centrax) and others Oxazepam Not Detected 50 ng/mL eg, Serax; also metabolite of nordiazepam and temazepam Temazepam Not Detected 50 ng/mL eg, Restoril; also a metabolite of diazepam Lorazepam Not Detected 60 ng/mL eg, Ativan Midazolam Not Detected 20 ng/mL eg, Versed Zolpidem Present 20 ng/mL eg, Ambien Reference interval Creatinine value (mg/dL) 200.0 20.0 - 400.0 mg/dL Patient: PAIN HYB 2, 2009288 ARUP Accession: 21-048-107698 4848 Chart continues on following page(s) ARUP Enhanced Reporting | February 17, 2021 | page 4 of 5 Drug Profile, Targeted with Interpretation by Tandem Mass Spectrometry and Enzyme Immunoassay, Urine Patient: PAIN HYB 2, 2009288 | Date of Birth | Gender: M | Physician: DR T.