Caffeine/Pentoxifylline Elisa Kit Instructions Product #106419 & 106416 Forensic Use Only
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Neuropsychopharmacology (2014) 39, 499–506 & 2014 American College of Neuropsychopharmacology. All rights reserved 0893-133X/14 www.neuropsychopharmacology.org Chronic Administration of the Methylxanthine Propentofylline Impairs Reinstatement to Cocaine by a GLT-1-Dependent Mechanism ,1 1,2 1 1 1 Kathryn J Reissner* , Robyn M Brown , Sade Spencer , Phuong K Tran , Charles A Thomas and 1 Peter W Kalivas 1 2 Department of Neurosciences, Medical University of South Carolina, Charleston, SC, USA; Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Australia In recent years, interactions between neurons and glia have been evaluated as mediators of neuropsychiatric diseases, including drug addiction. In particular, compounds that increase expression of the astroglial glutamate transporter GLT-1 (N-acetylcysteine and ceftriaxone) can decrease measures of drug seeking. However, it is unknown whether the compounds that influence broad measures of glial physiology can influence behavioral measures of drug relapse, nor is it clear whether the upregulated GLT-1 is functionally important for suppressing of drug seeking. To address these questions, we sought to determine whether the glial modulator and neuroprotective agent propentofylline (PPF) modifies drug seeking in rats using a reinstatement model of cocaine relapse. We found that 7 days of chronic (but not acute) administration of PPF significantly decreased both cue- and cocaine-induced reinstatement of cocaine seeking. We next determined whether the effect of systemic PPF on reinstatement depended upon its ability to restore expression of GLT-1 in the nucleus accumbens. PPF restored the cocaine-induced decrease in GLT-1 in the accumbens core; then, using an antisense strategy against glutamate transporter GLT-1, we found that restored transporter expression was necessary for PPF to inhibit cue-primed cocaine seeking. -
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 -
(Trental) Does Not Inhibit Dipyridamole-Induced Coronary Hyperemia: Implications for Dipyridamole-Thaffium-20 1 Myocardial Imaging
Pentoxifyffine (Trental) Does Not Inhibit Dipyridamole-Induced Coronary Hyperemia: Implications for Dipyridamole-Thaffium-20 1 Myocardial Imaging Kenneth A. Brown and Bryan K. Slinker Cardiology Unit ofihe University of Vermont College ofMedicine, Burlington, Vermont been found to be efficacious in the treatment of inter Dipyndamole-thallium-201imagingis often performedin mittent claudication because of its unique hemorrheo patientsunableto exercisebecauseof peripheralvascular logic effects (9). Thus, many patients with peripheral disease.Manyof these patientsare taking pentoxifylline vascular disease who undergo dipyridamole-thallium (Trental),a methylxanthinederivativewhichmayimprove 201 imaging may be taking pentoxifylline at the time intermittent claudication. Whether pentoxifylline inhibits di of their study. Although in vitro data from rat fat cells pyndamole-inducedcoronaryhyperamialike other math and hippocampal slices suggest that pentoxifylline is a ylxanthinas such as theophyllina and should be stopped much weaker adenosine antagonist than theophylline prior to dipyndamole-thallium-201 imaging is unknown. (7), it is not known whetherpentoxifylline significantly Therefore,we studiedthe hyperemicresponseto dipyn damolein sevenopen-chestanesthetizeddogs after pre inhibits dipyridamole-induced coronary hyperemia in treatmentwith either pantoxifylline(0, 7.5, or i 5 mg/kg vivo and should, therefore, be stopped prior to dipyri i.v.) or theophyllina(3 mg/kg i.v.). Baseline circumflex damole-thallium-20l imaging. Hence, we studied the -
(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. -
Customs Tariff - Schedule
CUSTOMS TARIFF - SCHEDULE 99 - i Chapter 99 SPECIAL CLASSIFICATION PROVISIONS - COMMERCIAL Notes. 1. The provisions of this Chapter are not subject to the rule of specificity in General Interpretative Rule 3 (a). 2. Goods which may be classified under the provisions of Chapter 99, if also eligible for classification under the provisions of Chapter 98, shall be classified in Chapter 98. 3. Goods may be classified under a tariff item in this Chapter and be entitled to the Most-Favoured-Nation Tariff or a preferential tariff rate of customs duty under this Chapter that applies to those goods according to the tariff treatment applicable to their country of origin only after classification under a tariff item in Chapters 1 to 97 has been determined and the conditions of any Chapter 99 provision and any applicable regulations or orders in relation thereto have been met. 4. The words and expressions used in this Chapter have the same meaning as in Chapters 1 to 97. Issued January 1, 2020 99 - 1 CUSTOMS TARIFF - SCHEDULE Tariff Unit of MFN Applicable SS Description of Goods Item Meas. Tariff Preferential Tariffs 9901.00.00 Articles and materials for use in the manufacture or repair of the Free CCCT, LDCT, GPT, UST, following to be employed in commercial fishing or the commercial MT, MUST, CIAT, CT, harvesting of marine plants: CRT, IT, NT, SLT, PT, COLT, JT, PAT, HNT, Artificial bait; KRT, CEUT, UAT, CPTPT: Free Carapace measures; Cordage, fishing lines (including marlines), rope and twine, of a circumference not exceeding 38 mm; Devices for keeping nets open; Fish hooks; Fishing nets and netting; Jiggers; Line floats; Lobster traps; Lures; Marker buoys of any material excluding wood; Net floats; Scallop drag nets; Spat collectors and collector holders; Swivels. -
TRENTAL (Pentoxifylline) Should Be Used During Pregnancy Only If the Potential Benefit Justifies the Potential Risk to the Fetus
TRENTAL® (pentoxifylline) Extended-Release Tablets, 400 mg DESCRIPTION TRENTAL® (pentoxifylline) extended-release tablets for oral administration contain 400 mg of the active drug and the following inactive ingredients: FD&C Red No. 3, hypromellose USP, magnesium stearate NF, polyethylene glycol NF, povidone USP, talc USP, titanium dioxide USP, and hydroxyethyl cellulose USP in an extended-release formulation. TRENTAL is a tri-substituted xanthine derivative designated chemically as 1-(5-oxohexyl)-3, 7 dimethylxanthine that, unlike theophylline, is a hemorrheologic agent, i.e. an agent that affects blood viscosity. Pentoxifylline is soluble in water and ethanol, and sparingly soluble in toluene. The CAS Registry Number is 6493-05-6. The chemical structure is: CLINICAL PHARMACOLOGY Mode of Action Pentoxifylline and its metabolites improve the flow properties of blood by decreasing its viscosity. In patients with chronic peripheral arterial disease, this increases blood flow to the affected microcirculation and enhances tissue oxygenation. The precise mode of action of pentoxifylline and the sequence of events leading to clinical improvement are still to be defined. Pentoxifylline administration has been shown to produce dose-related hemorrheologic effects, lowering blood viscosity, and improving erythrocyte flexibility. Leukocyte properties of hemorrheologic importance have been modified in animal and in vitro human studies. Pentoxifylline has been shown to increase leukocyte deformability and to inhibit neutrophil adhesion and activation. Tissue oxygen levels have been shown to be significantly increased by therapeutic doses of pentoxifylline in patients with peripheral arterial disease. Pharmacokinetics and Metabolism After oral administration in aqueous solution pentoxifylline is almost completely absorbed. It undergoes a first-pass effect and the various metabolites appear in plasma very soon after dosing. -
Prohibited Substances List
Prohibited Substances List This is the Equine Prohibited Substances List that was voted in at the FEI General Assembly in November 2009 alongside the new Equine Anti-Doping and Controlled Medication Regulations(EADCMR). Neither the List nor the EADCM Regulations are in current usage. Both come into effect on 1 January 2010. The current list of FEI prohibited substances remains in effect until 31 December 2009 and can be found at Annex II Vet Regs (11th edition) Changes in this List : Shaded row means that either removed or allowed at certain limits only SUBSTANCE ACTIVITY Banned Substances 1 Acebutolol Beta blocker 2 Acefylline Bronchodilator 3 Acemetacin NSAID 4 Acenocoumarol Anticoagulant 5 Acetanilid Analgesic/anti-pyretic 6 Acetohexamide Pancreatic stimulant 7 Acetominophen (Paracetamol) Analgesic/anti-pyretic 8 Acetophenazine Antipsychotic 9 Acetylmorphine Narcotic 10 Adinazolam Anxiolytic 11 Adiphenine Anti-spasmodic 12 Adrafinil Stimulant 13 Adrenaline Stimulant 14 Adrenochrome Haemostatic 15 Alclofenac NSAID 16 Alcuronium Muscle relaxant 17 Aldosterone Hormone 18 Alfentanil Narcotic 19 Allopurinol Xanthine oxidase inhibitor (anti-hyperuricaemia) 20 Almotriptan 5 HT agonist (anti-migraine) 21 Alphadolone acetate Neurosteriod 22 Alphaprodine Opiod analgesic 23 Alpidem Anxiolytic 24 Alprazolam Anxiolytic 25 Alprenolol Beta blocker 26 Althesin IV anaesthetic 27 Althiazide Diuretic 28 Altrenogest (in males and gelidngs) Oestrus suppression 29 Alverine Antispasmodic 30 Amantadine Dopaminergic 31 Ambenonium Cholinesterase inhibition 32 Ambucetamide Antispasmodic 33 Amethocaine Local anaesthetic 34 Amfepramone Stimulant 35 Amfetaminil Stimulant 36 Amidephrine Vasoconstrictor 37 Amiloride Diuretic 1 Prohibited Substances List This is the Equine Prohibited Substances List that was voted in at the FEI General Assembly in November 2009 alongside the new Equine Anti-Doping and Controlled Medication Regulations(EADCMR). -
Structure-Activity Relationship and Mechanistic Studies on The
University of Tennessee Health Science Center UTHSC Digital Commons Theses and Dissertations (ETD) College of Graduate Health Sciences 12-2008 Structure-Activity Relationship and Mechanistic Studies on the Chemopreventive Activity of Dipyridamole and Its Analogues Ja’Wanda Shavon Grant University of Tennessee Health Science Center Follow this and additional works at: https://dc.uthsc.edu/dissertations Part of the Pharmacy and Pharmaceutical Sciences Commons Recommended Citation Grant, Ja’Wanda Shavon , "Structure-Activity Relationship and Mechanistic Studies on the Chemopreventive Activity of Dipyridamole and Its Analogues" (2008). Theses and Dissertations (ETD). Paper 100. http://dx.doi.org/10.21007/ etd.cghs.2008.0114. This Dissertation is brought to you for free and open access by the College of Graduate Health Sciences at UTHSC Digital Commons. It has been accepted for inclusion in Theses and Dissertations (ETD) by an authorized administrator of UTHSC Digital Commons. For more information, please contact [email protected]. Structure-Activity Relationship and Mechanistic Studies on the Chemopreventive Activity of Dipyridamole and Its Analogues Document Type Dissertation Degree Name Doctor of Philosophy (PhD) Program Pharmaceutical Sciences Research Advisor John K. Buolamwini, Ph.D. Committee Richard E. Lee, Ph.D. Duane Miller, Ph.D. David Nelson, Ph.D. Jie Zheng, Ph.D. DOI 10.21007/etd.cghs.2008.0114 This dissertation is available at UTHSC Digital Commons: https://dc.uthsc.edu/dissertations/100 STRUCTURE-ACTIVITY RELATIONSHIP AND -
(12) Patent Application Publication (10) Pub. No.: US 2005/0142174A1 Assmus Et Al
US 2005O142174A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2005/0142174A1 ASSmus et al. (43) Pub. Date: Jun. 30, 2005 (54) ADHESIVE AND BINDING AGENT FOR (30) Foreign Application Priority Data DERMAL OR TRANSIDERMAL TREATMENT SYSTEMS Jan. 9, 2002 (DE)........................................ 10200578.8 (75) Inventors: Manfred Assmus, Bickenbach (DE); Publication Classification Erna Roth, Darmstadt (DE), Antoni (51) Int. Cl." .......................... A61K 31/485; A61 K 9/70 Boix, St. Joan (ES); Isabel Reig, St. (52) U.S. Cl. ............................................ 424/449; 514/282 Joan Despi (ES) s (57) ABSTRACT Correspondence Address: The invention relates to an adhesive and binding agent for OBLON, SPIVAK, MCCLELLAND, MAIER & dermal or transdermal treatment Systems, said agent con NEUSTADT, P.C. taining (a) a (meth)acrylate copolymer consisting of radi 1940 DUKE STREET cally polymerised C-sb>1</sb>to C-sb>4</sb>alkyl esters ALEXANDRIA, VA 22314 (US) of acrylic or methacrylic acid and (meth)acrylate monomers having a cationic ammonium group in the alkyl radical; (b) between 0.1 and 45 wt.%, in relation to (a), of an organic (73) Assignee: Roehm GMBH & Co. KG dicarboxylic or tricarboxylic acid, or of acrylate or (meth )acrylate polymers or copolymers containing acid groups; (21) Appl. No.: 10/499,818 (c) a skin penetration enhancer; and (d) optionally a phar maceutical active ingredient, a Softener and/or at least one (22) PCT Filed: Dec. 19, 2002 Standard addition agent. The inventive adhesive and binding agent is characterised in that the penetration enhancer (c) is (86) PCT No.: PCT/EPO2/14556 an alcohol comprising between 10 and 12 carbon atoms. -
Drugs and Medication Guidelines Brochure
Equine Medication Monitoring Program Drugs and Medication Guidelines January 2021 1 Introduction The California Equine Medication Monitoring Program (EMMP) is an industry funded program to ensure the integrity of public equine events and sales in California through the control of performance and disposition enhancing drugs and permitting limited therapeutic use of drugs and medications. The EMMP and the industry is dedicated and committed to promote the health, welfare and safety of the equine athlete. Owners, trainers, exhibitors, veterinarians and consignors of equines to public sales have a responsibility to be familiar with the California EMMP and the California Equine Medication Rule. California law (Food and Agricultural Code Sections 24000-24018) outlines the equine medication rule for public equine events in California. The owner, trainer and consignor have responsibility to ensure full compliance with all elements of the California Equine Medication Rule. Owners, trainers, exhibitors, veterinarians and consignors of equines to public sales must comply with both the California Equine Medication Rule and any sponsoring organization drug and medication rule for an event. The more stringent medication rule applies for the event. The California Equine Medication Rule is posted on the website: http://www.cdfa.ca.gov/ahfss/Animal_Health/emmp/ The information contained in this document provides advice regarding the California Equine Medication Rule and application of the rule to practical situations. The EMMP recognizes that situations arise where there is an indication for legitimate therapeutic treatment near the time of competition at equine events. The EMMP regulations permit the use of therapeutic medication in certain circumstances to accommodate legitimate therapy in compliance with the requirements of the rule. -
Exploring the Glial Mechanisms Underlying Central Neuropathic Pain in a Novel Rat Model of Spinal Cord Injury
i Exploring the Glial Mechanisms Underlying Central Neuropathic Pain in a Novel Rat Model of Spinal Cord Injury by Amanda Lynne Ellis B.A., University of Colorado, 2006 M.A., University of Colorado, 2011 A thesis submitted to the Faculty of the Graduate School of the University of Colorado in partial fulfillment of the requirement of the degree of Doctor of Philosophy Department of Psychology and Neuroscience 2014 ii This thesis entitled: Exploring the Glial Mechanisms Underlying Central Neuropathic Pain in a Novel Rat Model of Spinal Cord Injury written by Amanda Lynne Ellis has been approved for the Department of Psychology and Neuroscience ___________________________________ Dr. Linda Watkins ______________________________________________ Dr. Steven Maier ___________________________________________ Dr. Serge Campeau _______________________________________________ Dr. Benjamin Greenwood _______________________________________________ Dr. Michael Stallings Date____________ The final copy of this thesis has been examined by the signatories, and we Find that both the content and the form meet acceptable presentation standards Of scholarly work in the above mentioned discipline iii Abstract Ellis, Amanda Lynne (Ph.D., Psychology and Neuroscience) Glial Mechanisms of Central Neuropathic Pain Thesis directed by Distinguished Professor Linda Watkins Neuropathic pain is a debilitating condition that is usually intractable to treatment. Spinal cord injury (SCI) is the leading cause of central neuropathic pain (CNP), and patients often describe their pain as severe and intolerable. Although most of the focus in the pain literature has been on neurons, it is now well known that non-neuronal cells of the central nervous system called microglia and astrocytes (herein referred to as “glial cells” or “glia”) play a key role in the induction and maintenance of neuropathic pain. -
1 Package Leaflet: Information for the Patient Pentoxifyllin-Tchaikapharma
Package Leaflet: Information for the patient Pentoxifyllin-Tchaikapharma 400 mg prolonged-release tablets pentoxifylline Read all of this leaflet carefully before you start taking this medicine because it contains important information for you. - Keep this leaflet. You may need to read it again. - If you have any further questions, ask your doctor or pharmacist. - This medicine has been prescribed for you only. Do not pass it on to others. It may harm them, even if their symptoms are the same as yours. - If you get any side effects, talk to your doctor or pharmacist. This includes any possible side effects not listed in this leaflet. See section4. What is in this leaflet: 1. What Pentoxifyllin-Tchaikapharma is and what it is used for 2. What you need to know before you take Pentoxifyllin-Tchaikapharma 3. How to take Pentoxifyllin-Tchaikapharma 4. Possible side effects 5. How to store Pentoxifyllin-Tchaikapharma 6. Contents of the pack and other information 1. What Pentoxifyllin-Tchaikapharma is and what it is used for Pentoxifylline acts on the viscosity of the blood by reducing the binding of its components and increases the deformability of erythrocytes. This has a beneficial effect on blood circulation in diseases of the peripheral and cerebral arteries. This has a beneficial effect on blood circulation in diseases of the peripheral and cerebral arteries. This has a beneficial effect on the circulatory system diseases of the peripheral and cerebral arteries. Improves the blood supply to small blood vessels and the supply of tissues with oxygen. This medicine is used in: - Advanced disorders of peripheral arterial circulation of the limbs caused by atherosclerosis and diabetes and vascular spasms (intermittent claudication, diabetic macro- and microangiopathy, Raynaud's syndrome); - Diseases associated with venous circulation disorders; - Treatment of impaired blood supply to the brain and eyes.