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Anticonvulsants
ALZET® Bibliography References on the Administration of Anticonvulsive Agents Using ALZET Osmotic Pumps 1. Carbamazepine Q5784: K. Deseure, et al. Differential drug effects on spontaneous and evoked pain behavior in a model of trigeminal neuropathic pain. J Pain Res 2017;10(279-286 ALZET Comments: Carbamazepine, baclofen, clomipramine; DMSO, PEG, Ethyl Alcohol, Acetone; SC; Rat; 2ML1; Controls received mp w/ vehicle; animal info (7 weeks old); dimethyl sulfoxide, propylene glycol, ethyl alcohol, and acetone at a ratio of 42:42:15:1; post op. care (morphine 5 mg/day); behavioral testing (Facial grooming); Therapeutic indication (Trigeminal neuralgia, neuropathic pain); Dose (30 mg/day carbamazepine (the first-line drug treatment for trigeminal neuralgia), 1.06 mg/day baclofen, 4.18 mg/day clomipramine, and 5 mg/day morphine);. Q0269: S. M. Cain, et al. High resolution micro-SPECT scanning in rats using 125I beta-CIT: Effects of chronic treatment with carbamazepine. Epilepsia 2009;50(8):1962-1970 ALZET Comments: Carbamazepine; DMSO; propylene glycol; ethyl alcohol; acetone; SC; Rat; 2ML2; 14 days; Controls received mp w/ vehicle; animal info (adult, male, Sprague-Dawley, 160-270 g); functionality of mp verified by serum drug levels; 42% DMSO used; identified 3 mg/kg/day as the highest dose that could be reliably administered via minipumps over a 14-day period at 37 degrees Celsius, pg. 1969. P5195: H. C. Doheny, et al. A comparison of the efficacy of carbamazepine and the novel anti-epileptic drug levetiracetam in the tetanus toxin model of focal complex partial epilepsy. British Journal of Pharmacology 2002;135(6):1425-1434 ALZET Comments: Carbamazepine; levetiracetam; DMSO; Propylene glycol; ethanol, saline; IP; Rat; 7 days; Controls received mp/ vehicle; functionality of mp verified by drug serum levels; dose-response (text p.1428); carbamazepine was dissolved in 42.5% DMSO/42% Propylene glycol/15% ethanol. -
Chronic Pelvic Pain M
Guidelines on Chronic Pelvic Pain M. Fall (chair), A.P. Baranowski, S. Elneil, D. Engeler, J. Hughes, E.J. Messelink, F. Oberpenning, A.C. de C. Williams © European Association of Urology 2008 TABLE OF CONTENTS PAGE 1. INTRODUCTION 5 1.1 The guideline 5 1.1.1 Publication history 5 1.2 Level of evidence and grade recommendations 5 1.3 References 6 1.4 Definition of pain (World Health Organization [WHO]) 6 1.4.1 Innervation of the urogenital system 7 1.4.2 References 8 1.5 Pain evaluation and measurement 8 1.5.1 Pain evaluation 8 1.5.2 Pain measurement 8 1.5.3 References 9 2. CHRONIC PELVIC PAIN 9 2.1 Background 9 2.1.1 Introduction to urogenital pain syndromes 9 2.2 Definitions of chronic pelvic pain and terminology (Table 4) 11 2.3 Classification of chronic pelvic pain syndromes 12 Table 3: EAU classification of chronic urogenital pain syndromes (page 10) Table 4: Definitions of chronic pain terminology (page 11) Table 5: ESSIC classification of types of bladder pain syndrome according to the results of cystoscopy with hydrodistension and of biopsies (page 13) 2.4 References 13 2.5 An algorithm for chronic pelvic pain diagnosis and treatment 13 2.5.1 How to use the algorithm 13 2.6 Prostate pain syndrome (PPS) 15 2.6.1 Introduction 16 2.6.2 Definition 16 2.6.3 Pathogenesis 16 2.6.4 Diagnosis 17 2.6.5 Treatment 17 2.6.5.1 Alpha-blockers 17 2.6.5.2 Antibiotic therapy 17 2.6.5.3 Non-steroidal anti-inflammatory drugs (NSAIDs) 17 2.6.5.4 Corticosteroids 17 2.6.5.5 Opioids 17 2.6.5.6 5-alpha-reductase inhibitors 18 2.6.5.7 Allopurinol 18 2.6.5.8 -
Acetylcholine Signaling System in Progression of Lung Cancers
Pharmacology & Therapeutics 194 (2019) 222–254 Contents lists available at ScienceDirect Pharmacology & Therapeutics journal homepage: www.elsevier.com/locate/pharmthera Acetylcholine signaling system in progression of lung cancers Jamie R. Friedman a,1, Stephen D. Richbart a,1,JustinC.Merritta,KathleenC.Browna, Nicholas A. Nolan a, Austin T. Akers a, Jamie K. Lau b, Zachary R. Robateau a, Sarah L. Miles a,PiyaliDasguptaa,⁎ a Department of Biomedical Sciences, Joan C. Edwards School of Medicine, 1700 Third Avenue, Huntington, WV 25755 b Biology Department, Center for the Sciences, Box 6931, Radford University, Radford, Virginia 24142 article info abstract Available online 3 October 2018 The neurotransmitter acetylcholine (ACh) acts as an autocrine growth factor for human lung cancer. Several lines of evidence show that lung cancer cells express all of the proteins required for the uptake of choline (choline Keywords: transporter 1, choline transporter-like proteins) synthesis of ACh (choline acetyltransferase, carnitine acetyl- Lung cancer transferase), transport of ACh (vesicular acetylcholine transport, OCTs, OCTNs) and degradation of ACh (acetyl- Acetylcholine cholinesterase, butyrylcholinesterase). The released ACh binds back to nicotinic (nAChRs) and muscarinic Cholinergic receptors on lung cancer cells to accelerate their proliferation, migration and invasion. Out of all components Proliferation of the cholinergic pathway, the nAChR-signaling has been studied the most intensely. The reason for this trend Invasion Anti-cancer drugs is due to genome-wide data studies showing that nicotinic receptor subtypes are involved in lung cancer risk, the relationship between cigarette smoke and lung cancer risk as well as the rising popularity of electronic ciga- rettes considered by many as a “safe” alternative to smoking. -
United States Patent (19) (11) 4,310,524 Wiech Et Al
United States Patent (19) (11) 4,310,524 Wiech et al. 45 Jan. 12, 1982 (54) TCA COMPOSITION AND METHOD FOR McMillen et al., Fed. Proc., 38,592 (1979). RAPD ONSET ANTDEPRESSANT Sellinger et al., Fed. Proc., 38,592 (1979). THERAPY Pandey et al., Fed. Proc., 38,592 (1979). 75) Inventors: Norbert L. Wiech; Richard C. Ursillo, Primary Examiner-Stanley J. Friedman both of Cincinnati, Ohio Attorney, Agent, or Firm-Millen & White 73) Assignee: Richardson-Merrell, Inc., Wilton, Conn. (57 ABSTRACT A method is provided for treating depression in a pa (21) Appl. No.: 139,498 tient therefrom and requiring rapid symptomatic relief, (22 Filed: Apr. 11, 1980 which comprises administering to said patient concur 51) Int. Cl. .................... A61K 31/33; A61K 31/135 rently (a) an effective antidepressant amount of a tricy clic antidepressant or a pharmaceutically effective acid (52) ...... 424/244; 424/330 addition salt thereof, and (b) an amount of an a-adrener 58) Field of Search ................................ 424/244, 330 gic receptor blocking agent effective to achieve rapid (56) References Cited onset of the antidepressant action of (a), whereby the PUBLICATIONS onset of said antidepressant action is achieved within Chemical Abst., vol. 66-72828m, (1967), Kellett. from 1 to 7 days. Chemical Abst, vol. 68-94371a, (1968), Martelli et al. A pharmaceutical composition is also provided which is Chemical Abst., vol. 74-86.048j, (1971), Dixit et al. especially adapted for use with the foregoing method. Holmberg et al., Psychopharm., 2,93 (1961). Svensson, Symp. Med. Hoechst., 13, 245 (1978). 17 Claims, No Drawings 4,310,524 1. -
A Review of the Effects of Pain and Analgesia on Immune System Function and Inflammation: Relevance for Preclinical Studies
Comparative Medicine Vol 69, No 6 Copyright 2019 December 2019 by the American Association for Laboratory Animal Science Pages 520–534 Overview A Review of the Effects of Pain and Analgesia on Immune System Function and Inflammation: Relevance for Preclinical Studies George J DeMarco1* and Elizabeth A Nunamaker2 One of the most significant challenges facing investigators, laboratory animal veterinarians, and IACUCs, is how to bal- ance appropriate analgesic use, animal welfare, and analgesic impact on experimental results. This is particularly true for in vivo studies on immune system function and inflammatory disease. Often times the effects of analgesic drugs on a particu- lar immune function or model are incomplete or don’t exist. Further complicating the picture is evidence of the very tight integration and bidirectional functionality between the immune system and branches of the nervous system involved in nociception and pain. These relationships have advanced the concept of understanding pain as a protective neuroimmune function and recognizing pathologic pain as a neuroimmune disease. This review strives to summarize extant literature on the effects of pain and analgesia on immune system function and inflammation in the context of preclinical in vivo studies. The authors hope this work will help to guide selection of analgesics for preclinical studies of inflammatory disease and immune system function. Abbreviations and acronyms: CB,Endocannabinoid receptor; CD,Crohn disease; CFA, Complete Freund adjuvant; CGRP,Calcitonin gene-related -
Purinergic P2 Receptors As Targets for Novel Analgesics
Pharmacology & Therapeutics 110 (2006) 433 – 454 www.elsevier.com/locate/pharmthera Purinergic P2 receptors as targets for novel analgesics Geoffrey Burnstock * Autonomic Neuroscience Centre, Royal Free and University College Medical School, Rowland Hill Street, London NW3 2PF, UK Abstract Following hints in the early literature about adenosine 5V-triphosphate (ATP) injections producing pain, an ion-channel nucleotide receptor was cloned in 1995, P2X3 subtype, which was shown to be localized predominantly on small nociceptive sensory nerves. Since then, there has been an increasing number of papers exploring the role of P2X3 homomultimer and P2X2/3 heteromultimer receptors on sensory nerves in a wide range of organs, including skin, tongue, tooth pulp, intestine, bladder, and ureter that mediate the initiation of pain. Purinergic mechanosensory transduction has been proposed for visceral pain, where ATP released from epithelial cells lining the bladder, ureter, and intestine during distension acts on P2X3 and P2X2/3, and possibly P2Y, receptors on subepithelial sensory nerve fibers to send messages to the pain centers in the brain as well as initiating local reflexes. P1, P2X, and P2Y receptors also appear to be involved in nociceptive neural pathways in the spinal cord. P2X4 receptors on spinal microglia have been implicated in allodynia. The involvement of purinergic signaling in long-term neuropathic pain and inflammation as well as acute pain is discussed as well as the development of P2 receptor antagonists as novel analgesics. D -
Imaging Functional Brain Connectivity
Imaging Functional Brain Connectivity: pharmacological modulation, aging & Alzheimer’s disease Bernadet L. Klaassens 1 Table of contents Chapter 1 3 Introduction and aims Part I: Pharmacological challenge effects on brain connectivity in healthy young adults Chapter 2 10 Single-dose serotonergic stimulation shows widespread effects on functional brain connectivity (NeuroImage 2015 Nov; 122: 440-450) Chapter 3 31 Time related effects on functional brain connectivity after serotonergic and cholinergic neuromodulation (Human Brain Mapping 2017 Jan; 38 (1): 308-325) Part II: Functional brain connectivity and neuromodulation in older age and Alzheimer’s disease Chapter 4 60 Diminished posterior precuneus connectivity with the default mode network differentiates normal aging from Alzheimer’s disease (Frontiers in Aging Neuroscience 2017 Apr; 9: 1-13) Chapter 5 84 Serotonergic and cholinergic modulation of functional brain connectivity: a comparison between young and older adults ( NeuroImage 2018 Apr; 169: 312-322) Chapter 6 108 Imaging cholinergic and serotonergic neurotransmitter networks in Alzheimer’s disease in vivo (Submission at Alzheimer’s and Dementia) Chapter 7 131 Summary and general discussion 2 Chapter 1 Introduction and aims Brain function relies heavily on neural communication and connections. Better understanding of the mechanisms that are related to maintenance or deterioration of brain function requires a technique that takes into account the elaborate nature of the central nervous system (CNS). A useful method for that purpose is to assess the brain’s functional connectivity. Brain regions are functionally connected to each other when they exhibit correlating activation patterns (Friston et al., 1993), illustrating the complex organization of neural networks. Interactions between regions and within networks largely depend on chemical transmission between neurons. -
The Effect of Oxime Reactivators on the Muscarinic Receptors
Oxime reactivators and their in vivo and in vitro effects on nicotinic receptors Ondrej Soukup1,6, Jan Krusek4, Martina Kaniakova4, Uday Killi. Kumar3, Murat Oz5, Daniel Jun1,2, Josef Fusek1 and Kamil Kuca1,2 and Gunnar Tobin3 1Department of Toxicology and 2Center of Advanced Studies, Faculty of Military Health Sciences, University of Defence, Hradec Kralove, Czech Republic 3Institute of Neuroscience and Physiology, Department of Pharmacology, the Sahlgrenska Academy at University of Gothenburg, Sweden 4Institute of Physiology Academy of Sciences of the Czech Republic v.v.i., Prague, Czech Republic 5Department of Pharmacology and Therapeutics, Faculty of Medicine, United Arab Emirates University, Al Ain, United Arab Emirates 6University Hospital Hradec Kralove, Czech Republic Corresponding author: Ondrej Soukup ****************************************** Department of Toxicology Faculty of Military Health Sciences University of Defence Trebesska 1575 50001; Hradec Kralove Czech Republic Tel.: +420 973 255 151 Fax: +420 495 518 094 E-mail: [email protected] Summary: Current treatment of organophosphorus poisoning, resulting in overstimulation and desensitization of muscarinic and nicotinic receptors by acetylcholine (ACh), consists of the administration of atropine and oxime reactivators. However, no versatile oxime reactivator has been developed yet and some mortality still remains after application of standard atropine treatment, probably due to its lack of antinicotinic action. In our study, we focused on the interesting non-acetylcholinesterase property of oximes, i.e. antinicotinic effect of reactivators. Two standard reactivators (HI-6, obidoxime) and two new compounds (K027 and K203) were chosen and in vitro (patch clamp) and in vivo (nerve-evoked muscle contraction) testings were applied. Both examinations showed antinicotinic effects of the reactivators. -
Phytochem Referenzsubstanzen
High pure reference substances Phytochem Hochreine Standardsubstanzen for research and quality für Forschung und management Referenzsubstanzen Qualitätssicherung Nummer Name Synonym CAS FW Formel Literatur 01.286. ABIETIC ACID Sylvic acid [514-10-3] 302.46 C20H30O2 01.030. L-ABRINE N-a-Methyl-L-tryptophan [526-31-8] 218.26 C12H14N2O2 Merck Index 11,5 01.031. (+)-ABSCISIC ACID [21293-29-8] 264.33 C15H20O4 Merck Index 11,6 01.032. (+/-)-ABSCISIC ACID ABA; Dormin [14375-45-2] 264.33 C15H20O4 Merck Index 11,6 01.002. ABSINTHIN Absinthiin, Absynthin [1362-42-1] 496,64 C30H40O6 Merck Index 12,8 01.033. ACACETIN 5,7-Dihydroxy-4'-methoxyflavone; Linarigenin [480-44-4] 284.28 C16H12O5 Merck Index 11,9 01.287. ACACETIN Apigenin-4´methylester [480-44-4] 284.28 C16H12O5 01.034. ACACETIN-7-NEOHESPERIDOSIDE Fortunellin [20633-93-6] 610.60 C28H32O14 01.035. ACACETIN-7-RUTINOSIDE Linarin [480-36-4] 592.57 C28H32O14 Merck Index 11,5376 01.036. 2-ACETAMIDO-2-DEOXY-1,3,4,6-TETRA-O- a-D-Glucosamine pentaacetate 389.37 C16H23NO10 ACETYL-a-D-GLUCOPYRANOSE 01.037. 2-ACETAMIDO-2-DEOXY-1,3,4,6-TETRA-O- b-D-Glucosamine pentaacetate [7772-79-4] 389.37 C16H23NO10 ACETYL-b-D-GLUCOPYRANOSE> 01.038. 2-ACETAMIDO-2-DEOXY-3,4,6-TRI-O-ACETYL- Acetochloro-a-D-glucosamine [3068-34-6] 365.77 C14H20ClNO8 a-D-GLUCOPYRANOSYLCHLORIDE - 1 - High pure reference substances Phytochem Hochreine Standardsubstanzen for research and quality für Forschung und management Referenzsubstanzen Qualitätssicherung Nummer Name Synonym CAS FW Formel Literatur 01.039. -
Ovid MEDLINE(R)
Supplementary material BMJ Open Ovid MEDLINE(R) and Epub Ahead of Print, In-Process & Other Non-Indexed Citations and Daily <1946 to September 16, 2019> # Searches Results 1 exp Hypertension/ 247434 2 hypertens*.tw,kf. 420857 3 ((high* or elevat* or greater* or control*) adj4 (blood or systolic or diastolic) adj4 68657 pressure*).tw,kf. 4 1 or 2 or 3 501365 5 Sex Characteristics/ 52287 6 Sex/ 7632 7 Sex ratio/ 9049 8 Sex Factors/ 254781 9 ((sex* or gender* or man or men or male* or woman or women or female*) adj3 336361 (difference* or different or characteristic* or ratio* or factor* or imbalanc* or issue* or specific* or disparit* or dependen* or dimorphism* or gap or gaps or influenc* or discrepan* or distribut* or composition*)).tw,kf. 10 or/5-9 559186 11 4 and 10 24653 12 exp Antihypertensive Agents/ 254343 13 (antihypertensiv* or anti-hypertensiv* or ((anti?hyperten* or anti-hyperten*) adj5 52111 (therap* or treat* or effective*))).tw,kf. 14 Calcium Channel Blockers/ 36287 15 (calcium adj2 (channel* or exogenous*) adj2 (block* or inhibitor* or 20534 antagonist*)).tw,kf. 16 (agatoxin or amlodipine or anipamil or aranidipine or atagabalin or azelnidipine or 86627 azidodiltiazem or azidopamil or azidopine or belfosdil or benidipine or bepridil or brinazarone or calciseptine or caroverine or cilnidipine or clentiazem or clevidipine or columbianadin or conotoxin or cronidipine or darodipine or deacetyl n nordiltiazem or deacetyl n o dinordiltiazem or deacetyl o nordiltiazem or deacetyldiltiazem or dealkylnorverapamil or dealkylverapamil -
(19) 11 Patent Number: 5668117
US005668117A United States Patent (19) 11 Patent Number: 5,668,117 Shapiro 45 Date of Patent: Sep. 16, 1997 54 METHODS OF TREATING NEUROLOGICAL 4,673,669 6/1987 Yoshikumi et al. ...................... 514.f42 DSEASES AND ETOLOGICALLY RELATED 4,757,054 7/1988 Yoshikumi et al. ... 514742 SYMPTOMOLOGY USING CARBONYL 4,771,075 9/1988 Cavazza ............... ... 514/556 TRAPPNGAGENTS IN COMBINATION 4,801,581 1/1989 Yoshikumi et al. ...................... 514.f42 WITH PREVIOUSLY KNOWN 4,874,750 10/1989 Yoshikumi et al. ...................... 514/42 MEDICAMENTS 4,956,391 9/1990 Sapse .................. 514,810 4,957,906 9/1990 Yoshikumi et al. ...................... 514/25 tor: H . Shani 4,983,586 1/1991 Bodor....................................... 514/58 76 Inventor ES pr.) Price Ave 5,015,570 5/1991 Scangos et al. ............................ 435/6 5,037,851 8/1991 Cavazza ........... ... 514,912 5,252,489 10/1993 Macri ........................................ 436/87 21 Appl. No.: 62,201 5297,562 3/1994 Potter. ... 128/898 al 5,324,667 6/1994 Macri. ... 436/87 22 Filed: Jun. 29, 1993 5,324,668 6/1994 Macri ....................................... 436/87 Related U.S. Application Data I63 Continuation-in-part of set No. 26.617, Feb. 23, 1993, Primary Eminer ohn Kight abandoned, which is a continuation of Ser. No. 660.561, Assistant Examiner-Louise Leary Feb. 22, 1991, abandoned. Attorney, Agent, or Firm-D. J. Perrella (51) Int. Cl. ................... A01N 43/04; A01N 61/00; 57 ABSTRACT C07H1/00; C08B 37/08 52 U.S. C. ................................ 514/55; 514/54; 514/23; Therapeutic compositions comprising an effective amount 514/1: 514/811; 514/866; 514/878; 514/879; of at least one carbonyl trapping agent alone or in combi 514/903; 514/912; 436/518; 436/74; 536/1.11; nation with a therapeutically effective of a co-agent or 536/20 medicament are disclosed. -
Cicuta Douglasii) Tubers
Toxicon 108 (2015) 11e14 Contents lists available at ScienceDirect Toxicon journal homepage: www.elsevier.com/locate/toxicon Short communication The non-competitive blockade of GABAA receptors by an aqueous extract of water hemlock (Cicuta douglasii) tubers * Benedict T. Green a, , Camila Goulart b, 1, Kevin D. Welch a, James A. Pfister a, Isabelle McCollum a, Dale R. Gardner a a Poisonous Plant Research Laboratory, Agricultural Research Service, United States Department of Agriculture, Logan, UT, USA b Graduate Program in Animal Science, Universidade Federal de Goias, Goiania,^ Goias, Brazil article info abstract Article history: Water hemlocks (Cicuta spp.) are acutely toxic members of the Umbellierae family; the toxicity is due to Received 22 July 2015 the presence of C17-polyacetylenes such as cicutoxin. There is only limited evidence of noncompetitive Received in revised form antagonism by C17-polyacetylenes at GABAA receptors. In this work with WSS-1 cells, we documented 9 September 2015 the noncompetitive blockade of GABA receptors by an aqueous extract of water hemlock (Cicuta dou- Accepted 14 September 2015 A glasii) and modulated the actions of the extract with a pretreatment of 10 mM midazolam. Available online 28 September 2015 Published by Elsevier Ltd. Keywords: Water hemlock Cicutoxin C17-polyacetylenes Benzodiazepines Barbiturates Midazolam Water hemlocks (Cicuta spp.) are acutely toxic members of the antagonists of the GABAA receptor by binding to the picrotoxin Umbellierae, or carrot family, that grow in wet habitats such as binding site within the chloride channel to block ion flow through streambeds or marshlands, and have been considered one of the the channel (Ratra et al., 2001; Chen et al., 2006; 2011; Olsen, most toxic plants of North America for many years (Kingsbury, 2006).