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Prostaglandin D2 Synthase: Apoptotic Factor in Alzheimer Plasma, Inducer of Reactive Oxygen Species, Inflammatory Cytokines and Dialysis Dementia
www.nephropathol.com DOI:10.12860/JNP.2013.28 J Nephropathology. 2013; 2(3): 166-180 Journal of Nephropathology Prostaglandin D2 synthase: Apoptotic factor in alzheimer plasma, inducer of reactive oxygen species, inflammatory cytokines and dialysis dementia John K. Maesaka1,*, Bali Sodam1, Thomas Palaia1, Louis Ragolia1,Vecihi Batuman2, Nobuyuki Miyawaki 1, Shubha Shastry1, Steven Youmans3, Marwan El-Sabban4 1Department of Medicine, Winthrop-University Hospital, Mineola, N.Y., SUNY Medical School at Stony Brook, N.Y. USA. 2Department of Medicine, Tulane University School of Medicine. USA. 3Department of Biomedical Sciences, New York Institute of Technology, Westbury, N.Y. USA. 4Department of Anatomy, Cell Biology and Physiological Sciences, American University of Beirut, Beirut, Lebanon. ARTICLE INFO ABSTRACT Article type: Background: Apoptosis, reactive oxygen species (ROS) and inflammatory cytokines Original Article have all been implicated in the development of Alzheimer’s disease (AD). Article history: Objectives: The present study identifies the apoptotic factor that was responsible Received: 7 February 2013 for the fourfold increase in apoptotic rates that we previously noted when pig Accepted: 1 March 2013 proximal tubule, LLC-PK1, cells were exposed to AD plasma as compared to Published online: 1 July 2013 plasma from normal controls and multi-infarct dementia. Patients and Methods: The apoptotic factor was isolated from AD urine and identi- fied as lipocalin-type prostaglandin D2 synthase (L-PGDS). L-PGDS was found Keywords: Original Article Dialysis Dementia to be the major apoptotic factor in AD plasma as determined by inhibition of Alzheimer’s disease apoptosis approximating control levels by the cyclo-oxygenase (COX) 2 inhibitor, Apoptosis NS398, and the antibody to L-PGDS. -
Cannabinoids and Endocannabinoid System Changes in Intestinal Inflammation and Colorectal Cancer
cancers Review Cannabinoids and Endocannabinoid System Changes in Intestinal Inflammation and Colorectal Cancer Viktoriia Cherkasova, Olga Kovalchuk * and Igor Kovalchuk * Department of Biological Sciences, University of Lethbridge, Lethbridge, AB T1K 7X8, Canada; [email protected] * Correspondence: [email protected] (O.K.); [email protected] (I.K.) Simple Summary: In recent years, multiple preclinical studies have shown that changes in endo- cannabinoid system signaling may have various effects on intestinal inflammation and colorectal cancer. However, not all tumors can respond to cannabinoid therapy in the same manner. Given that colorectal cancer is a heterogeneous disease with different genomic landscapes, experiments with cannabinoids should involve different molecular subtypes, emerging mutations, and various stages of the disease. We hope that this review can help researchers form a comprehensive understanding of cannabinoid interactions in colorectal cancer and intestinal bowel diseases. We believe that selecting a particular experimental model based on the disease’s genetic landscape is a crucial step in the drug discovery, which eventually may tremendously benefit patient’s treatment outcomes and bring us one step closer to individualized medicine. Abstract: Despite the multiple preventive measures and treatment options, colorectal cancer holds a significant place in the world’s disease and mortality rates. The development of novel therapy is in Citation: Cherkasova, V.; Kovalchuk, critical need, and based on recent experimental data, cannabinoids could become excellent candidates. O.; Kovalchuk, I. Cannabinoids and This review covered known experimental studies regarding the effects of cannabinoids on intestinal Endocannabinoid System Changes in inflammation and colorectal cancer. In our opinion, because colorectal cancer is a heterogeneous Intestinal Inflammation and disease with different genomic landscapes, the choice of cannabinoids for tumor prevention and Colorectal Cancer. -
N-Acyl-Dopamines: Novel Synthetic CB1 Cannabinoid-Receptor Ligands
Biochem. J. (2000) 351, 817–824 (Printed in Great Britain) 817 N-acyl-dopamines: novel synthetic CB1 cannabinoid-receptor ligands and inhibitors of anandamide inactivation with cannabimimetic activity in vitro and in vivo Tiziana BISOGNO*, Dominique MELCK*, Mikhail Yu. BOBROV†, Natalia M. GRETSKAYA†, Vladimir V. BEZUGLOV†, Luciano DE PETROCELLIS‡ and Vincenzo DI MARZO*1 *Istituto per la Chimica di Molecole di Interesse Biologico, C.N.R., Via Toiano 6, 80072 Arco Felice, Napoli, Italy, †Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, R. A. S., 16/10 Miklukho-Maklaya Str., 117871 Moscow GSP7, Russia, and ‡Istituto di Cibernetica, C.N.R., Via Toiano 6, 80072 Arco Felice, Napoli, Italy We reported previously that synthetic amides of polyunsaturated selectivity for the anandamide transporter over FAAH. AA-DA fatty acids with bioactive amines can result in substances that (0.1–10 µM) did not displace D1 and D2 dopamine-receptor interact with proteins of the endogenous cannabinoid system high-affinity ligands from rat brain membranes, thus suggesting (ECS). Here we synthesized a series of N-acyl-dopamines that this compound has little affinity for these receptors. AA-DA (NADAs) and studied their effects on the anandamide membrane was more potent and efficacious than anandamide as a CB" transporter, the anandamide amidohydrolase (fatty acid amide agonist, as assessed by measuring the stimulatory effect on intra- hydrolase, FAAH) and the two cannabinoid receptor subtypes, cellular Ca#+ mobilization in undifferentiated N18TG2 neuro- CB" and CB#. NADAs competitively inhibited FAAH from blastoma cells. This effect of AA-DA was counteracted by the l µ N18TG2 cells (IC&! 19–100 M), as well as the binding of the CB" antagonist SR141716A. -
2-Arachidonoylglycerol a Signaling Lipid with Manifold Actions in the Brain
Progress in Lipid Research 71 (2018) 1–17 Contents lists available at ScienceDirect Progress in Lipid Research journal homepage: www.elsevier.com/locate/plipres Review 2-Arachidonoylglycerol: A signaling lipid with manifold actions in the brain T ⁎ Marc P. Baggelaara,1, Mauro Maccarroneb,c,2, Mario van der Stelta, ,2 a Department of Molecular Physiology, Leiden Institute of Chemistry, Leiden University, Einsteinweg 55, 2333 CC Leiden, The Netherlands. b Department of Medicine, Campus Bio-Medico University of Rome, Via Alvaro del Portillo 21, 00128 Rome, Italy c European Centre for Brain Research/IRCCS Santa Lucia Foundation, via del Fosso del Fiorano 65, 00143 Rome, Italy ABSTRACT 2-Arachidonoylglycerol (2-AG) is a signaling lipid in the central nervous system that is a key regulator of neurotransmitter release. 2-AG is an endocannabinoid that activates the cannabinoid CB1 receptor. It is involved in a wide array of (patho)physiological functions, such as emotion, cognition, energy balance, pain sensation and neuroinflammation. In this review, we describe the biosynthetic and metabolic pathways of 2-AG and how chemical and genetic perturbation of these pathways has led to insight in the biological role of this signaling lipid. Finally, we discuss the potential therapeutic benefits of modulating 2-AG levels in the brain. 1. Introduction [24–26], locomotor activity [27,28], learning and memory [29,30], epileptogenesis [31], neuroprotection [32], pain sensation [33], mood 2-Arachidonoylglycerol (2-AG) is one of the most extensively stu- [34,35], stress and anxiety [36], addiction [37], and reward [38]. CB1 died monoacylglycerols. It acts as an important signal and as an in- receptor signaling is tightly regulated by biosynthetic and catabolic termediate in lipid metabolism [1,2]. -
A Dissertation Entitled Uncovering Cannabinoid Signaling in C. Elegans
A Dissertation Entitled Uncovering Cannabinoid Signaling in C. elegans: A New Platform to Study the Effects of Medicinal Cannabis By Mitchell Duane Oakes Submitted to the Graduate Faculty as partial fulfillment of the requirements for the Doctor of Philosophy Degree in Biology ________________________________________ Dr. Richard Komuniecki, Committee Chair _______________________________________ Dr. Bruce Bamber, Committee Member ________________________________________ Dr. Patricia Komuniecki, Committee Member ________________________________________ Dr. Robert Steven, Committee Member ________________________________________ Dr. Ajith Karunarathne, Committee Member ________________________________________ Dr. Jianyang Du, Committee Member ________________________________________ Dr. Amanda Bryant-Friedrich, Dean College of Graduate Studies The University of Toledo August 2018 Copyright 2018, Mitchell Duane Oakes This document is copyrighted material. Under copyright law, no parts of this document may be reproduced without the expressed permission of the author. An Abstract of Uncovering Cannabinoid Signaling in C. elegans: A New Platform to Study the Effects of Medical Cannabis By Mitchell Duane Oakes Submitted to the Graduate Faculty as partial fulfillment of the requirements for the Doctor of Philosophy Degree in Biology The University of Toledo August 2018 Cannabis or marijuana, a popular recreational drug, alters sensory perception and exerts a range of medicinal benefits. The present study demonstrates that C. elegans exposed to -
Key Aspects to Consider About Beneficial and Harmful Effects on the Central Nervous System by the Endocannabinoid Modulation Linked to New Cardiovascular Therapies
Review Article Annals of Pharmacology and Pharmaceutics Published: 03 Dec, 2019 Key Aspects to Consider about Beneficial and Harmful Effects on the Central Nervous System by the Endocannabinoid Modulation Linked to New Cardiovascular Therapies Martin Gimenez VM1, Mocayar Maron FJ2, Kassuha DE1, Ferder L3 and Manucha W4,5* 1Research in Chemical Sciences, Catholic University of Cuyo, Argentina 2Department of Morphophysiology, National University of Cuyo, Argentina 3Department of Pediatrics, University of Miami, USA 4Department of Pathology, National Council of Scientific and Technological Research (IMBECU-CONICET), Argentina 5Department of Pathology, National University of Cuyo, Mendoza, Argentina Abstract The endocannabinoid system is closely related to the central nervous system and exerts a promising therapeutic potential on it and other systems such as the cardiovascular, mainly through its neuromodulatory, neuroprotective and neuroinflammatory effects. For this reason, when designing new treatments for different relevant pathologies such as hypertension, it is necessary to take into account the side effects that such therapies can cause at the neurological level. Deeping knowledge of each cannabinoid and the molecular mechanisms that can lead to undesired results is necessary. The OPEN ACCESS present review analyzes the psychoactive consequences of anandamide and other similar substances *Correspondence: such as other endocannabinoids, phytocannabinoids and synthetic cannabinoids, to assess their Walter Manucha, Department of little-explored -
1. Endocannabinoid System (ECS)
UNIVERSITÀ DI PISA Dipartimento di Farmacia Corso di Laurea Specialistica in Chimica e Tecnologia Farmaceutiche Tesi di Laurea: DESIGN AND SYNTHESIS OF HETEROCYCLIC DERIVATIVES AS POTENTIAL MAGL INHIBITORS Relatori: Prof. Marco Macchia Candidato: Glenda Tarchi Prof.ssa Clementina Manera (matricola N° 445314) Dott.ssa Chiara Arena Settore Scientifico Disciplinare: CHIM-08 ANNO ACCADEMICO 2013–2014 INDEX Sommario INDEX ......................................................................................... 3 1. Endocannabinoid system (ECS) ......................................... 6 1.1 Endocannabinoid receptors ........................................................... 7 1.2 Mechanism of endocannabinoid neuronal signaling ..................... 9 1.3 Endocannabinoids biosynthesis ................................................... 11 1.4 Enzymes involved in endocannabinoids degradation ................. 16 1.4.1 FAAH ........................................................................................................ 16 1.4.2 MAGL ....................................................................................................... 18 1.4.3 ABHD6 ..................................................................................................... 20 1.4.4 ABDH12 ................................................................................................... 21 2. MAGL like pharmacological target ................................ 23 2.1 The role of MAGL in pain and inflammation ............................. 24 2.1.1 Relation between -
DB Abs Cagliari Cong SIF 2007
33° Congresso Nazionale della SIF - Cagliari 6-9 giugno 2007 - Raccolta abstracts TOTALE ABSTRACTS VALIDI: 828 Ultimo aggiornamento: (167 simposi + 100 orali + 561 posters) 24-mag-07 Cod Autore (primo nome) Titolo abs Esp. Tema Data (N°) cognome-nome (titolo completo) O/P/I 1 Carnini Chiara CYSTEINYL LEUKOTRIENES IN HUMAN ENDOTHELIAL CELLS: SYNTHPEoSstIeSr AND ACTIVI1T6IES 07-giu 2 Ghelardini Carla ANTIHYPERALGESIC EFFECTS OF THE PYRROLIDINONE DERIVATIVEO rNaIlKe-13317 IN MdoOloDrEeLS OF N0E7-UgRiuOPATHIC PAIN 3 Cuzzocrea Salvatore PARG ACTIVITY MEDIATES POST-TRAUMATIC INFLAMMATORY REACOTrIaOleN AFTER EXnPeuErRoIMENTA0L9 S-gPiuINAL CORD TRAUMA 4 Cuzzocrea Salvatore ESTROGEN RECEPTOR ANTAGONIST ICI 182,780 INHIBITS THE ANTPI-IoNsFteLrAMMATORY1 E6FFECT OF07 G-gLiUu COCORTICOIDS 5 Cuzzocrea Salvatore GLYCOGEN SYNTHASE KINASE-3 INHIBITION ATTENUATES THE DEPVoEsLtOerPMENT OF B1L2EOMYCIN0-8IN-gDiuUCED LUNG INJURY 6 De sarro Angelina PROTECTIVE EFFECT OF HYPERICUM PERFORATUM IN ZYMOSAN-IPNoDsUteCrED MULTIPL2E2 ORGAN D08Y-SgFiuUNCTION SYNDROME 7 De sarro Angelina ROLE OF PEROXISOME PROLIFERATORS ACTIVATED RECEPTORS PAoLPstHeAr (PPAR- ) IN1 6ACUTE PA0N8C-gRiuEATITIS INDUCED BY CERULEIN 8 Esposito Emanuela GENETIC OR PHARMACOLOGICAL INHIBITION OF TNF- REDUCED SPOLrAalNeCHNIC ISCgHioEvaMnIiA AND R07E-PgEiuRFUSION INJURY 9 Martire Maria SELECTIVE REGULATION OF [3H]D-ASPARTATE RELEASE FROM HIPPPoOsCteArMPAL NERV4E ENDINGS07 B-gYi uLARGE-CONDUCTANCE CA2+- AND VOLTAGE-ACTIVATED K+ (BK) CHANNELS 10 Mey Valentina SYNERGISTIC CYTOTOXICITY AND PHARMACOGENETICS -
32120 Journal.Qxd
SLEEP PHYSIOLOGY Prostaglandin D Synthase (β-trace) in Healthy Human Sleep Wolfgang Jordan, MD1; Hayrettin Tumani, MD, PhD2; Stefan Cohrs, MD1; Sebastian Eggert1; Andrea Rodenbeck, DSc1; Edgar Brunner, MD, PhD3; Eckart Rüther, MD, PhD1; Göran Hajak, MD, PhD1,4 1Department of Psychiatry and Psychotherapy, University of Göttingen; 2Department of Neurology, Universitiy of Ulm; 3Department of Medical Statistics, University of Göttingen; 4Department of Psychiatry and Psychotherapy, University of Regensburg, Germany Study Objectives: The prostaglandin D system plays an important role in Results: Serum L-PGDS concentrations showed marked time-dependent animal sleep. In humans, alterations in the prostaglandin D system have changes with evening increases and the highest values at night (P< been found in diseases exhibiting sleep disturbances as a prominent .0005). This nocturnal increase was suppressed during total sleep depri- symptom, such as trypanosoma infection, systemic mastocytosis, bacteri- vation (P< .05), independent of external light conditions and melatonin Downloaded from https://academic.oup.com/sleep/article/27/5/867/2708439 by guest on 28 September 2021 al meningitis, major depression, or obstructive sleep apnea. Assessment secretion. Rapid eye movement sleep deprivation had no impact on cir- of this system’s activity in relation to human physiologic sleep was the tar- culating L-PGDS levels. get of the present study. Conclusions: The circadian L-PGDS pattern and its suppression by total Design: Serum concentrations of lipocalin-type prostaglandin D synthase sleep deprivation indicate an interaction of the prostaglandin D system (L-PGDS, former β-trace), and plasma levels of the pineal hormone mela- and human sleep regulation. L-PGDS measurements may well provide tonin were measured in 20 healthy humans (10 women, 10 men; aged: new insights into physiologic and pathologic sleep regulation in humans. -
SYNTHESIS of 3-HETEROCYCLE PHENYL N-ALKYL CARBAMATES and THEIR ACTIVITY AS FAAH INHIBITORS Doctoral Dissertation
TKK Dissertations 203 Espoo 2009 SYNTHESIS OF 3-HETEROCYCLE PHENYL N-ALKYL CARBAMATES AND THEIR ACTIVITY AS FAAH INHIBITORS Doctoral Dissertation Mikko Myllymäki Helsinki University of Technology Faculty of Chemistry and Materials Sciences Department of Chemistry TKK Dissertations 203 Espoo 2009 SYNTHESIS OF 3-HETEROCYCLE PHENYL N-ALKYL CARBAMATES AND THEIR ACTIVITY AS FAAH INHIBITORS Doctoral Dissertation Mikko Myllymäki Dissertation for the degree of Doctor of Philosophy to be presented with due permission of the Faculty of Chemistry and Materials Sciences for public examination and debate in Auditorium KE2 (Komppa Auditorium) at Helsinki University of Technology (Espoo, Finland) on the 19th of December, 2009, at 12 noon. Helsinki University of Technology Faculty of Chemistry and Materials Sciences Department of Chemistry Teknillinen korkeakoulu Kemian ja materiaalitieteiden tiedekunta Kemian laitos Distribution: Helsinki University of Technology Faculty of Chemistry and Materials Sciences Department of Chemistry P.O. Box 6100 (Kemistintie 1) FI - 02015 TKK FINLAND URL: http://chemistry.tkk.fi/ Tel. +358-9-470 22527 Fax +358-9-470 22538 E-mail: [email protected] © 2009 Mikko Myllymäki ISBN 978-952-248-240-2 ISBN 978-952-248-241-9 (PDF) ISSN 1795-2239 ISSN 1795-4584 (PDF) URL: http://lib.tkk.fi/Diss/2009/isbn9789522482419/ TKK-DISS-2686 Multiprint Oy Espoo 2009 3 AB HELSINKI UNIVERSITY OF TECHNOLOGY ABSTRACT OF DOCTORAL DISSERTATION P.O. BOX 1000, FI-02015 TKK http://www.tkk.fi Author Mikko Juhani Myllymäki Name of the dissertation -
Overactive Endocannabinoid Signaling Impairs Apolipoprotein E-Mediated Clearance of Triglyceride-Rich Lipoproteins
Overactive endocannabinoid signaling impairs apolipoprotein E-mediated clearance of triglyceride-rich lipoproteins Maxwell A. Ruby*, Daniel K. Nomura†, Carolyn S. S. Hudak†, Lara M. Mangravite*, Sally Chiu*, John E. Casida†‡, and Ronald M. Krauss*‡ *Children’s Hospital Oakland Research Institute, Oakland, CA 94609; and †Environmental Chemistry and Toxicology Laboratory, Department of Environmental Science, Policy and Management, University of California, Berkeley, CA 94720-3112 Contributed by John E. Casida, University of California, Berkeley, CA, July 25, 2008 (sent for review June 9, 2008) The endocannabinoid (EC) system regulates food intake and en- The EC system consists of the cannabinoid receptors, the ergy metabolism. Cannabinoid receptor type 1 (CB1) antagonists endocannabinoids (ECs), and the enzymes responsible for their show promise in the treatment of obesity and its metabolic synthesis and breakdown (14, 15). CB1 is a G protein-coupled consequences. Although the reduction in adiposity resulting from membrane receptor that transmits its response via Gi/o protein- therapy with CB1 antagonists may not account fully for the mediated reduction in adenylate cyclase activity (14). The ECs concomitant improvements in dyslipidemia, direct effects of over- anandamide and 2-arachidonoylglycerol (2-AG) are produced active EC signaling on plasma lipoprotein metabolism have not locally by N-acyl phosphatidylethanolamine phospholipase D been documented. The present study used a chemical approach to and by diacylglycerol lipase, respectively (14, 15). Signaling is evaluate the direct effects of increased EC signaling in mice by terminated primarily by enzymatic breakdown of anandamide by inducing acute elevations of endogenously produced cannabinoids fatty acid amide hydrolase (FAAH) and of 2-AG by monoacyl- through pharmacological inhibition of their enzymatic hydrolysis glycerol lipase (MAGL) (14–18). -
Laws, Rules, and Regulations
LAWS, RULES, AND REGULATIONS August 2020 Asa Hutchinson, Governor John Clay Kirtley, Pharm.D. Executive Director Arkansas Department of Health Arkansas State Board of Pharmacy 322 South Main Street, Suite 600 Little Rock, AR 72201 Phone: 501.682.0190 Fax: 501.682.0195 [email protected] www.pharmacyboard.arkansas.gov 10/8/2020 Arkansas State Board of Pharmacy Members Lenora Newsome, P.D. President, Smackover Rebecca Mitchell, Pharm.D. Vice President/Secretary, Greenbrier Deborah Mack, P.D. Member, Bentonville Lynn Crouse, Pharm.D. Member, Lake Village Brian Jolly, Pharm.D. Member, Beebe Carol Rader, RN Public Member, Fort Smith Amy Fore, MHSA, FACMPE, FACHE Public Member, Fort Smith 10/8/2020 Board of Pharmacy Law Book - Acts Table of Contents Pharmacy Practice Act A 17-92-101 Definitions……………………………………………………… 1-4 17-92-102 Exemptions…………………………………………………….. 4-5 17-92-103 Pharmacy laws unaffected……………………………………... 5 17-92-104 Privilege tax unaffected……………………………………….. 5 17-92-105 Prohibited acts – Penalties……………………………………... 6 17-92-106 Injunctions……………………………………………………… 6 17-92-107 Prosecutions – Disposition of fines……………………………. 6 17-92-108 Fees…………………………………………………………….. 6-10 17-92-109 Prescriptions for optometrists………………………………….. 10 17-92-110 Prescriptive authority of advance practice nurses……………… 10 17-92-111 Construction of Acts 1997, No. 1204………………………….. 10 17-92-112 Prescriptions for physician assistants…………………………. 10 17-92-201 Members – Qualifications……………………………………… 11 17-92-202 Members – Oath……………………………………………… 11 17-92-203 Members – Compensation…………………………………….. 11 17-92-204 Organization and proceedings…………………………………. 12 17-92-205 Rules and regulations – Enforcement………………………….. 12-13 17-92-206 Issuance of bulletins – Annual Reports………………………... 14 17-92-207 Maintenance of office………………………………………….