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Epithelial Delamination Is Protective During Pharmaceutical-Induced Enteropathy
Epithelial delamination is protective during pharmaceutical-induced enteropathy Scott T. Espenschieda, Mark R. Cronana, Molly A. Mattya, Olaf Muellera, Matthew R. Redinbob,c,d, David M. Tobina,e,f, and John F. Rawlsa,e,1 aDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710; bDepartment of Chemistry, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599; cDepartment of Biochemistry, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599; dDepartment of Microbiology and Immunology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599; eDepartment of Medicine, Duke University School of Medicine, Durham, NC 27710; and fDepartment of Immunology, Duke University School of Medicine, Durham, NC 27710 Edited by Dennis L. Kasper, Harvard Medical School, Boston, MA, and approved July 15, 2019 (received for review February 12, 2019) Intestinal epithelial cell (IEC) shedding is a fundamental response to in mediating intestinal responses to injury remains poorly un- intestinal damage, yet underlying mechanisms and functions have derstood for most xenobiotics. been difficult to define. Here we model chronic intestinal damage in Gastrointestinal pathology is common in people using phar- zebrafish larvae using the nonsteroidal antiinflammatory drug maceuticals, including nonsteroidal antiinflammatory drugs (NSAID) Glafenine. Glafenine induced the unfolded protein response (NSAIDs) (11). While gastric ulceration has historically been a (UPR) and inflammatory pathways in IECs, leading to delamination. defining clinical presentation of NSAID-induced enteropathy, Glafenine-induced inflammation was augmented by microbial colo- small intestinal pathology has also been observed, although the nizationandassociatedwithchanges in intestinal and environmental incidence may be underreported due to diagnostic limitations microbiotas. -
NINDS Custom Collection II
ACACETIN ACEBUTOLOL HYDROCHLORIDE ACECLIDINE HYDROCHLORIDE ACEMETACIN ACETAMINOPHEN ACETAMINOSALOL ACETANILIDE ACETARSOL ACETAZOLAMIDE ACETOHYDROXAMIC ACID ACETRIAZOIC ACID ACETYL TYROSINE ETHYL ESTER ACETYLCARNITINE ACETYLCHOLINE ACETYLCYSTEINE ACETYLGLUCOSAMINE ACETYLGLUTAMIC ACID ACETYL-L-LEUCINE ACETYLPHENYLALANINE ACETYLSEROTONIN ACETYLTRYPTOPHAN ACEXAMIC ACID ACIVICIN ACLACINOMYCIN A1 ACONITINE ACRIFLAVINIUM HYDROCHLORIDE ACRISORCIN ACTINONIN ACYCLOVIR ADENOSINE PHOSPHATE ADENOSINE ADRENALINE BITARTRATE AESCULIN AJMALINE AKLAVINE HYDROCHLORIDE ALANYL-dl-LEUCINE ALANYL-dl-PHENYLALANINE ALAPROCLATE ALBENDAZOLE ALBUTEROL ALEXIDINE HYDROCHLORIDE ALLANTOIN ALLOPURINOL ALMOTRIPTAN ALOIN ALPRENOLOL ALTRETAMINE ALVERINE CITRATE AMANTADINE HYDROCHLORIDE AMBROXOL HYDROCHLORIDE AMCINONIDE AMIKACIN SULFATE AMILORIDE HYDROCHLORIDE 3-AMINOBENZAMIDE gamma-AMINOBUTYRIC ACID AMINOCAPROIC ACID N- (2-AMINOETHYL)-4-CHLOROBENZAMIDE (RO-16-6491) AMINOGLUTETHIMIDE AMINOHIPPURIC ACID AMINOHYDROXYBUTYRIC ACID AMINOLEVULINIC ACID HYDROCHLORIDE AMINOPHENAZONE 3-AMINOPROPANESULPHONIC ACID AMINOPYRIDINE 9-AMINO-1,2,3,4-TETRAHYDROACRIDINE HYDROCHLORIDE AMINOTHIAZOLE AMIODARONE HYDROCHLORIDE AMIPRILOSE AMITRIPTYLINE HYDROCHLORIDE AMLODIPINE BESYLATE AMODIAQUINE DIHYDROCHLORIDE AMOXEPINE AMOXICILLIN AMPICILLIN SODIUM AMPROLIUM AMRINONE AMYGDALIN ANABASAMINE HYDROCHLORIDE ANABASINE HYDROCHLORIDE ANCITABINE HYDROCHLORIDE ANDROSTERONE SODIUM SULFATE ANIRACETAM ANISINDIONE ANISODAMINE ANISOMYCIN ANTAZOLINE PHOSPHATE ANTHRALIN ANTIMYCIN A (A1 shown) ANTIPYRINE APHYLLIC -
Nsaids: Dare to Compare 1997
NSAIDs TheRxFiles DARE TO COMPARE Produced by the Community Drug Utilization Program, a Saskatoon District Health/St. Paul's Hospital program July 1997 funded by Saskatchewan Health. For more information check v our website www.sdh.sk.ca/RxFiles or, contact Loren Regier C/O Pharmacy Department, Saskatoon City Hospital, 701 Queen St. Saskatoon, SK S7K 0M7, Ph (306)655-8506, Fax (306)655-8804; Email [email protected] We have come a long way from the days of willow Highlights bark. Today salicylates and non-steroidal anti- • All NSAIDs have similar efficacy and side inflammatory drugs (NSAIDs) comprise one of the effect profiles largest and most commonly prescribed groups of • In low risk patients, Ibuprofen and naproxen drugs worldwide.1 In Saskatchewan, over 20 may be first choice agents because they are different agents are available, accounting for more effective, well tolerated and inexpensive than 300,000 prescriptions and over $7 million in • Acetaminophen is the recommended first line sales each year (Saskatchewan Health-Drug Plan agent for osteoarthritis data 1996). Despite the wide selection, NSAIDs • are more alike than different. Although they do Misoprostol is the only approved agent for differ in chemical structure, pharmacokinetics, and prophylaxis of NSAID-induced ulcers and is to some degree pharmacodynamics, they share recommended in high risk patients if NSAIDS similar mechanisms of action, efficacy, and adverse cannot be avoided. effects. week or more to become established. For this EFFICACY reason, an adequate trial of 1-2 weeks should be NSAIDs work by inhibiting cyclooxygenase (COX) allowed before increasing the dose or changing to and subsequent prostaglandin synthesis as well as another NSAID. -
Glafenine-Induced Intestinal Injury in Zebrafish Is Ameliorated by -Opioid Signaling Via Enhancement of Atf6-Dependent Cellular Stress Responses
RESEARCH ARTICLE Disease Models & Mechanisms 6, 146-159 (2013) doi:10.1242/dmm.009852 Glafenine-induced intestinal injury in zebrafish is ameliorated by -opioid signaling via enhancement of Atf6-dependent cellular stress responses Jason R. Goldsmith1, Jordan L. Cocchiaro2, John F. Rawls2,3,*,‡ and Christian Jobin1,3,4,*,‡ SUMMARY Beside their analgesic properties, opiates exert beneficial effects on the intestinal wound healing response. In this study, we investigated the role of -opioid receptor (MOR) signaling on the unfolded protein response (UPR) using a novel zebrafish model of NSAID-induced intestinal injury. The NSAID glafenine was administered to zebrafish larvae at 5 days post-fertilization (dpf) for up to 24 hours in the presence or absence of the MOR- specific agonist DALDA. By analysis with histology, transmission electron microscopy and vital dye staining, glafenine-treated zebrafish showed evidence of endoplasmic reticulum and mitochondrial stress, with disrupted intestinal architecture and halted cell stress responses, alongside accumulation of apoptotic intestinal epithelial cells in the lumen. Although the early UPR marker BiP was induced with glafenine-induced injury, downstream atf6 and s-xbp1 expression were paradoxically not increased, explaining the halted cell stress responses. The -opioid agonist DALDA protected against glafenine-induced injury through induction of atf6-dependent UPR. Our findings show that DALDA prevents glafenine-induced epithelial damage through induction of effective UPR. DMM INTRODUCTION importance of the epithelium in maintaining intestinal homeostasis, Intestinal homeostasis is achieved in part by the maintenance of a understanding mechanisms involved in intestinal epithelial healing functional barrier composed of a single layer of intestinal epithelial and cell stress responses, and the identification of compounds that cells (IEC), which separates the host from the highly antigenic promote these processes, could lead to new therapeutic strategies lumenal milieu (Sartor, 2008). -
Of 20 PRODUCT MONOGRAPH FLURBIPROFEN Flurbiprofen Tablets BP 50 Mg and 100 Mg Anti-Inflammatory, Analgesic Agent AA PHARM
PRODUCT MONOGRAPH FLURBIPROFEN Flurbiprofen Tablets BP 50 mg and 100 mg Anti-inflammatory, analgesic agent AA PHARMA INC. DATE OF PREPARATION: 1165 Creditstone Road, Unit #1 April 16, 1991 Vaughan, Ontario L4K 4N7 DATE OF REVISION: February 7, 2019 Submission Control No. 223098 Page 1 of 20 PRODUCT MONOGRAPH NAME OF DRUG FLURBIPROFEN Flurbiprofen Tablets BP 50 mg and 100 mg PHARMACOLOGICAL CLASSIFICATION Anti-inflammatory, analgesic agent ACTIONS AND CLINICAL PHARMACOLOGY FLURBIPROFEN (flurbiprofen), a phenylalkanoic acid derivative, is a non-steroidal anti- inflammatory agent which also possesses analgesic and antipyretic activities. Its mode of action, like that of other non-steroidal anti-inflammatory agents, is not known. However, its therapeutic action is not due to pituitary adrenal stimulation. Flurbiprofen is an inhibitor of prostaglandin synthesis. The resulting decrease in prostaglandin synthesis may partially explain the drug's anti-inflammatory effect at the cellular level. Pharmacokinetics: Flurbiprofen is well absorbed after oral administration, reaching peak blood levels in approximately 1.5 hours (range 0.5 to 4 hours). Administration of flurbiprofen with food does not alter total drug availability but delays absorption. Excretion of flurbiprofen is virtually complete 24 hours after the last dose. The elimination half-life is 5.7 hours with 90% of the half-life values from 3-9 hours. There is no evidence of drug accumulation and flurbiprofen does not induce enzymes that alter its metabolism. Flurbiprofen is rapidly metabolized and excreted in the urine as free and unaltered intact drug (20-25%) and hydroxylated metabolites (60-80%). In animal models of inflammation the metabolites showed no activity. -
Patient Information Leaflet: Information for the User <Invented Name> 30
Patient Information Leaflet: Information for the user <Invented name> 30 mg/ml solution for injection ketorolac trometamol Read all of this leaflet carefully before you start using 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 nurse. • If you get any side effects, talk to your doctor or nurse. This includes any possible side effects not listed in this leaflet. See section 4. What is in this leaflet 1. What <Invented name> is and what it is used for 2. What you need to know before you are given <Invented name> 3. How <Invented name> is given 4. Possible side effects 5. How to store <Invented name> 6. Contents of the pack and other information 1. What <Invented name> is and what it is used for <Invented name> contains an active substance called ketorolac trometamol and belongs to a group of medicines called non-steroidal anti-inflammatory drugs (NSAIDs). Ketorolac is used in hospital, for short-term relief of moderate to severe pain after operations and in the case of acute kidney stone pain, in adults and adolescents ≥16 years. 2. What you need to know before you are given <Invented name> <Invented name> should not be used before or during surgery due to increased risk of bleeding. <Invented name> must not be given by epidural or intrathecal administration . Severe anaphylactic-like reactions have been observed in patients with a history of allergic reactions (symptoms of asthma, inflammation of the nasal mucosa or skin reactions) to the use of acetylsalicylic acid (e.g. -
2 Inhibitors and Non-Steroidal Anti-Inflammatory Drugs (Nsaids)
Drug Class Review on Cyclo-oxygenase (COX)-2 Inhibitors and Non-steroidal Anti-inflammatory Drugs (NSAIDs) Final Report Update 3 Evidence Tables November 2006 Original Report Date: May 2002 Update 1 Report Date: September 2003 Update 2 Report Date: May 2004 A literature scan of this topic is done periodically The purpose of this report is to make available information regarding the comparative effectiveness and safety profiles of different drugs within pharmaceutical classes. Reports are not usage guidelines, nor should they be read as an endorsement of, or recommendation for, any particular drug, use or approach. Oregon Health & Science University does not recommend or endorse any guideline or recommendation developed by users of these reports. Roger Chou, MD Mark Helfand, MD, MPH Kim Peterson, MS Tracy Dana, MLS Carol Roberts, BS Produced by Oregon Evidence-based Practice Center Oregon Health & Science University Mark Helfand, Director Copyright © 2006 by Oregon Health & Science University Portland, Oregon 97201. All rights reserved. Note: A scan of the medical literature relating to the topic is done periodically(see http://www.ohsu.edu/ohsuedu/research/policycenter/DERP/about/methods.cfm for scanning process description). Upon review of the last scan, the Drug Effectiveness Review Project governance group elected not to proceed with another full update of this report. Some portions of the report may not be up to date. Prior versions of this report can be accessed at the DERP website. Final Report Update 3 Drug Effectiveness Review Project TABLE OF CONTENTS Evidence Table 1. Systematic reviews…………………………………………………………………3 Evidence Table 2. Randomized-controlled trials………………………………………………………9 Evidence Table 3. -
Annrheumd00427-0020.Pdf
Annals of the Rheumatic Diseases, 1989; 48, 372-381 Evaluation of the effects of antiarthritic drugs on the secretion of proteoglycans by lapine chondrocytes using a novel assay procedure SIMON COLLIER AND PETER GHOSH From the Raymond Purves Research Laboratories (The University of Sydney) at the Royal North Shore Hospital of Sydney, St Leonards, NSW 2065, Australia SUMMARY A new method is described for separating free 35SO4- from 35SO4 labelled groteoglycans synthesised by rabbit articular chondrocytes cultured in the presence of excess 4 The procedure uses the low solubility product of barium sulphate to remove, by precipitation, free 35SO4- from culture medium. Optimum recovery of 35so4 labelled proteoglycans was achieved after papain digestion to release 35SO4-glycosaminoglycans, and addition of chondroitin sulphate before the precipitation step. Using this assay, we studied the effect of six drugs-indomethacin, diclofenac, sodium pentosan polysulphate, glycosaminoglycan polysulphate ester, tiaprofenic acid, and ketoprofen-on the secretion into the medium of labelled proteoglycans by lapine chondrocytes. The six drugs were tested at 0< 1, 1, 10, 50, and 100 I.g/ml over four consecutive 48 hour culture periods. A consistent concentration-response pattern was found for the four non-steroidal anti-inflammatory drugs (NSAIDs) studied. Generally they inhibited proteoglycan secretion at 50 and 100 [ig/ml but had no effect at lower concentrations. Inhibition of secretion was strongest with indomethacin and diclofenac at 50 and 100 ig/ml. In contrast with the NSAIDs studied, the two sulphated polysaccharides (sodium pentosan polysulphate and glycosaminoglycan polysulphate ester) at low concentrations increased proteoglycan secretion by chondrocytes, with maximal stimulation occurring at 1 [ig/ml. -
Treatment for Acute Pain: an Evidence Map Technical Brief Number 33
Technical Brief Number 33 R Treatment for Acute Pain: An Evidence Map Technical Brief Number 33 Treatment for Acute Pain: An Evidence Map Prepared for: Agency for Healthcare Research and Quality U.S. Department of Health and Human Services 5600 Fishers Lane Rockville, MD 20857 www.ahrq.gov Contract No. 290-2015-0000-81 Prepared by: Minnesota Evidence-based Practice Center Minneapolis, MN Investigators: Michelle Brasure, Ph.D., M.S.P.H., M.L.I.S. Victoria A. Nelson, M.Sc. Shellina Scheiner, PharmD, B.C.G.P. Mary L. Forte, Ph.D., D.C. Mary Butler, Ph.D., M.B.A. Sanket Nagarkar, D.D.S., M.P.H. Jayati Saha, Ph.D. Timothy J. Wilt, M.D., M.P.H. AHRQ Publication No. 19(20)-EHC022-EF October 2019 Key Messages Purpose of review The purpose of this evidence map is to provide a high-level overview of the current guidelines and systematic reviews on pharmacologic and nonpharmacologic treatments for acute pain. We map the evidence for several acute pain conditions including postoperative pain, dental pain, neck pain, back pain, renal colic, acute migraine, and sickle cell crisis. Improved understanding of the interventions studied for each of these acute pain conditions will provide insight on which topics are ready for comprehensive comparative effectiveness review. Key messages • Few systematic reviews provide a comprehensive rigorous assessment of all potential interventions, including nondrug interventions, to treat pain attributable to each acute pain condition. Acute pain conditions that may need a comprehensive systematic review or overview of systematic reviews include postoperative postdischarge pain, acute back pain, acute neck pain, renal colic, and acute migraine. -
Read This for Safe and Effective Use of Your Medicine
PATIENT MEDICATION INFORMATION READ THIS FOR SAFE AND EFFECTIVE USE OF YOUR MEDICINE VIMOVO® naproxen/esomeprazole modified release tablets Read this carefully before you start taking VIMOVO and each time you get a refill. This leaflet is a summary and will not tell you everything about this drug. Talk to your healthcare professional about your medical condition and treatment and ask if there is any new information about VIMOVO. Serious Warnings and Precautions If you have, or previously had, any of the following medical conditions, see your health care provider to discuss treatment options other than VIMOVO: • Heart Attack or Angina • Stroke or Mini-stroke • Loss of Vision • Current Pregnancy (less than 28 weeks) • Congestive Heart Failure What is VIMOVO used for? VIMOVO is used in adults to treat the signs and symptoms of: • Osteoarthritis • Rheumatoid arthritis • Ankylosing spondylitis VIMOVO helps to reduce pain, swelling, redness and heat (inflammation). It is used for people who: • need to take an anti-inflammatory medicine. • and are at risk of getting a stomach ulcer (sore) or an ulcer in the small intestine (gut). How does VIMOVO work? VIMOVO contains 2 drugs which work together. • Naproxen belongs to a group of medicines called “nonsteroidal anti-inflammatory drugs” (NSAIDs). It reduces the substances in your body which cause pain and swelling. • Esomeprazole belongs to a group of medicines called “proton pump inhibitors” (PPIs). It reduces the amount of acid produced by your stomach. • Naproxen can damage the stomach but esomeprazole helps reduce this damage. • VIMOVO only treats the symptoms of pain and inflammation of the illness as long as you use it. -
Licofelone Enhances the Efficacy of Paclitaxel in Ovarian Cancer by Reversing Drug
Author Manuscript Published OnlineFirst on June 11, 2018; DOI: 10.1158/0008-5472.CAN-17-3993 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Licofelone enhances the efficacy of paclitaxel in ovarian cancer by reversing drug resistance and tumor stem-like properties Jeff Hirst1, Harsh B. Pathak1, Stephen Hyter1, Ziyan Y. Pessetto1, Thuc Ly1, Stefan Graw2, Devin C. Koestler2,3, Adam J. Krieg4,5, Katherine F. Roby3,6,7, and Andrew K. Godwin1,3 1Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, USA 2Department of Biostatistics, University of Kansas Medical Center, Kansas City, KS, USA 3University of Kansas Cancer Center, University of Kansas Medical Center, Kansas City, KS, USA 4Department of Obstetrics and Gynecology, Oregon Health & Science University, Portland, OR, USA 5Division of Reproductive and Developmental Sciences, Oregon National Primate Research Center, Beaverton, OR, USA 6Institute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, KS, USA 7Department of Anatomy & Cell Biology, University of Kansas Medical Center, Kansas City, KS, USA Corresponding author: Andrew K. Godwin 3901 Rainbow Boulevard, MS 3040 Kansas City, KS 66160 Email: [email protected] Phone: 913-945-6373 Fax (913) 945-6327 DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST -1- Downloaded from cancerres.aacrjournals.org on September 26, 2021. © 2018 American Association for Cancer Research. Author Manuscript Published OnlineFirst on June 11, 2018; DOI: 10.1158/0008-5472.CAN-17-3993 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. The authors declare no potential conflicts of interest. -
Inflammatory Drugs (Nsaids) for People with Or at Risk of COVID-19
Evidence review Acute use of non-steroidal anti- inflammatory drugs (NSAIDs) for people with or at risk of COVID-19 Publication date: April 2020 This evidence review sets out the best available evidence on acute use of non- steroidal anti-inflammatory drugs (NSAIDs) for people with or at risk of COVID-19. It should be read in conjunction with the evidence summary, which gives the key messages. Evidence review commissioned by NHS England Disclaimer The content of this evidence review was up-to-date on 24 March 2020. See summaries of product characteristics (SPCs), British national formulary (BNF) or the MHRA or NICE websites for up-to-date information. For details on the date the searches for evidence were conducted see the search strategy. Copyright © NICE 2020. All rights reserved. Subject to Notice of rights. ISBN: 978-1-4731-3763-9 Contents Contents ...................................................................................................... 1 Background ................................................................................................. 2 Intervention .................................................................................................. 2 Clinical problem ........................................................................................... 3 Objective ...................................................................................................... 3 Methodology ................................................................................................ 4 Summary of included studies