DOCSLIB.ORG

Characterization of Strychnine Binding Sites in the Rodent

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Characterization of Strychnine Binding Sites in the Rodent CHARACTERIZATION OF STRYCHNINE BINDING SITES IN THE RODENT SPINAL CORD BY VINCENT MAURICE O’CONNOR UNIVERSITY COLLEGE LONDON A thesis submitted for the degree of Doctor of Philosophy from the University of London, 1992. I ProQuest Number: 10608898 All rights reserved INFORMATION TO ALL USERS The quality of this reproduction is dependent upon the quality of the copy submitted. In the unlikely event that the author did not send a com plete manuscript and there are missing pages, these will be noted. Also, if material had to be removed, a note will indicate the deletion. uest ProQuest 10608898 Published by ProQuest LLC(2017). Copyright of the Dissertation is held by the Author. All rights reserved. This work is protected against unauthorized copying under Title 17, United States C ode Microform Edition © ProQuest LLC. ProQuest LLC. 789 East Eisenhower Parkway P.O. Box 1346 Ann Arbor, Ml 48106- 1346 This thesis is dedicated to the select band o f people, including the most recent arrivals and the sorely missed departed, that I hold closest in my affections. "At the end of the day" they make It all worthwhile. Remember, in the words of the famous actor whose name at present escapes me; "Nobody said it would be easy". Although my own feeling is that Nobody was probably wrong. II Thesis abstract The convulsant alkaloid strychnine is a selective and highly potent antagonist at postsynaptic receptor for the inhibitory neurotransmitter glycine . These properties have led to the extensive use of strychnine as a ligand to probe the postsynaptic glycine receptor. Despite the recent increased understanding of the molecular structure of this receptor protein there is still much dispute as to the nature of the interaction between glycine and strychnine. In an attempt to more clearly define this interaction the experiments described, combine the techniques of protein modification and ligand binding. These investigations also revealed a novel [3H]-strychnine binding site in the rodent CNS and attempts were made to characterize this phenomenon. The results described suggest that glycine is a fully competitive inhibitor of [3H]- strychnine binding and its reported action as a partial competitive inhibitor is an artefact of the assay conditions. The disruption of [3H]-strychnine binding by residue selective protein modifying reagents suggests some overlap in the strychnine and glycine binding sites at the receptor. Protection studies confirm this and the results are best explained by overlapping yet conformationally distinct recognition sites for strychnine and glycine. Experiments which describe protein modification and ligand protection of strychnine binding antisera highlight possible congruence in the molecular recognition at the antisera and the receptor. This is of interest in the light of proposed models of the strychnine binding site at the postsynaptic glycine receptor. Modification of spinal cord membranes by the arginine selective reagent 2,3- butanedione (BD) reveals a low affinity and high capacity [3H]-strychnine binding site which is not detectable in untreated membranes. This binding site showed a similar distribution in the CNS as the high affinity site. However, experiments using affinity purified glycine receptor and crude membrane preparations from the mutant mouse spastic indicated that the BD-induced binding site is not located on the postsynaptic glycine receptor. Competition studies revealed that [3H]-strychnine binding sites in untreated and BD-treated membranes have different structural determinants. The ability to effectively inhibit [3H]-strychnine binding to the BD-induced site by cation channel blockers is in accord with reports that strychnine can interact with various cation channels to open or block them. In addition several compounds that inhibit the BD-induced [3H]-strychnine binding can also modulate the reaction of BD with spinal cord membranes if present during the treatment, suggesting a conformational dependent modification. Upon exposure to ultraviolet light [3H]-strychnine is specifically incorporated into a low molecular weight peptide in BD-treated membranes in addition to the ligand binding subunit of the inhibitory glycine receptor, which is the only peptide photolabelled in untreated membranes. The significance of this biochemical and pharmacological characterization of this previously undescribed strychnine binding site is presently unclear. However, the uneven distribution in the CNS and the interaction with important therapeutic agents; local anaesthetics and anti-arrhythmics, indicate the possible biological importance of the novel strychnine binding site. Ill ACKNOWLEDGEMENTS I would like to thank Jonathan Fry for his scientific supervision and optimism throughout the time I have been at University College. I am grateful to the Department and its members for their encouragement in all aspects of my education. I am particularly indebted to: Christine Williams, for her skilful and patient preparation of plates and drug structures, experimental assistance and advice on parenting. Keith Caddy and my buddy Alex who in combination contrived to enable my figures to be printed, although I am grateful for the assistance of many others with regard to this matter. Mabel Kendrick for laboratory luxuries which includes the steady supply of confectionaries. Ian Martin for supplying the glycine receptor alignments along with discussion on my trips to Cambridge or his to London. Dennis Haylett for discussion and supplying several compounds especially the channel blockers that were initially screened. Also I would like to thank the individuals and companies listed in Chapter Two for the generous supply of drugs. In particular I would like to thank G.A.R. Johnston and Hue Tran for synthesizing 2- aminostrychnine and thereby enabling us to bypass the shortage of commercially available compound. I would like to thank my peers at University College especially Boris Barbour, Margaret "Bridgett" Carey and Gerard "de Pad" Christoffi for scientific discussion and a series of lighter moments that helped make my time so stimulating. I would also like to acknowledge the MRC for providing my stipend. In addition I am grateful to the MRC, The Physiological Society, The Biochemical Society and the Department for providing the funding that enabled me to attend conferences and courses. In particular I am grateful to all those who encouraged and made it possible for me to attend MBL, the scientific paradise at Woods Hole. This thesis is my own account of investigations carried out by myself under the supervision of Jonathan Fry. IV ABBREVIATIONS 2-AS 2-aminostrychnine 5-HT 5-hydroxytryptamine Ach acetylcholine B bound ligand BD 2,3-butanedione Bm« maximal number of binding sites BSA bovine serum albumin CAD cationic amphipathic drug cDNA cloned deoxyribonucleic acid CHAPS 3-[(3-Cholamidopropyl)-dimethylammonio]-l- propanesulphonate CHD 1,2-cyclohexanedione CNS central nervous system cpm counts per minute CQS camphorquinone- 10-sulphate D-600 methoxy verapamil DEP diethylpyrocarbonate dpm disintegrations per minute DSA diasotized sulphanilate DT diazonium tetratzole DTT dithiothreitol EDTA ethylenediaminetetraacetic acid FI flurescein isothiocyanate GABA y-amino-N-butyric acid IAA iodoacetamide IC50 concentration of displacer which inhibits 50% of control binding Ig immunoglobulin Iso-THAZ 5,6,7,8-tetrahydro-4H-isooxazolo[3,4]azepin-3-ol Ki association rate constant k.i dissociation rate constant kd kilodalton Kd equilibrium dissociation constant K j equilibrium inhibition constant KLH keyhole limpet haemocyanin M merthiolate mAb monoclonal antibody mRNA messenger ribonucleic acid NA noradrenaline NBS N-bromosuccinimide NEM N-ethylmaleimide NMDA N-methyl-D-aspartic acid PAGE polyacrylamide gel electrophoresis PBB phosphate buffered borate PBS phosphate buffered saline PCR polymeraze chain reaction PEG polyethylene glycol PEI polyethylenimine V PG phenylglyoxal PLP pyridoxal phosphate PMSF phenylmethane sulphonyl fluoride pPG p-hydroxy-phenylglyoxal PTC phosphatidylcholine SBTI soya bean trypsin inhibitor SDS sodium dodecyl sulphate SEM standard error of the mean spa spastic TBPS t-butylbicyclophosphorothionate TCA trichloroacetic acid TEA tetraethylammonium TEMED NNN *,N-tetramethylethylenediamine TNBS trinitrobenzosulphonic acid TNM tetranitromethane UV ultraviolet Single letter code for amino acids A alanine C cysteine D aspartic acid E glutamic acid F phenylalanine G glycine H histidine I isoleucine K lysine L leucine M methionine N asparagine P proline Q glutamine R arginine S serine T threonine V valine W tryptophan Y tyrosine VI CONTENTS PAGE Title I Dedication II Abstract m Acknowledgements IV Abbreviations V Chapter One Introduction i 1.1 Introduction i 1.2 Actions of strychnine on CNS inhibition. i 1.3 Establishing glycine as an inhibitory transmitter in CNS. 3 1.4 Use of strychnine as a molecular probe to study the inhibitory glycine receptor. 4 1.4.a Distribution of glycine receptors in the CNS. 5 1.4.b Ionic modulation of [3H]-strychnine binding. 8 1.5 Biochemical characterization of the inhibitory glycine receptor. 10 1.5.a Solubilization and affinity purification of the inhibitory glycine receptor. 10 1.5.b Photolabelling the inhibitory glycine receptor. 11 1.5.C Antibodies specific for the inhibitory glycine receptor. 12 1.5.d Subunit associations in the inhibitory glycine receptor. 13 1.5.e Developmental regulation of [3H]-strychnine binding and inhibitory glycine receptor. 16 1.6 Molecular Genetic Analysis
Load more

Recommended publications
  • Amnestic Concentrations of Sevoflurane Inhibit Synaptic
    Anesthesiology 2008; 108:447–56 Copyright © 2008, the American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc. Amnestic Concentrations of Sevoflurane Inhibit Synaptic Plasticity of Hippocampal CA1 Neurons through ␥-Aminobutyric Acid–mediated Mechanisms Junko Ishizeki, M.D.,* Koichi Nishikawa, M.D., Ph.D.,† Kazuhiro Kubo, M.D.,‡ Shigeru Saito, M.D., Ph.D.,§ Fumio Goto, M.D., Ph.D.࿣ Background: The cellular mechanisms of anesthetic-induced for surgical procedures do not have recollection of ac- amnesia are still poorly understood. The current study exam- tually being awake despite being awake and cooperative ined sevoflurane at various concentrations in the CA1 region of during the procedure.1 Galinkin et al.2 compared sub- rat hippocampal slices for effects on excitatory synaptic trans- Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/108/3/447/366512/0000542-200803000-00017.pdf by guest on 29 September 2021 mission and on long-term potentiation (LTP), as a possible jective, psychomotor, cognitive, and analgesic effects of mechanism contributing to anesthetic-induced loss of recall. sevoflurane (0.3% and 0.6%) with those of nitrous oxide Methods: Population spikes and field excitatory postsynaptic at equal minimum alveolar concentrations (MACs) in potentials were recorded using extracellular electrodes after healthy volunteers. They found that sevoflurane pro- electrical stimulation of Schaffer-collateral-commissural fiber inputs. Paired pulse facilitation was used as a measure of pre- duced a greater degree of amnesia and psychomotor synaptic effects of the anesthetic. LTP was induced using tetanic impairment than did an equal MAC of nitrous oxide but stimulation (100 Hz, 1 s). Sevoflurane at concentrations from had no analgesic actions.
    [Show full text]
  • Picrotoxin-Like Channel Blockers of GABAA Receptors
    COMMENTARY Picrotoxin-like channel blockers of GABAA receptors Richard W. Olsen* Department of Molecular and Medical Pharmacology, Geffen School of Medicine, University of California, Los Angeles, CA 90095-1735 icrotoxin (PTX) is the prototypic vous system. Instead of an acetylcholine antagonist of GABAA receptors (ACh) target, the cage convulsants are (GABARs), the primary media- noncompetitive GABAR antagonists act- tors of inhibitory neurotransmis- ing at the PTX site: they inhibit GABAR Psion (rapid and tonic) in the nervous currents and synapses in mammalian neu- system. Picrotoxinin (Fig. 1A), the active rons and inhibit [3H]dihydropicrotoxinin ingredient in this plant convulsant, struc- binding to GABAR sites in brain mem- turally does not resemble GABA, a sim- branes (7, 9). A potent example, t-butyl ple, small amino acid, but it is a polycylic bicyclophosphorothionate, is a major re- compound with no nitrogen atom. The search tool used to assay GABARs by compound somehow prevents ion flow radio-ligand binding (10). through the chloride channel activated by This drug target appears to be the site GABA in the GABAR, a member of the of action of the experimental convulsant cys-loop, ligand-gated ion channel super- pentylenetetrazol (1, 4) and numerous family. Unlike the competitive GABAR polychlorinated hydrocarbon insecticides, antagonist bicuculline, PTX is clearly a including dieldrin, lindane, and fipronil, noncompetitive antagonist (NCA), acting compounds that have been applied in not at the GABA recognition site but per- huge amounts to the environment with haps within the ion channel. Thus PTX major agricultural economic impact (2). ͞ appears to be an excellent example of al- Some of the other potent toxicants insec- losteric modulation, which is extremely ticides were also radiolabeled and used to important in protein function in general characterize receptor action, allowing and especially for GABAR (1).
    [Show full text]
  • GABA Receptors
    D Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews Review No.7 / 1-2011 GABA receptors Wolfgang Froestl , CNS & Chemistry Expert, AC Immune SA, PSE Building B - EPFL, CH-1015 Lausanne, Phone: +41 21 693 91 43, FAX: +41 21 693 91 20, E-mail: [email protected] GABA Activation of the GABA A receptor leads to an influx of chloride GABA ( -aminobutyric acid; Figure 1) is the most important and ions and to a hyperpolarization of the membrane. 16 subunits with γ most abundant inhibitory neurotransmitter in the mammalian molecular weights between 50 and 65 kD have been identified brain 1,2 , where it was first discovered in 1950 3-5 . It is a small achiral so far, 6 subunits, 3 subunits, 3 subunits, and the , , α β γ δ ε θ molecule with molecular weight of 103 g/mol and high water solu - and subunits 8,9 . π bility. At 25°C one gram of water can dissolve 1.3 grams of GABA. 2 Such a hydrophilic molecule (log P = -2.13, PSA = 63.3 Å ) cannot In the meantime all GABA A receptor binding sites have been eluci - cross the blood brain barrier. It is produced in the brain by decarb- dated in great detail. The GABA site is located at the interface oxylation of L-glutamic acid by the enzyme glutamic acid decarb- between and subunits. Benzodiazepines interact with subunit α β oxylase (GAD, EC 4.1.1.15). It is a neutral amino acid with pK = combinations ( ) ( ) , which is the most abundant combi - 1 α1 2 β2 2 γ2 4.23 and pK = 10.43.
    [Show full text]
  • Exploring the Activity of an Inhibitory Neurosteroid at GABAA Receptors
    1 Exploring the activity of an inhibitory neurosteroid at GABAA receptors Sandra Seljeset A thesis submitted to University College London for the Degree of Doctor of Philosophy November 2016 Department of Neuroscience, Physiology and Pharmacology University College London Gower Street WC1E 6BT 2 Declaration I, Sandra Seljeset, confirm that the work presented in this thesis is my own. Where information has been derived from other sources, I can confirm that this has been indicated in the thesis. 3 Abstract The GABAA receptor is the main mediator of inhibitory neurotransmission in the central nervous system. Its activity is regulated by various endogenous molecules that act either by directly modulating the receptor or by affecting the presynaptic release of GABA. Neurosteroids are an important class of endogenous modulators, and can either potentiate or inhibit GABAA receptor function. Whereas the binding site and physiological roles of the potentiating neurosteroids are well characterised, less is known about the role of inhibitory neurosteroids in modulating GABAA receptors. Using hippocampal cultures and recombinant GABAA receptors expressed in HEK cells, the binding and functional profile of the inhibitory neurosteroid pregnenolone sulphate (PS) were studied using whole-cell patch-clamp recordings. In HEK cells, PS inhibited steady-state GABA currents more than peak currents. Receptor subtype selectivity was minimal, except that the ρ1 receptor was largely insensitive. PS showed state-dependence but little voltage-sensitivity and did not compete with the open-channel blocker picrotoxinin for binding, suggesting that the channel pore is an unlikely binding site. By using ρ1-α1/β2/γ2L receptor chimeras and point mutations, the binding site for PS was probed.
    [Show full text]
  • Chronic Social Isolation Reduces 5-HT Neuronal Activity Via Upregulated SK3 Calcium-Activated Potassium Channels Derya Sargin1, David K Oliver1, Evelyn K Lambe1,2,3*
    SHORT REPORT Chronic social isolation reduces 5-HT neuronal activity via upregulated SK3 calcium-activated potassium channels Derya Sargin1, David K Oliver1, Evelyn K Lambe1,2,3* 1Department of Physiology, University of Toronto, Toronto, Canada; 2Department of Obstetrics and Gynaecology, University of Toronto, Toronto, Canada; 3Department of Psychiatry, University of Toronto, Toronto, Canada Abstract The activity of serotonin (5-HT) neurons is critical for mood regulation. In a mouse model of chronic social isolation, a known risk factor for depressive illness, we show that 5-HT neurons in the dorsal raphe nucleus are less responsive to stimulation. Probing the responsible cellular mechanisms pinpoints a disturbance in the expression and function of small-conductance Ca2+-activated K+ (SK) channels and reveals an important role for both SK2 and SK3 channels in normal regulation of 5-HT neuronal excitability. Chronic social isolation renders 5-HT neurons insensitive to SK2 blockade, however inhibition of the upregulated SK3 channels restores normal excitability. In vivo, we demonstrate that inhibiting SK channels normalizes chronic social isolation- induced anxiety/depressive-like behaviors. Our experiments reveal a causal link for the first time between SK channel dysregulation and 5-HT neuron activity in a lifelong stress paradigm, suggesting these channels as targets for the development of novel therapies for mood disorders. DOI: 10.7554/eLife.21416.001 Introduction *For correspondence: evelyn. Major depression is a prevalent and debilitating disease for which standard treatments remain inef- [email protected] fective. Social isolation has long been implicated as a risk factor for depression in humans Competing interests: The (Cacioppo et al., 2002,2006; Holt-Lunstad et al., 2010) and induces anxiety- and depressive-like authors declare that no behaviors in rodents (Koike et al., 2009; Wallace et al., 2009; Dang et al., 2015; Shimizu et al., competing interests exist.
    [Show full text]
  • Increased NMDA Receptor Inhibition at an Increased Sevoflurane MAC Robert J Brosnan* and Roberto Thiesen
    Brosnan and Thiesen BMC Anesthesiology 2012, 12:9 http://www.biomedcentral.com/1471-2253/12/9 RESEARCH ARTICLE Open Access Increased NMDA receptor inhibition at an increased Sevoflurane MAC Robert J Brosnan* and Roberto Thiesen Abstract Background: Sevoflurane potently enhances glycine receptor currents and more modestly decreases NMDA receptor currents, each of which may contribute to immobility. This modest NMDA receptor antagonism by sevoflurane at a minimum alveolar concentration (MAC) could be reciprocally related to large potentiation of other inhibitory ion channels. If so, then reduced glycine receptor potency should increase NMDA receptor antagonism by sevoflurane at MAC. Methods: Indwelling lumbar subarachnoid catheters were surgically placed in 14 anesthetized rats. Rats were anesthetized with sevoflurane the next day, and a pre-infusion sevoflurane MAC was measured in duplicate using a tail clamp method. Artificial CSF (aCSF) containing either 0 or 4 mg/mL strychnine was then infused intrathecally at 4 μL/min, and the post-infusion baseline sevoflurane MAC was measured. Finally, aCSF containing strychnine (either 0 or 4 mg/mL) plus 0.4 mg/mL dizocilpine (MK-801) was administered intrathecally at 4 μL/min, and the post- dizocilpine sevoflurane MAC was measured. Results: Pre-infusion sevoflurane MAC was 2.26%. Intrathecal aCSF alone did not affect MAC, but intrathecal strychnine significantly increased sevoflurane requirement. Addition of dizocilpine significantly decreased MAC in all rats, but this decrease was two times larger in rats without intrathecal strychnine compared to rats with intrathecal strychnine, a statistically significant (P < 0.005) difference that is consistent with increased NMDA receptor antagonism by sevoflurane in rats receiving strychnine.
    [Show full text]
  • Waste Disposal Guide
    Waste Disposal Guide How to Properly Dispose of Waste Materials Generated at Michigan State University Environmental Health & Safety (EHS) / Office of Radiation, Chemical & Biological Safety (ORCBS) C124 Research Complex‐Engineering East Lansing, MI 48824‐1326 Revised April 2009 CONTACT INFORMATION Campus Emergency: 911 ORCBS Phone Number: (517) 355-0153 ORCBS Fax Number: (517) 353-4871 ORCBS E-mail Address: [email protected] ORCBS Web Address: http://www.orcbs.msu.edu TABLE OF CONTENTS Sections Introduction ................................................................................................................... 4 Hazardous Waste Defined ............................................................................................ 5 Requirements for Chemical Waste ............................................................................... 6 Classification of Chemical Waste .................................................................................. 7 Containers ..................................................................................................................... 8 Container Label ............................................................................................................. 9 General Labeling & Packaging Procedures .................................................................. 9 Specific Labeling & Packaging Procedures ............................................................. 9-15 Scheduling a Chemical Waste Pick-up ......................................................................
    [Show full text]
  • AMANITA MUSCARIA: Mycopharmacological Outline and Personal Experiences
    • -_._----------------------- .....•.----:: AMANITA MUSCARIA: Mycopharmacological Outline and Personal Experiences by Francesco Festi and Antonio Bianchi Amanita muscaria, also known as Fly Agaric, is a yellow-to-orange capped wild mushroom. It grows in symbir-, is with arboreal trees such as Birch, Pine or Fir, in both Europe and the Americas. Its his- tory has it associated with both shamanic and magical practices for at least the last 2,000 years, and it is probably the Soma intoxicant spoken of in the Indian Rig-Vedas. The following piece details both the generic as well as the esoteric history and pharmacological pro- files of the Amanita muscaria. It also introduces research which J shows that psychoactivity related to this species is seasonally- determinant. This determinant can mean the difference between poi- soning and pleasant, healing applications, which include psychedelic experiences. Connections between the physiology of sleep and the plant's inner chemistry is also outlined. if" This study is divided into two parts, reflecting two comple- l"" ~ ,j. mentary but different approaches to the same topic. The first (" "~l>;,;,~ ~ study, presented by Francesco Festi, presents a critical over- .~ view of the ~-:<'-.:=l.=';i.:31. ethnobotanical, chemical and phar- macological d~:.:: -.c. ~_~.::-_ .:::e :-efe:-::-e j to the Amanita muscaria (through 198'5 In :he se.:,='~_·: :;-.r:. also Italian author and mycologist Antc nio Bianchi reports on personal experiences with the Amar.i:a muscaria taken from European samples. The following experimental data - far from constituting any final answers - are only a proposal and (hopefully) an excitement for further investigations.
    [Show full text]
  • Glutamate-Gated Inhibitory Currents of Central Pattern Generator Neurons in the Lobster Stomatogastric Ganglion
    The Journal of Neuroscience, October 1995, 75(10): 6631-6639 Glutamate-Gated Inhibitory Currents of Central Pattern Generator Neurons in the Lobster Stomatogastric Ganglion Thomas A. Cleland and Allen I. Selverston Biology Department, University of California at San Diego, La Jolla, California 92093-0357 Inhibitory glutamatergic neurotransmission is an elemental (Johnsonand Hooper, 1992), and have served as model systems “building block” of the oscillatory networks within the for understanding the function of biological neural networks crustacean stomatogastric ganglion (STG). This study con- (Kristan, 1980; Getting, 1989). Inhibitory glutamatergicsynaptic stitutes the initial characterization of glutamatergic cur- transmissionis a major building block of the reciprocal inhibi- rents in isolated STG neurons in primary culture. Super- tory pairs and recurrent cyclic inhibitory chains of the neurons fusion of 1 mM L-glutamate evoked a current response in that comprise these oscillatory CPGs (Marder and Paupardin- 45 of 65 neurons examined. The evoked current incorpo- Tritsch, 1978; Marder and Eisen, 1984). The chemical modula- rated two kinetically distinct components in variable pro- tion of these glutamatergic synapsescontributes heavily to con- portion: a fast desensitizing component and a slower com- trol of oscillatory phase relationships among the participating ponent. The current was mediated by an outwardly recti- neurons (Johnson et al., 1994), and changesin such phasere- fying conductance increase and reversed at -46.6 + 5.3 lationshipsin turn directly mediate changesin behavioral output mV. Reducing the external chloride concentration by 50% (Heinzel et al., 1993). deflected the glutamate equilibrium potential (E,,,) by +14 The glutamatergicIPSP in situ is primarily dependenton chlo- mV, while increasing external potassium threefold shifted ride, but also sometimesexhibits a smaller potassium depen- E,,, by up to +6 mV.
    [Show full text]
  • Chemical Resistance of Plastics
    (c) Bürkle GmbH 2010 Important Important information The tables “Chemical resistance of plastics”, “Plastics and their properties” and “Viscosity of liquids" as well as the information about chemical resistance given in the particular product descriptions have been drawn up based on information provided by various raw material manufacturers. These values are based solely on laboratory tests with raw materials. Plastic components produced from these raw materials are frequently subject to influences that cannot be recognized in laboratory tests (temperature, pressure, material stress, effects of chemicals, construction features, etc.). For this reason the values given are only to be regarded as being guidelines. In critical cases it is essential that a test is carried out first. No legal claims can be derived from this information; nor do we accept any liability for it. A knowledge of the chemical and mechanical Copyright This table has been published and updated by Bürkle GmbH, D-79415 Bad Bellingen as a work of reference. This Copyright clause must not be removed. The table may be freely passed on and copied, provided that Extensions, additions and translations If your own experiences with materials and media could be used to extend this table then we would be pleased to receive any additional information. Please send an E-Mail to [email protected]. We would also like to receive translations into other languages. Please visit our website at http://www.buerkle.de from time to Thanks Our special thanks to Franz Kass ([email protected]), who has completed and extended these lists with great enthusiasm and his excellent specialist knowledge.
    [Show full text]
  • Loba Chemie Pvt
    TABLE OF CONTENT INTRODUCTION Contact US ii MD Letter iii Company Profile iv Latest Information v Label vi Certifications vii GMP Compliant Pharma Facility viii QC Capability ix R&D x Logistic xi COA xii SDS xiii Packing xiv Quality xvi Terms Of Sales xvii Application xviii Product Highlights xix Nanopowder & Carbon Nanotubes xxvii List of New Products xxviii ALPHABETICAL PRODUCT LISTING Price List Chemical 01-155 Ecosafe Safety Products 156-160 Macherey-Nagel Filtration Products 161-181 [email protected] I CONTACT US Contact us for more information on any of our products and services HEAD OFFICE - MUMBAI Loba Chemie Pvt. Ltd., Jehangir Villa, 107, Wode House Road, Colaba, Mumbai-400005 Maharashtra, India Tel: +91(022) 6663 6663 Fax: +91(022) 6663 6699 MANUFACTURING UNIT (TARAPUR) Loba Chemie Pvt. Ltd., Plot No.: D-22, M.I.D.C. Tarapur, Boisar, Taluka: Palghar, Thane-401506 Maharashtra, India Ph: +91(02525) 300 001 Stay up to date about our range and availability www.lobachemie.com Get in touch with us General Enquiry: [email protected] Technical Query: [email protected] Domestic Sales: [email protected] Export Sales: [email protected] Follow us on: ii www.lobachemie.com WELCOME AT LOBA CHEMIE Dear Valued Reader Another exciting year has gone by and we would like to start the New Year, as usual, with a new catalogue featuring more innova- tive highest quality range of routine and novel Laboratory Chemi- cal and Fine Reagents. With our more than 4 decads of expertise in Laboratory Chemical and Fine Reagents we not only bring you a complete Laboratory at your fingertips but in addition with our expertise we have palced our brand of products in a very competitive position for years to come.
    [Show full text]
  • |||||III USOO5547541A United States Patent (19) 11) Patent Number: 5,547,541 Hansen Et Al
    |||||III USOO5547541A United States Patent (19) 11) Patent Number: 5,547,541 Hansen et al. 45) Date of Patent: Aug. 20, 1996 54) METHOD FOR DENSEFYING FIBERS USING OTHER PUBLICATIONS A DENSIFYINGAGENT Gugliemelli et al., "Base-Hydrolyzed Starch-Polyacryloni (75) Inventors: Michael R. Hansen, Seattle; Richard trile (S-PAN) Graft Copolymer. S-PAN-1:1, PAN. M. W. H. Young, Sr., Renton, both of Wash. 794,000*", J. of Applied Copolymer Science, 13:2007-2017 (1969). (73) Assignee: Weyerhaeuser Company, Federal Way, Weaver et al., "Hydrolyzed Starch-Polyacrylonitrile Graft Wash. Copolymers: Effect of Structure on Properties', J. of Applied Polymer Science, 15:3015–3024 (1971). Weaver et al., "Highly Absorbent Starch-Based Polymer." 21 Appl. No.: 197483 Northern Regional Research Laboratory, Agricultural 22) Filed: Feb. 16, 1994 Research Service, U.S. Dept. of Agriculture, Peoria, Illinois, pp. 169-177. Related U.S. Application Data "Super slurpers: Time for change?,” Chemical Week, pp. 21-22 (Jul. 24, 1974). (63) Continuation-in-part of Ser. No. 931,059, Aug. 17, 1992, S. Lammie, "Use of Glycerine as a Softener for Paper Ser. No. 931,277, Aug. 17, 1992, Ser. No. 931,213, Aug. 17, 1992, Pat. No. 5,300,192, Ser. No. 931,278, Aug. 17, 1992, Products." The World's Paper Trade Review, Dec. 13, 1962, Pat. No. 5,352,480, Ser. No. 931,284, Aug. 17, 1992, Pat. p. 2050. No. 5,308,896, Ser. No. 931,279, Aug. 17, 1992, Ser. No. Lindsay, "Absorbent Starch Based Co-polymers- Their 107,469, Aug. 17, 1993, Ser. No. 108,219, Aug.
    [Show full text]