Chemical Mechanical Polishing (Cmp) of Cobalt-Containing Substrate
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The G Protein-Coupled Glutamate Receptors As Novel Molecular Targets in Schizophrenia Treatment— a Narrative Review
Journal of Clinical Medicine Review The G Protein-Coupled Glutamate Receptors as Novel Molecular Targets in Schizophrenia Treatment— A Narrative Review Waldemar Kryszkowski 1 and Tomasz Boczek 2,* 1 General Psychiatric Ward, Babinski Memorial Hospital in Lodz, 91229 Lodz, Poland; [email protected] 2 Department of Molecular Neurochemistry, Medical University of Lodz, 92215 Lodz, Poland * Correspondence: [email protected] Abstract: Schizophrenia is a severe neuropsychiatric disease with an unknown etiology. The research into the neurobiology of this disease led to several models aimed at explaining the link between perturbations in brain function and the manifestation of psychotic symptoms. The glutamatergic hypothesis postulates that disrupted glutamate neurotransmission may mediate cognitive and psychosocial impairments by affecting the connections between the cortex and the thalamus. In this regard, the greatest attention has been given to ionotropic NMDA receptor hypofunction. However, converging data indicates metabotropic glutamate receptors as crucial for cognitive and psychomotor function. The distribution of these receptors in the brain regions related to schizophrenia and their regulatory role in glutamate release make them promising molecular targets for novel antipsychotics. This article reviews the progress in the research on the role of metabotropic glutamate receptors in schizophrenia etiopathology. Citation: Kryszkowski, W.; Boczek, T. The G Protein-Coupled Glutamate Keywords: schizophrenia; metabotropic glutamate receptors; positive allosteric modulators; negative Receptors as Novel Molecular Targets allosteric modulators; drug development; animal models of schizophrenia; clinical trials in Schizophrenia Treatment—A Narrative Review. J. Clin. Med. 2021, 10, 1475. https://doi.org/10.3390/ jcm10071475 1. Introduction Academic Editors: Andreas Reif, Schizophrenia is a common debilitating disease affecting about 0.3–1% of the human Blazej Misiak and Jerzy Samochowiec population worldwide [1]. -
Buffers a Guide for the Preparation and Use of Buffers in Biological Systems Calbiochem® Buffers a Guide for the Preparation and Use of Buffers in Biological Systems
Buffers A guide for the preparation and use of buffers in biological systems Calbiochem® Buffers A guide for the preparation and use of buffers in biological systems Chandra Mohan, Ph.D. EMD, San Diego, California © EMD, an affiliate of Merck KGaA, Darmstadt, Germany. All rights reserved. A word to our valued customers We are pleased to present to you the newest edition of Buffers: A Guide for the Preparation and Use of Buffers in Biological Systems. This practical resource has been especially revamped for use by researchers in the biological sciences. This publication is a part of our continuing commitment to provide useful product information and exceptional service to you, our customers. You will find this booklet a highly useful resource, whether you are just beginning your research work or training the newest researchers in your laboratory. Over the past several years, EMD Biosciences has clearly emerged as a world leader in providing highly innovative products for your research needs in Signal Transduction, including the areas of Cancer Biology, Alzheimer’s Disease, Diabetes, Hypertension, Inflammation, and Apoptosis. Please call us today for a free copy of our LATEST Catalog that includes tools for signal transduction and life science research. If you have used our products in the past, we thank you for your support and confidence in our products, and if you are just beginning your research career, please call us and give us the opportunity to demonstrate our exceptional customer and technical service. Corrine Fetherston Sr. Director, Marketing ii Table of Contents: Why does Calbiochem® Biochemicals Publish a Booklet on Buffers? . -
Customs Tariff - Schedule
CUSTOMS TARIFF - SCHEDULE 99 - i Chapter 99 SPECIAL CLASSIFICATION PROVISIONS - COMMERCIAL Notes. 1. The provisions of this Chapter are not subject to the rule of specificity in General Interpretative Rule 3 (a). 2. Goods which may be classified under the provisions of Chapter 99, if also eligible for classification under the provisions of Chapter 98, shall be classified in Chapter 98. 3. Goods may be classified under a tariff item in this Chapter and be entitled to the Most-Favoured-Nation Tariff or a preferential tariff rate of customs duty under this Chapter that applies to those goods according to the tariff treatment applicable to their country of origin only after classification under a tariff item in Chapters 1 to 97 has been determined and the conditions of any Chapter 99 provision and any applicable regulations or orders in relation thereto have been met. 4. The words and expressions used in this Chapter have the same meaning as in Chapters 1 to 97. Issued January 1, 2020 99 - 1 CUSTOMS TARIFF - SCHEDULE Tariff Unit of MFN Applicable SS Description of Goods Item Meas. Tariff Preferential Tariffs 9901.00.00 Articles and materials for use in the manufacture or repair of the Free CCCT, LDCT, GPT, UST, following to be employed in commercial fishing or the commercial MT, MUST, CIAT, CT, harvesting of marine plants: CRT, IT, NT, SLT, PT, COLT, JT, PAT, HNT, Artificial bait; KRT, CEUT, UAT, CPTPT: Free Carapace measures; Cordage, fishing lines (including marlines), rope and twine, of a circumference not exceeding 38 mm; Devices for keeping nets open; Fish hooks; Fishing nets and netting; Jiggers; Line floats; Lobster traps; Lures; Marker buoys of any material excluding wood; Net floats; Scallop drag nets; Spat collectors and collector holders; Swivels. -
PHARMACEUTICAL APPENDIX to the TARIFF SCHEDULE 2 Table 1
Harmonized Tariff Schedule of the United States (2020) Revision 19 Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE Harmonized Tariff Schedule of the United States (2020) Revision 19 Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 2 Table 1. This table enumerates products described by International Non-proprietary Names INN which shall be entered free of duty under general note 13 to the tariff schedule. The Chemical Abstracts Service CAS registry numbers also set forth in this table are included to assist in the identification of the products concerned. For purposes of the tariff schedule, any references to a product enumerated in this table includes such product by whatever name known. -
Activation of Group I Metabotropic Glutamate Receptors Reduces Neuronal Apoptosis but Increases Necrotic Cell Death in Vitro
Cell Death and Differentiation (2000) 7, 470 ± 476 ã 2000 Macmillan Publishers Ltd All rights reserved 1350-9047/00 $15.00 www.nature.com/cdd Activation of group I metabotropic glutamate receptors reduces neuronal apoptosis but increases necrotic cell death in vitro JW Allen1,2, SM Knoblach1,3 and AI Faden*,1,3,4 hydroxyphenylglycine; DHPG, dihydroxyphenylglycine; MK801, dizocilpine; LDH, lactate dehydrogenase; MCPG, -methyl-4- 1 Institute for Cognitive and Computational Sciences, Georgetown University carboxyphenylglycine; mGluR, metabotropic glutamate receptors; Medical Center, Washington, DC 20007, USA OGD, oxygen-glucose deprivation; TBI, traumatic brain injury 2 Interdisciplinary Program in Neuroscience, Georgetown University Medical Center, Washington, DC 20007, USA 3 Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20007, USA Introduction 4 Department of Pharmacology, Georgetown University Medical Center, Washington, DC 20007, USA Activation of both ionotropic and metabotropic glutamate * Corresponding author: AI Faden, EP-04 Research Building, 3970 Reservoir receptors has been implicated in the pathophysiology of Road, N.W. Washington, DC 20007, USA. Tel: (202) 687 0492; Fax: (202) 687 stroke and CNS trauma. It has been well established that 0617; E-mail: [email protected] blockade of ionotropic glutamate receptors provides neuro- protection in vitro and in vivo.1±5 Recent studies have suggested that metabotropic glutamate receptors (mGluR) Received 23.7.99; revised 19.1.00; accepted 7.2.00 are also activated following traumatic brain injury (TBI)6±9 or Edited by FD Miller cerebral ischemia,10 or in vitro neuronal trauma7,9 or ischemia,11,12 leading to neuroprotection or exacerbation depending upon the mGluR subtype activated. -
Biological Buffers and Ultra Pure Reagents
Biological Buffers and Ultra Pure Reagents Are MP Buffers in your corner? One Call. One Source. A World of Ultra Pure Biochemicals. www.mpbio.com Theoretical Considerations Since buffers are essential for controlling the pH in many Since, under equilibrium conditions, the rates of dissociation and biological and biochemical reactions, it is important to have a association must be equal, they may be expressed as: basic understanding of how buffers control the hydrogen ion concentration. Although a lengthy, detailed discussion is impractical, + - k1 (HAc) = k2 (H ) (Ac ) some explanation of the buffering phenomena is important. Or Let us begin with a discussion of the equilibrium constant (K) for + - weak acids and bases. Acids and bases which do not completely k1 = (H ) (Ac ) dissociate in solution, but instead exist as an equilibrium mixture of k (HAc) undissociated and dissociated species, are termed weak acids and 2 bases. The most common example of a weak acid is acetic acid. If we now let k1/k2 = Ka , the equilibrium constant, the equilibrium In solution, acetic acid exists as an equilibrium mixture of acetate expression becomes: ions, hydrogen ions, and undissociated acetic acid. The equilibrium between these species may be expressed as follows: + - Ka = (H ) (Ac ) k1 (HAc) + - HAc ⇌ H + Ac which may be rearranged to express the hydrogen ion concentration k2 in terms of the equilibrium constant and the concentrations of undissociated acetic acid and acetate ions as follows: where k1 is the dissociation rate constant of acetic acid to acetate and hydrogen ions and k is the association rate constant of the ion 2 (H+) = K (HAc) species to form acetic acid. -
Electrophoresis Tech Note 5956
electrophoresis tech note 5956 Precision Plus Protein™ Dual Xtra Standards — New Protein Standards with an Extended Range from 2 to 250 kD Sansan Lin, Jonathan E. Kohn, Joseph Siino, Dennis C. Yee, and the standard were used to estimate the molecular weights Michael Urban, Bio-Rad Laboratories, Inc., 6000 James Watson Drive, of five known sample proteins. The results presented here Hercules, CA 94547 USA. demonstrate that the Precision Plus Protein Dual Xtra Introduction standards offer a convenient and reliable method to estimate The Precision Plus Protein Dual Xtra standards are expanded the molecular weight of proteins on a variety of gel types. range molecular weight standards for protein electrophoresis composed of 12 recombinant proteins and peptides with Methods molecular weights ranging from 2 to 250 kD. The Dual Xtra Sample Preparation Precision Plus Protein Dual Xtra standards were used standards are prestained with two colors for easy band according to manufacturer’s specifications. A total of referencing during electrophoresis and blot transfer. 10 μl of Dual Xtra standards was loaded onto each lane. Protein standards are tools commonly used with one- All other purified proteins were purchased from Sigma- dimensional electrophoresis to determine the molecular Aldrich. Sample proteins were suspended in Laemmli sample weight of unknown proteins (Bio-Rad Bulletin 3133). In buffer containing b-mercaptoethanol (Bio-Rad Laboratories, polyacrylamide gel electrophoresis (PAGE), proteins are Inc.) and heated at 85°C for 6 min prior to loading. driven through the gel under an electric field, during which Gel Electrophoresis and Molecular Weight Analysis the gel matrix acts as a sieve to separate proteins based on For migration analysis a total of 10 μl of Precision Plus size (SDS-PAGE), or charge and shape (native PAGE). -
Buyers' Guide
Buyers’ Guide S119 Buyers’ Guide Suppliers’ Contact Details Amersham Biosciences UK Limited The Menarini Group Amersham Place www.menarini.com Little Chalfont Buckinghamshire HP7 9NA Moravek Biochemicals UK 577 Mercury Lane www5.amershambiosciences.com Brea Ca 92821 Avanti Polar Lipids Inc USA 700 Industrial Park Drive www.moravek.com Alabaster AL 35007 Roche Pharmaceuticals USA F. Hoffmann-La Roche Ltd www.avantilipids.com Pharmaceuticals Division Grenzacherstrasse 124 Bachem Bioscience Inc. CH-4070 Basel 3700 Horizon Drive Switzerland King of Prussia Telephone þ 41-61-688 1111 PA 19406 Unites States Telefax þ 41-61-691 9391 www.bachem.org www.roche.com Boehringer Ingelheim Ltd Ellesfield Avenue SIGMA Chemicals/Sigma-Aldrich Bracknell P.O. Box 14508 Berks RG12 8YS St. Louis, MO 63178-9916 UK USA www.boehringer-ingelheim.co.uk www.sigma-aldrich.com Calbiochem Tocris Cookson Ltd. EMD Biosciences, Inc. Northpoint, Fourth Way 10394 Pacific Center Court Avonmouth San Diego Bristol CA 92121 BS11 8TA USA UK www.emdbiosciences.com www.tocris.com S120 Buyers’ Guide Compound Supplier Buyers’ Guide a-methyl-5-HT a-Methyl-5-hydroxytryptamine Tocris ab-meATP ab-methylene-adenosine 5’-triphosphate Sigma-Aldrich bg-meATP bg-methylene-adenosine 5’-triphosphate Sigma-Aldrich (-)-(S)-BAYK8664 (-)-(S)-methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluromethylphenyl)-pyridine-5-carboxylate Sigma-Aldrich, Tocris (+)7-OH-DPAT (+)-7-hydroxy-2-aminopropylaminotetralin Sigma-Aldrich a-dendrotoxin Sigma-Aldrich (RS)PPG (R,S)-4-phosphonophenylglycine Tocris (S)-3,4-DCPG -
Amino Acids by G.C.BARRETT
1 Amino Acids By G.C.BARRETT 1 Introduction The chemistry and biochemistry of the amino acids as represented in the 1992 literature, is covered in this Chapter. The usual policy for this Specialist Periodical Report has been continued, with almost exclusive attention in this Chapter, to the literature covering the natural occurrence, chemistry, and analysis methodology for the amino acids. Routine literature covering the natural distribution of well-known amino acids is excluded. The discussion offered is brief for most of the papers cited, so that adequate commentary can be offered for papers describing significant advances in synthetic methodology and mechanistically-interesting chemistry. Patent literature is almost wholly excluded but this is easily reached through Section 34 of Chemical Abstracts. It is worth noting that the relative number of patents carried in Section 34 of Chemical Abstracts is increasing (e.g. Section 34 of Chem-Abs., 1992, Vol. 116, Issue No. 11 contains 45 patent abstracts, 77 abstracts of papers and reviews), reflecting the perception that amino acids and peptides are capable of returning rich commercial rewards due to their important physiological roles and consequent pharmaceutical status. However, there is no slowing of the flow of journal papers and secondary literature, as far as the amino acids are concerned. The coverage in this Chapter is arranged into sections as used in all previous Volumes of this Specialist Periodical Report, and major Journals and Chemical Abstracts (to Volume 118, issue 11) have -
Evidence for Metabotropic Glutamate Receptor Activation in the Induction of Depolarization-Induced Suppression of Inhibition in Hippocampal CA1
The Journal of Neuroscience, July 1, 1998, 18(13):4870–4882 Evidence for Metabotropic Glutamate Receptor Activation in the Induction of Depolarization-Induced Suppression of Inhibition in Hippocampal CA1 Wade Morishita, Sergei A. Kirov, and Bradley E. Alger Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201 Depolarization-induced suppression of inhibition (DSI) is a tran- (1S,3R)-ACPD-induced IPSC suppression and markedly re- sient reduction of GABAA receptor-mediated IPSCs that is duced DSI, whereas group III antagonists had no effect on DSI. mediated by a retrograde signal from principal cells to interneu- Many other similarities between DSI and the (1S,3R)-ACPD- rons. Using whole-cell recordings, we tested the hypothesis induced suppression of IPSCs also were found. Our data sug- that mGluRs are involved in the DSI process in hippocampal gest that a glutamate-like substance released from pyramidal CA1, as has been proposed for cerebellar DSI. Group II mGluR cells could mediate CA1 DSI by reducing GABA release from agonists failed to affect either evoked monosynaptic IPSCs or interneurons via the activation of group I mGluRs. DSI, and forskolin, which blocks cerebellar DSI, did not affect CA1 DSI. Group I and group III mGluR agonists reduced IPSCs, Key words: IPSP; GABA; retrograde signal; voltage clamp; but only group I agonists occluded DSI. (S)-MCPG blocked mGluR; synaptic inhibition Depolarization-induced suppression of inhibition (DSI) is a phe- decrease cAMP production (Conn et al., 1994), which can reduce nomenon seen in both hippocampal CA1 pyramidal cells (Pitler GABA release (Capogna et al., 1995). -
<<Presentation Title>>
Sihuan Pharmaceutical Holdings Group Ltd. 四環醫藥控股集團有限公司 2013 Interim Results Presentation Stock Code : 0460 Disclaimer The sole purpose of this Presentation (the “Presentation”) is to assist the recipient in deciding whether it wishes to proceed with a further investigation of Sihuan Pharmaceutical Holdings Group Ltd. (the “Company”) and it is not intended to form the basis of any decision to purchase securities, interests or assets in or of the Company. This Presentation does not constitute or contain an offer or invitation or recommendation or solicitation for the sale or purchase of securities, interests or assets in or of the Company and neither this document nor anything contained herein shall form the basis of, or be relied upon in connection with, any contract or commitment whatsoever. Any decision to purchase or subscribe for securities in any offering must be made solely on the basis of the information contained in the prospectus or offering circular issued by the company in connection with such offerings. All the information in this Presentation has been provided by the Company and has not been independently verified. No representation or warranty, express or implied, is or will be made in or in relation to, and no responsibility or liability is or will be accepted by the Company or any of its subsidiaries as to the appropriateness, accuracy, completeness or reliability of, this Presentation or any other written or oral information made available to any interested party or its advisers and any liability therefore is hereby expressly disclaimed. And no reliance should be placed on the accuracy, fairness, completeness or correctness of the information contained in this Presentation. -
Microglial Glutathione and Glutamate: Regulation Mechanisms
Microglial glutathione and glutamate: Regulation mechanisms Victoria Anne Honey Fry UCL Institute of Neurology A thesis submitted for the degree of Doctor of Philosophy (Ph.D.) 1 I, Victoria Fry, confirm that the work presented in this thesis is my own. Where information has been derived from other sources, I confirm that this has been indicated in the thesis. 2 Abstract Microglia, the immune cells of the central nervous system (CNS), are important in the protection of the CNS, but may be implicated in the pathogenesis of neuroinflammatory disease. Upon activation, microglia produce reactive oxygen and nitrogen species; intracellular antioxidants are therefore likely to be important in their self-defence. Here, it was confirmed that cultured microglia contain high levels of glutathione, the predominant intracellular antioxidant in mammalian cells. The activation of microglia with lipopolysaccharide (LPS) or LPS + interferon- was shown to affect their glutathione levels. GSH levels in primary microglia and those of the BV-2 cell line increased upon activation, whilst levels in N9 microglial cells decreased. - Microglial glutathione synthesis is dependent upon cystine uptake via the xc transporter, which exchanges cystine and glutamate. Glutamate is an excitatory neurotransmitter whose extracellular concentration is tightly regulated by excitatory amino acid transporters, as high levels cause toxicity to neurones and other CNS cell types through overstimulation of - glutamate receptors or by causing reversal of xc transporters. Following exposure to LPS, increased extracellular glutamate and increased levels of messenger ribonucleic acid - (mRNA) for xCT, the specific subunit of xc , were observed in BV-2 and primary microglial cells, suggesting upregulated GSH synthesis.