Appendix G: High Hazard Chemicals
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Pertussis Toxin
Pertussis Toxin Publication Number MAN0004270 Revision Date 09 May 2011 Catalog Number: PHZ1174 Quantity: 50 μg Lot Number: See product label. Appearance: Lyophilized solid. Origin: Bordetella pertussis. Purity: >99%. This preparation migrates as five distinct bands when analyzed by SDS–Urea PAGE. The five bands correspond to one A protomer subunit, designated S1 (Mr=26.2 kDa), and four B oligomer subunits, designated S2- S5 (Mr’s= 21.9, 21.9, 12.1, and 10.9 kDa, respectively). Summary: Islet-activating protein Pertussis toxin consists of an A protomer subunit (S1) which possesses both NAD+ glycohydrolase and ADP–ribosyltransferase activities, and B oligomer subunits (S2, S3, S4, and S5) which are responsible for attachment of the native toxin to eukaryotic cell surfaces. Pertussis toxin uncouples G proteins from receptors by ADP ribosylating a cysteine residue near the carboxyl terminus of the α subunit. Biological Activity: The lowest concentration which produces a clustered growth pattern with CHO cells is 0.03 ng/mL. The adenylate cyclase activity of this preparation is 20.1 picomoles/minute/μg in the presence of 1 μg calmodulin. Reconstitution Reconstitute the contents of this vial with 500 μL sterile, distilled water. The composition of the solution will be Recommendation: 50 μg Pertussis toxin, 10 mM sodium phosphate, pH 7.0, 50 mM sodium chloride. Because Pertussis toxin is relatively insoluble, the resulting suspension should be made uniform by gentle mixing prior to withdrawing aliquots. It is important to note that this suspension should not be sterile-filtered. This preparation is not activated. For use with intact cells or extracts, activation is not necessary. -
Bacillus Anthracis Edema Factor Substrate Specificity: Evidence for New Modes of Action
Toxins 2012, 4, 505-535; doi:10.3390/toxins4070505 OPEN ACCESS toxins ISSN 2072–6651 www.mdpi.com/journal/toxins Review Bacillus anthracis Edema Factor Substrate Specificity: Evidence for New Modes of Action Martin Göttle 1,*, Stefan Dove 2 and Roland Seifert 3 1 Department of Neurology, Emory University School of Medicine, 6302 Woodruff Memorial Research Building, 101 Woodruff Circle, Atlanta, GA 30322, USA 2 Department of Medicinal/Pharmaceutical Chemistry II, University of Regensburg, D-93040 Regensburg, Germany; E-Mail: [email protected] 3 Institute of Pharmacology, Medical School of Hannover, Carl-Neuberg-Str. 1, D-30625 Hannover, Germany; E-Mail: [email protected] * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +1-404-727-1678; Fax: +1-404-727-3157. Received: 23 April 2012; in revised form: 15 June 2012 / Accepted: 27 June 2012 / Published: 6 July 2012 Abstract: Since the isolation of Bacillus anthracis exotoxins in the 1960s, the detrimental activity of edema factor (EF) was considered as adenylyl cyclase activity only. Yet the catalytic site of EF was recently shown to accomplish cyclization of cytidine 5′-triphosphate, uridine 5′-triphosphate and inosine 5′-triphosphate, in addition to adenosine 5′-triphosphate. This review discusses the broad EF substrate specificity and possible implications of intracellular accumulation of cyclic cytidine 3′:5′-monophosphate, cyclic uridine 3′:5′-monophosphate and cyclic inosine 3′:5′-monophosphate on cellular functions vital for host defense. In particular, cAMP-independent mechanisms of action of EF on host cell signaling via protein kinase A, protein kinase G, phosphodiesterases and CNG channels are discussed. -
The Role of Streptococcal and Staphylococcal Exotoxins and Proteases in Human Necrotizing Soft Tissue Infections
toxins Review The Role of Streptococcal and Staphylococcal Exotoxins and Proteases in Human Necrotizing Soft Tissue Infections Patience Shumba 1, Srikanth Mairpady Shambat 2 and Nikolai Siemens 1,* 1 Center for Functional Genomics of Microbes, Department of Molecular Genetics and Infection Biology, University of Greifswald, D-17489 Greifswald, Germany; [email protected] 2 Division of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, University of Zurich, CH-8091 Zurich, Switzerland; [email protected] * Correspondence: [email protected]; Tel.: +49-3834-420-5711 Received: 20 May 2019; Accepted: 10 June 2019; Published: 11 June 2019 Abstract: Necrotizing soft tissue infections (NSTIs) are critical clinical conditions characterized by extensive necrosis of any layer of the soft tissue and systemic toxicity. Group A streptococci (GAS) and Staphylococcus aureus are two major pathogens associated with monomicrobial NSTIs. In the tissue environment, both Gram-positive bacteria secrete a variety of molecules, including pore-forming exotoxins, superantigens, and proteases with cytolytic and immunomodulatory functions. The present review summarizes the current knowledge about streptococcal and staphylococcal toxins in NSTIs with a special focus on their contribution to disease progression, tissue pathology, and immune evasion strategies. Keywords: Streptococcus pyogenes; group A streptococcus; Staphylococcus aureus; skin infections; necrotizing soft tissue infections; pore-forming toxins; superantigens; immunomodulatory proteases; immune responses Key Contribution: Group A streptococcal and Staphylococcus aureus toxins manipulate host physiological and immunological responses to promote disease severity and progression. 1. Introduction Necrotizing soft tissue infections (NSTIs) are rare and represent a more severe rapidly progressing form of soft tissue infections that account for significant morbidity and mortality [1]. -
Review Cholera Toxin Structure, Gene Regulation and Pathophysiological
Cell. Mol. Life Sci. 65 (2008) 1347 – 1360 1420-682X/08/091347-14 Cellular and Molecular Life Sciences DOI 10.1007/s00018-008-7496-5 Birkhuser Verlag, Basel, 2008 Review Cholera toxin structure, gene regulation and pathophysiological and immunological aspects J. Sncheza and J. Holmgrenb,* a Facultad de Medicina, UAEM, Av. Universidad 1001, Col. Chamilpa, CP62210 (Mexico) b Department of Microbiology and Immunology and Gothenburg University Vaccine Research Institute (GUVAX), University of Gçteborg, Box 435, Gothenburg, 405 30 (Sweden), e-mail: [email protected] Received 25 October 2007; accepted 12 December 2007 Online First 19 February 2008 Abstract. Many notions regarding the function, struc- have recently been discovered. Regarding the cell ture and regulation of cholera toxin expression have intoxication process, the mode of entry and intra- remained essentially unaltered in the last 15 years. At cellular transport of cholera toxin are becoming the same time, recent findings have generated addi- clearer. In the immunological field, the strong oral tional perspectives. For example, the cholera toxin immunogenicity of the non-toxic B subunit of cholera genes are now known to be carried by a non-lytic toxin (CTB) has been exploited in the development of bacteriophage, a previously unsuspected condition. a now widely licensed oral cholera vaccine. Addition- Understanding of how the expression of cholera toxin ally, CTB has been shown to induce tolerance against genes is controlled by the bacterium at the molecular co-administered (linked) foreign antigens in some level has advanced significantly and relationships with autoimmune and allergic diseases. cell-density-associated (quorum-sensing) responses Keywords. -
How Do Pathogenic Microorganisms Develop Cross-Kingdom Host Jumps? Peter Van Baarlen1, Alex Van Belkum2, Richard C
Molecular mechanisms of pathogenicity: how do pathogenic microorganisms develop cross-kingdom host jumps? Peter van Baarlen1, Alex van Belkum2, Richard C. Summerbell3, Pedro W. Crous3 & Bart P.H.J. Thomma1 1Laboratory of Phytopathology, Wageningen University, Wageningen, The Netherlands; 2Department of Medical Microbiology and Infectious Diseases, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands; and 3CBS Fungal Biodiversity Centre, Utrecht, The Netherlands Correspondence: Bart P.H.J. Thomma, Abstract Downloaded from https://academic.oup.com/femsre/article/31/3/239/2367343 by guest on 27 September 2021 Laboratory of Phytopathology, Wageningen University, Binnenhaven 5, 6709 PD It is common knowledge that pathogenic viruses can change hosts, with avian Wageningen, The Netherlands. Tel.: 10031 influenza, the HIV, and the causal agent of variant Creutzfeldt–Jacob encephalitis 317 484536; fax: 10031 317 483412; as well-known examples. Less well known, however, is that host jumps also occur e-mail: [email protected] with more complex pathogenic microorganisms such as bacteria and fungi. In extreme cases, these host jumps even cross kingdom of life barriers. A number of Received 3 July 2006; revised 22 December requirements need to be met to enable a microorganism to cross such kingdom 2006; accepted 23 December 2006. barriers. Potential cross-kingdom pathogenic microorganisms must be able to First published online 26 February 2007. come into close and frequent contact with potential hosts, and must be able to overcome or evade host defences. Reproduction on, in, or near the new host will DOI:10.1111/j.1574-6976.2007.00065.x ensure the transmission or release of successful genotypes. -
New Markers in the Mycotox Profile
New Markers in the MycoTOX Profile We are happy to announce the addition of four new mycotoxin markers to our MycoTOX Profile. The test now includes 11 mycotoxins from 40 species of mold, making it by far the most comprehensive and competitively priced mycotoxin test available. It also still more sensitive and accurate than other tests available, because we use LC/MS/MS technology. Here is an overview of the four new mycotoxin markers: Gliotoxin Gliotoxin (GTX) is produced by the mold genus Aspergillus. Aspergillus spreads in the environment by releasing conidia which are capable of infiltrating the small alveolar airways of individuals. In order to evade the body’s defenses Aspergillus releases Gliotoxin to inhibit the immune system. One of the targets of Gliotoxin is PtdIns (3,4,5) P3. This results in the downregulation of phagocytic immune defense, which can lead to the exacerbation of polymicrobial infections. Gliotoxin impairs the activation of T-cells and induces apoptosis in monocytes and in monocyte-derived dendritic cells. These impairments can lead to multiple neurological syndromes. Mycophenolic Acid Mycophenolic Acid (MPA) produced by the Penicillium fungus. MPA is an immunosuppressant which inhibits the proliferation of B and T lymphocytes. MPA exposure can increase the risk of opportunistic infections such as Clostridia and Candida. MPA is associated with miscarriage and congenital malformations when the woman is exposed in pregnancy. Dihydrocitrinone Dihydrocitrinone is a metabolite of Citrinin (CTN), which is a mycotoxin that is produced by the mold species Aspergillus, Penicillium, and Monascus. CTN exposure can lead to nephropathy, because of its ability to increase permeability of mitochondrial membranes in the kidneys. -
Fungal Keratitis: Immune Recognition, Neutrophil-Hyphae Interactions, And
FUNGAL KERATITIS: IMMUNE RECOGNITION, NEUTROPHIL-HYPHAE INTERACTIONS, AND FUNGAL ANTI-OXIDATIVE DEFENSES by SIXTO MANUEL LEAL JR. Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy Thesis Advisor: Eric Pearlman, Ph.D. Department of Pathology CASE WESTERN RESERVE UNIVERSITY August, 2012 CASE WESTERN RESERVE UNIVERSITY SCHOOL OF GRADUATE STUDIES We hereby approve the dissertation of ______________________________________________________ candidate for the Ph.D. degree *. (signed)_______________________________________________ (chair of the committee) ________________________________________________ ________________________________________________ ________________________________________________ ________________________________________________ ________________________________________________ (date) _______________________ *We also certify that written approval has been obtained for any proprietary material contained therein. Dedication I dedicate this cumulative work to the invisible hand that has blessed my personal and academic life with incredible people, guidance, talent, courage, perseverance, and productivity. 3 Table of Contents List of Figures 7 List of Tables 9 Acknowledgements 10 List of Abbreviations 12 Abstract 14 Chapter 1. Introduction Fungi in their natural environment 16 Fungi and human disease 18 Fungi that cause human corneal infection 21 Fungal keratitis- Clinical characteristics and outcome 22 Anti-microbial Defenses at the Ocular Surface 23 Immune Recognition of Fungi 27 β2 integrins -
Biological Toxins Fact Sheet
Work with FACT SHEET Biological Toxins The University of Utah Institutional Biosafety Committee (IBC) reviews registrations for work with, possession of, use of, and transfer of acute biological toxins (mammalian LD50 <100 µg/kg body weight) or toxins that fall under the Federal Select Agent Guidelines, as well as the organisms, both natural and recombinant, which produce these toxins Toxins Requiring IBC Registration Laboratory Practices Guidelines for working with biological toxins can be found The following toxins require registration with the IBC. The list in Appendix I of the Biosafety in Microbiological and is not comprehensive. Any toxin with an LD50 greater than 100 µg/kg body weight, or on the select agent list requires Biomedical Laboratories registration. Principal investigators should confirm whether or (http://www.cdc.gov/biosafety/publications/bmbl5/i not the toxins they propose to work with require IBC ndex.htm). These are summarized below. registration by contacting the OEHS Biosafety Officer at [email protected] or 801-581-6590. Routine operations with dilute toxin solutions are Abrin conducted using Biosafety Level 2 (BSL2) practices and Aflatoxin these must be detailed in the IBC protocol and will be Bacillus anthracis edema factor verified during the inspection by OEHS staff prior to IBC Bacillus anthracis lethal toxin Botulinum neurotoxins approval. BSL2 Inspection checklists can be found here Brevetoxin (http://oehs.utah.edu/research-safety/biosafety/ Cholera toxin biosafety-laboratory-audits). All personnel working with Clostridium difficile toxin biological toxins or accessing a toxin laboratory must be Clostridium perfringens toxins Conotoxins trained in the theory and practice of the toxins to be used, Dendrotoxin (DTX) with special emphasis on the nature of the hazards Diacetoxyscirpenol (DAS) associated with laboratory operations and should be Diphtheria toxin familiar with the signs and symptoms of toxin exposure. -
Pdf 309.57 K
Proceeding of the 6th ICEE Conference 29-31 May 2012 ENMC-2 1/6 6th International Conference Military Technical College on Kobry El-Kobbah, Chemical & Environmental Cairo, Egypt Engineering 29 -31 May, 2012. ENMC-2 SENSITIVITY AND DETONATION PARAMETERS OF 4, 6-DIAZIDO-N-NITRO-1, 3, 5-TRIAZIN-2-AMINE Tomáš Musil*, Robert Matyáš*, Ondřej Němec*, Martin Künze* Abstract Highly dense nitrogen-rich compounds are potential high performance energetic materials for use in industrial scene or military. 4,6-Diazido-N-nitro-1,3,5-triazin-2- amine (DANT) is relatively a new substance on which characterization and detonation parameters were tested. The sensitivity of DANT to impact, friction and electric discharge was also determined. Sensitivity to impact is between PETN and RDX, sensitivity to friction is higher as PETN. DANT´s relative strength is 108 % of TNT. We also calculated and measured detonation parameters such as pressure and detonation velocity. Theoretical detonation parameters are 8 205 m.s-1 and 30.3 GPa. Temperature of autoignition is 156 °C. Keywords: 4,6-Diazido-N-nitro-1,3,5-triazin-2-amine; DANT, detonation parameters, sensitivity * Institute of Energetic Materials, Faculty of Chemical Technology, University of Pardubice, Studentska 95, 532 10 Pardubice, Czech Republic. [email protected] 1/6 Proceeding of the 6th ICEE Conference 29-31 May 2012 ENMC-2 2/6 1. Introduction 4,6-Diazido-N-nitro-1,3,5-triazin-2-amine (DANT, see scheme 1) – this relatively simple molecule was first reported only four years ago by Fronabarger et al. [1]. The more extensive study of this molecule focused on its synthesis, analysis, structure and its sensitivity to mechanical stimuli was published recently by us [2]. -
Batrachotoxin Time-Resolved Absorption And
Dental, Oral and Maxillofacial Research Mini Review ISSN: 2633-4291 Batrachotoxin time-resolved absorption and resonance FT-IR and raman biospectroscopy and density functional theory (DFT) investigation of vibronic-mode coupling structure in vibrational spectra analysis: A spectroscopic study on an anti-gum cancer drug Alireza Heidari1,2*, Jennifer Esposito1 and Angela Caissutti1 1Faculty of Chemistry, California South University, 14731 Comet St. Irvine, CA 92604, USA 2American International Standards Institute, Irvine, CA 3800, USA Abstract Gum cancers are cancers that arise from the gum. They are due to the development of abnormal cells that have the ability to invade or spread to other parts of the body. There are three main types of gum cancers: basal-cell gum cancer (BCC), squamous-cell gum cancer (SCC) and melanoma. Batrachotoxin (BTX) is an anti- gum cancer extremely potent cardiotoxic and neurotoxic steroidal alkaloid found in certain species of beetles, birds, and frogs. Batrachotoxin was derived from the Greek word βάτραχος bátrachos "frog". Structurally-related chemical compounds are often referred to collectively as batrachotoxins. It is an extremely poisonous alkaloid. In certain frogs this alkaloid is present mostly on the gum. Such frogs are among those used for poisoning darts. Batrachotoxin binds to and irreversibly opens the sodium channels of nerve cells and prevents them from closing, resulting in paralysis-no antidote is known. Parameters such as FT -IR and Raman vibrational wavelengths and intensities for single crystal Batrachotoxin are calculated using density functional theory and were compared with empirical results. The investigation about vibrational spectrum of cycle dimers in crystal with carboxyl groups from each molecule of acid was shown that it leads to create Hydrogen bonds for adjacent molecules. -
Chemical Chemical Hazard and Compatibility Information
Chemical Chemical Hazard and Compatibility Information Acetic Acid HAZARDS & STORAGE: Corrosive and combustible liquid. Serious health hazard. Reacts with oxidizing and alkali materials. Keep above freezing point (62 degrees F) to avoid rupture of carboys and glass containers.. INCOMPATIBILITIES: 2-amino-ethanol, Acetaldehyde, Acetic anhydride, Acids, Alcohol, Amines, 2-Amino-ethanol, Ammonia, Ammonium nitrate, 5-Azidotetrazole, Bases, Bromine pentafluoride, Caustics (strong), Chlorosulfonic acid, Chromic Acid, Chromium trioxide, Chlorine trifluoride, Ethylene imine, Ethylene glycol, Ethylene diamine, Hydrogen cyanide, Hydrogen peroxide, Hydrogen sulfide, Hydroxyl compounds, Ketones, Nitric Acid, Oleum, Oxidizers (strong), P(OCN)3, Perchloric acid, Permanganates, Peroxides, Phenols, Phosphorus isocyanate, Phosphorus trichloride, Potassium hydroxide, Potassium permanganate, Potassium-tert-butoxide, Sodium hydroxide, Sodium peroxide, Sulfuric acid, n-Xylene. Acetone HAZARDS & STORAGE: Store in a cool, dry, well ventilated place. INCOMPATIBILITIES: Acids, Bromine trifluoride, Bromine, Bromoform, Carbon, Chloroform, Chromium oxide, Chromium trioxide, Chromyl chloride, Dioxygen difluoride, Fluorine oxide, Hydrogen peroxide, 2-Methyl-1,2-butadiene, NaOBr, Nitric acid, Nitrosyl chloride, Nitrosyl perchlorate, Nitryl perchlorate, NOCl, Oxidizing materials, Permonosulfuric acid, Peroxomonosulfuric acid, Potassium-tert-butoxide, Sulfur dichloride, Sulfuric acid, thio-Diglycol, Thiotrithiazyl perchlorate, Trichloromelamine, 2,4,6-Trichloro-1,3,5-triazine -
Properties of Explosives.Pdf
Properties of Explosives Explosive VOD Density %OB Formula Notes Acetone peroxide 5290 1.2 -159 C9H18O6 Amatol 40/60 7440 1.59 Amatol 50/50 6430 1.55 Cast Amatol 60/40 5760 1.5 Amatol 80/20 5100 1.5 Cast Ammonal 6230 English Ammonal 4580 service Ammonal T 6871 1.59 Ammon-carbonite 3380 1.06 Ammonit 1 3600 1 Ammonium nitrate 2460 +20.0 NH4NO3 Lead tube Ammonium nitrate 2500 1.4 +20.0 NH4NO3 Liquid Ammonium nitrate/sulphate 60/40 2430 0.9 Ammonium perchlorate 3800 +34.0 NH4ClO4 Ammonium picrate (Explosive D) 7150 1.6 C6H2(NO2)3ONH4 APEX 220/329 5800 1.25 Baratol 90/10 5900 1.65 Baronal 5450 2.32 Blackpowder 400 1.6 BTF 8490 1.86 Carbonite 2440 1.46 Carbonit I 3042 Carbonit II 2472 Cheddite 02 4020 1.04 Cheddite 60bis 01 2901 1.17 Cheddite 60M 3000 1.3 Cheditte No. 2 2365 1 Chloratit No. 2 4000 1.5 Chloratit No. 3 2700 1.7 92% KClO3 Chloratit No. 3 3500 1.4 90% KClO3 Chlorotrinitrobenzene 6800 1.66 Composition A3 8470 1.64 Composition A-3 8100 1.59 Composition B 7800 1.65 Composition B-3 7890 1.72 Cast Composition C-2 7660 1.57 Composition C-3 7630 1.6 Composition C4 8370 1.66 Composition C-4 8040 1.59 Cyanuric triazide 5600 1.15 Cyanuric triazide 5500 1.02 Cyanuric triazide 7500 1.54 Cyclotetramethylene tetranitramine 9100 1.9 -21.6 C4H8N8O8 (Octogen, HMX) Cyclotol 60/40 7900 1.72 Cyclotol 65/35 7975 1.72 Cast Cyclotol 70/30 8060 1.73 Cyclotol 75/25 8035 1.7 Cast Cyclotol 75/25 7938 1.71 Cast Cyclotol 75/25 8300 1.76 Cyclotrimethylene trinitirosamine 7300 1.42 Cyclotrimethylenetrinitramine (RDX, 8180 1.65 -21.6 C3H6N6O6 cyclonite) Cyclotrimethylenetrinitramine