What Are the Health Effects from Exposure to Carbon Monoxide?
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18,8 Quaternary Structure of Proteins
570 CHAPTERt8 Amino Acids,Peptides, and Proteins 18,8Quaternary structure of proteins AIMS: Todefine the termssubunit dnd quaternarystructure. Io describethe quoternorystructure of hemoglobin.To distinguishomong oxyhemoglobin,deoxyhemoglobin, ond methemoglobin. Someproteins consist of more than one pollpeptide chain. Theseindiuid- ual chains are calledsubunits of the protein. Proteins composedof subunits In some proteins, polypeptide are said to haue quaternary structure. Many proteins have structures that chains aggregateto form contain subunits. Proteins consistingof dimers (two subunits), tetramers quaternary structures. (four subunits), and hexamers (six subunits) are fairly common. The pro- teins that comprise the individual subunits may be identical, or they may be different. Like the secondary and tertiary structures, the quaternary structure of a protein is determined by its primary structure. The pollpep- tide chains of subunits are held in place by the same forces that determine tertiary structure-hydrogen bonds, salt bridges, and sometimes disulfide bridges-except the forces are betweenthe polypeptide chains of the sub- units instead of within them. Hydrophobic aliphatic and aromatic side chains of subunits can aggregateto exclude water. Hemoglobin-the globular oxygen-transport protein of blood-is an example of a protein that has a quaternary structure. Max Perutz, also of the Medical ResearchCouncil laboratories,determined the structure of horse blood hemoglobin in 1959.Hemoglobin is a larger molecule than myoglo- bin. The hemoglobin molecule has a molar mass of 64,500.It contains about 5000 individual atoms, excluding hydrogens, in 574 amino acid residues. The quaternary structure of hemoglobin consistsof four peptide sub- units. TWo of the subunits are identical and are called the alpha subunits. -
Highly Selective Addition of Organic Dichalcogenides to Carbon-Carbon Unsaturated Bonds
Highly Selective Addition of Organic Dichalcogenides to Carbon-Carbon Unsaturated Bonds Akiya Ogawa and Noboru Sonoda Department of Applied Chemistry, Faculty of Engineering, Osaka University, Abstract: Highly chemo-, regio- and/or stereoselective addition of organic dichalcogenides to carbon-carbon unsaturated bonds has been achieved based on two different methodologies for activation of the chalcogen-chalcogen bonds, i.e., by the aid of transition metal catalysts and by photoirradiation. The former is the novel transition metal-catalyzed reactions of organic dichalcogenides with acetylenes via oxidative addition of dichalcogenides to low valent transition metal complexes such as Pd(PPh3)4. The latter is the photoinitiated radical addition of organic dichalcogenides to carbon-carbon unsaturated bonds via homolytic cleavage of the chalcogen-chalcogen bonds to generate the corresponding chalcogen-centered radicals as the key species. 1. Introduction The clarification of the specific chemical properties of heteroatoms and the development of useful synthetic reactions based on these characteristic features have been the subject of continuing interest (ref. 1). This paper deals with new synthetic methods for introducing group 16 elements into organic molecules, particularly, synthetic reactions based on the activation of organic dichalcogenides, i.e., disulfides, diselenides, and ditellurides, by transition metal catalysts and by photoirradiation. In transition metal-catalyzed reactions, metal sulfides (RS-ML) are formed as the key species, whereas the thiyl radicals (ArS•E) play important roles in photoinitiated reactions. These species exhibit different selectivities toward the addition process to carbon-carbon unsaturated compounds. The intermediates formed in situ by the addition, i.e., vinylic metals and vinylic radicals, could successfully be subjected to further manipulation leading to useful synthetic transformations. -
The History of Carbon Monoxide Intoxication
medicina Review The History of Carbon Monoxide Intoxication Ioannis-Fivos Megas 1 , Justus P. Beier 2 and Gerrit Grieb 1,2,* 1 Department of Plastic Surgery and Hand Surgery, Gemeinschaftskrankenhaus Havelhoehe, Kladower Damm 221, 14089 Berlin, Germany; fi[email protected] 2 Burn Center, Department of Plastic Surgery and Hand Surgery, University Hospital RWTH Aachen, Pauwelsstrasse 30, 52074 Aachen, Germany; [email protected] * Correspondence: [email protected] Abstract: Intoxication with carbon monoxide in organisms needing oxygen has probably existed on Earth as long as fire and its smoke. What was observed in antiquity and the Middle Ages, and usually ended fatally, was first successfully treated in the last century. Since then, diagnostics and treatments have undergone exciting developments, in particular specific treatments such as hyperbaric oxygen therapy. In this review, different historic aspects of the etiology, diagnosis and treatment of carbon monoxide intoxication are described and discussed. Keywords: carbon monoxide; CO intoxication; COHb; inhalation injury 1. Introduction and Overview Intoxication with carbon monoxide in organisms needing oxygen for survival has probably existed on Earth as long as fire and its smoke. Whenever the respiratory tract of living beings comes into contact with the smoke from a flame, CO intoxication and/or in- Citation: Megas, I.-F.; Beier, J.P.; halation injury may take place. Although the therapeutic potential of carbon monoxide has Grieb, G. The History of Carbon also been increasingly studied in recent history [1], the toxic effects historically dominate a Monoxide Intoxication. Medicina 2021, 57, 400. https://doi.org/10.3390/ much longer period of time. medicina57050400 As a colorless, odorless and tasteless gas, CO is produced by the incomplete combus- tion of hydrocarbons and poses an invisible danger. -
The Role of Methemoglobin and Carboxyhemoglobin in COVID-19: a Review
Journal of Clinical Medicine Review The Role of Methemoglobin and Carboxyhemoglobin in COVID-19: A Review Felix Scholkmann 1,2,*, Tanja Restin 2, Marco Ferrari 3 and Valentina Quaresima 3 1 Biomedical Optics Research Laboratory, Department of Neonatology, University Hospital Zurich, University of Zurich, 8091 Zurich, Switzerland 2 Newborn Research Zurich, Department of Neonatology, University Hospital Zurich, University of Zurich, 8091 Zurich, Switzerland; [email protected] 3 Department of Life, Health and Environmental Sciences, University of L’Aquila, 67100 L’Aquila, Italy; [email protected] (M.F.); [email protected] (V.Q.) * Correspondence: [email protected]; Tel.: +41-4-4255-9326 Abstract: Following the outbreak of a novel coronavirus (SARS-CoV-2) associated with pneumonia in China (Corona Virus Disease 2019, COVID-19) at the end of 2019, the world is currently facing a global pandemic of infections with SARS-CoV-2 and cases of COVID-19. Since severely ill patients often show elevated methemoglobin (MetHb) and carboxyhemoglobin (COHb) concentrations in their blood as a marker of disease severity, we aimed to summarize the currently available published study results (case reports and cross-sectional studies) on MetHb and COHb concentrations in the blood of COVID-19 patients. To this end, a systematic literature research was performed. For the case of MetHb, seven publications were identified (five case reports and two cross-sectional studies), and for the case of COHb, three studies were found (two cross-sectional studies and one case report). The findings reported in the publications show that an increase in MetHb and COHb can happen in COVID-19 patients, especially in critically ill ones, and that MetHb and COHb can increase to dangerously high levels during the course of the disease in some patients. -
Respiratory Physiology - Part B Experimental Determination of Anatomical Dead Space Value (Human 9 - Version Sept
Comp. Vert. Physiology- BI 244 Respiratory Physiology - Part B Experimental Determination of Anatomical Dead Space Value (Human 9 - Version Sept. 10, 2013) [This version has been modified to also serve as a tutorial in how to run HUMAN's artificial organs] Part of the respiratory physiology computer simulation work for this week allows you to obtain a hand-on feeling for the effects of anatomical dead space on alveolar ventilation. The functional importance of dead space can explored via employing HUMAN's artificial respirator to vary the respiration rate and tidal volume. DEAD SPACE DETERMINATION Introduction The lack of unidirectional respiratory medium flow in non-avian air ventilators creates the existence of an anatomical dead space. The anatomical dead space of an air ventilator is a fixed volume not normally under physiological control. However, the relative importance of dead space is adjustable by appropriate respiratory maneuvers. For example, recall the use by panting animals of their dead space to reduce a potentially harmful respiratory alkalosis while hyperventilating. In general, for any given level of lung ventilation, the fraction of the tidal volume attributed to dead space will affect the resulting level of alveolar ventilation, and therefore the efficiency (in terms of gas exchange) of that ventilation. [You should, of course, refresh your knowledge of total lung ventilation, tidal volume alveolar ventilation.] Your objective here is to observe the effects of a constant "unknown" dead space on resulting alveolar ventilation by respiring the model at a variety of tidal volume-frequency combinations. You are then asked to calculate the functional dead space based on the data you collect. -
Carbon Monoxide (CO), Known As the Invisible Killer, Is a Colorless
FACT SHEET Program: Fire Equipment & Systems CARBON MONOXIDE DETECTORS – RESIDENTIAL UNITS Carbon monoxide (CO), known as the Invisible Killer, is a colorless, odorless, poisonous gas that results from incomplete burning of fuels such as natural gas, propane, oil, wood, coal, and gasoline. Exposure to carbon monoxide can cause flu-like symptoms and can be fatal. Residential buildings that contain fossil burning fuel equipment (i.e., oil, gas, wood, coal, etc.) or contain enclosed parking are required to have carbon monoxide detectors. What are the symptoms of CO poisoning? CO poisoning victims may initially suffer flu-like symptoms including nausea, fatigue, headaches, dizziness, confusion and breathing difficulty. Because CO poisoning often causes a victim's blood pressure to rise, the victim's skin may take on a pink or red cast. How does CO affect the human body? When victims inhale CO, the toxic gas enters the bloodstream and replaces the oxygen molecules found on the critical blood component - hemoglobin, depriving the heart and brain of the oxygen necessary to function. Mild exposure: Often described as flu-like symptoms, including slight headache, nausea, vomiting, fatigue. Medium exposure: Severe throbbing headache, drowsiness, confusion, fast heart rate. Extreme exposure: Unconsciousness, convulsions, cardio respiratory failure, death. Many cases of reported carbon monoxide poisoning indicate that while victims are aware they are not well, they become so disoriented, that they are unable to save themselves by either exiting the building or calling for assistance. Young children and household pets are typically the first affected. If you think you have symptoms of carbon monoxide poisoning or your CO alarm is sounding, contact the Fire Department (911) or University Operations Center (5-5560) and leave the building immediately. -
Hemoglobin : Its Protein of Molecular Weight 64,450 , in Human Beings It
Hemoglobin : its protein of molecular weight 64,450 , in human beings it is enclose in the RBC .if it were in plasma, some of it leaks through the capillary membrane into the tissue space or through the glomerular membrane of the kidney into the glomerular filtrate each time the blood passes through the capillaries , high free plasma concentration of Hb increased blood viscosity and osmotic pressure. So for Hb to remain in the bloodstream , it must exist in the RBCs ,its major function is to carry O2 to the tissue and also it transport CO2 from the tissues to the lungs Normal hemoglobin type: Hb A: Its normal adult Hb . Its molecule consist of four polypeptide chains ,2 alpha (α) chains (each of which contains 141 amino acids) and 2 beta chains (each of which contains 146 amino acids).thus Hb A is designated α2 and β2. Hb A is predominant type of Hb in adult (95- 97% of total Hb) . Hb A2 : in the normal adult about 25% of the total Hb is Hb A2 in which chain are replaced by delta chains and is designated 2 α 2δ2 . Each δ chain also contain 146 amino acid but 10 amino acid differ from those in the β chain . Hb F (Fetal Hb): it is the main Hb in fetus and new born . It is 2α 2γ,gamma(γ) chain also has 146 amino acid but 37 amino acid differ from those in β chain, Hb F is replaced gradually by adult Hb soon after birth, usually at about 6 months to one year of age, the normal adult Hb predominates . -
Metabolic Stable Isotope Fractionation
Photograph by author, Gina M.A. Carroll Metabolic Stable Isotope Fractionation: Biogeochemical Approaches to Diagnosing Sickle Cell and Thalassemia Anemia in the Archaeological Record MSc Thesis Faculty of Archaeology MSc Proefschrift Faculteit der Archaeologie Gina M.A. Carroll 1 Photograph by Gina. M.A. Carroll Taken with permission from the Municipal Museum of Écija, Spain April 2014 Gina M.A. Carroll Alberta, Canada Leiden, The Netherlands [email protected] 1 Metabolic Stable Isotope Fractionation: Biogeochemical Approaches to Diagnosing Sickle Cell and Thalassemia Anemia in the Archaeological Record. MSc Thesis MSc Proefschrift Gina M.A. Carroll Human Osteology and Funerary s1371266 Archaeology MSc Thesis Archaeology University of Leiden Faculty of Archaeology ARCH 1044WY Prof. Dr. Waters-Rist Leiden, The Netherlands & Prof. Dr. Inskip Leiden, 26 May 2015 Final Draft. 2 TABLE OF CONTENTS DEDICATIONS ...................................................................................................................... 9 ACKNOWLEDGEMENTS .................................................................................................. 10 CHAPTER 1 INTRODUCTION ....................................................................... 12-30 1. BRIEF HISTORY OF ARCHAEOLOGICAL RESEARCH ........................................ 13 1.1. The Anemias in Archaeology ....................................................... 14 1.2. The Application of Stable Isotopes in Palaeopathology ............... 18 2. HYPOTHESIS ................................................................................................ -
Ocean Storage
277 6 Ocean storage Coordinating Lead Authors Ken Caldeira (United States), Makoto Akai (Japan) Lead Authors Peter Brewer (United States), Baixin Chen (China), Peter Haugan (Norway), Toru Iwama (Japan), Paul Johnston (United Kingdom), Haroon Kheshgi (United States), Qingquan Li (China), Takashi Ohsumi (Japan), Hans Pörtner (Germany), Chris Sabine (United States), Yoshihisa Shirayama (Japan), Jolyon Thomson (United Kingdom) Contributing Authors Jim Barry (United States), Lara Hansen (United States) Review Editors Brad De Young (Canada), Fortunat Joos (Switzerland) 278 IPCC Special Report on Carbon dioxide Capture and Storage Contents EXECUTIVE SUMMARY 279 6.7 Environmental impacts, risks, and risk management 298 6.1 Introduction and background 279 6.7.1 Introduction to biological impacts and risk 298 6.1.1 Intentional storage of CO2 in the ocean 279 6.7.2 Physiological effects of CO2 301 6.1.2 Relevant background in physical and chemical 6.7.3 From physiological mechanisms to ecosystems 305 oceanography 281 6.7.4 Biological consequences for water column release scenarios 306 6.2 Approaches to release CO2 into the ocean 282 6.7.5 Biological consequences associated with CO2 6.2.1 Approaches to releasing CO2 that has been captured, lakes 307 compressed, and transported into the ocean 282 6.7.6 Contaminants in CO2 streams 307 6.2.2 CO2 storage by dissolution of carbonate minerals 290 6.7.7 Risk management 307 6.2.3 Other ocean storage approaches 291 6.7.8 Social aspects; public and stakeholder perception 307 6.3 Capacity and fractions retained -
Elevated Carboxyhemoglobin in a Marine Mammal, the Northern
© 2014. Published by The Company of Biologists Ltd | The Journal of Experimental Biology (2014) 217, 1752-1757 doi:10.1242/jeb.100677 RESEARCH ARTICLE Elevated carboxyhemoglobin in a marine mammal, the northern elephant seal Michael S. Tift1,2,*, Paul J. Ponganis1 and Daniel E. Crocker2 ABSTRACT storage capacity (decreased arterial O2 content), thus limiting Low concentrations of endogenous carbon monoxide (CO), mitochondrial respiration. However, CO is also generated generated primarily through degradation of heme from heme- endogenously in low concentrations, and functions in proteins, have been shown to maintain physiological function of neurotransmission and in protection of tissues and cells against organs and to exert cytoprotective effects. However, high inflammation, apoptosis and ischemia–reperfusion injuries (Snyder concentrations of carboxyhemoglobin (COHb), formed by CO binding et al., 1998; Kevin and Laffey, 2008; Mustafa et al., 2009; Kajimura to hemoglobin, potentially prevent adequate O2 delivery to tissues by et al., 2010; Prabhakar, 2012). Therefore, low concentrations of CO lowering arterial O2 content. Elevated heme-protein concentrations, can provide beneficial and therapeutic effects up to a specific as found in marine mammals, are likely associated with greater heme concentration, at which elevated CO then leads to detrimental effects degradation, more endogenous CO production and, consequently, from reduced O2 delivery. These relatively recent findings give CO elevated COHb concentrations. Therefore, we measured COHb in a new functional perspective and emphasize the importance of elephant seals, a species with large blood volumes and elevated understanding the biological effects of specific CO concentrations hemoglobin and myoglobin concentrations. The levels of COHb were in the body which can be viewed as therapeutic. -
Published on May 14, 2008 As Doi: 10.1183/09031936.00126507 ERJ
ERJ Express. Published on May 14, 2008 as doi: 10.1183/09031936.00126507 ACCURACY AND RELIABILITY OF PULSE OXIMETRY AT DIFFERENT PaCO2 LEVELS Authors: Muñoz Xa,b,d , Torres Fc , Sampol Ga,d , Rios Jc , Martí Sa,d , Escrich Eb a) Servei de Pneumologia,Hospital Universitari Vall d’Hebron, Barcelona, Spain b) Departament de Biología Cel·lular, de Fisiologia i d’Immunologia, UAB, Barcelona, Spain c) Laboratorio de Bioestadística i Epidemiología (Universitat Autònoma de Barcelona); Servei de Farmacologia Clínica, IDIBAPS, (Hospital Clínic), Barcelona d) CIBER de Enfermedades Respiratorias (Ciberes) Correspondence to: Dr. Xavier Muñoz Servei de Pneumologia Hospital Vall d'Hebron Pº Vall d'Hebron, 119-129 08035 Barcelona Spain Telf: 00 34 93 2746157 Fax: 00 34 93 2746083 E-mail: [email protected] Short title: ACCURACY OF PULSE OXIMETRY AND PaCO2 LEVELS The first two authors have contributed equally to this study. Copyright 2008 by the European Respiratory Society. ABSTRACT Aim: To assess whether arterial carbon dioxide pressure (PaCO2) has an impact on agreement between oxygen saturation measured with pulse oximetry (SpO2) or arterial blood gas co- oximetry (SaO2). Methods: A study was performed on SaO2 and SpO2 determinations obtained simultaneously from 846 patients under assessment for long-term home oxygen therapy in a specialized outpatient clinic. Both measurements were taken with patients seated and breathing room air. Agreement between SaO2 and SpO2 results was analyzed by the Bland-Altman method and the Lin concordance coefficient. In addition, potential interactions of PaO2 or PaCO2 on agreement were analyzed by adjusted multivariate analysis. Results: At comparison of SaO2 and SpO2 results, the Bland-Altman technique yielded a bias (95% CI) of -1.24 (-6.86; 4.38) and -1.32 (-7.78; 5.15) when PaCO2 was higher than 48 mmHg or PaO2 lower than 54 mmHg, respectively. -
Titanium Dioxide Production Final Rule: Mandatory Reporting of Greenhouse Gases
Titanium Dioxide Production Final Rule: Mandatory Reporting of Greenhouse Gases Under the Mandatory Reporting of Greenhouse Gases (GHGs) rule, owners or operators of facilities that contain titanium dioxide production processes (as defined below) must report emissions from titanium dioxide production and all other source categories located at the facility for which methods are defined in the rule. Owners or operators are required to collect emission data; calculate GHG emissions; and follow the specified procedures for quality assurance, missing data, recordkeeping, and reporting. How Is This Source Category Defined? The titanium dioxide production source category consists of any facility that uses the chloride process to produce titanium dioxide. What GHGs Must Be Reported? Each titanium dioxide production facility must report carbon dioxide (CO2) process emissions from each chloride process line. In addition, each facility must report GHG emissions for other source categories for which calculation methods are provided in the rule. For example, facilities must report CO2, nitrous oxide (N2O), and methane (CH4) emissions from each stationary combustion unit on site by following the requirements of 40 CFR part 98, subpart C (General Stationary Fuel Combustion Sources). Please refer to the relevant information sheet for a summary of the rule requirements for calculating and reporting emissions from any other source categories at the facility. How Must GHG Emissions Be Calculated? Reporters must calculate CO2 process emissions using one of two methods, as appropriate: • Installing and operating a continuous emission monitoring system (CEMS) according to the requirements specified in 40 CFR part 98, subpart C. • Calculating the process CO2 emissions for each process line using monthly measurements of the mass and carbon content of calcined petroleum coke.