European Chemicals Agency
The European Chemicals Agency is an agency of the European Union which manages the technical and administrative aspects of the implementation of the European Union regulation called Registration, Evaluation and Restriction of Chemicals. ECHA is the driving force among regulatory authorities in implementing the EU's chemicals legislation. ECHA helps companies to comply with the legislation, advances the safe use of chemicals, provides information on chemicals and addresses chemicals of concern, it is located in Finland. The agency headed by Executive Director Bjorn Hansen, started working on 1 June 2007; the REACH Regulation requires companies to provide information on the hazards and safe use of chemical substances that they manufacture or import. Companies register this information with ECHA and it is freely available on their website. So far, thousands of the most hazardous and the most used substances have been registered; the information is technical but gives detail on the impact of each chemical on people and the environment.
This gives European consumers the right to ask retailers whether the goods they buy contain dangerous substances. The Classification and Packaging Regulation introduces a globally harmonised system for classifying and labelling chemicals into the EU; this worldwide system makes it easier for workers and consumers to know the effects of chemicals and how to use products safely because the labels on products are now the same throughout the world. Companies need to notify ECHA of the labelling of their chemicals. So far, ECHA has received over 5 million notifications for more than 100 000 substances; the information is available on their website. Consumers can check chemicals in the products. Biocidal products include, for example, insect disinfectants used in hospitals; the Biocidal Products Regulation ensures that there is enough information about these products so that consumers can use them safely. ECHA is responsible for implementing the regulation; the law on Prior Informed Consent sets guidelines for the import of hazardous chemicals.
Through this mechanism, countries due to receive hazardous chemicals are informed in advance and have the possibility of rejecting their import. Substances that may have serious effects on human health and the environment are identified as Substances of Very High Concern 1; these are substances which cause cancer, mutation or are toxic to reproduction as well as substances which persist in the body or the environment and do not break down. Other substances considered. Companies manufacturing or importing articles containing these substances in a concentration above 0,1% weight of the article, have legal obligations, they are required to inform users about the presence of the substance and therefore how to use it safely. Consumers have the right to ask the retailer whether these substances are present in the products they buy. Once a substance has been identified in the EU as being of high concern, it will be added to a list; this list is available on ECHA's website and shows consumers and industry which chemicals are identified as SVHCs.
Substances placed on the Candidate List can move to another list. This means that, after a given date, companies will not be allowed to place the substance on the market or to use it, unless they have been given prior authorisation to do so by ECHA. One of the main aims of this listing process is to phase out SVHCs where possible. In its 2018 substance evaluation progress report, ECHA said chemical companies failed to provide “important safety information” in nearly three quarters of cases checked that year. "The numbers show a similar picture to previous years" the report said. The agency noted that member states need to develop risk management measures to control unsafe commercial use of chemicals in 71% of the substances checked. Executive Director Bjorn Hansen called non-compliance with REACH a "worry". Industry group CEFIC acknowledged the problem; the European Environmental Bureau called for faster enforcement to minimise chemical exposure. European Chemicals Bureau Official website
Prostaglandin-endoperoxide synthase 2
Prostaglandin-endoperoxide synthase 2 known as cyclooxygenase-2 or COX-2, is an enzyme that in humans is encoded by the PTGS2 gene. In humans it is one of two cyclooxygenases, it is involved in the conversion of arachidonic acid to prostaglandin H2, an important precursor of prostacyclin, expressed in inflammation. PTGS2, converts arachidonic acid to prostaglandin endoperoxide H2. PGHSs are targets for NSAIDs and PTGS2 specific inhibitors called coxibs. PGHS-2 is a sequence homodimer; each monomer of the enzyme has a PTGS active site. The PTGS enzymes catalyze the conversion of arachidonic acid to prostaglandins in two steps. First, hydrogen is abstracted from carbon 13 of arachidonic acid, two molecules of oxygen are added by the PTGS2, giving PGG2. Second, PGG2 is reduced to PGH2 in the peroxidase active site; the synthesized PGH2 is converted to prostaglandins, prostacyclin, or thromboxane A2 by tissue-specific isomerases. While metabolizing arachidonic acid to PGG2, COX-2 converts this fatty acid to small amounts of a racemic mixture of 15-Hydroxyicosatetraenoic acids composed of ~22% 15-HETE and ~78% 15-HETE stereoisomers as well as a small amount of 11-HETE.
The two 15-HETE stereoisomers have intrinsic biological activities but more can be further metabolized to a major class of agents, the lipoxins. Furthermore, aspirin-treated COX-2 metabolizes arachidonic acid exclusively to 15-HETE which product can be further metabolized to epi-lipoxins; the lipoxins and epi-lipoxins are potent anti-inflammatory agents and may contribute to the overall activities of the two COX's as well as to aspirin. COX-2 is inhibited by calcitriol. Both the peroxidase and PTGS activities are inactivated during catalysis by mechanism-based, first-order processes, which means that PGHS-2 peroxidase or PTGS activities fall to zero within 1–2 minutes in the presence of sufficient substrates; the conversion of arachidonic acid to PGG2 can be shown as a series of radical reactions analogous to polyunsaturated fatty acid autoxidation. The 13-pro -hydrogen is abstracted and dioxygen traps the pentadienyl radical at carbon 11; the 11-peroxyl radical cyclizes at carbon 9 and the carbon-centered radical generated at C-8 cyclizes at carbon 12, generating the endoperoxide.
The allylic radical generated is trapped by dioxygen at carbon 15 to form the 15- -peroxyl radical. This is supported by the following evidence: 1) a significant kinetic isotope effect is observed for the abstraction of the 13-pro -hydrogen. Another mechanism in which the 13-pro -hydrogen is deprotonated and the carbanion is oxidized to a radical is theoretically possible. However, oxygenation of 10,10-difluoroarachidonic acid to 11--hydroxyeicosa-5,8,12,14-tetraenoic acid is not consistent with the generation of a carbanion intermediate because it would eliminate fluoride to form a conjugated diene; the absence of endoperoxide-containing products derived from 10,10-difluoroarachidonic acid has been thought to indicate the importance of a C-10 carbocation in PGG2 synthesis. However, the cationic mechanism requires that endoperoxide formation comes before the removal of the 13-pro -hydrogen; this is not consistent with the results of the isotope experiments of arachidonic acid oxygenation. PTGS2 exists as each monomer with a molecular mass of about 70 kDa.
The tertiary and quaternary structures of PTGS1 and PTGS2 enzymes are identical. Each subunit has three different structural domains: a short N-terminal epidermal growth factor domain. PTGS enzymes are monotopic membrane proteins. PTGS1 and PTGS2 are bifunctional enzymes that carry out two consecutive chemical reactions in spatially distinct but mechanistically coupled active sites. Both the cyclooxygenase and the peroxidase active sites are located in the catalytic domain, which accounts for 80% of the protein; the catalytic domain is homologous to mammalian peroxidases such as myeloperoxidase. It has been found that human PTGS2 functions as a conformational heterodimer having a catalytic monomer and an allosteric monomer. Heme binds only to the peroxidase site of E-cat while substrates, as well as certain inhibitors, bind the COX site of E-cat. E-cat is regulated by E-allo in a way dependent on. Substrate and non-substrate fatty acid and some PTGS inhibitors preferentially bind to the PTGS site of E-allo.
Arachidonic acid can bind to E-cat and E-allo, but the affinity of AA for E-allo is 25 times that for Ecat. Palmitic acid, an efficacious stimulator of huPGHS-2, binds only E-allo in palmitic acid/murine PGHS-2 co-crystals. Non-substrate FAs can potentiate or attenuate PTGS inhibitors depending on the fatty acid and whether the inhibitor binds E-cat or E-allo. Studies suggest that the concentration and composition of the free fatty acid pool in the environment in which PGHS-2 functions in cells referred to as the FA tone, is a key factor reg
The Jmol applet, among other abilities, offers an alternative to the Chime plug-in, no longer under active development. While Jmol has many features that Chime lacks, it does not claim to reproduce all Chime functions, most notably, the Sculpt mode. Chime requires plug-in installation and Internet Explorer 6.0 or Firefox 2.0 on Microsoft Windows, or Netscape Communicator 4.8 on Mac OS 9. Jmol operates on a wide variety of platforms. For example, Jmol is functional in Mozilla Firefox, Internet Explorer, Google Chrome, Safari. Chemistry Development Kit Comparison of software for molecular mechanics modeling Jmol extension for MediaWiki List of molecular graphics systems Molecular graphics Molecule editor Proteopedia PyMOL SAMSON Official website Wiki with listings of websites and moodles Willighagen, Egon. "Fast and Scriptable Molecular Graphics in Web Browsers without Java3D". Doi:10.1038/npre.2007.50.1
Nonsteroidal anti-inflammatory drug
Nonsteroidal anti-inflammatory drugs are a drug class that reduce pain, decrease fever, prevent blood clots and, in higher doses, decrease inflammation. Side effects depend on the specific drug, but include an increased risk of gastrointestinal ulcers and bleeds, heart attack and kidney disease; the term nonsteroidal distinguishes these drugs from steroids, which while having a similar eicosanoid-depressing, anti-inflammatory action, have a broad range of other effects. First used in 1960, the term served to distance these medications from steroids, which where stigmatised at the time due to the connotations with anabolic steroid abuse. NSAIDs work by inhibiting the activity of cyclooxygenase enzymes. In cells, these enzymes are involved in the synthesis of key biological mediators, namely prostaglandins which are involved in inflammation, thromboxanes which are involved in blood clotting. There are two types of NSAID available: COX-2 selective. Most NSAIDs are non-selective, inhibit the activity of both COX-1 and COX-2.
These NSAIDs, while reducing inflammation inhibit platelet aggregation and increase the risk of gastrointestinal ulcers/bleeds. COX-2 selective inhibitors have less gastrointestinal side effects, but promote thrombosis and increase the risk of heart attack; as a result, COX-2 selective inhibitors are contraindicated due to the high risk of undiagnosed vascular disease. These differential effects are due to the different roles and tissue localisations of each COX isoenzyme. By inhibiting physiological COX activity, all NSAIDs increase the risk of kidney disease and, through a related mechanism, heart attack; the most prominent NSAIDs are aspirin and naproxen, all available over the counter in most countries. Paracetamol is not considered an NSAID because it has only minor anti-inflammatory activity, it treats pain by blocking COX-2 in the central nervous system, but not much in the rest of the body. NSAIDs are used for the treatment of acute or chronic conditions where pain and inflammation are present.
NSAIDs are used for the symptomatic relief of the following conditions: Aspirin, the only NSAID able to irreversibly inhibit COX-1, is indicated for antithrombosis through inhibition of platelet aggregation. This is useful for the management of arterial thrombosis and prevention of adverse cardiovascular events like heart attacks. Aspirin inhibits platelet aggregation by inhibiting the action of thromboxane A2. In a more specific application, the reduction in prostaglandins is used to close a patent ductus arteriosus in neonates if it has not done so physiologically after 24 hours. NSAIDs are useful in the management of post-operative dental pain following invasive dental procedures such as dental extraction; when not contra-indicated they are favoured over the use of paracetamol alone due to the anti-inflammatory effect they provide. When used in combination with paracetamol the analgesic effect has been proven to be improved. There is weak evidence suggesting that taking pre-operative analgesia can reduce the length of post operative pain associated with placing orthodontic spacers under local anaesthetic.
Combination of NSAIDs with pregabalin as preemptive analgesia has shown promising results for decreasing post operative pain intensity. The effectiveness of NSAID's for treating non-cancer chronic pain and cancer-related pain in children and adolescents is not clear. There have not been sufficient numbers of high-quality randomized controlled trials conducted. NSAIDs may be used with caution by people with the following conditions: Irritable bowel syndrome Persons who are over age 50, who have a family history of GI problems Persons who have had past GI problems from NSAID useNSAIDs should be avoided by people with the following conditions: The widespread use of NSAIDs has meant that the adverse effects of these drugs have become common. Use of NSAIDs increases risk of a range of gastrointestinal problems, kidney disease and adverse cardiovascular events; as used for post-operative pain, there is evidence of increased risk of kidney complications. Their use following gastrointestinal surgery remains controversial, given mixed evidence of increased risk of leakage from any bowel anastomosis created.
An estimated 10–20% of NSAID patients experience dyspepsia. In the 1990s high doses of prescription NSAIDs were associated with serious upper gastrointestinal adverse events, including bleeding. Over the past decade, deaths associated with gastric bleeding have declined. NSAIDs, like all drugs, may interact with other medications. For example, concurrent use of NSAIDs and quinolones may increase the risk of quinolones' adverse central nervous system effects, including seizure. There is an argument over the benefits and risks of NSAIDs for treating chronic musculoskeletal pain; each drug has a benefit-risk profile and balancing the risk of no treatment with the competing potential risks of various therapies is the clinician's responsibility. If a COX-2 inhibitor is taken, a traditional NSAID should not be taken at the same time. In addition, people on daily aspirin therapy must be careful if they use other NSAIDs, as these may inhibit the cardioprotective effects of aspirin. Rofecoxib was shown to produce fewer gastrointestinal adverse drug reactions compared with naproxen.
This study, the VIGOR trial, raised the issue of the cardiovascular safety of the coxibs. A statistically significant increase in the incidence of myocardial infarctions was observed in patients on rofecoxib. Further data, from the APPROVe trial, s
Salicylic acid is a lipophilic monohydroxybenzoic acid, a type of phenolic acid, a beta hydroxy acid. It has the formula C7H6O3; this colorless crystalline organic acid is used in organic synthesis and functions as a plant hormone. It is derived from the metabolism of salicin. In addition to serving as an important active metabolite of aspirin, which acts in part as a prodrug to salicylic acid, it is best known for its use as a key ingredient in topical anti-acne products; the salts and esters of salicylic acid are known as salicylates. It is on the WHO Model List of Essential Medicines, the most important medications needed in a basic health system. Salicylic acid as a medication is used most to help remove the outer layer of the skin; as such, it is used to treat warts, acne, ringworm and ichthyosis. Similar to other hydroxy acids, salicylic acid is a key ingredient in many skincare products for the treatment of seborrhoeic dermatitis, psoriasis, corns, keratosis pilaris, acanthosis nigricans and warts.
Salicylic acid is used in the production of other pharmaceuticals, including 4-aminosalicylic acid and landetimide. Salicylic acid was one of the original starting materials for making acetylsalicylic acid in 1897. Bismuth subsalicylate, a salt of bismuth and salicylic acid, is the active ingredient in stomach relief aids such as Pepto-Bismol, is the main ingredient of Kaopectate and "displays anti-inflammatory action and acts as an antacid and mild antibiotic". Other derivatives include methyl salicylate used as a liniment to soothe joint and muscle pain and choline salicylate used topically to relieve the pain of mouth ulcers. Salicylic acid is used as a bactericidal and an antiseptic. Sodium salicylate is a useful phosphor in the vacuum ultraviolet spectral range, with nearly flat quantum efficiency for wavelengths between 10 and 100 nm, it fluoresces in the blue at 420 nm. It is prepared on a clean surface by spraying a saturated solution of the salt in methanol followed by evaporation. Aspirin can be prepared by the esterification of the phenolic hydroxyl group of salicylic acid with the acetyl group from acetic anhydride or acetyl chloride.
Salicylic acid directly and irreversibly inhibits the activity of both types of cyclo-oxygenases to decrease the formation of precursors of prostaglandins and thromboxanes from arachidonic acid. Salicylate may competitively inhibit prostaglandin formation. Salicylate's antirheumatic actions are a result of its anti-inflammatory mechanisms. Salicylic acid works by causing the cells of the epidermis to slough off more preventing pores from clogging up, allowing room for new cell growth. Salicylic acid inhibits the oxidation of uridine-5-diphosphoglucose competitively with nicotinamide adenosine dinucleotide and noncompetitively with UDPG, it competitively inhibits the transferring of glucuronyl group of uridine-5-phosphoglucuronic acid to the phenolic acceptor. The wound-healing retardation action of salicylates is due to its inhibitory action on mucopolysaccharide synthesis; as a topical agent and as a beta-hydroxy acid, salicylic acid is capable of penetrating and breaking down fats and lipids, causing moderate chemical burns of the skin at high concentrations.
It may damage the lining of pores if the solvent is acetone or an oil. Over-the-counter limits are set at 2% for topical preparations expected to be left on the face and 3% for those expected to be washed off, such as acne cleansers or shampoo. For wart removal, such a solution should be applied once or twice a day – more frequent use may lead to an increase in side-effects without an increase in efficacy; some people are hypersensitive to related compounds. If high concentrations of salicylic ointment are applied to a large percentage of body surface, high levels of salicylic acid can enter the blood, requiring hemodialysis to avoid further complications. Salicylic acid has the formula C6H4COOH, it is known as 2-hydroxybenzoic acid. It is poorly soluble in water. Salicylic acid is biosynthesized from the amino acid phenylalanine. In Arabidopsis thaliana it can be synthesized via a phenylalanine-independent pathway. Sodium salicylate is commercially prepared by treating sodium phenolate with carbon dioxide at high pressure and high temperature – a method known as the Kolbe-Schmitt reaction.
Acidification of the product with sulfuric acid gives salicylic acid: It can be prepared by the hydrolysis of aspirin or methyl salicylate with a strong acid or base. Hippocrates, Pliny the Elder and others knew that willow bark could ease pain and reduce fevers, it was used in China to treat these conditions. This remedy is mentioned in texts from ancient Egypt and Assyria; the Cherokee and other Native Americans used an infusion of the bark for fever and other medicinal purposes. In 2014, archaeologists identified traces of salicylic acid on 7th century pottery fragments found in east central Colorado; the Reverend Edward Stone, a vicar from Chipping Norton, Engla
Simplified molecular-input line-entry system
The simplified molecular-input line-entry system is a specification in the form of a line notation for describing the structure of chemical species using short ASCII strings. SMILES strings can be imported by most molecule editors for conversion back into two-dimensional drawings or three-dimensional models of the molecules; the original SMILES specification was initiated in the 1980s. It has since been extended. In 2007, an open standard called. Other linear notations include the Wiswesser line notation, ROSDAL, SYBYL Line Notation; the original SMILES specification was initiated by David Weininger at the USEPA Mid-Continent Ecology Division Laboratory in Duluth in the 1980s. Acknowledged for their parts in the early development were "Gilman Veith and Rose Russo and Albert Leo and Corwin Hansch for supporting the work, Arthur Weininger and Jeremy Scofield for assistance in programming the system." The Environmental Protection Agency funded the initial project to develop SMILES. It has since been modified and extended by others, most notably by Daylight Chemical Information Systems.
In 2007, an open standard called "OpenSMILES" was developed by the Blue Obelisk open-source chemistry community. Other'linear' notations include the Wiswesser Line Notation, ROSDAL and SLN. In July 2006, the IUPAC introduced the InChI as a standard for formula representation. SMILES is considered to have the advantage of being more human-readable than InChI; the term SMILES refers to a line notation for encoding molecular structures and specific instances should be called SMILES strings. However, the term SMILES is commonly used to refer to both a single SMILES string and a number of SMILES strings; the terms "canonical" and "isomeric" can lead to some confusion when applied to SMILES. The terms are not mutually exclusive. A number of valid SMILES strings can be written for a molecule. For example, CCO, OCC and CC all specify the structure of ethanol. Algorithms have been developed to generate the same SMILES string for a given molecule; this SMILES is unique for each structure, although dependent on the canonicalization algorithm used to generate it, is termed the canonical SMILES.
These algorithms first convert the SMILES to an internal representation of the molecular structure. Various algorithms for generating canonical SMILES have been developed and include those by Daylight Chemical Information Systems, OpenEye Scientific Software, MEDIT, Chemical Computing Group, MolSoft LLC, the Chemistry Development Kit. A common application of canonical SMILES is indexing and ensuring uniqueness of molecules in a database; the original paper that described the CANGEN algorithm claimed to generate unique SMILES strings for graphs representing molecules, but the algorithm fails for a number of simple cases and cannot be considered a correct method for representing a graph canonically. There is no systematic comparison across commercial software to test if such flaws exist in those packages. SMILES notation allows the specification of configuration at tetrahedral centers, double bond geometry; these are structural features that cannot be specified by connectivity alone and SMILES which encode this information are termed isomeric SMILES.
A notable feature of these rules is. The term isomeric SMILES is applied to SMILES in which isotopes are specified. In terms of a graph-based computational procedure, SMILES is a string obtained by printing the symbol nodes encountered in a depth-first tree traversal of a chemical graph; the chemical graph is first trimmed to remove hydrogen atoms and cycles are broken to turn it into a spanning tree. Where cycles have been broken, numeric suffix labels are included to indicate the connected nodes. Parentheses are used to indicate points of branching on the tree; the resultant SMILES form depends on the choices: of the bonds chosen to break cycles, of the starting atom used for the depth-first traversal, of the order in which branches are listed when encountered. Atoms are represented by the standard abbreviation of the chemical elements, in square brackets, such as for gold. Brackets may be omitted in the common case of atoms which: are in the "organic subset" of B, C, N, O, P, S, F, Cl, Br, or I, have no formal charge, have the number of hydrogens attached implied by the SMILES valence model, are the normal isotopes, are not chiral centers.
All other elements must be enclosed in brackets, have charges and hydrogens shown explicitly. For instance, the SMILES for water may be written as either O or. Hydrogen may be written as a separate atom; when brackets are used, the symbol H is added if the atom in brackets is bonded to one or more hydrogen, followed by the number of hydrogen atoms if greater than 1 by the sign + for a positive charge or by - for a negative charge. For example, for ammonium. If there is more than one charge, it is written as digit.
The melting point of a substance is the temperature at which it changes state from solid to liquid. At the melting point the solid and liquid phase exist in equilibrium; the melting point of a substance depends on pressure and is specified at a standard pressure such as 1 atmosphere or 100 kPa. When considered as the temperature of the reverse change from liquid to solid, it is referred to as the freezing point or crystallization point; because of the ability of some substances to supercool, the freezing point is not considered as a characteristic property of a substance. When the "characteristic freezing point" of a substance is determined, in fact the actual methodology is always "the principle of observing the disappearance rather than the formation of ice", that is, the melting point. For most substances and freezing points are equal. For example, the melting point and freezing point of mercury is 234.32 kelvins. However, certain substances possess differing solid-liquid transition temperatures.
For example, agar melts at 85 °C and solidifies from 31 °C. The melting point of ice at 1 atmosphere of pressure is close to 0 °C. In the presence of nucleating substances, the freezing point of water is not always the same as the melting point. In the absence of nucleators water can exist as a supercooled liquid down to −48.3 °C before freezing. The chemical element with the highest melting point is tungsten, at 3,414 °C; the often-cited carbon does not melt at ambient pressure but sublimes at about 3,726.85 °C. Tantalum hafnium carbide is a refractory compound with a high melting point of 4215 K. At the other end of the scale, helium does not freeze at all at normal pressure at temperatures arbitrarily close to absolute zero. Many laboratory techniques exist for the determination of melting points. A Kofler bench is a metal strip with a temperature gradient. Any substance can be placed on a section of the strip, revealing its thermal behaviour at the temperature at that point. Differential scanning calorimetry gives information on melting point together with its enthalpy of fusion.
A basic melting point apparatus for the analysis of crystalline solids consists of an oil bath with a transparent window and a simple magnifier. The several grains of a solid are placed in a thin glass tube and immersed in the oil bath; the oil bath is heated and with the aid of the magnifier melting of the individual crystals at a certain temperature can be observed. In large/small devices, the sample is placed in a heating block, optical detection is automated; the measurement can be made continuously with an operating process. For instance, oil refineries measure the freeze point of diesel fuel online, meaning that the sample is taken from the process and measured automatically; this allows for more frequent measurements as the sample does not have to be manually collected and taken to a remote laboratory. For refractory materials the high melting point may be determined by heating the material in a black body furnace and measuring the black-body temperature with an optical pyrometer. For the highest melting materials, this may require extrapolation by several hundred degrees.
The spectral radiance from an incandescent body is known to be a function of its temperature. An optical pyrometer matches the radiance of a body under study to the radiance of a source, calibrated as a function of temperature. In this way, the measurement of the absolute magnitude of the intensity of radiation is unnecessary. However, known temperatures must be used to determine the calibration of the pyrometer. For temperatures above the calibration range of the source, an extrapolation technique must be employed; this extrapolation is accomplished by using Planck's law of radiation. The constants in this equation are not known with sufficient accuracy, causing errors in the extrapolation to become larger at higher temperatures. However, standard techniques have been developed to perform this extrapolation. Consider the case of using gold as the source. In this technique, the current through the filament of the pyrometer is adjusted until the light intensity of the filament matches that of a black-body at the melting point of gold.
This establishes the primary calibration temperature and can be expressed in terms of current through the pyrometer lamp. With the same current setting, the pyrometer is sighted on another black-body at a higher temperature. An absorbing medium of known transmission is inserted between this black-body; the temperature of the black-body is adjusted until a match exists between its intensity and that of the pyrometer filament. The true higher temperature of the black-body is determined from Planck's Law; the absorbing medium is removed and the current through the filament is adjusted to match the filament intensity to that of the black-body. This establishes a second calibration point for the pyrometer; this step is repeated to carry the calibration to hi