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nephrotoxicity A pathologic state that can be induced by chemicals (nephrotoxicants) and in which the normal homeostatic functioning of the kidney is impaired. It is often associated with necrosis of the proximal tubule. neurotoxicity This is a general term referring to all toxic effects on the nervous system, including toxic effects measured as behavioral abnormalities. Because the nervous system is complex, both structurally and functionally, and has considerable functional reserve, the study of neurotoxicity is a many-faceted branch of toxicology. It involves electrophysiology, receptor function, pathology, behavior, and other aspects. No Observed Effect Level (NOEL) This is the highest dose level of a chemical that, in a given toxicity test, causes no observable effect in the test animals. The NOEL for a given chemical varies with the route and duration of exposure and the nature of the adverse effect (i.e., the indicator of toxicity). The NOEL for the most sensitive test species and the most sensitive indicator of toxicity is usually employed for regulatory purposes. Effects considered are usually adverse effects, and this value may be called the No Observed Adverse Effects Level (NOAEL). Occupational Safety and Health Administration (OSHA) In the United States, OSHA is the government agency concerned with health and safety in the workplace. Through the administration of the Occupational Safety and Health Act, OSHA sets the standards for worker exposure to speci c chemicals, for air concentration values, and for monitoring procedures. OSHA is also concerned with research (through the National Institute for Occupational Safety and Health, NIOSH), information, education, and training in occupational safety and health. oncogenes Oncogenes are genes that, when activated in cells, can transform the cells from normal to neoplastic. Sometimes oncogenes are carried into normal cells by infecting viruses, particularly, RNA viruses or retroviruses. In some cases, however, the oncogene is already present in the normal human cell, and it needs only a mutation or other activating event to change it from a harmless and possible essential gene, called proto-oncogene, into a cancer-producing gene. More than 30 oncogenes have been identi ed in humans. oxidative phosphorylation The conservation of chemical energy extracted from fuel oxidations by the phosphorylation of adenosine diphosphate (ADP) by inorganic phosphate to form adenosine triphosphate (ATP) is accomplished in several ways. The majority of ATP is formed by respiratory chain-linked oxidative phosphorylation associated with the electron transport system in the mitochondrial inner membrane. The oxidations are tightly coupled to phosphorylations through a chemiosmotic mechanism in which H+ are pumped across the inner mitochondrial membrane. Uncouplers of oxidative phosphorylation serve as H+ ionophores to dissipate the H+ gradient, and thus uncouple the phosphorylations from the oxidations. oxidative stress Damage to cells and cellular constituents and processes by reactive oxygen species generated in situ. Oxidative stress may be involved in such toxic interactions as DNA damage, lipid peroxidation, and pulmonary and cardiac toxicity. Because of the transitory nature of most reactive oxygen species, although oxidative stress is often invoked as a mechanism of toxicity, rigorous proof may be lacking. partition coef cient This is a measure of the relative lipid solubility of a chemical and is determined by measuring the partitioning of the compound between an organic phase and an aqueous phase (e.g., octanol and water). The partition coef cient is important in studies of the uptake of toxicants because compounds with high
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coef cients (lipophilic compounds) are usually taken up more readily by organisms and tissues. pharmacokinetics The study of the quantitative relationship between absorption, distribution, and excretion of chemicals and their metabolites. It involves derivation of rate constants for each of these processes and their integration into mathematical models that can predict the distribution of the chemical throughout the body compartments at any point in time after administration. Pharmacokinetics have been carried out most extensively in the case of clinical drugs. When applied speci cally to toxicants, the term toxicokinetics is often used. phase I reactions These reactions introduce a reactive polar group into lipophilic xenobiotics. In most cases this group becomes the site for conjugation during phase II reactions. Such reactions include microsomal monooxygenations, cytosolic and mitochondrial oxidations, cooxidations in the prostaglandin synthetase reaction, reductions, hydrolyses, and epoxide hydrolases. The products of phase I reactions may be potent electrophiles that can be conjugated and detoxi ed in phase II reactions or that may react with nucleophilic groups on cellular constituents, thereby causing toxicity. phase II reactions Reactions involving the conjugation with endogenous substrates of phase I products and other xenobiotics that contain functional groups such as hydroxyl, amino, carboxyl, epoxide, or halogen. The endogenous metabolites include sugars, amino acids, glutathione, and sulfate. The conjugation products, with rare exceptions, are more polar, less toxic, and more readily excreted than are their parent compounds. There are two general types of conjugations: type I (e.g., glycoside and sulfate formation), in which an activated conjugating agent combines with substrate to yield the conjugated product, and type II (e.g., amino acid conjugation), in which the substrate is activated and then combines with an amino acid to yield a conjugated product. poison (toxicant) A poison (toxicant) is any substance that causes a harmful effect when administered to a living organism. Due to a popular connotation that poisons are, by de nition, fatal in their effects and that their administration is usually involved with attempted homicide or suicide, most toxicologists prefer the less prejudicial term toxicant. Poison is a quantitative concept. Almost any substance is harmful at some dose and, at the same time, is harmless at a very low dose. There is a range of possible effects, from subtle long-term chronic toxicity to immediate lethality. pollution This is contamination of soil, water, food, or the atmosphere by the discharge or admixture of noxious materials. A pollutant is any chemical or substance contamination the environment and contributing to pollution. portals of entry The sites at which xenobiotics enter the body. They include the skin, the gastrointestinal (GI) tract, and the respiratory system. potentiation See synergism and potentiation. procarcinogen See carcinogen, ultimate. promotion The facilitation of the growth and development of neoplastic cells into a tumor. This process is manifested by enhancement of carcinogenesis when the agent is given after a carcinogen. pulmonary toxicity This term refers to the effects of compounds that exert their toxic effects on the respiratory system, primarily the lungs. quantitative structure activity relationships (QSAR) The relationship between the physical and/or chemical properties of chemicals and their ability to cause a particular
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