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1

Hartley, James Holroyd. Saccharide accelerated hydrolysis of boronic acid imines. Birmingham: University of Birmingham, 2000.

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2

Vecil, Giacomo G. Pharmacological characterization of excitatory amino acid-induced polyphosphoinositide hydrolysis. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1992.

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3

F, Harris John, and Forest Products Laboratory (U.S.), eds. Two-stage, dilute sulfuric acid hydrolysis of wood: An investigation of fundamentals. [Madison, Wis.]: U.S. Dept. of Agriculture, Forest Service, Forest Products Laboratory, 1985.

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4

Zerbe, John I. Investigation of fundamentals of two-stage, dilute sulfuric acid hydrolysis of wood. [Madison, Wis.?: Forest Products Laboratory, 1988.

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5

Zerbe, John I. Investigation of fundamentals of two-stage, dilute sulfuric acid hydrolysis of wood. [Madison, Wis.?: Forest Products Laboratory, 1988.

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6

Brenner, Walter. High temperature dilute acid hydrolysis of waste cellulose: Batch and continuous processes. Cincinnati, OH: Hazardous Waste Engineering Research Laboratory, U.S. Environmental Protection Agency, 1986.

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7

Zerbe, John I. Investigation of fundamentals of two-stage, dilute sulfuric acid hydrolysis of wood. [Madison, Wis.?: Forest Products Laboratory, 1988.

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8

1940-, Harris John Frank, and Forest Products Laboratory (U.S.), eds. Two-stage, dilute sulfuric acid hydrolysis of wood: An investigation of fundamentals. [Madison, Wis.]: U.S. Dept. of Agriculture, Forest Service, Forest Products Laboratory, 1985.

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9

1940-, Harris John Frank, and Forest Products Laboratory (U.S.), eds. Two-stage, dilute sulfuric acid hydrolysis of wood: An investigation of fundamentals. [Madison, Wis.]: U.S. Dept. of Agriculture, Forest Service, Forest Products Laboratory, 1985.

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10

1940-, Harris John Frank, and Forest Products Laboratory (U.S.), eds. Two-stage, dilute sulfuric acid hydrolysis of wood: An investigation of fundamentals. [Madison, Wis.]: U.S. Dept. of Agriculture, Forest Service, Forest Products Laboratory, 1985.

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11

Maloney, Mark T. An engineering analysis of the production of xylose by dilute acid hydrolysis of hardwood hemicellulose. Madison, WI: Forest Products Laboratory, 1987.

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12

Maloney, Mark T. An engineering analysis of the production of xylose by dilute acid hydrolysis of hardwood hemicellulose. Madison, WI: Forest Products Laboratory, 1987.

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13

Maloney, Mark T. An engineering analysis of the production of xylose by dilute acid hydrolysis of hardwood hemicellulose. Madison, WI: Forest Products Laboratory, 1987.

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14

Occupational Medicine and Hygiene Laboratory. Aromatic isocyanates in air: Field method using acid hydrolysis, diazotisation and coupling with N-2-aminoethyl-1-naphthylamine. Bootle: Health and Safety Executive, 1985.

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15

Humbird, David. Process design and economics for biochemical conversion of lignocellulosic biomass to ethanol: Dilute-acid pretreatment and enzymatic hydrolysis of corn stover. Golden, CO: National Renewable Energy Laboratory, 2011.

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16

Sheng wu zhi ji yi xian bing suan hua xue yu ji shu. Beijing Shi: Hua xue gong ye chu ban she, 2009.

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17

Atmospheric Research and Exposure Assessment Laboratory (U.S.), ed. Analytical method evaluation for ethylene oxide emissions from commercial dilute-acid hydrolytic control units: Project summary. Research Triangle Park, NC: U.S. Environmental Protection Agency, Atmospheric Research and Exposure Assessment Laboratory, 1989.

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18

Burton, R. J. Mild acid hydrolysis of wood. 1986.

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19

Two-stage, dilute sulfuric acid hydrolysis of wood: An investigation of fundamentals. [Madison, Wis.]: U.S. Dept. of Agriculture, Forest Service, Forest Products Laboratory, 1985.

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20

Lignocellulosic biomass to ethanol process design and economics utilizing co-current dilute acid prehydrolysis and enzymatic hydrolysis current and futuristic scenarios. Golden, Colo. (1617 Cole Boulevard, Golden 80401-3393): National Renewable Energy Laboratory, 1999.

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21

Hydrolysis of dihydrouridine and related compounds. [Washington, DC: National Aeronautics and Space Administration, 1996.

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22

Columb, Malachy O. Local anaesthetic agents. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0017.

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Local anaesthetic agents cause a pharmacologically induced reversible neuropathy characterized by axonal conduction blockade. They act by blocking the sodium ionophore and exhibit membrane stabilizing activity by inhibiting initiation and propagation of action potentials. They are weak bases consisting of three components: a lipophilic aromatic ring, a link, and a hydrophilic amine. The chemical link classifies them as esters or amides. Local anaesthetics diffuse through the axolemma as unionized free-base and block the ionophore in the quaternary ammonium ionized form. The speed of onset of block is therefore dependent on the pKa of the agent and the ambient tissue pH. Esters undergo hydrolysis by plasma esterases and amides are metabolized by hepatic microsomal mixed-function oxidases. Local anaesthetics are bound in the blood to α‎1-acid glycoproteins. Pharmacological potency is dependent on the lipid solubility of the drug as is the potential for systemic toxicity. The blood concentrations required to cause cardiovascular system (CVS) collapse and early central nervous system (CNS) toxicity are used to quantify the CVS:CNS toxicity ratio. Local anaesthetics also have the potential to induce direct neuronal damage. Intravenous lipid emulsion is used for the treatment of systemic toxicity but the scientific evidence is inconsistent. With regard to the pipecoloxylidine local anaesthetics, early evidence indicated that the S- was less toxic than the R-enantiomer. However, clinical research using minimum local analgesic concentration designs suggests that reduced systemic toxicity and motor block sparing is mainly explained by potency rather than enantiomerism.
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23

Olkkola, Klaus T., Hugo E. M. Vereecke, and Martin Luginbühl. Drug interactions in anaesthetic practice. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0021.

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When two or more drugs are administered simultaneously, the pharmacological response may be greater or less than the sum of the effects of the individual drugs. One drug may antagonize or potentiate the effects of the other and there may be also qualitative differences in response. Although some drug interactions increase the toxicity or result in loss of therapeutic effect, others are beneficial. Indeed, modern anaesthetic techniques depend on beneficial drug interactions. A sound combination of drugs helps clinicians to increase both the efficacy and safety of drug treatment. Drugs may interact on a pharmaceutical, pharmacodynamic, or pharmacokinetic basis. Many pharmacodynamic interactions are predictable and can be avoided by the use of common sense. However, it is much more difficult to predict the likelihood of pharmacokinetic and pharmaceutical interactions despite good prior knowledge of pharmacokinetics and chemical properties of individual drugs. Pharmaceutical drug interactions usually occur before the drug is given to the patient and they are caused by chemical (such as acid–base, salt formation, oxidation–reduction, hydrolysis, or epimerization) or physical (such as adsorption/absorption or emulsion breaking) reactions. When drugs have a pharmacokinetic interaction, one drug alters the absorption, distribution, or the elimination of the other drug. Many pharmacokinetic drug interactions are due to inhibition or induction of cytochrome P450 enzymes. Pharmacodynamic drug interactions are caused by drugs having an effect on the same receptors or the same physiological system. This chapter gives anaesthetists an overview of clinically relevant perioperative drug interactions.
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