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Books on the topic 'Active oxidants'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Lester, Packer, ed. Oxidants and antioxidants. San Diego: Academic Press, 1999.

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2

Baraboĭ, V. A. Okislitelʹno-antioksidantnyĭ gomeostaz v norme i patologii. Kiev: Chernobylʹinterinform, 1997.

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3

Kronhausen, Eberhard. Formula for life: The anti-oxidant, free-radical, detoxification program. New York: Morrow, 1989.

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4

International, Conference on Oxygen and Life (3rd 2000 Kyoto Japan). Oxygen and life: Oxygenases, oxidases, and lipid mediators : proceedings of the 3rd International Conference on Oxygen and Life which was held in Kyoto, between 26 and 29 November 2000. Amsterdam: Elsevier, 2002.

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5

1942-, Sies H., ed. Oxidative stress: Oxidants and antioxidants. London: Academic Press, 1991.

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6

(Editor), John N. Abelson, Melvin I. Simon (Editor), and Helmut Sies (Editor), eds. Methods in Enzymology, Volume 299: Oxidants and Antioxidants, Part A (Methods in Enzymology). Academic Press, 1998.

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7

(Editor), Jens Thiele, and Peter Elsner (Editor), eds. Oxidants and Antioxidants in Cutaneous Biology (Current Problems in Dermatology). S. Karger Publishers (USA), 2001.

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8

Fuchs, Jürgen. Environmental Stressors in Health and Disease (Oxidative Stress and Disease). CRC, 2001.

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9

F, Ursini, and Davies Kelvin J. A, eds. The oxygen paradox. Padova, Italy: CLEUP University Press, 1995.

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10

1957-, Fuchs Jürgen, and Packer Lester, eds. Environmental stressors in health and disease. New York: M. Dekker, 2001.

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11

Balz, Frei, ed. Natural antioxidants in human health and disease. San Diego: Academic Press, 1994.

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12

Catherine, Rice-Evans, ed. Free radicals, oxidant stress and drug action. London: Richelieu Press, 1987.

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13

Lameire, N. Haemodialysis And Oxidant Stress (Reprint of Blood Purification Ser. 17). Edited by N. Lameire. Karger, 1999.

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14

Redox Regulation of Cell Signaling and Its Clinical Application (Oxidative Stress and Disease, 3). CRC, 1999.

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15

Yodoi, Junji. Redox Regulation of Cell Signaling and Its Clinical Application. Taylor & Francis Group, 1999.

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16

Yodoi, Junji. Redox Regulation of Cell Signaling and Its Clinical Application. Taylor & Francis Group, 1999.

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17

Ware, Lorraine B. Pathophysiology of acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0108.

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The acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure characterized by the acute onset of non-cardiogenic pulmonary oedema due to increased lung endothelial and alveolar epithelial permeability. Common predisposing clinical conditions include sepsis, pneumonia, severe traumatic injury, and aspiration of gastric contents. Environmental factors, such as alcohol abuse and cigarette smoke exposure may increase the risk of developing ARDS in those at risk. Pathologically, ARDS is characterized by diffuse alveolar damage with neutrophilic alveolitis, haemorrhage, hyaline membrane formation, and pulmonary oedema. A variety of cellular and molecular mechanisms contribute to the pathophysiology of ARDS, including exuberant inflammation, neutrophil recruitment and activation, oxidant injury, endothelial activation and injury, lung epithelial injury and/or necrosis, and activation of coagulation in the airspace. Mechanical ventilation can exacerbate lung inflammation and injury, particularly if delivered with high tidal volumes and/or pressures. Resolution of ARDS is complex and requires coordinated activation of multiple resolution pathways that include alveolar epithelial repair, clearance of pulmonary oedema through active ion transport, apoptosis, and clearance of intra-alveolar neutrophils, resolution of inflammation and fibrinolysis of fibrin-rich hyaline membranes. In some patients, activation of profibrotic pathways leads to significant lung fibrosis with resultant prolonged respiratory failure and failure of resolution.

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18

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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