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Relevant bibliographies by topics / Oxidative stress ; nitrotyrosine ; inflammation / Books

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Books on the topic 'Oxidative stress ; nitrotyrosine ; inflammation'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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1

Bondy, Stephen C., and Arezoo Campbell, eds. Inflammation, Aging, and Oxidative Stress. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-33486-8.

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2

Farooqui, Akhlaq A. Inflammation and Oxidative Stress in Neurological Disorders. Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-04111-7.

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3

Soares, Raquel, and Carla Costa, eds. Oxidative Stress, Inflammation and Angiogenesis in the Metabolic Syndrome. Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-1-4020-9701-0.

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4

Carla, Costa, and SpringerLink (Online service), eds. Oxidative Stress, Inflammation and Angiogenesis in the Metabolic Syndrome. Springer Netherlands, 2009.

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5

Kong, Ah-Ng Tony. Inflammation, oxidative stress, and cancer: Dietary approaches for cancer prevention. Taylor & Francis, 2014.

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6

Camps, Jordi, ed. Oxidative Stress and Inflammation in Non-communicable Diseases - Molecular Mechanisms and Perspectives in Therapeutics. Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-07320-0.

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7

Italy) International Conference on Environmental Stressors in Biology and Medicine (2nd 2011 Siena. Environmental stressors in biology and medicine. Edited by Valacchi Giuseppe. Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2012.

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8

Bondy, Stephen C., and Arezoo Campbell. Inflammation, Aging, and Oxidative Stress. Springer, 2018.

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9

Surh, Young-Joon. Oxidative Stress, Inflammation, and Health. Taylor & Francis Group, 2005.

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10

Kong, Ah-Ng Tony, ed. Inflammation, Oxidative Stress, and Cancer. CRC Press, 2016. http://dx.doi.org/10.1201/b15323.

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11

Young-Joon, Surh, and Packer Lester, eds. Oxidative stress, inflammation, and health. Taylor & Francis, 2005.

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12

1957-, Chauhan Abha, Chauhan Ved, and Brown Ted 1946-, eds. Autism: Oxidative stress, inflammation, and immune abnormalities. Taylor & Francis, 2010.

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13

1957-, Chauhan Abha, Chauhan Ved, and Brown Ted 1946-, eds. Autism: Oxidative stress, inflammation, and immune abnormalities. Taylor & Francis, 2010.

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14

Chauhan, Abha, Ted Brown, and Ved Chauhan. Autism: Oxidative Stress, Inflammation, and Immune Abnormalities. Taylor & Francis Group, 2009.

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15

1957-, Chauhan Abha, Chauhan Ved, and Brown Ted 1946-, eds. Autism: Oxidative stress, inflammation, and immune abnormalities. Taylor & Francis, 2010.

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16

Chauhan, Abha, Ted Brown, and Ved Chauhan. Autism: Oxidative Stress, Inflammation and Immune Abnormalities. CRC, 2009.

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17

Soares, Raquel, and Carla Costa. Oxidative Stress, Inflammation and Angiogenesis in the Metabolic Syndrome. Springer, 2010.

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18

Kong, Ah-Ng Tony. Inflammation, Oxidative Stress, and Cancer: Dietary Approaches for Cancer Prevention. Taylor & Francis Group, 2016.

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19

M, Matata Bashir, and Elahi Maqsood M, eds. Oxidative stress: Clinical and biomedical implications. Nova Biomedical Books, 2007.

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20

Oxidative Stress: Clinical and Biomedical Implications. Nova Biomedical Books, 2007.

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21

(Editor), Lester Packer, and Helmut Sies (Editor), eds. Oxidative Stress and Inflammatory Mechanisms in Obesity, Diabetes, and the Metabolic Syndrome (Oxidative Stress and Disease). CRC, 2007.

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22

Farooqui, Akhlaq A. A. Inflammation and Oxidative Stress in Neurological Disorders: Effect of Lifestyle, Genes, and Age. Springer, 2016.

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23

Farooqui, Akhlaq A. Inflammation and Oxidative Stress in Neurological Disorders: Effect of Lifestyle, Genes, and Age. Springer, 2014.

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24

Camps, Jordi. Oxidative Stress and Inflammation in Non-communicable Diseases - Molecular Mechanisms and Perspectives in Therapeutics. Springer, 2014.

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25

Oxidative Stress and Inflammation as Targets for Novel Preventive and Therapeutic Approches in Non Communicable Diseases. MDPI, 2020. http://dx.doi.org/10.3390/books978-3-03928-936-3.

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26

N. Liu, J.Q. Wang, Z.Y. Liu, Y.K. Chen, and J.P. Wang. Tetramethylpyrazine attenuates necrotic enteritis by reducing gut oxidative stress, inflammation, opportunistic bacteria and endotoxins in broilers. Verlag Eugen Ulmer, 2018. http://dx.doi.org/10.1399/eps.2018.233.

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27

Oxidative stress and inflammatory mechanisms in obesity, diabetes, and the metabolic syndrome. CRC Press/Taylor & Francis, 2007.

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28

Lester, Packer, and Sies H. 1942-, eds. Oxidative stress and inflammatory mechanisms in obesity, diabetes, and the metabolic syndrome. CRC Press, 2008.

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29

Oxidative stress and inflammatory mechanisms in obesity, diabetes, and the metabolic syndrome. CRC Press, 2008.

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30

Particle Toxicology. CRC, 2006.

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31

DSc, Donaldson Kenneth, and Borm Paul, eds. Particle toxicology. CRC Press/Taylor & Francis Group, 2007.

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32

Falk, Katherine, Barbara Bartlik, and Janet Mindes. Inflammation and the Gut–Brain–Mood Connection (DRAFT). Edited by Madeleine M. Castellanos. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190225889.003.0014.

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Inflammation, oxidative stress, dysbiosis, and increased gut permeability (leaky gut) are now understood to be among the causative factors in depression, other psychiatric illnesses, and sexual dysfunction. This new appreciation of psychiatric illness as a systemic illness, occurring in the body as well as in the brain, offers new ways to understand and treat sexual problems such as polycystic ovary syndrome and erectile dysfunction. Leaky gut can be caused by medications such as antibiotics, NSAIDS, or aspirin; drinking alcohol; or the proinflammatory standard American diet. As conventional t

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33

Becker, Jeffrey. Nutraceutical Treatments for Addiction Recovery. Edited by Shahla J. Modir and George E. Muñoz. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190275334.003.0020.

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Current medical treatment in substance-use disorders and addiction recovery often fails to address the underlying molecular pathophysiologic mechanisms of addiction morbidity. Psychopharmacology and behavioral interventions do not directly address the cellular patterns of dysfunction in addiction but natural treatments can and should be employed in a research-based manner to support existing treatment protocols. Research into addiction pathophysiology is clear: removing the offending agent through sobriety is often not enough to restore natural premorbid physiology. Drug-induced oxidative stre

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34

Annane, Djillali, and B. Jérôme Aboab. Management of carbon monoxide poisoning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0328.

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CO poisoning is the commonest cause of toxic death. Carbon monoxide is colourless, odourless, and tasteless, and is produced under various conditions. When people inhale CO, the gas diffuses rapidly to the body and replaces oxygen at the level of haemoglobin, myoglobin, and other oxygen carriers. Subsequently, CO causes oxygen deprivation of all body tissues. CO also induces oxidative stress and systemic inflammation. After CO poisoning a broad variety of symptoms may occur. Survivors of CO poisoning often present with persistent neurological sequels or develop delayed neurological symptoms. T

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35

Poff, Angela M., Shannon L. Kesl, and Dominic P. D’Agostino. Ketone Supplementation for Health and Disease. Edited by Dominic P. D’Agostino. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0032.

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Exogenous ketone supplements rapidly elevate blood ketones in a dose-dependent manner regardless of dietary intake, making them a practical method of inducing therapeutic ketosis for medical use. It is thought that ketone supplementation could be used as a stand-alone therapy, or as a way to further augment the therapeutic efficacy of the ketogenic diet. Ketone supplementation could increase treatment compliance by allowing many patients to maintain a more normal lifestyle with a less restrictive diet. The therapeutic effects of ketone supplementation are likely mediated in part by a stabiliza

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36

Jay, Taylor R., Shane M. Bemiller, Lee E. Neilson, Paul J. Cheng-Hathaway, and Bruce T. Lamb. Neuroinflammation and Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0004.

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Neuroinflammation has long been associated with many neurodegenerative diseases (NDDs). Immune-related genetic and environmental risk factors have recently been identified for NDDs, suggesting that neuroinflammation can play an active role in modifying NDD pathologies. Immune cells that underlie this neuroinflammatory response can have both beneficial and detrimental roles in NDDs. These cells can engage in clearance of debris and provide important survival factors to neighboring neurons. However, these cells can also release inflammatory molecules that promote oxidative stress and excitotoxic

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37

Guzik, Tomasz J., and Rhian M. Touyz. Vascular pathophysiology of hypertension. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0019.

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Hypertension is a multifactorial disease, in which vascular dysfunction plays a prominent role. It occurs in over 30% of adults worldwide and an additional 30% are at high risk of developing the disease. Vascular pathology is both a cause of the disease and a key manifestation of hypertension-associated target-organ damage. It leads to clinical symptoms and is a key risk factor for cardiovascular disease. All layers of the vascular wall and the endothelium are involved in the pathogenesis of hypertension. Pathogenetic mechanisms, whereby vascular damage contributes to hypertension, are linked

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38

Hausenloy, Derek, and Derek Yellon, eds. Novel Cardioprotective Strategies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0011.

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• Despite optimal therapy, the mortality and morbidity of coronary heart disease remains significant. Hence, novel treatment strategies of cardioprotection are required to improve clinical outcomes in these patients• Experimental studies have provided a plethora of therapeutic strategies for reducing myocardial injury, but the translation of these findings into the clinical setting has been largely disappointing. Many of these unsuccessful clinical studies have relied upon individually targeting established mediators of lethal reperfusion injury such as oxidative stress, inflammation, calcium

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39

Hughes, Jeremy. Proteinuria as a direct cause of progression. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.

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Proximal tubular cells reabsorb any filtered proteins during health via cell surface receptors such as megalin and cubulin so that very low levels of protein are present in the excreted urine. Significant proteinuria is a common finding in patients with many renal diseases. Proteinuria is a marker of glomerular damage and podocyte loss and injury in particular. The degree of proteinuria at presentation or during the course of the disease correlates with long-term outcome in many renal diseases. Proteinuria per se may be nephrotoxic and thus directly relevant to the progression of renal disease

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40

Frew, Anthony. Air pollution. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0341.

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Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household

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