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Books on the topic 'Oxidative stress responses'

Author: Grafiati

Published: 7 September 2021

Last updated: 29 July 2025

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1

Requena, Jose M. Stress response in microbiology. Caister Academic Press, 2012.

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2

1946-, Pasquier C., ed. Oxidative stress, cell activation and viral infection. Birkhäuser Verlag, 1994.

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3

O'Farrell, Francis J. An investigation of the response to lymphoid cells to oxidative stress. The Author], 1996.

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4

Soosay, Ashley Edward. A Gene complementation strategy in cloning an oxidative stress response gene of campylobacter jejuni. National Library of Canada, 1998.

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5

Poljsak, Borut, and Irina Milisav. What Doesn't Kill Us, Makes Us Stronger: Reducing Oxidative Stress and Damage Through Adaptive Stress Responses. Nova Science Publishers, Incorporated, 2014.

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6

Kim, Raymond H. DJ-1 regulates tumour suppression by PTEN and cellular responses to oxidative stress in Parkinson's disease. 2006.

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7

Breusegem, Frank Van, and Ron Mittler. Oxidative Stress Response in Plants. Elsevier Science & Technology, 2023.

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8

Breusegem, Frank Van, and Ron Mittler. Oxidative Stress Response in Plants. Elsevier Science & Technology Books, 2023.

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9

Gasz, Balazs. Inflammatory Response and Oxidative Stress Related to Cardiopulmonary Bypass. VDM Verlag, 2008.

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10

The unfolded protein response und cellular stress. Elsevier, 2011.

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11

Khan, Nafees, ed. Plant Response and Tolerance to Abiotic Oxidative Stress: Antioxidant Machinery as a Paradigm of Defense. MDPI, 2023. http://dx.doi.org/10.3390/books978-3-0365-7783-8.

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12

Pantola, R. C. Intracellular Copper Accumulation and Biochemical Changes in Response to Cu Induced Oxidative Stress in Brassica Species. GRIN Verlag GmbH, 2016.

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13

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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14

Madl, Ulrike. Pathophysiology of glucose control. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0258.

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Hyperglycaemia is a frequent phenomenon in critically-ill patients, associated with increased morbidity and mortality. Hyperglycaemia results in cellular glucose overload and toxic adverse effects of glycolysis and oxidative phosphorylation, especially in tissues with insulin-independent glucose uptake, and acute hyperglycaemia can exert a variety of negative effects. It is the main side effect of intensive insulin therapy. Both severe and moderate hypoglycaemia are independent risk factors of mortality in critically-ill patients. Prolonged hypoglycaemia induces neuronal damage, but may also h

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15

Laumbach, Robert, and Michael Gochfeld. Toxicology. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190662677.003.0007.

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This chapter describes the basic principles of toxicology and their application to occupational and environmental health. Topics covered include pathways that toxic substances may take from sources in the environment to molecular targets in the cells of the body where toxic effects occur. These pathways include routes of exposure, absorption into the body, distribution to organs and tissues, metabolism, storage, and excretion. The various types of toxicological endpoints are discussed, along with the concepts of dose-response relationships, threshold doses, and the basis of interindividual dif

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16

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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17

Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi, and Brian B. Ratliff. Pathophysiology of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0221.

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In the intricate maze of proposed mechanisms, modifiers, modulators, and sensitizers for acute kidney injury (AKI) and diverse causes inducing it, this chapter focuses on several common and undisputable strands which do exist.Structurally, the loss of the brush border, desquamation of tubular epithelial cells, and obstruction of the tubular lumen are commonly observed, albeit to various degrees. These morphologic hallmarks of AKI are accompanied by functional defects, most consistently reflected in the decreased glomerular filtration rate and variable degree of reduction in renal blood flow, a

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18

Ho, Vanessa P., and Philip S. Barie. Acute acalculous cholecystitis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0188.

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Acute acalculous cholecystitis (AAC) may occur in surgical or injured, critically-ill, and systemically-ill patients, with diabetes mellitus, malignant disease, abdominal vasculitis, congestive heart failure, cholesterol embolization, shock, and cardiac arrest. Children may also be affected, especially following a viral illness. The pathogenesis of AAC is complex and multifactorial. Ischaemia/reperfusion injury and the associated pro-inflammatory response and oxidative tissue stress, appear to be the central mechanisms, but bile stasis, opioid therapy, positive-pressure ventilation, and parent

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19

Nicholson, Grainne, and George M. Hall. Neuroendocrine physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0008.

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This chapter describes the hormonal, metabolic, and inflammatory response to surgery—commonly known as the surgical stress response. The changes in protein, carbohydrate, and fat metabolism to provide fuel for oxidation are outlined as well as changes in salt and water metabolism. Psychological sequelae of fatigue and malaise are also common in patients undergoing surgery. Attenuating the metabolic and endocrine changes associated with surgery may reduce postoperative morbidity and expedite recovery; the choice of anaesthetic drugs and techniques (regional vs general anaesthesia) and the incre

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20

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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