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Книги з теми "Oxidative stress factors"

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Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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1

Packer, Lester, and Karel W. A. Wirtz, eds. Signalling Mechanisms — from Transcription Factors to Oxidative Stress. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79675-3.

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2

Saavedra-Molina, Alfredo. Mitochondrial dysfunctions related to oxidative stress. Hauppauge, N.Y: Nova Science Publishers, 2010.

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3

Packer, Lester, and Karel W. A. Wirtz. Signalling Mechanisms -- from Transcription Factors to Oxidative Stress. Springer London, Limited, 2013.

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4

Signalling mechanisms-- from transcription factors to oxidative stress. [Berlin: Springer-Verlag, 1995.

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5

Packer, Lester, and Karel W. A. Wirtz. Signalling Mechanisms - From Transcription Factors to Oxidative Stress. Springer London, Limited, 2012.

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6

Josse, Andrea R. Almonds, glycemic excursions, oxidative stress and risk factors for coronary heart disease. 2006.

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7

Hinds, Terry D. Jr, David E. Stec, and Barbara Wegiel, eds. Oxidative Stress, Antioxidants, Transcription Factors, and Assimilation of Signal Transduction Pathways in Obesity-Related Disorders. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-527-5.

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8

Shultz, Lawrence B. Cell Apoptosis: Regulation and Environmental Factors. Nova Science Publishers Inc, 2006.

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9

B, Shultz Lawrence, ed. Cell apoptosis: Regulation and environmental factors. New York: Nova Biomedical Books, 2007.

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10

Focus On Atherosclerosis Research. Nova Science Publishers, 2004.

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11

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 have adverse cardiovascular effects. Several risk factors predispose critically-ill patients to hypoglycaemic events. Rapid glucose fluctuations may induce oxidative stress and lead to vascular damage. Glucose complexity is a marker of endogenous glucose regulation. Association between hyperglycaemia and outcome is weaker in diabetic critically-ill patients than in non-diabetic patients. Pre-admission glucose control in diabetic critically-ill patients plays a role in the response to glucose control and mortality.

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12

Yalin, Nefize, Danilo Arnone, and Allan Y. Young. Bidirectional relationships between general medical conditions and bipolar disorder: treatment considerations. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0019.

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Increased medical co-morbidity is one of the underlying causes of excess and premature mortality in bipolar disorder. This increased prevalence of medical conditions is likely to result from a range of different factors. Some attention in recent years has been devoted to intrinsic illness factors resulting in excessive allostatic load and oxidative stress potentially predisposing to physical morbidity. Some other contributors have also been identified as unhealthy lifestyle habits and unwanted effects of pharmacological treatment. Irrespective of causality, risk minimization can be obtained by systematically addressing physical needs into the management of bipolar disorder. This can be achieved with a range of interventions including regular monitoring of physical health, tailored management of unhealthy lifestyle choices, and pharmacological optimization.

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13

Morales-Gonzalez, Jose Antonio, Angel Morales-Gonzalez, and Eduardo Osiris Madrigal-Santillan, eds. A Master Regulator of Oxidative Stress - The Transcription Factor Nrf2. InTech, 2016. http://dx.doi.org/10.5772/62743.

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14

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 treatments for these conditions do not address sources of systemic inflammation, this integrative medicine approach is of great value for clinicians and can help relieve the suffering of patients and their loved ones.

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15

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 damage in surrounding neurons, and aberrantly clear healthy cells and structures from the brain. In turn, the cells within the brain play important roles in determining the phenotype and function of these immune cells, and changes in the interaction among these cells in the context of disease can lead to detrimental immune cell activation. There has been recent interest in developing inflammation-related biomarkers to help diagnose NDDs and immune-targeted therapeutics.

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16

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. There is poor correlation between carboxyhaemoglobin levels and clinical symptoms. The presence of coma, underlying co-morbid conditions and need for mechanical ventilation are the main prognostic factors. Management includes prompt extraction from the toxic environment and breathing 100% oxygen, although the role and practicalities of hyperbaric oxygen therapy remain controversial.

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17

Sliwa, Karen, and Denise Hilfiker-Kleiner. Peripartum cardiomyopathy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0374.

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Pregnancy-related heart disease is increasing worldwide and peripartum cardiomyopathy (PPCM) is an important contributor to early (<42 days postpartum) and late (up to 1 year postpartum) maternal death. PPCM is an idiopathic form of cardiomyopathy, presenting with heart failure secondary to left ventricular dysfunction towards the end of pregnancy, or in the months following delivery, where no other cause of heart failure is identified. It is a diagnosis of exclusion. Incidence and prognosis varies according to geography and is likely due to multiple factors. The recent specific pathophysiological hypothesis which states that the oxidative stress–cathepsin D-16 kDa prolactin cascade plays a key role in the development of PPCM in experimental models and in humans suggests that a therapeutic approach involving blockade of this pathway with bromocriptine may be a novel disease-specific approach. Despite ongoing research, numerous uncertainties regarding the incidence, pathophysiology, treatment, and prognosis of PPCM patients remain, indicating the need for further investigation. The establishment of the international registry on PPCM, under the umbrella of the EuroObservational research programme, will provide novel information and address many uncertainties.

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18

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 rather than simply acting as a marker of the severity of glomerular injury and podocytes loss. Seminal studies used the atypical renal anatomy of the axolotl to instill proteins directly into the tubular lumen without requiring passage through the glomerulus. This indicated that tubular protein could be cytotoxic and induce interstitial inflammation and fibrosis in the peritubular region. Cell culture studies demonstrate that exposure to proteins results in proximal tubular cell activation and the production of pro-inflammatory and pro-fibrotic mediators. Proximal tubular cell death occurred in some studies reinforcing the potential of protein to exert cytotoxic effects via oxidative stress or endoplasmic reticulum stress. Analysis of renal biopsy material from both experimental studies using models of proteinuric disease or patients with various proteinuric diseases provided evidence of activation of transcription factors and production of chemokines and pro-inflammatory mediators by proximal tubular cells. These data strongly suggest that although proteinuria is the result of glomerular disease it also represents an important cause of progression in patients with chronic kidney disease associated with proteinuria.

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19

Remesal, Ana. Effects of Oxidative Stress and Antenatal Corticosteroids on the Pulmonary Expression of Vascular Endothelial Growth Factor (VEGF) and Alveolarization. INTECH Open Access Publisher, 2012.

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20

Xu, Kui, Joseph C. LaManna, and Michelle A. Puchowicz. Ketogenic Diet, Aging, and Neurodegeneration. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0024.

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The brain is normally completely dependent on glucose, but is capable of using ketones as an alternate energy source, as occurs with prolonged starvation or chronic feeding of a ketogenic diet. Research has shown that ketosis is neuroprotective against ischemic insults in rodents. This review focuses on investigating the mechanistic links to neuroprotection by ketosis in the aged. Recovery from stroke and other pathophysiological conditions in the aged is challenging. Cerebral metabolic rate for glucose, cerebral blood flow, and the defenses against oxidative stress are known to decline with age, suggesting dysfunction of the neurovascular unit. One mechanism of neuroprotection by ketosis involves succinate-induced stabilization of hypoxic inducible factor-1alpha (HIF1α‎) and its downstream effects on intermediary metabolism. The chapter hypothesizes that ketone bodies play a role in the restoration of energy balance (stabilization of ATP supply) and act as signaling molecules through the up-regulation of salvation pathways targeted by HIF1α‎.

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21

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 to increased peripheral vascular resistance. At the vascular level, processes leading to change sin peripheral resistance include hyper-contractility of vascular smooth muscle cells, endothelial dysfunction, and structural remodelling, due to aberrant vascular signalling, oxidative and inflammatory responses. Increased vascular stiffness due to vascular remodelling, adventitial fibrosis, and inflammation are key processes involved in sustained and established hypertension. These mechanisms are linked to vascular smooth muscle and fibroblast proliferation, migration, extracellular matrix remodelling, calcification, and inflammation. Apart from the key role in the pathogenesis of hypertension, hypertensive vasculopathy also predisposes to atherosclerosis, another risk factor for cardiovascular disease. This is linked to increased transmural pressure, blood flow, and shear stress alterations in hypertension, as well as endothelial dysfunction and vascular stiffness. Therefore, understanding the mechanisms and identifying potential novel treatments targeting hypertensive vasculopathy are of primary importance in vascular medicine.

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