Titlebook: Inflammation and Oxidative Stress in Neurological Disorders; Effect of Lifestyle, Akhlaq A. Farooqui Book 2014 Springer International Publi

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Akhlaq A. Farooquif the crystal classes, studying their effects on the form of the constitutive equations of these materials. After a section of exercises, the last sections describe the program LinElasticityTensor, written with Mathematica., which allows to determine the elasticity tensor of linear elasticity of dif

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alysis of these narrow regions by Prandtl’s approach. Then, we apply the general theory of ordinary waves to perfect fluids in order to prove the existence of longitudinal waves in compressible fluids. Finally, we apply the Rankine–Hugoniot conditions to analyze the behavior of shock waves in perfec

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Inflammation and Oxidative Stress in Neurological DisordersEffect of Lifestyle,

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Contribution of Dietary Fat in Neuroinflammation,formation of above mentioned lipid mediators occurs slowly. The resolution of neuroinflammation is mediated by arachidonic acid-derived lipoxins and eicosapentaenoic acid and docosahexaenoic acid-derived resolvins, protectins, and maresins. Although, some information is available on the generation o

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Contribution of Dietary Fat in the Induction of Oxidative Stress,e eicosanoids, 4-HNE, IsoP, IsoF, IsoK, Ac and MDA. Increased plasma levels of these metabolites have been associated with neurotraumatic and neurodegenerative diseases. Resolvins and protectins/neuroprotectins, the EPA and DHA-derived lipid mediators regulate immune systems by inhibiting signal tra

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Contribution of Dietary Carbohydrates in Induction of Oxidative Stress,disease. At high levels glucose is not only converted into fructose through polyol pathway, but is also metabolized into advanced glycated end products (AGEs), which bind with serum lipids and proteins to form glycated/fructated proteins. These proteins not only show impaired functions, but are also

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Contribution of Transcription Factors and Genes in the Induction of Oxidative Stress,g apoptosis. Thus, at low levels, ROS and RNS-mediated activation of Nrf2, AP1, NF-kB, HIF-1α, p53, and FOXO effectively neutralizes and removes excess oxidants to restore redox homeostasis, but at high levels, ROS and RNS over-stimulate transcription factors resulting into malfunction of cellular a