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Książki na temat „Nitrite Stress”

Autor: Grafiati

Data publikacji: 6 września 2023

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Sprawdź 41 najlepszych książek naukowych na temat „Nitrite Stress”.

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1

Dillow, Jonathan J. A. Estimates of the loads of nitrite + nitrate in the flow of Bassett Creek to the Maryland Coastal Bays adjacent to Assateague Island National Seashore, water years 2003-2004. Reston, Va: U.S. Dept. of Interior, U.S. Geological Survey, 2006.

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2

E, Groseclose Lance, i United States. National Aeronautics and Space Administration., red. Flexural stress rupture and creep of commercial silicon nitrides. [Washington, DC: National Aeronautics and Space Administration, 1991.

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3

Jorgensen, Eric E. Ecosystem stress from chronic exposure to low levels of nitrate. Cincinnati, Ohio: National Risk Management Research Laboratory, 2005.

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4

Khan, M. Nasir, Mohammad Mobin, Firoz Mohammad i Francisco J. Corpas, red. Nitric Oxide Action in Abiotic Stress Responses in Plants. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17804-2.

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5

Lamattina, Lorenzo, i Joseph C. Polacco, red. Nitric Oxide in Plant Growth, Development and Stress Physiology. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/11563280.

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6

Khan, M. Nasir, Mohammad Mobin, Firoz Mohammad i Francisco J. Corpas, red. Nitric Oxide in Plants: Metabolism and Role in Stress Physiology. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-06710-0.

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7

Packer, Lester, i Enrique Cadenas. Nitric oxide: Oxidative and nitrosative stress in redox regulation of cell signaling. San Diego, Calif: Elsevier/Academic Press, 2008.

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8

Abdul-Aziz, Ali. Design evaluation using finite element analysis of cooled silicon nitride plates for a turbine blade application. [Cleveland, Ohio]: National Aeronautics and Space Administration, Glenn Research Center, 2001.

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9

Abdul-Aziz, Ali. Design evaluation using finite element analysis of cooled silicon nitride plates for a turbine blade application. [Cleveland, Ohio]: National Aeronautics and Space Administration, Glenn Research Center, 2001.

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10

M, Matata Bashir, i Elahi Maqsood M, red. Oxidative stress: Clinical and biomedical implications. New York: Nova Biomedical Books, 2007.

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11

Pittman, John R. Spring contributions to water quality and nitrate loads in the Suwannee River during base flow in July 1995. [Tallahassee, FL]: U.S. Geological Survey, 1997.

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12

Abdul-Aziz, Ali. Influence of cooling hole geometry and material conductivity on the thermal response of cooled silicon nitride plate. Cleveland, Ohio: National Aeronautics and Space Administration, Glenn Research Center, 2002.

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13

Explaining 'unexplained illnesses': Disease Paradigm for Chronic Fatigue Syndrome, Multiple Chemical Sensitivity, Fibromyalgia, Post-Traumatic Stress Disorder, Gulf War Syndrome and Others. Binghamton, NY: Harrington Park Press, 2007.

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14

Val, Vallyathan, Shi Xianglin Ph D i Castranova Vincent, red. Oxygen/nitrogen radicals: Lung injury and disease. New York: Marcel Dekker, Inc., 2004.

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15

Poor, Peter, Antonio Ferrante, Noushina Iqbal i M. Iqbal R. Khan. Nitric Oxide in Developing Plant Stress Resilience. Elsevier Science & Technology, 2022.

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16

Ferrante, Antonio, Noushina Iqbal, M. Iqbal R. Khan i Péter Poór. Nitric Oxide in Developing Plant Stress Resilience. Elsevier Science & Technology Books, 2022.

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17

Mohammad, Firoz, M. Nasir Khan, Mohammad Mobin i Francisco J. Corpas. Nitric Oxide Action in Abiotic Stress Responses in Plants. Springer, 2015.

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18

Mohammad, Firoz, M. Nasir Khan, Mohammad Mobin i Francisco J. Corpas. Nitric Oxide Action in Abiotic Stress Responses in Plants. Springer, 2015.

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19

Mohammad, Firoz, M. Nasir Khan, Mohammad Mobin i Francisco J. Corpas. Nitric Oxide Action in Abiotic Stress Responses in Plants. Springer, 2016.

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20

Zilliox, Lindsay, i James W. Russell. Diabetic and Prediabetic Neuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0115.

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Impaired glucose regulation (IGR) constitutes a spectrum of impaired glucose and metabolic regulation that can result in neuropathy. Several different pathways of injury in the diabetic peripheral nervous system that include metabolic dysregulation induced by metabolic syndrome induce oxidative stress, failure of nitric oxide regulation, and dysfunction of certain key signaling pathways. Oxidative stress can directly injure both dorsal route ganglion neurons and axons. Modulation of the nitric oxide system may have detrimental effects on endothelial function and neuronal survival. Reactive oxidative species can alter mitochondrial function, protein and DNA structure, interfere with signaling pathways, and deplete antioxidant defenses. Advanced glycelation end (AGE) products and formation of ROS are activated by and in turn regulate key signal transduction pathways.

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21

Polacco, J. C., i Lorenzo Lamattina. Nitric Oxide in Plant Growth, Development and Stress Physiology. Springer Berlin / Heidelberg, 2010.

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22

Mohammad, Firoz, M. Nasir Khan, Mohammad Mobin i Francisco J. Corpas. Nitric Oxide in Plants: Metabolism and Role in Stress Physiology. Springer London, Limited, 2014.

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23

Khan, Nafees A. Regulation of Metal Stress Toxicity in Plants by Nitric Oxide. Elsevier Science & Technology, 2022.

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24

Mohammad, Firoz, M. Nasir Khan, Mohammad Mobin i Francisco J. Corpas. Nitric Oxide in Plants: Metabolism and Role in Stress Physiology. Springer, 2014.

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25

Khan, Nafees A. Regulation of Metal Stress Toxicity in Plants by Nitric Oxide. Elsevier Science & Technology Books, 2022.

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26

Mohammad, Firoz, M. Nasir Khan, Mohammad Mobin i Francisco J. Corpas. Nitric Oxide in Plants: Metabolism and Role in Stress Physiology. Springer, 2016.

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27

(Editor), Santiago Lamas, i Enrique Cadenas (Editor), red. Nitric Oxide, Cell Signaling, and Gene Expression (Oxidative Stress and Disease). CRC, 2005.

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28

(Editor), Lorenzo Lamattina, i Joseph C. Polacco (Editor), red. Nitric Oxide in Plant Growth, Development and Stress Physiology (Plant Cell Monographs). Springer, 2007.

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29

Nitric Oxide in Plant Growth, Development and Stress Physiology (Plant Cell Monographs Book 6). Springer, 2007.

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30

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

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31

Nitric Oxide, Part G Oxidative and Nitrosative Stress in Redox Regulation of Cell Signaling. Elsevier, 2008. http://dx.doi.org/10.1016/s0076-6879(08)x0007-2.

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32

Bakke, Paul D. The spatial and temporal variability of nitrate in streams of the Bull Run Watershed, Oregon. 1993.

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33

Pall, Martin. Explaining Unexplained Illnesses: Disease Paradigm for Chronic Fatigue Syndrome, Multiple Chemical Sensitivity, Fibromyalgia, Post-Traumatic Stress Disorder, Gulf War Syndrome and Others. Taylor & Francis Group, 2013.

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34

Curry, Nicola, i Raza Alikhan. Normal platelet function. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0281.

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The platelet is a small (2–4 µm in diameter), discoid, anucleate cell that circulates in the blood. In health, it plays a vital role in haemostasis, and in disease it contributes to disorders of bleeding and thrombosis. Platelets are produced from the surface of megakaryocytes in the bone marrow, under tight homeostatic control regulated by the cytokine thrombopoietin. Platelets have a lifespan of approximately 7–10 days, and usually circulate in the blood stream in a quiescent state. Intact, undamaged vessel walls help to maintain platelets in this inactive state by releasing nitric oxide, which acts both to dilate the vessel wall and to inhibit platelet adhesion, activation, and aggregation. After trauma to the blood vessel wall, platelets are activated and, acting in concert with the endothelium and coagulation factors, form a stable clot. This chapter addresses platelet structure and function, and the response of platelets to vessel injury.

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35

Suri, Ajay, i Jean R. McEwan. Anti-anginal agents in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0037.

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Angina is chest pain resulting from the lack of blood supply to heart muscle most commonly due to obstructive atherosclerotic. Intensive care unit patients are subject to various stresses that will increase the demand on the heart and are in a pro-thrombotic state. Patients in an intensive treatment unit may be sedated and so cardiac ischaemia may be detected by electrocardiogram, haemodynamic monitoring, and echocardiographic imaging of function. These signs may indicate critical coronary perfusion heralding a myocardial infarction and are alleviated by anti-anginal drugs. Beta-blockers and calcium channel blockers are the usual first-line treatments for angina, but may not be ideal in the critically-ill patient. Nitrates reduce blood pressure without typically affecting heart rate. Nicorandil is a similar mechanism of action and tends to be given orally, while ivabridine, an If channel blocker, is a newer anti-anginal, which acts by reducing heart rate, while not affecting blood pressure. Ranolazine is the one of the newest anti-anginal agents and is believed to alter the transcellular late sodium current thereby decreasing sodium entry into ischaemic myocardial cells.

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36

Nakamura, Tomohiro, i Stuart A. Lipton. Neurodegenerative Diseases as Protein Misfolding Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0002.

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Neurodegenerative diseases (NDDs) often represent disorders of protein folding. Rather than large aggregates, recent evidence suggests that soluble oligomers of misfolded proteins are the most neurotoxic species. Emerging evidence points to small, soluble oligomers of misfolded proteins as the cause of synaptic dysfunction and loss, the major pathological correlate to disease progression in many NDDs including Alzheimer’s disease. The protein quality control machinery of the cell, which includes molecular chaperones as found in the endoplasmic reticulum (ER), the ubiquitin-proteasome system (UPS), and various forms of autophagy, can counterbalance the accumulation of misfolded proteins to some extent. Their ability to eliminate the neurotoxic effects of misfolded proteins, however, declines with age. A plausible explanation for the age-dependent deterioration of the quality control machinery involves compromise of these systems by excessive generation of reactive oxygen species (ROS), such as superoxide anion (O2-), and reactive nitrogen species (RNS), such as nitric oxide (NO). The resulting redox stress contributes to the accumulation of misfolded proteins. Here, we focus on aberrantly increased generation of NO-related species since this process appears to accelerate the manifestation of key neuropathological features, including protein misfolding. We review the chemical mechanisms of posttranslational modification by RNS such as protein S-nitrosylation of critical cysteine thiol groups and nitration of tyrosine residues, showing how they contribute to the pathogenesis of NDDs.

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37

Pall, Martin L. Explaining 'Unexplained Illnesses': Disease Paradigm for Chronic Fatigue Syndrome, Multiple Chemical Sensitivity, Fibromyalgia, Post-Traumatic Stress Disorder, and Gulf War Syndrome. Harrington Park Press, 2007.

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38

Pall, Martin L. Explaining 'Unexplained Illnesses': Disease Paradigm for Chronic Fatigue Syndrome, Multiple Chemical Sensitivity, Fibromyalgia, Post-Traumatic Stress Disorder, and Gulf War Syndrome. Haworth Medical Pr, 2007.

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39

G, Poli, Packer Lester i Cadenas Enrique, red. Free radicals in brain pathophysiology. New York: Dekker, 2000.

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40

(Editor), Val Vallyathan, Vincent Castranova (Editor) i Xianglin Shi (Editor), red. Oxygen/Nitrogen Radicals: Lung Injury and Disease (Lung Biology in Health and Disease). Informa Healthcare, 2004.

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41

Oxygen/Nitrogen Radicals: Cell Injury and Disease. Springer, 2011.

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