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Books on the topic 'Metabolic activation'

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Published: 4 June 2021
Last updated: 25 April 2022

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1

Lau, Grace S. N. Metabolic activation of drugs and other xenobiotics in hepatocellular carcinoma. Hong Kong: Chinese University Press, 1997.

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2

Roland, Per E. Brain activation. New York: Wiley-Liss, 1993.

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3

Sideman, S., and R. Beyar, eds. Activation, Metabolism and Perfusion of the Heart. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3313-2.

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4

Regulation of enzyme activity. Oxford: IRL Press, 1988.

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5

E, Adams Gerald, and North Atlantic Treaty Organization. Scientific Affairs Division., eds. Selective activation of drugs by redox processes. New York: Plenum Press, 1990.

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6

Sideman, S. Activation, Metabolism and Perfusion of the Heart: Simulation and experimental models. Dordrecht: Springer Netherlands, 1987.

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7

Hedgehog signaling activation in human cancer and its clinical implications. New York: Springer, 2011.

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8

International Symposium "Brain Activation and CBF Control" ( 2001 Tokyo, Japan). Brain activation and CBF control: Proceedings of the Satellite meeting on Brain Activation and Cerebral Blood Flow Control, held in Tokyo, Japan 5-8 June 2001. Edited by Tomita M, Kanno I, and Hamel E. Amsterdam: Elsevier, 2002.

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9

Convegno nazionale Meccanismi di attivazione e tossicità degli xenobiotici (1st 1987 Istituto superiore di sanità). 1st Italian Symposium Mechanisms of Activation and Toxicity of Xenobiotics: Istituto superiore di Sanità, Rome, 26-27 March 1987 : abstract book. Roma: Il Istituto, 1987.

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10

Nederkoorn, Paul H. J. Signal transduction by G protein-coupled receptors: Bioenergetics and G protein activation : proton transfer and GTP synthesis to explain the experimental findings. New York: Springer, 1997.

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11

Post-transcriptional regulation by STAR proteins : control of RNA metabolism in development and disease. New York: Springer Science+Business Media, LLC, 2010.

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12

Ng, Linda Fung-yee. Metabolic Activation of Drugs (Young Scholars Dissertation Awards). Columbia University Press, 1997.

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13

Anari, Mohammad Reza. Cytochrome P450 peroxidase/peroxygenase-dependent metabolic activation of xenobiotics. 1997.

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14

E, Gram Theodore, ed. Metabolic activation and toxicity of chemical agents to lung tissue and cells. New York: Pergamon Press, 1993.

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15

Metabolic Activation and Toxicity of Chemical Agents to Lung Tissue and Cells. Elsevier, 1993. http://dx.doi.org/10.1016/c2009-0-00832-0.

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16

Activation And Detoxification Enzymes Functions And Implications. Springer, 2011.

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17

Eyre, Russel James. Species differences in the metabolic activation of trichloroethylene by the cysteine S-conjugate pathway in B6C3F1 mice and F344 rats. 1994.

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18

Magalhaes, Eric, Angelo Polito, Andréa Polito, and Tarek Sharshar. Sepsis-Associated Encephalopathy. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0032.

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Brain dysfunction is a major complication of sepsis and is characterized by alteration of consciousness, ranging from delirium to coma and marked electroencephalographic changes. It reflects a constellation of dynamic biological mechanisms, including neurotransmitter imbalance, macro- and microcirculatory dysfunction resulting in ischaemia, endothelial activation, alteration of the blood-brain barrier impairment with passage of neurotoxic mediators, activation of microglial cells within the central nervous system, cumulatively resulting in a neuroinflammatory state. Sepsis-associated brain dysfunction is associated with increased mortality and long-term cognitive decline, whose mechanisms might include microglial activation, axonopathy, or cerebral microinfarction. There is no specific treatment, other than the management of the underlying septic source, correction of physiological and metabolic abnormalities, and limiting the use of medications with neurotoxic effects.
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19

Roland, Per E. Brain Activation. 2nd ed. Wiley-Liss, 2006.

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20

Connor, Thomas, and Patrick H. Maxwell. Von Hippel–Lindau disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0332.

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Von Hippel–Lindau (VHL) disease is a dominantly inherited familial cancer syndrome caused by germline mutations in the VHL tumour suppressor gene. The most frequent manifestations of VHL disease are retinal and central nervous system haemangioblastomas, clear cell renal cell carcinomas, and phaeochromocytomas. Genetic testing and active screening for clinical manifestations is now started in childhood and has greatly improved the prognosis for patients with VHL disease. The VHL protein plays a critical role in regulating the cellular response to changes in oxygen tension. Loss of VHL function results in constitutive activation of a range of angiogenic and metabolic pathways. New drug therapies have been developed that reverse some of the cellular consequences of VHL loss of function in kidney cancer.
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21

Young, Allan H., and Mario F. Juruena. Hypothalamic–pituitary–adrenal axis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0006.

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Increased adrenocortical secretion of hormones, primarily cortisol in depression, is one of the most consistent findings in neuropsychiatry. The maintenance of the internal homeostatic state of an individual is facilitated by the ability to circulate glucocorticoids to exert negative feedback on the secretion of hypothalamic–pituitary–adrenal (HPA) hormones through binding to mineralocorticoid and glucocorticoid receptors, thus limiting the vulnerability to diseases related to psychological stress in genetically predisposed individuals. The HPA axis response to stress can be thought of as a crucial part of the organism’s response to stress: acute responses are generally adaptive, but excessive or prolonged responses can lead to deleterious effects. A spectrum of conditions may be associated with increased and prolonged activation of the HPA axis, including depression, poorly controlled diabetes mellitus, and metabolic syndrome. HPA axis dysregulation and hypercortisolaemia may further contribute to a hyperglycaemic or poorly controlled diabetic state.
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22

Monaco, Claudia, and Giuseppina Caligiuri. Molecular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0014.

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The development of the atherosclerotic plaque relies on specific cognate interactions between ligands and receptors with the ability to regulate cell recruitment, inflammatory signalling, and the production of powerful inflammatory and bioactive lipid mediators. This chapter describes how signalling is engaged by cell-cell surface interactions when the endothelium interacts with platelets and leukocytes enhancing leukocyte recruitment during atherogenesis. It also exemplifies intracellular signalling pathways induced by the activation of innate immune receptors, the most potent activators of inflammation in physiology and disease. Differences are highlighted in innate signalling pathways in metabolic diseases such as atherosclerosis compared to canonical immunological responses. Finally, the key lipid mediators whose production can affect endothelial function, inflammation, and atherosclerosis development are summarized. This Chapter will take you through these fundamental steps in the development of the atherosclerotic plaque by summarizing very recent knowledge in the field and highlighting recent or ongoing clinical trials that may enrich our ability to target cardiovascular disease in the future.
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23

(Editor), M. Tomita, I. Kanno (Editor), and E. Hamel (Editor), eds. Brain Activation and CBF Control. Elsevier, 2002.

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24

A, Elfarra Adnan, ed. Advances in bioactivation research. New York: Springer, 2008.

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25

Bouchama, Abderrezak. Pathophysiology and management of hyperthermia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0353.

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Hyperthermia is a state of elevated core temperature that rises rapidly above 40°C, secondary to failure of thermoregulation. Hyperthermia has many causes, but it is the hallmark of three conditions—heatstroke, malignant hyperthermia, and neuroleptic malignant syndrome. The clinical and metabolic alterations of hyperthermia, if left untreated, can culminate in multiple organ system failure and death. High temperature causes direct cellular death and tissue damage. The extent of tissue injury is a function of the degree and duration of hyperthermia. Heat-induced ischaemia-reperfusion injury, and exacerbated activation of inflammation and coagulation are also contributory. Hyperthermia is a true medical emergency with rapid progression to multiple organ system failure and death. The primary therapeutic goal is to reduce body temperature as quickly as possible using physical cooling methods, and if indicated, the use of pharmacological treatment to accelerate cooling. There is no evidence of the superiority of one cooling technique over another. Non-invasive techniques that are easy to use and well-tolerated are preferred. Pharmacological cooling with Dantrolene sodium is crucial in the treatment of malignant hyperthermia.
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26

Kurosaki, Fumiya. Induction and Activation of Plant Secondary Metabolism by External Stimuli. INTECH Open Access Publisher, 2012.

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27

S, Sideman, Beyar Rafael, Tekhniyon Makhon tekhnologi le-Yiśraʼel, Rutgers University, and Henry Goldberg Workshop (3rd : 1986 : Rutgers University), eds. Activation, metabolism, and perfusion of the heart: Simulation and experimental models. Dordrecht, Netherlands: Nijhoff, 1987.

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28

Annas, Anita. Metabolism-Dependent Activation of Food and Environmental Mutagens in Endothelial Cells. Uppsala Universitet, 2000.

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29

Activation, Metabolism and Perfusion of the Heart: Simulation and experimental models. Springer, 2011.

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30

Fred, Snyder, ed. Platelet-activating factor and related lipid mediators. New York: Plenum Press, 1987.

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31

1937-, Politzer Peter, and Martin F. J, eds. Chemical carcinogens: Activation mechanisms, structural and electronic factors, and reactivity. Amsterdam: Elsevier, 1988.

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32

Chardin, Pierre Teilhard de. Activation of Energy: Enlightening Reflections on Spiritual Energy. Harvest Books, 2002.

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33

Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0022.

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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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34

Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_002.

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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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35

Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_003.

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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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36

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

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37

Alan, Wiseman, ed. Enzyme induction, mutagen activation, and carcinogen testing in yeast. Chichester, West Sussex, England: E. Horwood, 1987.

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38

Xie, Jingwu. Hedgehog signaling activation in human cancer and its clinical implications. Springer, 2011.

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39

Xie, Jingwu. Hedgehog signaling activation in human cancer and its clinical implications. Springer, 2014.

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40

Benton, Richard Lee. The effect of methylprednisolone treatment on astroglial activation and glutamate metabolism following spinal cord injury. [s.n.], 2000.

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41

L, Purich Daniel, ed. Enzyme kinetics and mechanism. San Diego: Academic Press, 2002.

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42

Folkers, Gerd, Raimund Mannhold, Thomas Wieland, Hugo Kubinyi, and Roland Seifert. G Protein-Coupled Receptors As Drug Targets: Analysis of Activation and Constitutive Activity. Wiley & Sons, Incorporated, John, 2006.

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43

Folkers, Gerd, Raimund Mannhold, Thomas Wieland, Hugo Kubinyi, and Roland Seifert. G Protein-Coupled Receptors As Drug Targets: Analysis of Activation and Constitutive Activity. Wiley-VCH Verlag GmbH, 2006.

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44

Roland, Seifert, and Wieland Thomas, eds. G protein-coupled receptors as drug targets: Analysis of activation and constitutive activity. Weinheim: Wiley-VCH, 2005.

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45

Clarke, Andrew. Temperature and reaction rate. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780199551668.003.0007.

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All other things being equal, physiological reaction rate increases roughly exponentially with temperature. Organisms that have adapted over evolutionary time to live at different temperatures can have enzyme variants that exhibit similar kinetics at the temperatures to which they have adapted to operate. Within species whose distribution covers a range of temperatures, there may be differential expression of enzyme variants with different kinetics across the distribution. Enzymes adapted to different optimum temperatures differ in their amino acid sequence and thermal stability. The Gibbs energy of activation tends to be slightly lower in enzyme variants adapted to lower temperatures, but the big change is a decrease in the enthalpy of activation, with a corresponding change in the entropy of activation, both associated with a more open, flexible structure. Despite evolutionary adjustments to individual enzymes involved in intermediary metabolism (ATP regeneration), many whole-organism processes operate faster in tropical ectotherms compared with temperate or polar ectotherms. Examples include locomotion (muscle power output), ATP regeneration (mitochondrial function), nervous conduction and growth.
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46

Daci, Evis. The Role of the Plasminogen Activator/Plasmin Pathway in Bone Metabolism (Acta Biomedica Lovanuensia, 223). Leuven Univ Pr, 2000.

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47

G Protein-Coupled Receptors as Drug Targets: Analysis of Activation and Constitutive Activity (Methods and Principles in Medicinal Chemistry). Wiley-VCH, 2006.

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48

O’Neal, M. Angela. Pain in the Back. Edited by Angela O’Neal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190609917.003.0006.

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This case explores how bone health can be affected by antiepileptic drugs (AEDs), and why this is an important issue in women with epilepsy (WWE). AEDs affect bone health through activation of the cytochrome P450 system in the liver, leading to increased metabolism of vitamin D. The enzyme-inducing AEDs include phenytoin, carbamazepine, phenobarbital, and primidone. Risk factors for osteoporosis include female gender, low body mass, inadequate vitamin D intake, and smoking. The specific AEDs used and the length of treatment confer additional risks. Furthermore, in WWE, risks are magnified related to falls, either from seizures or related to medication toxicity. Screening with bone density and measures to promote bone health are extremely important in these at-risk women.
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49

Arachidonate Related Lipid Mediators, Volume 187: Volume 187: Arachidonate Related Lipid Mediators (Methods in Enzymology). Academic Press, 1990.

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50

C, Murphy Robert, and Fitzpatrick Frank A, eds. Arachidonate related lipid mediators. San Diego: Academic Press, 1990.

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