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Books on the topic 'Metabolic inhibition'

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Published: 4 June 2021
Last updated: 7 February 2022

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1

Yu, Wai Haung. Desferrioxamine analysis by high performance liquid chromatography, stability and metabolic inhibition by monoamine oxidase inhibitors. Ottawa: National Library of Canada, 1994.

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2

Ahlström, Marie. Cytochrome P450, metabolism and inhibition: Computational and experimental studies. Göteborg: Göteborg University, 2007.

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3

Wagner, Sylvie. Studies on metabolism and inhibition of melanoma mouse cell line. Sudbury, Ont: Laurentian University, 1994.

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4

Bitnun, Ari. Metabolic abnormalities associated with protease inhibitor therapy in HIV-infected children. Ottawa: National Library of Canada, 2003.

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5

Fernandes, Leona Caterina. Pharmacologic effects and safety of tranylcypromine inhibition of nicotine metabolism in humans. Ottawa: National Library of Canada, 2002.

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6

Kathiramalainathan, Kalyani. Modification of codeing metabolism and abuse liability by inhibition of cytochrome P450 2D6. Ottawa: National Library of Canada, 1996.

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7

A, Stafford Jeffrey, ed. Kinase inhibitor drugs. Hoboken, N.J: J. Wiley, 2009.

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8

Cancer: Between glycolysis and physical constraint. Berlin: Springer, 2004.

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9

Huq, Rokaiya. Energy metabolism in human MCF-7 ADR and ADR-9 breast cancer cells treated with P-glycoprotein inhibitor PSC 833. Sudbury, Ont: Laurentian University, 2000.

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10

Cheung, Hermia. Effect of dopamine depletion on D1 receptor binding in rat brain; and metabolism studies of D1 agonist R-[11C]SKF 82957 and phosphodiesterase-4 inhibitor R-[11C}rolipram. Ottawa: National Library of Canada, 2003.

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11

Metabolic Inhibition of a Toluene-Enriched Microbial Population Due to Lead (Pb2 ); Verification of a Free Metal ION Toxicity Model. Storming Media, 1997.

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12

Sada, Nagisa, and Tsuyoshi Inoue. Lactate Dehydrogenase. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0029.

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Glucose is transported into neurons and used as an energy source. It is also transported into astrocytes, a type of glial cell, and converted to lactate, which is then released to neurons and used as another energy source. The latter is called the astrocyte-neuron lactate shuttle. Although the lactate shuttle is a metabolic pathway, it also plays important roles in neuronal activities and brain functions. We recently reported that this metabolic pathway is involved in the antiepileptic effects of the ketogenic diet. Lactate dehydrogenase (LDH) is a metabolic enzyme that mediates the lactate shuttle, and its inhibition hyperpolarizes neurons and suppresses seizures. This enzyme is also a molecular target of stiripentol, a clinically used antiepileptic drug for Dravet syndrome. This review provides an overview of electrical regulation by the astrocyte-neuron lactate shuttle, and then introduces LDH as a metabolic target against epilepsy.
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13

D’Mello, Ajay. Mitochondrial Disease. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0047.

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Mitochondrial disease is now considered to be an important cause for a diverse range of neurological, muscular, cardiac and endocrine disorders. Initially thought to be a rare group of disorders, it is now increasingly common for children with mitochondrial disease to present for a surgical procedure. While the mitochondrial respiratory chain is the essential finally common pathway for aerobic metabolism, mitochondria also play a role in a several important cellular processes. A variety of anesthetic techniques have been successfully used for this group of patients. However, the possibility of complications due to inhibition of mitochondrial function by anesthetic agents and surgical stress is a worry for the physician managing these patients. Anesthetic management focuses on disease symptoms at presentation, maintaining normoglycemia, while preventing further metabolic stress and complications that worsen lactic acidosis.
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14

Inhibition of Polyamine Metabolism. Elsevier, 1987. http://dx.doi.org/10.1016/b978-0-12-481835-4.x5001-7.

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15

Bleck, Thomas P. Pathophysiology and causes of seizures. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0231.

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Seizures result from imbalances between excitation and inhibition, and between neuronal synchrony and dyssynchrony. Current models implicate the cerebral cortex in the genesis of seizures, although thalamic mechanisms (particularly the thalamic reticular formation) are involved in the synchronization of cortical neurons. Often, the precipitants of a seizure in the critical care setting are pharmacological. Several mechanisms linked to critical illness can lead to seizures. Failure to remove glutamate and potassium from the extracellular space, functions performed predominantly by astrocytes, occurs in trauma, hypoxia, ischaemia, and hypoglycaemia. Loss of normal inhibition occurs during withdrawal from alcohol and other hypnosedative agents, or in the presence of GABA. Conditions such as cerebral trauma, haemorrhages, abscesses, and neoplasms all produce physical distortions of the adjacent neurons, astrocytes, and the extracellular space. Deposition of iron in the cortex from the breakdown of haemoglobin appears particularly epileptogenic. Although acute metabolic disturbances can commonly produce seizures in critically-ill patients, an underlying and potentially treatable structural lesion must always be considered and excluded.
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16

Poff, Angela M., Shannon L. Kesl, and Dominic P. D’Agostino. Ketone Supplementation for Health and Disease. Edited by Dominic P. D’Agostino. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0032.

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Exogenous ketone supplements rapidly elevate blood ketones in a dose-dependent manner regardless of dietary intake, making them a practical method of inducing therapeutic ketosis for medical use. It is thought that ketone supplementation could be used as a stand-alone therapy, or as a way to further augment the therapeutic efficacy of the ketogenic diet. Ketone supplementation could increase treatment compliance by allowing many patients to maintain a more normal lifestyle with a less restrictive diet. The therapeutic effects of ketone supplementation are likely mediated in part by a stabilization of blood glucose and insulin levels, an increase in metabolic efficiency, and an inhibition of oxidative stress and inflammation. Ketone supplements may also serve as an effective preventative medicine due to their potential ability to protect and enhance mitochondrial health and function. Indeed, preliminary evidence suggests there are a number of conditions for which exogenous ketone supplementation may be beneficial.
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17

McCann, Peter P., and Anthony E. Pegg. Inhibition of Polyamine Metabolism: Biological Significance and Basis for New Therapies. Academic Pr, 1987.

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18

P, McCann Peter, Pegg Anthony E, and Sjoerdsma Albert 1924-, eds. Inhibition of polyamine metabolism: Biological significance and basis for new therapies. Orlando: Academic Press, 1987.

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19

McCann, Peter P., and Anthony E. Pegg. Inhibition of Polyamine Metabolism: Biological Significance and Basis for New Therapies. Academic Pr, 1987.

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20

(Editor), William R. Miller, and Richard Santen (Editor), eds. Aromatase Inhibition and Breast Cancer. CRC, 2001.

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21

Zedeck, Morris S., and Martin Lipkin. Inhibition of Tumor Induction and Development. Springer, 2013.

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22

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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23

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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24

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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25

Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0032.

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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
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26

Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_001.

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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
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27

Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_002.

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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
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28

1943-, Greenwald Robert A., Golub Lorne M, and New York Academy of Sciences., eds. Inhibition of matrix metalloproteinases: Therapeutic potential. New York, N.Y: New York Academy of Sciences, 1994.

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29

Hitchings, George H. Inhibition of Folate Metabolism in Chemotherapy: The Origins and Uses of Co-trimoxazole. Brand: Springer, 2011.

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30

Chuang, Lu, and Li A. P, eds. Enzyme inhibition in drug discovery and development: The good and the bad. Hoboken, N.J: John Wiley, 2009.

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31

Li, Albert P., and Chuang Lu. Enzyme Inhibition in Drug Discovery and Development: The Good and the Bad. Wiley & Sons, Incorporated, John, 2010.

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32

D, Satoh Tetsuo Ph, and Gupta Ramesh C. 1949-, eds. Anticholinesterase pesticides: Metabolism, neurotoxicity, and epidemiology. Hoboken, N.J: Wiley, 2010.

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33

(Editor), H. John Smith, and Claire Simons (Editor), eds. Proteinase and Peptidase Inhibition: Recent Potential Targets for Drug Development. CRC, 2002.

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34

1930-, Smith H. J., and Simons Claire, eds. Proteinase and peptidase inhibition: Recent potential targets for drug development. London: Taylor & Francis, 2002.

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35

Kim, Young. Aerobic cometabolism of chlorinated aliphatic hydrocarbons by a butane-grown mixed culture: Transformation abilities, kinetics and inhibition. 2000.

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36

Yang, Zhihong, and Xiu-Fen Ming. Adventitia and perivascular adipose tissue—the integral unit in vascular disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0020.

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Obesity and obesity-associated metabolic disorders are highly associated with cardiovascular disease. Abnormal ectopic deposition and accumulation of adipose tissue in organs, including perivascular space (perivascular adipose tissue, PVAT) in obesity are emerging to contribute to vascular disease development through pathological paracrine and/or endocrine secretion of cytokines, namely adipokines, which are vasoactive factors including vascular relaxing and contracting factors, smooth muscle growth promoting and inhibiting factors, and pro- and anti-inflammatory factors. In obesity, production of these factors from PVAT is altered and in imbalance which favours vascular contraction, pathological remodelling, and inflammation. In cross-talk with the endothelium, the functional changes of adventitia and PVAT are detrimental and importantly contribute to the acceleration of vascular atherosclerosis and complications associated with obesity and metabolic disorders
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37

(Editor), Robert A. Greenwald, Stanley Zucker (Editor), and Lorne M. Golub (Editor), eds. Inhibition of Matrix Metalloproteinases: Therapeutic Applications (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1999.

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38

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B9 (folate) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0012.

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Folate is a coenzyme in multiple biochemical pathways involving one-carbon metabolism, including amino acid metabolism, DNA and RNA synthesis, homocysteine metabolism, and methylation of DNA. The most overt consequence of folate deficiency is megaloblastic anaemia caused by the inhibition of DNA synthesis in red blood cell production. Folate deficiency may also influence the ability to maintain DNA methylation patterns in replicating cells, resulting in lasting phenotypic changes. Embryogenesis and fetal growth require higher levels of folate, which must be supplied maternally during pregnancy. A link between low maternal folate levels and the occurrence of neural tube defects has long been recognized. Other effects in pregnancy include increased risks of pre-eclampsia and placental vascular disorders. The general recommendation is for supplementation prior to conception and throughout pregnancy with 400 #amp;#x03BC;g of folic acid in tablet form, in addition to dietary sources, which can reduce the risk of neural tube defects.
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39

M, Yu Peter, Boulton A. A, and Tipton Keith F, eds. Current neurochemical and pharmacological aspects of biogenic amines: Their function, oxidative deamination, and inhibition. Amsterdam: Elsevier, 1995.

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40

M, Yu Peter, Boulton A. A, and Tipton Keith F, eds. Current neurochemical and pharmacological aspects of biogenic amines: Their function, oxidative deamination, and inhibition. Amsterdam: Elsevier, 1995.

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41

Harney, Dennis J. A kinetic study of the enzyme systems deaminating phenylalanine and tyrosine using the specific PAL inhibitor 2-aminoindan-2-phosphonic acid (AIP). 1996.

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42

Stafstrom, Carl E., and Thomas P. Sutula. 2-Deoxyglucose. Edited by Dominic P. D’Agostino. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0036.

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Metabolic regulation of excitability is increasingly appreciated as a strategy to control seizures and reduce pathogenesis. Inhibiting or bypassing glycolysis may be one way in which the ketogenic diet suppresses seizures. 2-deoxy-D-glucose (2DG) is a glucose analog that partially inhibits glycolysis and has antiseizure effects in several acute and chronic seizure models. The mechanisms underlying the acute and chronic effects of 2DG are being investigated. Preliminary studies provide evidence that the acute anticonvulsant actions of 2DG involve activity-dependent presynaptic suppression of excitatory synaptic transmission during network synchronization. The chronic effects of 2DG entail reduction of the expression of brain-derived neurotrophic factor and its receptor, tyrosine kinase B. Preclinical toxicology studies demonstrate that 2DG has a favorable toxicity profile at doses effective for seizure protection. Currently available preclinical studies support 2DG as a novel first-in-class metabolic treatment for epilepsy with an antiglycolytic mechanism distinct from all other anticonvulsants.
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43

Kortgen, Andreas, and Michael Bauer. The effect of acute hepatic failure on drug handling in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0197.

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Impaired hepatic function is a common event in intensive care unit patients and as the liver plays a central role in drug metabolism and excretion this may lead to profound changes in pharmacokinetics. Underlying mechanisms are altered enzyme function of phase I and phase II metabolism, altered transporter protein function together with cholestasis and hepatic perfusion disorders. Moreover, multidrug therapy may lead to induction and inhibition of these enzymes and transporter proteins. In addition, changes in plasma protein binding and volumes of distribution of drugs are common. Altogether, these changes may not only lead to sometimes unpredictable plasma levels of xenobiotics, but also to drug-induced liver injury when hepatocellular accumulation of noxious substances occurs. Concomitant renal dysfunction may further complicate this situation. Pharmacodynamic alterations might also occur. In conclusion, the clinician must carefully evaluate medication given to patients with hepatic failure. Therapeutic drug monitoring should be performed wherever available to guide therapy.
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44

(Editor), Robert A. Greenwald, New York Academy of Sciences (Corporate Author), and Lorne M. Golub (Editor), eds. Inhibition of Matrix Metalloproteinases: Therapeutic Potential (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1994.

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45

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 differences and interspecies differences in response to exposure to toxic substances. The diversity of cellular and molecular mechanisms of toxicity, including enzyme induction and inhibition, oxidative stress, mutagenesis, carcinogenesis, and teratogenesis, are discussed and the chapter concludes with examples of practical applications in clinical evaluation and in toxicity testing.
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46

(Editor), Robert A. Greenwald, New York Academy of Sciences (Corporate Author), and Lorne M. Golub (Editor), eds. Inhibition of Matrix Metalloproteinases: Therapeutic Potential (Annals of the New York Academy of Sciences, Vol 732). New York Academy of Sciences, 1994.

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47

(Editor), Janice E. Chambers, and Patricia E. Levi (Editor), eds. Organophosphates: Chemistry, Fate, and Effects. Academic Press, 1992.

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48

(Editor), Janice E. Chambers, and Patricia E. Levi (Editor), eds. Organophosphates: Chemistry, Fate, and Effects. Academic Press, 1992.

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49

E, Chambers Janice, and Levi Patricia E, eds. Organophosphates: Chemistry, fate, and effects. San Diego: Academic Press, 1992.

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50

Iversen, Leslie. Endocannabinoids. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190846848.003.0004.

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The endocannabinoids are part of a large family of lipid signaling molecules derived from arachidonic acid, including the prostaglandins and leukotrienes, which are important mediators of inflammation. Far less is known about the newer members of the endocannabinoid group, and it remains unclear whether they all play important functional roles. This chapter reviews the multiple members of this family and their biosynthesis and inactivation. Physiological functions, including retrograde synaptic signaling, control of energy metabolism, regulation of pain sensitivity, and cardiovascular control, are discussed. In addition, the chapter reports the synthesis of novel agonists, antagonists, and compounds inhibiting endocannabinoid inactivation as novel medicines.
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