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Books on the topic 'Metabolic function'

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Published: 4 June 2021
Last updated: 14 February 2022

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1

name, No. Metabolic profiling: Its role in biomarker discovery and gene function analysis. Boston, MA: Kluwer Academic, 2003.

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2

Harrigan, George G., and Royston Goodacre, eds. Metabolic Profiling: Its Role in Biomarker Discovery and Gene Function Analysis. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0333-0.

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3

Brown, A. M. Metabolic substrates other than glucose support axon function in central white mater. New York, N.Y: Wiley-Liss, Inc., 2001.

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4

Canada. Dept. of Fisheries and Oceans. Physical and Chemical Sciences Branch. Protocols for measuring mixed function oxygenases of fish liver. Mont-Joli, Qué: Physical and Chemical Sciences Branch, Dept. of Fisheries and Oceans, 1991.

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5

Bronner, Felix, Mary C. Farach-Carson, and Helmtrud I. Roach, eds. Bone-Metabolic Functions and Modulators. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2745-1.

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6

Dhalla, Naranjan S., Grant N. Pierce, and Robert E. Beamish, eds. Heart Function and Metabolism. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2053-1.

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7

Yazaki, Yoshio, and Seibu Mochizuki, eds. Cellular Function and Metabolism. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3078-7.

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8

Storey, Kenneth B., ed. Functional Metabolism. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2004. http://dx.doi.org/10.1002/047167558x.

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9

Moss, Joel, and Peter Zahradka, eds. ADP-Ribosylation: Metabolic Effects and Regulatory Functions. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2614-8.

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10

Workshop Conference Hoechst-Werk Albert (1987 Frankfurt, Germany). Muscle ischaemia: Functional and metabolic aspects. Edited by Hudlicka O and Okyayuz-Baklouti I. München: C. Wolf, 1988.

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11

Dirnagl, Ulrich, Arno Villringer, and Karl M. Einhäupl, eds. Optical Imaging of Brain Function and Metabolism. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4899-2468-1.

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12

Optical Imaging of Brain Function andMetabolism (Conference) (1991 Garmisch-Partenkirchen, Germany). Optical imaging of brain function and metabolism. New York: Plenum, 1993.

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13

International Conference on Integration of Mitochondrial Function (1987 Chapel Hill, N.C.). Integration of mitochondrial function. New York: Plenum Press, 1988.

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14

Histones: Class, structure, and function. Hauppauge, N.Y: Nova Science Publishers, 2011.

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15

1931-, Mortlock Robert P., ed. The Evolution of metabolic function. Boca Raton [Fla.]: CRC Press, 1992.

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16

Metabolic function of the lungs. Philadelphia: W. B. Saunders, 1989.

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17

Krywawych, Steve. Metabolic Acidosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0081.

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Hydrogen ion turnover in resting adults exceeds 500 mole/24 hours and maintenance of hydrogen ion balance is an essential requirement for normal cellular, organ and body function. A variety of mechanisms co-operate to ensure that the hydrogen concentration in plasma can be tightly controlled between 35 to 46 nano moles per litre and any deviation being rapidly compensated. Inherited metabolic diseases can to a variable degree impact to disturb this equilibrium. The underlying causes responsible for this outcome are disease dependent and may occur due to generation of overwhelming quantities of hydrogen per se, or at the level of renal reabsorption or generation of bicarbonate or due to tissue hypoxia resulting from either poor pulmonary or cardiac function.
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18

Herken, E. Genazzani H. Central Nervous System: Studies on Metabolic Regulation and Function. Springer, 2011.

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19

Central Nervous System: Studies on Metabolic Regulation and Function. Springer, 2011.

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20

Nasimudeen, Abdul. Normal respiratory function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0125.

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Respiration has two components: external respiration, which enables the absorption of O2 and the removal of CO2, and internal respiration, which enables the utilization of O2 and production of CO2 and mediates gas exchange between the cells and their fluid medium. This chapter addresses the mechanics of respiration; gas exchange in the lungs; the pulmonary circulation; lung defence mechanisms; and the metabolic and endocrine functions of the lungs.
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21

Rowland, Thomas W. Cardiovascular function. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0011.

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The circulatory response to increased metabolic demands of endurance exercise is best explained by a model in which volume of circulatory flow is governed by alterations in peripheral vascular resistance. These dynamics of the cardiovascular response to an acute bout of progressive endurance exercise are similar in children and adults, and, when adjusted for body size, true cardiovascular fitness (ability to generate cardiac output) is no different in healthy, untrained pre- and postpubertal individuals. As in adults, the capacity to eject stroke volume at maximal exercise differentiates levels of physiological fitness (maximal oxygen uptake) between individual children. Stroke volume at exhaustive exercise, in turn, appears to be governed by factors which influence left ventricular diastolic size rather than those which dictate myocardial systolic and diastolic function.
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22

Rowland, Thomas W. Cardiovascular function. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199232482.003.0019.

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While the critical nature of blood perfusion during exercise is well recognized, many questions remain incompletely answered. What are the mechanisms by which circulation of blood is increased during exercise? By what means is circulatory flow tightly linked to tissue metabolic demands? What limits increases in circulatory flow during exhaustive exercise? By what mechanism does repeated exercise (i.e. fitness training) improve cardiovascular capacity? And—germane to the present discussion—are the answers to any or all of these questions diff erent in children than adults? Chapter 19 considers these issues, summarizing available information in the paediatric population from the perspectives of three different exercise models: progressive treadmill or cycle ergometer exercise to exhaustion, sustained constant-load submaximal exercise (cardiovascular drift ), and isometric or resistance exercise.
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23

O’Callaghan, Chris A. Renal function. Edited by Rutger Ploeg. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0126.

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The kidneys play a central role in homeostasis by maintaining extracellular fluid composition and volume. They do this by continuous filtration of plasma in the renal glomeruli and then subsequent modification of the filtered fluid as it passes along the nephron. The filtration process excludes large molecules, but most small molecules and ions are freely filtered. The filtrate that is produced in the glomeruli has a similar composition to plasma with respect to small molecules and ions. Most of the water and solutes are reabsorbed along the tubules and this process requires high levels of metabolic activity. In addition, a range of compounds and ions are secreted into the tubules along the nephron. Renal function is central to homeostasis and an appreciation of normal renal physiology is essential to understand the role of the kidney in a wide variety of disease processes.
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24

G, Harrigan George, and Goodacre Royston, eds. Metabolic profiling: Its role in biomarker discovery and gene function analysis. Boston, Mass: Kluwer Academic, 2003.

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25

F, Guillon, and European AIR concerted action, eds. Plant polysaccharides in human nutrition: Structure, function, digestive fate & metabolic effects. Nantes, France: Institut National de la Recherche Agronomique, 1997.

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26

Metabolic Profiling: Its Role in Biomarker Discovery and Gene Function Analysis. Springer, 2011.

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27

(Editor), George G. Harrigan, and Royston Goodacre (Editor), eds. Metabolic Profiling: Its Role in Biomarker Discovery and Gene Function Analysis. Springer, 2003.

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28

Alreja, Meenakshi, Carol F. Elias, and Jennifer W. Hill, eds. From precocious puberty to infertility: metabolic control of the reproductive function. Frontiers Media SA, 2013. http://dx.doi.org/10.3389/978-2-88919-133-8.

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29

McManus, Alison M., and Neil Armstrong. Pulmonary function. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0010.

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The principles of pulmonary ventilation are the same for children and adults. Ventilation adjusts to alterations in metabolic demand in the child; but for a given exercise intensity there is a greater ventilation when expressed relative to body mass and a higher energetic cost of breathing in the child compared to the adult. Limited evidence suggests child-adult differences may be a result of immature chemoreception, a greater drive to breathe, differences in airway dimensions, and the mechanical work of breathing. There are few studies investigating the dynamic ventilatory response to moderate intensity exercise and none to heavy or very heavy intensity exercise in the child. Little attention has been devoted to the developmental pattern of ventilatory control, although there is evidence of altered chemoreceptive modulation of breathing in the child. Considerable research will be necessary before we have a full appreciation of pulmonary function during exercise in the child.
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30

Phillips, Andrew J. K. The function of sleep. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198778240.003.0003.

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The function of sleep was a longstanding mystery in neuroscience, but there is now compelling empirical evidence for several key functions of sleep. Elucidating these functions and their underlying pathways is a hot area for the field of sleep research today, and many open questions remain. What we have gleaned from recent data is that it is important to view sleep as a synthesis of processes that enable improved functioning during wakefulness. There is no single universal function of sleep, but rather a collection of synergistic functions that are each of varying importance to different species. In humans, sleep plays critical roles in consolidating memories, restoring energy stores in the brain, clearing wastes from the brain, immune function, metabolic function, and overall health.
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31

Korkeila, Maarit, Bengt Lindholm, and Peter Stenvinkel. The obese patient (metabolic syndrome). Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0168.

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Overweight and obesity cause pathophysiological changes in renal function and increase the risk for chronic kidney disease in otherwise healthy subjects. This should not be a surprise as the risk factors for metabolic syndrome largely overlap with those for chronic kidney disease. Intentional weight loss has beneficial effects on risk factors, but long term effects are less clear. Bariatric surgery does seem to achieve rapid benefits on blood pressure and proteinuria as well as on other aspects of metabolic syndrome, but its long term implications for kidney function are less clear cut as there may be an increased risk of nephrolithiasis, and possibly AKI and other complications.Obesity in haemodialysis patients is one of those paradoxical examples of reverse epidemiology where a factor associated with negative outcomes in the general population is associated with better outcomes in dialysis patients. The same is true for high blood cholesterol values. Interpretation is complicated by complex competing outcomes and confounders.
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32

Abracchio, Maria P., and Michael Williams. Purinergic and Pyrimidinergic Signalling II: Cardiovascular, Respiratory, Immune, Metabolic and Gastrointestinal Tract Function. Springer, 2014.

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33

The effects of hand cooling during strenuous exercise on metabolic and cardiorespiratory function. 1990.

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34

The effects of hand cooling during strenuous exercise on metabolic and cardiorespiratory function. 1988.

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35

Fugmann, Andreas. Effects of Acute Metabolic Interventions on Hemodynamics, Endothelial Function and Forearm Glucose Uptake. Uppsala Universitet, 2001.

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36

Shaffu, Shireen, and James Taylor. Normal function of the musculoskeletal system. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0263.

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The musculoskeletal system consists of specialized connective tissue whose primary function is to allow locomotion. The tissues of the musculoskeletal system are bones, muscles, tendons, and ligaments. In particular, the bony skeleton also has the task of protecting vital internal organs, contains the bone marrow, and is an intrinsic part of the metabolic pathways involved in calcium homeostasis. Motion is allowed by specialized articulating structures, the joints.
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37

Cheng, Ning, Susan A. Masino, and Jong M. Rho. Metabolic Therapy for Autism Spectrum Disorder and Comorbidities. Edited by Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0014.

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Autism spectrum disorder (ASD) is a heretogenous developmental disorder characterized by deficits in sociability and communication and by repetitive and/or restrictive behaviors. Currently, only comorbid manifestations can be alleviated (such as seizures and sleep disturbance) not core behavioral symptoms. Recent studies have increasingly implicated mitochondrial dysfunction as a cause of ASD. Mitochondria play an integral role in many cellular functions and are susceptible to many pathophysiological insults. Derangements in mitochondrial structure and function provide a scientific rationale for experimental therapeutics. Meanwhile, the high-fat, low-carbohydrate ketogenic diet (KD) has been shown to enhance mitochondrial function through a multiplicity of mechanisms. Reviewed herein is clinical and basic laboratory evidence for the use of metabolism-based therapies such as the KD in the treatment of ASD, as well as emerging comorbid models of epilepsy and autism. Future research directions aimed at validating such therapeutic approaches and identifying novel mechanistic targets are discussed.
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38

Martínez-François, Juan Ramón, Nika N. Danial, and Gary Yellen. Metabolic Seizure Resistance via BAD and KATP Channels. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0028.

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On a ketogenic diet, ketone bodies provide an alternative fuel, replacing much of the glucose used ordinarily by the brain. This switch is thought to underlie its anticonvulsant effects. Brain fuel utilization can also be modified by a nondietary approach: genetic alteration of the protein BAD, which has known roles in regulating both apoptosis and glucose metabolism. When the metabolic function of BAD is genetically altered in mice, it produces reduced glucose and increased ketone body metabolism in neurons and astrocytes. This effect is related to regulation of BAD by phosphorylation and is independent of its apoptotic function. Mice with BAD modifications that produce decreased glucose metabolism exhibit a marked increase in the activity of neuronal ATP-sensitive potassium (KATP) channels and strong resistance to behavioral and electrographic seizures in vivo. This seizure resistance is lost upon genetic ablation of KATP channels, suggesting that KATP channels mediate BAD’s anticonvulsant effect.
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39

Ellinson, Michelle, and Tommy Rampling. Normal nutritional function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0331.

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Normal nutritional function requires a healthy diet. Healthy eating incorporates a variety of nutrients that are essential for energy expenditure, prevention of disease, and maintenance of normal physiological function. An unhealthy diet can result in malnutrition, and this contributes to illness and death throughout the world. The core principle of healthy eating is obtaining an adequate balance, and the diseases resulting from overnourishment differ greatly from those resulting from undernourishment. In the third world, diets tend to rely heavily on staple crops, and can be very seasonal. Energy sources are predominantly cereals, whereas meat and fish are limited. Malnutrition tends to occur from a lack of essential nutrients, leading to conditions such as vitamin deficiencies, kwashiorkor, and iodine deficiency syndromes. In first-world countries, people have more freedom to choose what they eat. Thus, diets tend to be high in fat and dense in energy. Obesity, diabetes, coronary heart disease, cancer, and hypertension are major contributors to morbidity and mortality. A healthy diet should contain adequate proportions of carbohydrates, fats, proteins, vitamins, and trace elements. The intake of these constituents is sporadic, with meals constituting major boluses of potential energy. Energy expenditure, conversely, is continuous. The human body has, therefore, developed complex mechanisms directing nutrients into storage when in excess, and mobilizing these stores as they are needed, and it is essential that sufficient energy is always available to maintain the basal metabolic rate, which is the amount of energy expended while at rest in a neutrally temperate environment. This energy is sufficient only for the functioning of the vital organs, such as the heart, the lungs, the liver, the kidneys, and the CNS.
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40

Edward, Bittar E., ed. Metabolic pumps and intracellular homeostasis, hormones and cell function, intercellular communication, cell motility and contractility. Greenwich, Conn: JAI Press, 1992.

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41

Bower, Mark, Louise Robinson, and Sarah Cox. Endocrine and metabolic complications of advanced cancer. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0142.

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Cancer produces endocrine and metabolic complications in two ways. Firstly, the primary tumour or its metastases may interfere with the function of endocrine glands, kidneys, or liver by invasion or obstruction. Secondly, tumours may give rise to remote effects without local spread and these actions are termed paraneoplastic manifestations of malignancy. Generally, these paraneoplastic syndromes arise from secretion by tumours of hormones, cytokines, and growth factors, but also occur when normal cells secrete products in response to the presence of tumour. This chapter reviews the pathogenesis, epidemiology, and management of the commonest paraneoplastic endocrinopathies including hypercalcaemia, Cushing’s syndrome, the syndrome of inappropriate antidiuresis, non-islet cell tumour hypoglycaemia, enteropancreatic hormone syndromes, Carcinoid syndrome, phaeochromocytoma, gonadotrophin secretion syndromes, prolactin and oxytocin secretion, and paraneoplastic pyrexia. The chapter concludes with a brief discussion of the management of metabolic disease in the context of advanced malignancy including hyperglycaemia, thyroid dysfunction, metabolic bone disease, renal failure, liver failure, and lactic acidosis.
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42

Ostrow, J. Donald. Bile Pigments and Jaundice: Molecular, Metabolic, and Medical Aspects (Liver: Normal Function and Disease Series, Vol 4). Marcel Dekker, 1986.

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43

Grunnet, Niels, and Bjorn Quistorff. Regulation of Hepatic Function: Metabolic and Structural Interactions: Proceedings (Alfred Benzon Symposium, No. 30) (Alfred Benzon Symposium). Mosby, 1991.

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44

Neligan, Patrick J., and Clifford S. Deutschman. Management of metabolic acidosis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0256.

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Metabolic acidosis (MA) commonly complicates critical illness, usually manifesting as a fall in arterial pH (<7.4) accompanied by a concomitant fall in serum bicarbonate concentration. Acidosis caused by unmeasured anions (UMA), can be distinguished from Hyperchloraemic acidosis by demonstrating a widening of the anion gap (AG). AG should be corrected for albumin and lactate. The base deficit (BD) calculates degree of metabolic acidosis and represents the amount of strong cation required to restore the pH to 7.4. Neither the AG nor the BD specify the cause of acidosis, and are unhelpful in the setting of mixed disorders. The base deficit gap (BDG) is used to calculate the effect of free water, sodium, chloride and albumin on the BD. It is the difference between BDcalc and BDmeasured (on a blood gas) and represents UMA. The strong ion gap more robustly calculates the amount of UMA than AG or BDG, and may be more accurate at predicting outcomes in the emergency room. Lactic acidosis is due to hypovolaemia until otherwise proven. In the majority of cases aggressive fluid resuscitation is warranted. In the presence of normal tissue blood flow regional hypoperfusion, poisoning or exogenous catecholamines should be considered. Ketoacidosis is due to intracellular glucose deficiency, caused by hypoinsulinaemia or starvation. The former is treated with isotonic crystalloid and insulin. Renal acidosis is treated with renal replacement therapy or recovery of renal function.
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45

C. H. Kim and H. K. Kang*. Effect of dietary supplementation with a chlorella by-product on the performance, immune response and metabolic function in laying hens. Verlag Eugen Ulmer, 2015. http://dx.doi.org/10.1399/eps.2015.108.

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46

Bonnet, Marie-Pierre, and Anne Alice Chantry. Placenta and uteroplacental perfusion. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0003.

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The placenta is a complex and changing organ necessary for normal fetal growth and development and for maintenance of a healthy pregnancy. It has three major functions: a protective function of the fetus, an endocrine function, and a metabolic function. The main functional unit of the placenta is the chorionic villous, responsible for the majority of the fetal–maternal exchanges. Migration of trophoblastic cells induces a remodelling of the uterine arteries, with vasodilatated and compliant vessels, unresponsive to maternal vasomotor control. Therefore, any significant change in maternal blood pressure, in particular in the context of general or regional anaesthesia, can directly impact on uteroplacental perfusion. Most anaesthetic drugs cross the placental barrier, but without significant consequences on the fetal well-being.
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47

Adam, Sheila, Sue Osborne, and John Welch. Renal problems. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199696260.003.0007.

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The kidneys normally excrete metabolic waste products in urine while maintaining fluid, electrolyte, and acid–base balance. However, critical illness frequently leads to renal impairment, loss of these functions, and potentially life-threatening complications. This chapter describes the functional anatomy and physiology of the renal system, important risk factors for acute kidney injury, and how renal function can be monitored and maintained. The methods, advantages, disadvantages, and practical management of different types of renal replacement therapy are discussed, together with essential aspects of holistic patient care.
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48

Golper, Thomas A., Andrew A. Udy, and Jeffrey Lipman. Drug dosing in acute kidney injury. Edited by William G. Bennett. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0364.

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Drug dosing in acute kidney injury (AKI) is one of the broadest topics in human medicine. It requires an understanding of markedly altered and constantly changing physiology under many disease situations, the use of the drugs to treat those variety of diseases, and the concept of drug removal during blood cleansing therapies. Early in AKI kidney function may be supraphysiologic, while later in the course there may be no kidney function. As function deteriorates other metabolic pathways are altered in unpredictable ways. Furthermore, the underlying disorders that lead to AKI alter metabolic pathways. Heart failure is accompanied by vasoconstriction in the muscle, skin and splanchnic beds, while brain and cardiac blood flow proportionally increase. Third spacing occurs and lungs can become congested. As either kidney or liver function deteriorates, there may be increased or decreased drug sensitivity at the receptor level. Acidosis accompanies several failing organs. Protein synthesis is qualitatively and quantitatively altered. Sepsis affects tissue permeability. All these abnormalities influence drug pharmacokinetics and dynamics. AKI is accompanied by therapeutic interventions that alter intrinsic metabolism which is in turn complicated by kidney replacement therapy (KRT). So metabolism and removal are both altered and constantly changing. Drug management in AKI is exceedingly complex and is only beginning to be understood. Thus, we approach this discussion in a physiological manner. Critically ill patients pass through phases of illness, sometimes rapidly, other times slowly. The recognition of the phases and the need to adjust medication administration strategies is crucial to improving outcomes. An early phase involving supraphysiologic kidney function may be contributory to therapeutic failures that result in the complication of later AKI and kidney function failure.
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49

Fraser, Jamie L., Frédéric Sedel, and Charles P. Vendetti. Disorders of Cobalamin and Folate Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0027.

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Cobalamin C deficiency (cblC) and related disorders of intracellular cobalamin metabolism may present at any time from the prenatal period through adolescence/adulthood and are due to deficiency of the cobalamin cofactors adenosylcobalamin and methylcobalamin. Chronic complications of cblC depend on the age at presentation and may include poor growth, renal dysfunction, neuropsychiatric manifestations, intellectual disability, strokes, progressive leukoencephalopathy and spinal cord degeneration, psychiatric manifestations and executive function deficits, and optic nerve and retinal anomalies. While less common than in isolated MMA, acute metabolic decompensation may occur in cblC patients due to accumulation of methylmalonic acid and associate metabolites and should be managed as in isolated MMA in conjunction with a metabolic consultant. The most common inborn error of folate (vitamin B9) metabolism relevant for adult patients is methylenetetrahydrofolate reductase (MTHFR) deficiency. Manifestations are primarily neurological, but the disorder may present in a substantial number of adults with psychiatric symptoms. Early recognition with adequate treatment is crucial.
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50

The effect of acetylsalicylic acid administration on metabolic, cardiovascular, and thermoregulatory function in young males during acute exercise in hot and neutral environments. 1986.

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