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1
Arimura, Gen-ichiro, and Massimo Maffei, eds. Plant Specialized Metabolism. Boca Raton : Taylor & Francis, 2017.: CRC Press, 2016. http://dx.doi.org/10.1201/9781315370453.
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2
Moore, Bradley S. Marine Enzymes and Specialized Metabolism - Part A. Elsevier Science & Technology, 2018.
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3
Marine Enzymes and Specialized Metabolism - Part A. Elsevier, 2018. http://dx.doi.org/10.1016/s0076-6879(18)x0006-8.
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Marine Enzymes and Specialized Metabolism - Part B. Elsevier, 2018. http://dx.doi.org/10.1016/s0076-6879(18)x0007-x.
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Moore, Bradley S. Marine Enzymes and Specialized Metabolism - Part B. Elsevier Science & Technology, 2018.
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6
Plant Specialized Metabolism: Genomics, Biochemistry, and Biological Functions. Taylor & Francis Group, 2016.
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7
Suzuki, Hideyuki, and Tomonobu Kusano. Polyamines: A Universal Molecular Nexus for Growth, Survival, and Specialized Metabolism. Springer, 2015.
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8
Hollak, Carla E. M., and Robin Lachmann, eds. Inherited Metabolic Disease in Adults. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.001.0001.
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As clinical management of inherited metabolic diseases (IMDs) has improved, more patients affected by these conditions are surviving into adulthood. This trend, coupled with the widespread recognition that IMDs can present differently and for the first time during adulthood, makes the need for a working knowledge of these diseases more important than ever.Inherited Metabolic Disease in Adults offers an authoritative clinical guide to the adult manifestations of these challenging and myriad conditions. These include both the classic pediatric-onset conditions and a number of new diseases that can manifest at any age. It is the first book to give a clear and concise overview of how this group of conditions affects adult patients, a topic that will become a growing imperative for physicians across primary and specialized care.
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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.
10
Ellison, Aaron M., and Lubomír Adamec. Introduction: what is a carnivorous plant? Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198779841.003.0001.
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The approximately 800 species of carnivorous plant together provide a classic example of convergent evolution. The known carnivorous species and genera represent nine independent angiosperm lineages. They are united by a suite of five essential traits that together make up the ‘carnivorous syndrome:’ (1) capturing or trapping prey in specialized. usually attractive, traps; (2) killing the captured prey; (3) digesting the prey; (4) absorption of metabolites (nutrients) from the killed and digested prey; and (5) use of these metabolites for plant growth and development. Although many other ‘paracarnivorous’ plants have one or two of these traits, only plants that have all five of them that function in a coordinated way can be considered true carnivorous plants.
11
Gibson, Glenn R., and Marcel B. Roberfroid. Colonic Microbiota, Nutrition and Health. Springer, 1999.
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12
Clarke, Andrew. Endothermy. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780199551668.003.0010.
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Endothermy is the maintenance of a high and relatively constant internal body temperature, where the principal source of heat is a high metabolic rate at rest. The main sources of this heat are the visceral organs (especially the liver, spleen and gut), which tend to be larger and with greater metabolic capacity than in ectotherms. An important contribution also comes from heat produced by muscular activity during routine daily activity. Among living animals, only mammals and birds are true endotherms. Body temperatures are generally higher in bird than in mammals, and in both groups mean body temperature varies with lineage, environmental temperature and diet. Within the thermoneutral zone (TNZ) endotherms regulate their body temperature by controlling the loss of sensible heat. Below the TNZ, endotherms generate extra heat by uprating the metabolic rate of viscera, shivering, increased activity and in some mammals, switching on a specialised heat generating tissue (brown adipose tissue, BAT). Above the TNZ, endotherms lose heat by evaporation of water. Endotherms vary their insulation seasonally and depending on climate. Endothermy evolved independently in mammals and birds, but the precise timing of its evolution is not clear in either lineage.
13
Giuseffi, Jennifer, John McPherson, Chad Wagner, and E. Wesley Ely. Acute cognitive disorders: recognition and management of delirium in the cardiovascular intensive care unit. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0074.
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Delirium is the most common acute cognitive disorder seen in critically ill patients in the cardiovascular intensive care unit. It is defined as a disturbance of consciousness and cognition that develops suddenly and fluctuates over time. Delirious patients can become hyperactive, hypoactive, or both. The occurrence of delirium during hospitalization is associated with increased in-hospital and long-term morbidity and mortality. The cause of delirium is multifactorial and may include imbalances in neurotransmitters, inflammatory mediators, metabolic disturbances, impaired sleep, and the use of sedatives and analgesics. Patients with advanced age, dementia, chronic illness, extensive vascular disease, and low cardiac output are at particular risk of developing delirium. Specialized bedside assessment tools are now available to rapidly diagnose delirium, even in mechanically ventilated patients. Increased awareness of delirium risk factors, in addition to non-pharmacological and pharmacological treatments for delirium, can be effective in reducing the incidence of delirium in cardiac patients and in minimizing adverse outcomes, once delirium occurs.
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McPherson, John, Jennifer Giuseffi, Chad Wagner, and E. Wesley Ely. Acute cognitive disorders: recognition and management of delirium in the cardiovascular intensive care unit. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0074_update_001.
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Delirium is the most common acute cognitive disorder seen in critically ill patients in the cardiovascular intensive care unit. It is defined as a disturbance of consciousness and cognition that develops suddenly and fluctuates over time. Delirious patients can become hyperactive, hypoactive, or both. The occurrence of delirium during hospitalization is associated with increased in-hospital and long-term morbidity and mortality. The cause of delirium is multifactorial and may include imbalances in neurotransmitters, inflammatory mediators, metabolic disturbances, impaired sleep, and the use of sedatives and analgesics. Patients with advanced age, dementia, chronic illness, extensive vascular disease, and low cardiac output are at particular risk of developing delirium. Specialized bedside assessment tools are now available to rapidly diagnose delirium, even in mechanically ventilated patients. Increased awareness of delirium risk factors, in addition to non-pharmacological and pharmacological treatments for delirium, can be effective in reducing the incidence of delirium in cardiac patients and in minimizing adverse outcomes, once delirium occurs.
15
Suffredini, Anthony F., and J. Perren Cobb. Genetic and molecular expression patterns in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0031.
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Investigators who study RNA, proteins, or metabolites use analytic platforms that simultaneously measure changes in the relative abundance of thousands of molecules in a single biological sample. Over the last decade, the application of these high-throughput, genome-wide platforms to study critical illness and injury has generated huge quantities of data that require specialized computational skills for analysis. These investigations hold promise for improving our understanding of the host response, thereby transforming the practice of intensive care. This chapter summarizes recent technological and computational approaches used in genomics, proteomics, and metabolomics. While major advances have been made with these approaches when applied to chronic diseases, the acute nature of critical illness and injury has unique challenges. The rapidity of initiating events, the trajectory of inflammation that follows injury or infection and the interplay of host responses to a replicating infection, all have major effects on changes in gene and molecular expression. This complexity is further accentuated by measurement that may vary with the timing and type of tissue sampled after the critical event. In addition, the hunt for novel molecular markers holds promise for identifying patients at risk for severe illness and for enabling more individualized therapy.
16
Sprague, Stuart M., and James M. Pullman. Spectrum of bone pathologies in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0122.
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Histologic bone abnormalities begin very early in the course of chronic kidney disease. The KDIGO guidelines recommend that bone disease in patients with chronic kidney disease should be diagnosed on the basis of bone biopsy examination, with bone histomorphometry. They have also proposed a new classification system (TMV), using three key features of bone histology—turnover, mineralization, and volume—to describe bone disease in these patients. However, bone biopsy is still rarely performed today, as it involves an invasive procedure and highly specialized laboratory techniques. High-turnover bone disease (osteitis fibrosa cystica) is mainly related to secondary hyperparathyroidism and is characterized by increased rates of both bone formation and resorption, with extensive osteoclast and osteoblast activity, and a progressive increase in peritrabecular marrow space fibrosis. On the other hand, low-turnover (adynamic) bone disease involves a decline in osteoblast and osteoclast activities, reduced new bone formation and mineralization, and endosteal fibrosis. The pathophysiological mechanisms of adynamic bone include vitamin D deficiency, hyperphosphataemia, metabolic acidosis, inflammation, low oestrogen and testosterone levels, bone resistance to parathyroid hormone, and high serum fibroblast growth factor 23. Mixed uraemic osteodystrophy describes a combination of osteitis fibrosa and mineralization defect. In the past few decades, an increase in the prevalence of mixed uraemic osteodystrophy and adynamic bone disease has been observed.
17
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.
18
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.
Full textAbstract:
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.
19
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.
Full textAbstract:
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.
20
Kipnis, Eric, and Benoit Vallet. Tissue perfusion monitoring in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0138.
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Resuscitation endpoints have shifted away from restoring normal values of routinely assessed haemodynamic parameters (central venous pressure, mean arterial pressure, cardiac output) towards optimizing parameters that reflect adequate tissue perfusion. Tissue perfusion-based endpoints have changed outcomes, particularly in sepsis. Tissue perfusion can be explored by monitoring the end result of perfusion, namely tissue oxygenation, metabolic markers, and tissue blood flow. Tissue oxygenation can be directly monitored locally through invasive electrodes or non-invasively using light absorbance (pulse oximetry (SpO2) or tissue (StO2)). Global oxygenation may be monitored in blood, either intermittently through blood gas analysis, or continuously with specialized catheters. Central venous saturation (ScvO2) indirectly assesses tissue oxygenation as the net balance between global O2 delivery and uptake, decreasing when delivery does not meet demand. Lactate, a by-product of anaerobic glycolysis, increases when oxygenation is inadequate, and can be measured either globally in blood, or locally in tissues by microdialysis. Likewise, CO2 (a by-product of cellular respiration) and PCO2 can be measured globally in blood or locally in accessible mucosal tissues (sublingual, gastric) by capnography or tonometry. Increasing PCO2 gradients, either tissue-to-arterial or venous-to-arterial, are due to inadequate perfusion. Metabolically, the oxidoreductive status of mitochondria can be assessed locally through NADH fluorescence, which increases in situations of inadequate oxygenation/perfusion. Finally, local tissue blood flow may be measured by laser-Doppler or visualized through intravital microscopic imaging. These perfusion/oxygenation resuscitation endpoints are increasingly used and studied in critical care.