Books: 'Complex physiology'

1

Rammensee, Hans-Georg. MHC ligands and peptide motifs. Austin, Tex: Landes Bioscience, 1997.

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2

Aizawa, Miki. Major histocompatibility complex of the rat, rattus norvegicus. Sapporo: Hokkaido University School of Medicine, 1988.

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3

Bianca, C. Towards a mathematical theory of complex biological systems. Singapore: World Scientific, 2011.

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4

Aizawa, Miki. Major histocompatibility complex of the rat, Rattus norvegicus: Its structure and function. Sapporo: Hokkaido University School of Medicine, 1988.

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5

The new executive brain: Frontal lobes in a complex world. New York: Oxford University Press, 2009.

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6

Dehmer, Matthias. Towards an Information Theory of Complex Networks: Statistical Methods and Applications. Boston: Springer Science+Business Media, LLC, 2011.

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7

New aspects of complement structure and function. Austin, TX: R.G. Landes, 1994.

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8

Dahlem Workshop on Complex Organismal Functions: Integration and Evolution in Vertebrates (1988 Berlin, Germany). Complex organismal functions: Integration and evolution in vertebrates : report of the Dahlem Workshop on Complex Organismal Functions--Integration and Evolution in Vertebrates, Berlin 1988, August 28-September 2. Edited by Wake David B and Roth, Gerhard, 1942 Aug. 15-. Chichester [England]: Wiley, 1989.

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9

K, Dana Syamal, Roy Prodyot K, and Kurths J. (Jürgen) 1953-, eds. Complex dynamics in physiological systems: From heart to brain. [Dordrecht]: Springer, 2009.

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10

Harding, Clifford V. MHC molecules and antigen processing. Austin, Tex: R.G. Landes Co., 1997.

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11

International Society for Invertebrate Neurobiology. Symposium. Neurobiology of invertebrates: Simple and complex regulatory systems : proceedings of the Symposium of the International Society for Invertebrate Neurobiology, Tihany, Hungary, June 27-July 2, 1995. Budapest: Akadémiai Kiadó, 1996.

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12

International Meeting on the Function of Thiamin Diphosphate Enzymes (1990 Blaubeuren, Germany). Biochemistry and physiology of thiamin diphosphate enzymes: Proceedings of the International Meeting on the Function of Thiamin Diphosphate Enzymes, held in Blaubeuren, October 1990. Weinheim: VCH, 1991.

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13

Inuzuka, Hiroyuki. SCF and APC E3 ubiquitin ligases in tumorigenesis. Cham: Springer, 2014.

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14

Achkasov, Evgeniy, Andrey Pugaev, Maksim Zabelin, and Vladislav Posudnevskiy. Acute pancreatitis: clinic, diagnosis, treatment. ru: INFRA-M Academic Publishing LLC., 2019. http://dx.doi.org/10.12737/995531.

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The textbook consistently highlights the issues of anatomy and physiology of the pancreas, etiology, pathogenesis, classification, clinical picture, diagnosis and treatment of acute pancreatitis. Special attention is paid to determining the severity and prognosis of the disease. Modern approaches to treatment taking into account the severity of the disease, features of suppression of secretory activity of the pancreas and the role of nutritional support in the complex treatment of acute pancreatitis are presented. Attention is drawn to the timing of minimally invasive interventions for uninfected and infected postnecrotic fluid formations, as well as methods of surgical treatment in the phase of purulent-necrotic complications of acute pancreatitis. For the first time in the educational edition psychological aspects of rehabilitation of surgical patients are presented. Mastering the material of the textbook is facilitated by test tasks and questions for self-control. Meets the requirements of the Federal state educational standards of higher education of the last generation. It is intended for students of medical universities, clinical residents and doctors studying in the system of additional professional education, specialty "Surgery".

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15

Sneyd, James, Richard Bertram, Joel Tabak, Wondimu Teka, Theodore Vo, Martin Wechselberger, and Vivien Kirk. Mathematical Analysis of Complex Cellular Activity. Springer, 2015.

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16

Bittihn, Philip. Complex Structure and Dynamics of the Heart. Springer, 2016.

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17

Bittihn, Philip. Complex Structure and Dynamics of the Heart. Springer, 2014.

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18

Miller, Robert, 1943 Aug. 29-, Ivanit͡s︡kiĭ A. M, and Balaban P. M, eds. Complex brain functions: Conceptual advances in Russian neuroscience. Amsterdam, Netherlands: Harwood Academic, 2000.

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19

(Editor), Robert G. Urban, and Roman M. Chicz (Editor), eds. Mhc Molecules: Expression, Assembly and Function (Medical Intelligence Unit). Chapman & Hall, 1996.

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20

L, Kraus Steven, ed. TMJ disorders: Management of the craniomandibular complex. New York: Churchill Livingstone, 1988.

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21

Miller, Lauren A., and Mary N. Towner. Pregnancy Physiology. Edited by Emma Ciafaloni, Cheryl Bushnell, and Loralei L. Thornburg. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190667351.003.0004.

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This chapter discusses the complex physiologic changes that take place in the immune and nervous system of the pregnant patient. Shifts in cellular production and function as well as the dramatic alterations in hormone concentrations observed in pregnancy are described. The chapter also reviews the current understanding of the major gestational hormones’ roles within the immune and nervous system. We will also summarize the current state of knowledge regarding the physiologic effects of pregnancy, focusing on the effects of estrogen, progesterone, and prolactin on the female immune system and central and peripheral nervous systems. Whenever possible, the clinical relevance of such immunologic and neurologic adaptations to pregnancy will be highlighted.

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22

1948-, Bejan Adrian, Mamut Eden, and NATO Advanced Study Institute on Thermodynamics and the Optimization of Complex Energy Systems (1998 : Neptun, Romania), eds. Theromodynamic optimization of complex energy systems. Dordrecht: Kluwer Academic Publishers, 1999.

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23

Miller, Robert, 1943 Aug. 29- and Wickens J, eds. Brain dynamics and the striatal complex. Amsterdam, Netherlands: Harwood Academic, 2000.

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24

(Editor), Robert Miller, and Alexey M. Ivanitsky (Editor), eds. Complex Brain Functions: Conceptual Advances in Russian Neuroscience (Conceptual Advances in Brain Research). CRC, 2000.

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25

Naumenko, E. V. Central Regulation of the Pituitary-Adrenal Complex. Springer, 2012.

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26

(Editor), A. Quarteroni, L. Formaggia (Editor), and A. Veneziani (Editor), eds. Complex Systems in Biomedicine. Springer, 2006.

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27

(Editor), D. B. Wake, and G. Roth (Editor), eds. Complex Organismal Functions: Integration and Evolution in Vertebrates. John Wiley & Sons, 1989.

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28

1944-, Krammer E. B., ed. The Motoneuronal organization of the spinal accessory nuclear complex. Berlin: Springer-Verlag, 1987.

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29

O’Flaherty, Brendan M., Chia-Chun Hsu, M. Anzar Abbas, and Donald G. Rainnie. Cellular Physiology of the Basolateral Complex of the Amygdala and Its Modulation by Stress. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0003.

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Fear is a critical emotional response that allows an organism to safely navigate through dangerous environments. The neural systems underlying the fear response have been well characterized, and include the amygdala, hippocampus, prefrontal cortex, bed nucleus of stria terminalis, nucleus accumbens, and others. While normally these brain regions coordinate to produce an appropriate fear response, the fear network in humans can become dysregulated after a traumatic event. The resulting phenotype of hyperarousal, avoidance, and re-experiencing of fear known as post-traumatic stress disorder (PTSD) is a growing problem in the United States. This chapter focuses on the role of the basolateral complex (BLC) of the amygdala, which has been implicated in the neuropathology of PTSD, particularly the hyperarousal, fear generalization, and fear extinction deficits characteristic of the disorder, as well as aspects of the microcircuitry, network connectivity, and neuromodulation of the BLC that may be involved in the pathophysiology of PTSD.

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30

Kasahara, Masanori. Major Histocompatibility Complex: Evolution, Structure, and Function. Springer, 2000.

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31

(Editor), Viktor K. Jirsa, and A. R. McIntosh (Editor), eds. Handbook of Brain Connectivity (Understanding Complex Systems). Springer, 2007.

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32

Gordon, Joanna K., and Mark C. Bellamy. Gastrointestinal physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0004.

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The physiology of the human gut and gastrointestinal tract is complex. Studying it is difficult, and much of what we know relies on extrapolation from animal models. The interactions between normal physiology, deranged physiology, and anaesthetic drugs and procedures are likewise extremely complex, and in some cases paradoxical. A clear understanding of these is likely to be beneficial in achieving best clinical outcomes in anaesthesia for patients undergoing gastrointestinal tract procedures, but also for the critically ill patient undergoing coincidental anaesthetic procedures. Strategies aimed at monitoring the function of the gastrointestinal tract during anaesthesia have in the past been used as research tools, but have potential for use as therapeutic guides. However, further development of these technologies and clinical trials of their application are required, before any firm recommendation in this area can be made.

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33

Girard, Thierry, and Thomas Erb. Fetal and neonatal physiology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0004.

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Knowledge of fetal and neonatal physiology is a prerequisite for physicians involved in the care for mother and child during pregnancy and fetal surgery as well as for the care of a newborn. This chapter focuses on essential aspects of fetal growth, and respiratory and cardiovascular physiology including the complex transition from intra- to extrauterine life. In essence, this transition involves every organ system and knowledge of the most important aspects is a prerequisite to understanding pathophysiology of this transition. Key points regarding the nervous system, nociception, metabolism, that is, fluid homeostasis, kidneys, and liver, and the integumentary system are also addressed.

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34

Kovacs, William J., and Sergio R. Ojeda, eds. Textbook of Endocrine Physiology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199744121.001.0001.

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The sixth edition of this highly popular text retains its comprehensive coverage of endocrine basics from previous editions while featuring entirely new chapters on several topics, including the assessment of endocrine function, sexual differentiation, growth regulation, the thyroid, the adrenals, and calcium homeostasis. Chapters have been updated and reorganized to make information easily accessible in concise form, and new figures and tables have been added to enhance the presentation of complex concepts. Fundamental principles of endocrine physiology are reinforced with illustrative examples from clinical observation and the limitations of current knowledge are properly identified. The ideal resource for students entering the field, the Textbook of Endocrine Physiology aims to provide for all a solid basis in fundamentals of endocrinology and for some, inspiration for the pursuit of advanced medical or graduate studies in the field.

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35

Blaser, Annika Reintam, and Adam M. Deane. Normal physiology of nutrition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0201.

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Energy is derived from three major categories of macronutrient—carbohydrate, lipid, and protein. While energy requirements to maintain stable weight can be estimated, it is uncertain if meeting these energy requirements improves outcomes in the critically ill. In health, excess energy is stored via non-oxidative metabolism and during periods of inadequate energy delivery catabolism of storage products occurs. Both storing and using the stores cost energy, each may require up to quarter of energy contained in stored nutrient. Excess carbohydrate stored as glycogen is easily available, albeit in a limited amount. Storage of lipid is the largest energy repository, but requires complex metabolism and is limited by low oxidative capacity. Protein catabolism normally contributes less than 5% of energy requirements, but during periods of inadequate energy delivery or increased catabolism there is a marked increase in endogenous protein breakdown.

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36

(Editor), Adrian Bejan, and Eden Mamut (Editor), eds. Thermodynamic Optimization of Complex Energy Systems (Nato Science Partnership, 3). Springer, 1999.

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37

Complex Sports Biodynamics With Practical Applications In Tennis. Springer, 2009.

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38

Delaney, Anthony. Physiology of body fluids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0068.

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An understanding of the physiology of body fluids is essential when considering appropriate fluid resuscitation and fluid replacement therapy in critically-ill patients. In healthy humans, the body is composed of approximately 60% water, distributed between intracellular and an extracellular compartments. The extracellular compartment is divided into intravascular, interstitial and transcellular compartments. The movement of fluids between the intravascular and interstitial compartments, is classically described as being governed by Starling forces, leading to a small net efflux of fluid from the intravascular to the interstitial compartment. More recent evidence suggests that a model incorporating the effect of the endothelial glycoclayx layer, a web of glycoproteins and proteoglycans that are bound on the luminal side of the vascular endothelium, better explains the observed distribution of fluids. The movement of fluid to and from the intracellular compartment and the interstitial fluid compartment, is governed by the relative osmolarities of the two compartments. Body fluid status is governed by the difference between fluid inputs and outputs; fluid input is regulated by the thirst mechanism, with fluid outputs consisting of gastrointestinal, renal, and insensible losses. The regulation of intracellular fluid status is largely governed by the regulation of the interstitial fluid osmolarity, which is regulated by the secretion of antidiuretic hormone from the posterior pituitary gland. The regulation of extracellular volume status is regulated by a complex neuro-endocrine mechanism, designed to regulate sodium in the extracellular fluid.

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39

Gow, Neil A. R., and Alistair J. P. Brown. Physiology and metabolism of fungal pathogens. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0003.

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The metabolism and physiology of an invading fungal pathogen determine the outcome of its interaction with the host. The pathogen must be able to assimilate nutrients to grow and colonize diverse host niches. Meanwhile, the host attempts to restrict this growth by withholding some essential nutrients, by imposing stresses, and by inducing innate immune defences. These interactions involve complex regulatory networks that ultimately dictate the equilibrium between pathogen killing and the establishment of commensal or pathogenic associations.

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40

Price, Chane, Zahid Huq, Eellan Sivanesan, and Constantine Sarantopoulos. Pain Pathways and Pain Physiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457006.003.0001.

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Pain is a multidimensional sensory experience that is mediated by complex peripheral and central neuroanatomical pathways and mechanisms. Typically, noxious stimuli activate specific peripheral nerve terminals onto Aδ‎ and C nerve fibers that convey pain and generate signals that are relayed and processed in the spinal cord and then conveyed via the spinothalamic tracts to the contralateral thalamus and from there to the brain. Acute pain is self-limited and resolves with the healing process, but conditions of extensive injury or inflammation sensitize the pain pathways and generate aberrant, augmented responses. Peripheral and central sensitization of neurons (as a result of spatially and temporally excessive inflammation or intense afferent signal traffic) may result in hyperexcitability and chronicity of pain, with spontaneous pain and abnormal evoked responses to stimuli (allodynia, hyperalgesia). Finally, neuropathic pain follows injury or disease to nerves as a result of hyperexcitability augmented by various sensitizing mechanisms.

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41

Petrella, Carla, Giuseppe Nisticò, and Robert Nisticò. Gut–brain axis: Physiology and pathology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0007.

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A large body of research has shown the presence of a complex pathway of communication between gut and brain. It is now recognized that, through this pathway, microbiota can influence intestinal homeostasis and modulate brain plasticity in normal and pathological conditions. This chapter provides an overview of preclinical and clinical evidence supporting the possible mechanisms whereby microbiota can influence gastrointestinal function and stress-related behaviour. Since normalization of gut flora can prevent changes in behaviour, the authors further postulate that the gut–brain axis might represent a possible target for pharmacological and dietary strategies aimed at improving intestinal and mental health.

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42

Baudouin, Simon, and Steve Ball. Normal physiology of the endocrine system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0249.

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The endocrine system describes an array of chemical signals (hormones). Working in concert with the nervous system, the endocrine system forms a complex neurohumoral network, communicating changes in the environment to facilitate adaptive responses and serving to integrate those responses in a coherent, coordinated manner. The endocrine system has inherent rhythmicity, which has important implications for the integration and coordination of metabolism, and how we measure endocrine signals in clinical settings. At a cellular level, hormone action is mediated through a series of discrete, but interacting signal transduction pathways. This chapter outlines a functional design approach to endocrinology; providing a framework covering the principles of hormone regulation and hormone action—critical for understanding the role of the endocrine system in physiology and pathophysiology.

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43

T, Mohanakumar, ed. The role of MHC and non-MHC antigens in allograft immunity. Austin: R.G. Landes Co., 1994.

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44

Di, Napoli Mario, and Wójcik Cezary 1968-, eds. The ubiquitin proteasome system in the central nervous system: From physiology to pathology : 2008 update. Hauppauge, NY: Nova Science, 2009.

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45

Bernal, William, and Alberto Quaglia. Normal physiology of the hepatic system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0173.

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Hepatic blood inflow is from two sources—high-pressure, well-oxygenated blood from the hepatic artery and low-pressure, partly deoxygenated blood from the portal vein. Hepatic inflow is maintained by variation in flows in these two systems. Although less than a third of total blood flow is delivered via the hepatic artery, it is responsible for the majority of hepatic oxygen supply. The liver can be subdivided into eight functionally independent segments, each with its own vascular inflow, outflow, and biliary drainage. The tri-dimensional hepatic microstructure is complex with geographic heterogeneity of hepatocellular function, and resistance to toxic, ischaemic, and metabolic damage. The liver is central to a wide variety of synthetic, metabolic, and detoxification functions. The overall balance of activity may be altered rapidly in response to systemic inflammatory stimuli.

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46

(Editor), Mario Di Napoli, and Cezary Wojcik (Editor), eds. The Ubiquitin Proteasome System in the Central Nervous System: From Physiology to Pathology. Nova Science Pub Inc, 2008.

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47

1964-, Beim Graben P., ed. Lectures in supercomputational neuroscience: Dynamics in complex brain networks. Berlin: Springer, 2008.

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48

Colvin, Lesley A., and Marie T. Fallon. Pain physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0009.

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The International Association for the Study of Pain defines pain as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage’. A good understanding of the physiology of pain processing is important, with recent advances in basic science, functional neuroimaging, and clinical pain syndromes contributing to our understanding. It is also important to differentiate between nociception, the process of detecting noxious stimuli, and pain perception, which is a much more complex process, integrating biological, psychological, and social factors. The somatosensory nervous system, from peripheral nociceptors, to sensory nerves and spinal cord synapses has many potential sites for modulation, with ascending pathways to the brain, balanced by ‘top-down’ control from higher centres. Under certain circumstances, for example, after tissue injury from trauma or surgery, there will be continued nociceptive input, with resultant changes in the whole somatosensory nervous system that lead to development of chronic pain syndromes. In such cases, even when the original injury has healed, the pathophysiological changes in the nervous system itself lead to ongoing pain, with peripheral or central sensitization, or both. Additionally, in some chronic pain syndromes, for example, chronic widespread pain, it has been postulated that abnormalities in central processing may be the initiating factor, with some evidence for this from neuroimaging studies. Further work is needed to fully understand pain neurobiology in order to advance our management.

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49

Blaser, Annika Reintam, and Adam M. Deane. Normal physiology of the gastrointestinal system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0172.

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The gastrointestinal (GI) system is responsible for digestion and absorption, but also has important endocrine, immune and barrier functions. Additionally, the GI system plays a major role in fluid, electrolyte and acid-base balance. The GI system is regulated by complex myogenic, neural and humoral mechanisms, and, in health, these are affected by the presence of luminal nutrient, thereby modulating function of the GI system. Accordingly, GI function varies depending on whether a person is fasted or in the postprandial state. Adequate fasting and postprandial perfusion, motility and exocrine secretion are required for ‘normal’ functioning. The protective mechanisms of the GI system consist of physical (intact gut mucosa), non-immune (gastric acid, intestinal mucin, bile and peristalsis) and immune (gut-associated lymphoid tissue, GALT) elements. Disruption of GI protection is a putative mechanism underlying the development of multiple-organ dysfunction syndrome. Maintenance of GI function is increasingly recognised as an important factor underlying survival in critical illness.

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50

1938-, Volanakis John E., and Frank Michael M, eds. The human complement system in health and disease. New York: M. Dekker, 1998.

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Books on the topic 'Complex physiology'

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