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1
Junwei, Huang, ed. IOS Web Kai fa ru men jing dian: Shi yong HTML, CSS, JavaScript he Ajax. Beijing: Qing hua da xue chu ban she, 2013.
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2
Guan, Dongsheng. Yao zhang wo iOS kai fa, xian zhang wo iPhone shang de mei yi ge gan ying qi. Taibei Shi: Jia kui zi xun, 2016.
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3
iPhone 6 di biao zui qiang mi ji da ji he!: Zhao chu ni mei xiang guo de huo yong fa, jie kai yin cang ban de li ji gong lüe. Taibei Shi: Dian nao ren wen hua, 2015.
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4
Singh, B. P., and R. Prasad. Fundamentals and Applications of Heavy Ion Collisions: Below 10 MeV/ Nucleon Energies. Cambridge University Press, 2018.
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5
Mason, Peggy. The Neuron at Rest. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0009.
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Neuronal membrane potential depends on the distribution of ions across the plasma membrane and the permeability of the membrane to those ions afforded by transmembrane proteins. Ions cannot pass through a lipid bilayer but enter or exit neurons through ion channels. When activated by voltage or a ligand, ion channels open to form a pore through which selective ions can pass. The ion channels that support a resting membrane potential are critical to setting a cell’s excitability. From the distribution of an ionic species, the Nernst potential can be used to predict the steady-state potential for that one ion. Neurons are permeable to potassium, sodium, and chloride ions at rest. The Goldman-Hodgkin-Katz equation takes into consideration the influence of multiple ionic species and can be used to predict neuronal membrane potential. Finally, how synaptic inputs affect neurons through synaptic currents and changes in membrane resistance is described.
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Slimp, Jefferson C. Neurophysiology of Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0003.
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Any discussion of the pathomechanisms and treatments of MS benefits from an understanding of the physiology of the neuronal membrane and the action potential. Neurons and glia, are important for signal propagation, synaptic function, and neural development. The neuronal cell membrane, maintains different ionic environments inside and outside the cell, separating charge across the membrane and facilitating electrical excitability. Ion channels allow flow of sodium, potassium, and calcium ions across the membrane at selected times. At rest, potassium ion efflux across the membrane establishes the nerve membrane resting potential. When activated by a voltage change to threshold, sodium influx generates an action potential, or a sudden alteration in membrane potentials, that can be conducted along an axon. The myelin sheaths around an axon, increase the speed of conduction and conserve energy. The pathology of MS disrupts the myelin structures, disturbs conduction, and leads to neurodegeneration. Ion channels have been the target of investigation for both restoration of conduction and neuroprotection.
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Jef ferys, John G. R. Cortical activity: single cell, cell assemblages, and networks. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0004.
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This chapter describes how the activity of neurons produces electrical potentials that can be recorded at the levels of single cells, small groups of neurons, and larger neuronal networks. It outlines how the movement of ions across neuronal membranes produces action potentials and synaptic potentials. It considers how the spatial arrangement of specific ion channels on the neuronal surface can produce potentials that can be recorded from the extracellular space. Finally, it outlines how the layered cellular structure of the neocortex can result in summation of signals from many neurons to be large enough to record through the scalp as evoked potentials or the electroencephalogram.
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Zwarts, Machiel J. Nerve, muscle, and neuromuscular junction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0001.
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Essential to all living creatures is the ability to convey information. In addition motor responses are required, for example running. This all is possible due to the ability of specialized cells to conduct information along the cell membrane by means of action potentials (AP) made possible by the charged cell membrane, which has selective permeability for different ions. Voltage and ligand sensitive ion channels are responsible for sudden changes in selective permeability of the membrane resulting in local depolarization of the membrane. The neuromuscular junction is a highly specialized region of the distal motor axon that is responsible for the transferring of activation from nerve to muscle. All these systems and subsystems can fail and a thorough understanding is necessary in order to understand the changes a clinical neurophysiologist can encounter while recording from the human nervous system in cases of disorders of brain, nerve and muscle.
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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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Steinhäuser, Christian, Gerald Seifert, and Joachim W. Deitmer. Physiology of Astrocytes: Ion Channels and Ion Transporters. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199794591.003.0016.
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This is a digitally enhanced text. Readers can also see the coverage of this topic area in the second edition of Neuroglia. The second edition of Neuroglia was first published digitally in Oxford Scholarship Online and the bibliographic details provided, if cited, will direct people to that version of the text. Readers can also see the coverage of this topic area in the ...
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Kumar, Deepak, and Richard Carrington. Hip resurfacing. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.007014.
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♦ Hip resurfacing has emerged as an alternative method of hip arthroplasty for younger patients♦ It is technically more demanding than total hip replacement♦ The reported early and mid-term results are good with revision rates below 5% at 7 years♦ Long term effect of raised levels of metal ions remains a major concern♦ Long term clinical follow up and further research must continue.
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Park, Susanna B., Cindy S.-Y. Lin, and Matthew C. Kiernan. Axonal excitability: molecular basis and assessment in the clinic. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0009.
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Axonal excitability techniques were developed to assess axonal resting membrane potential and ion channel function in vivo, and thereby provide greater molecular understanding of the activity of voltage gated ion channels and ion pumps underlying nerve and membrane function. Axonal excitability studies provide complimentary information to conventional nerve conduction studies, using submaximal stimuli to examine the properties underlying the excitability of the axon. Such techniques have been developed both as a research technique to examine disease pathophysiology and as a clinical investigation technique. This chapter provides an overview of axonal excitability techniques, addressing the role of key ion channels and pumps in membrane function and highlighting examples of clinical case studies, where such techniques have been utilized, including motor neuronopathies, tracking progression of chemotherapy-induced peripheral neuropathy, and assessing treatment response in chronic inflammatory demyelinating polyneuropathy.
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Heine, Christopher L. Malignant Hyperthermia. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0025.
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In this chapter we discuss the pathophysiology of malignant hyperthermia, identify those who are known to be susceptible to MH, delineate how best to prepare the operating for those patients, and provide step by step treatment recommendations for patients that develop MH. Malignant hyperthermia (MH) is a pharmacogenetic disease. When susceptible individuals are exposed to a triggering agent, a hypermetabolic response develops. Succinylcholine and halogenated, inhaled anesthetics are triggers of MH. The MH reaction is initiated by a rapid influx of calcium ions into the myoplasm that triggers uncontrolled muscle contraction. Prompt recognition and treatment of the reaction is critical to a successful outcome.
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Linglart, Agnès, and Anne-Sophie Lambert. Approach to the patient with hypocalcaemia. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0038.
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Calcium homeostasis is maintained through a fine balance between calcium absorption, parathyroid hormone secretion and action, vitamin D production and action, cellular compartmentalization of calcium ions, and renal function. Although the extracellular calcium level does not vary with age, the maintenance of calcium faces the significant mineral requirement of skeletal growth and bone mass acquisition during childhood. Acquired or genetic defects in any determinants of blood calcium (i.e. vitamin D, parathyroid hormone, calcium absorption, etc.) may manifest as hypocalcaemia, especially during childhood/adolescence. The discovery of hypocalcaemia in a patient should trigger two clinical responses: (1) therapy to restore the calcium level to normal and (2) investigations to determine the cause of hypo/hypercalcaemia.
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Casey, Coreen. Target fragmentation in the interaction of 12-16 MEV/NUCLEON ³²S with ¹⁶⁵HO. 1988.
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16
Hatfield, Anthea. Metabolism. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199666041.003.0024.
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This chapter tells you how homeostasis in the body is achieved. Contributing factors such as stress, hormones, and the automatic nervous system are integrated into the discussion in a thoughtful way. The problem of cold postoperative patients is thoroughly referenced to modern investigation. Diabetes, how surgery destabilizes diabetics, and how to use insulin is explained. Malignant hyperthermia, thyroid storm, and acid—base disorders are all problems that can occur in the recovery room and guidelines for the management of these patients are outlined. Hydrogen ions affect haemoglobin and biochemical reactions and can cause acidosis and alkalosis—this chapter outlines how to interpret the blood gas results. How to distinguish between respiratory and metabolic causes of acid—base disorders is simply and clearly explained.
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Traul, David E. Postoperative Visual Loss in Spine Surgery. Edited by David E. Traul and Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0026.
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Postoperative visual loss (POVL) is a rare but devastating condition associated with many types of nonocular surgery. In spine surgery, the most common causes of POVL are ischemic optic neuropathy (ION), central retinal artery occlusion (CRAO), and cortical blindness. Although the association of POVL with spine surgery has long been recognized, the low incidence of this complication hinders the identification of patient and perioperative risk factors and limits our understanding of the causes of POVL. In adult spine surgery, POVL is most frequently attributed to ION whereas CRAO is more commonly seen in cardiac procedures. POVL due to cortical blindness has the highest incidence in pediatric spine surgery. While several risk factors for POVL have been identified in spine surgery, there are currently no standardized practice guidelines to eliminate the risk for POVL. Currently, there are no effective treatments for POVL, and recovery from ION and CRAO is limited.
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Mason, Peggy. Neurotransmitter Release. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0011.
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The biochemical and physiological processes of neurotransmitter release from an active zone, a specialized region of synaptic membrane, are examined. Synaptic vesicles containing neurotransmitters are docked at the active zone and then primed for release by SNARE complexes that bring them into extreme proximity to the plasma membrane. Entry of calcium ions through voltage-gated calcium channels triggers synaptic vesicle fusion with the synaptic terminal membrane and the consequent diffusion of neurotransmitter into the synaptic cleft. Release results when the fusion pore bridging the synaptic vesicle and plasma membrane widens and neurotransmitter from the inside of the synaptic vesicle diffuses into the synaptic cleft. Membrane from the active zone membrane is endocytosed, and synaptic vesicle proteins are then reassembled into recycled synaptic vesicles, allowing for more rounds of neurotransmitter release.
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Montgomery, Erwin B. Principles of Electrophysiology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190259600.003.0003.
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In many ways, post-operative DBS programming is “prescribing electricity” in much the same sense as “prescribing medications.” The principles of pharmacokinetics and pharmacodynamics that guide the rational use of medications find parallels in DBS. Many drugs have their effect by binding to ligand-gated channels, particularly channels that control the flow of electrical charges, in the form of ions across the cell membrane of the neuron in the soma. The binding of drugs to receptors can open the receptor to approximate the normal opening by endogenous neurotransmitters, or to block the channel from opening when endogenous neurotransmitters are released. In the case of DBS, the electrical charges manipulated in the nervous system similarly affect neuronal membrane channels; however, these initially and primarily are voltage gated ionic conductance channels, which are described in detail in this chapter.
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Amzica, Florin, and Fernando H. Lopes da Silva. Cellular Substrates of Brain Rhythms. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0002.
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The purpose of this chapter is to familiarize the reader with the basic electrical patterns of the electroencephalogram (EEG). Brain cells (mainly neurons and glia) are organized in multiple levels of intricate networks. The cellular membranes are semipermeable media between extracellular and intracellular solutions, populated by ions and other electrically charged molecules. This represents the basis of electrical currents flowing across cellular membranes, further generating electromagnetic fields that radiate to the scalp electrodes, which record changes in the activity of brain cells. This chapter presents these concepts together with the mechanisms of building up the EEG signal. The chapter discusses the various behavioral conditions and neurophysiological mechanisms that modulate the activity of cells leading to the most common EEG patterns, such as the cellular interactions for alpha, beta, gamma, slow, delta, and theta oscillations, DC shifts, and some particular waveforms such as sleep spindles and K-complexes and nu-complexes.
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Hopkins, Philip M. Neuromuscular physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0007.
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The pharmacological interventions that constitute general anaesthesia are targeted at producing unconsciousness and an immobile patient even in response to noxious stimuli. Surgical anaesthesia also requires skeletal muscle relaxation, the degree of which depends on the site and nature of the surgical procedure. The anaesthetist therefore needs an advanced level of knowledge and understanding of the function of nerves, synapses, and muscle in order to understand, from first principles, how the drugs they use every day mediate their effects. Nerves and muscle cells are termed excitable cells because the electrical potential across their cell membranes (membrane potential) can be rapidly and profoundly altered because of the presence of specialized ion channels. Some drugs, such as local anaesthetics, act on ion channels involved in nerve conduction while many others act on synaptic transmission, the neurochemical communication between neurons or between a neuron and its effector organ. The neuromuscular junction is a synapse of specific interest to anaesthetists because it is the site of action of neuromuscular blocking drugs. This chapter covers the fundamentals of cellular electrophysiology, structure and function of key ion channels, and the physiology of nerves, synapses, and skeletal muscle.
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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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Nagy, Istvan. The capsaicin receptor. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0027.
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The landmark paper discussed in this chapter is ‘The capsaicin receptor: A heat activated ion channel in the pain pathway’, published by Caterina et al. in 1997. The identification of the molecular basis for the sensitivity of a major proportion of nociceptive primary sensory neurons for capsaicin, the pungent agent in chilli pepper, was undoubtedly one of the most significant pain-related discoveries in the twentieth century, for at least three reasons. First, the mechanism for capsaicin-induced responses could unequivocally be explained. Second, the discovery heralded the starting point for the development of a highly promising, mechanism-based means of analgesia. Third, the discovery also sparked studies which resulted in the discovery of the major cation channel family, the transient receptor potential (TRP) ion channel family, several members of which have also become putative targets for the development of analgesics.
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Cavanna, Andrea E. Antiepileptic drugs and behaviour: mechanisms of action. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198791577.003.0002.
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Antiepileptic drugs (AEDs) exert their pharmacological properties on both epileptic seizures and behaviour through different mechanisms of action. These include modulation of ion (mainly sodium and calcium) conductance through voltage-gated channels located within the neuronal membrane, as well as facilitation of inhibitory (GABAergic) neurotransmission and inhibition of excitatory (glutamatergic) neurotransmission, resulting in regulation of neuronal excitability.
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W, Drew D. A novel MeV ion microbeam technique for measuring diffusion of small molecules in polymeric & biological matrices. 1996.
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Murer, Heini, Jürg Biber, and Carsten A. Wagner. Phosphate homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0025.
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Inorganic phosphate ions (H2PO4−/ HPO42−) (abbreviated as Pi) are involved in formation of bone and generation of high-energy bonds (e.g. ATP), metabolic pathways, and regulation of cellular functions. In addition, Pi is a component of biological membranes and nucleic acids. Only about 1% of total body Pi content is present in extracellular fluids, at a plasma concentration in adults within the range 0.8–1.4 mMol/L (at pH 7.4 mostly as HPO42−), with diurnal variations of approximately 0.2 mM. A small amount of plasma Pi is bound to proteins or forms complexes with calcium. Under normal, balanced conditions, absorption of dietary Pi along the small intestine equals the output of Pi via kidney and faeces. Renal excretion of Pi represents the key determinant for the adjustment of normal Pi plasma concentrations. Renal reabsorption of Pi occurs along the proximal tubules by sodium-dependent Pi cotransporters that are strictly localized at the apical brush border membrane. Parathyroid hormone (PTH) and FGF23 are key regulators amongst a myriad of factors controlling excretion of Pi in urine, mostly by changes of the apical abundance of Na/Pi cotransporters. Hypophosphataemia may result in osteomalacia, rickets, muscle weakness, and haemolysis. Hyperphosphataemia can lead to hyperparathyroidism and severe calcifications in different tissues.
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Rodrigues Diniz Morais, Ione. Construindo o ser professor: (geo)grafias da trajetória de vida. Editora SertãoCult, 2021. http://dx.doi.org/10.35260/67960425-2021.
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Construindo o Ser professor: (geo)grafias da trajetória de vida constitui uma narrativa acerca dos itinerários percorridos em busca dessa construção, reconhecidamente inacabada, que contempla as terras e grafias que marcam meu existir. Nessa narrativa em que fui tecelã de minha história, costurando os retalhos da vida para confeccionar o tecido que conferiu corpus a esta escrita, bordei pessoas, eventos e lugares que fazem parte do enredo e dos cenários dessa trajetória. MORAIS, Ione Rodrigues Diniz. Construindo o ser professor: (geo) grafias da trajetória de vida. Sobral-CE: SertãoCult, 2021.
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Garcia-Pavia, Pablo, and Fernando Dominguez. Left ventricular non-compaction: genetics and embryology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0362.
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Left ventricular non-compaction (LVNC) is a rare disorder that is considered an ‘unclassified cardiomyopathy’ by the European Society of Cardiology. Several different gene mutations related to LVNC have been identified, involving sarcomeric, cytoskeletal, Z-line, ion channel, mitochondrial, and signalling proteins. However, there is broad genetic overlap between LVNC and other inherited cardiac diseases such as dilated cardiomyopathy and hypertrophic cardiomyopathy. LVNC could also be part of multisystemic genetic entities such as Barth syndrome, or accompany congenital heart defects.
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Marini, Carla, and Renzo Guerrini. Biological Basis of Primary Generalized Epilepsies—Genetics. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0036.
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Primary generalized epilepsies account for 30% of all epilepsies. These age-related epilepsies without structural brain lesions and normal development have a high heritability. Based on the main seizure type and their age of onset, four main subsyndromes are recognized. Rare autosomal dominant families carry mutations in a few genes involved in ion channel functions, whereas common genes are yet to be discovered. The complex inheritance involving multiple genes is the major limiting factor preventing to uncover their genetic architecture. Understanding genetic determinants is the key to unraveling the neurobiology and to improve therapies for these disorders.
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Ho, Kwok M. Kidney and acid–base physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0005.
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Anatomically the kidney consists of the cortex, medulla, and renal pelvis. The kidneys have approximately 2 million nephrons and receive 20% of the resting cardiac output making the kidneys the richest blood flow per gram of tissue in the body. A high blood and plasma flow to the kidneys is essential for the generation of a large amount of glomerular filtrate, up to 125 ml min−1, to regulate the fluid and electrolyte balance of the body. The kidneys also have many other important physiological functions, including excretion of metabolic wastes or toxins, regulation of blood volume and pressure, and also production and metabolism of many hormones. Although plasma creatinine concentration has been frequently used to estimate glomerular filtration rate by the Modification of Diet in Renal Disease (MDRD) equation in stable chronic kidney diseases, the MDRD equation has limitations and does not reflect glomerular filtration rate accurately in healthy individuals or patients with acute kidney injury. An optimal acid–base environment is essential for many body functions, including haemoglobin–oxygen dissociation, transcellular shift of electrolytes, membrane excitability, function of many enzymes, and energy production. Based on the concepts of electrochemical neutrality, law of conservation of mass, and law of mass action, according to Stewart’s approach, hydrogen ion concentration is determined by three independent variables: (1) carbon dioxide tension, (2) total concentrations of weak acids such as albumin and phosphate, and (3) strong ion difference, also known as SID. It is important to understand that the main advantage of Stewart over the bicarbonate-centred approach is in the interpretation of metabolic acidosis.
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Storey, Elsdon. Ataxias. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0007.
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This chapter explores the historical development of understanding about the structure, function, and disorders of the cerebellum. The chosen papers represent the following development: the discovery that the cerebellum is concerned with movement control rather than movement generation; the first recognition of a distinct spinocerebellar disorder; recognition of the existence of dominantly-inherited ataxias; the delineation of the classic motor features of ataxia; the formal recognition of paraneoplastic cerebellar degenerations; the description of truncal ataxia due to anterior vermal damage in chronic alcoholics; the demonstration of long-term depression at the parallel fibre; the discovery of the first gene (ATXN 1) for a dominantly-inherited spinocerebellar ataxia; the revelation that episodic ataxia type 2 is an ion channel disorder; and the recognition of a cerebellar role in cognition and emotional regulation.
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Miquerol, Lucile. Origin and development of the cardiac conduction system. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0015.
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The cardiac conduction system represents the ‘wiring’ of the heart and orchestrates the propagation of the electrical activity to synchronize heartbeats. It is built from specialized cardiomyocytes expressing a subset of ion channels and gap junctions indispensable for their electrophysiological properties. Although representing only a very small volume of the heart, the conduction system plays a crucial role in the appearance of cardiac arrhythmias. The cells forming the conduction system are derived from the same cardiac progenitors as the working cardiomyocytes, and the choice between these two fates is acquired during embryonic development. The components of the conduction system are progressively established during cardiac morphogenesis and converge to form an integrated electrical system in the definitive heart. This chapter will discuss recent advances using mouse genetic approaches which have improved understanding of the cellular origin and the transcriptional regulatory networks involved in the development of the conduction system.
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Postma, Alex V., David Sedmera, Frantisek Vostarek, Vincent M. Christoffels, and Connie R. Bezzina. Developmental aspects of cardiac arrhythmias. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0027.
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The rhythmic and synchronized contraction of atria and ventricles is essential for efficient pumping of blood throughout the body. This process relies on the proper generation and conduction of the cardiac electrical impulse. Electrophysiological properties differ in various regions of the heart, revealing intrinsic heterogeneities rooted, at least in part, in regional differences in expression of ion channel and gap junction subunit genes. A causal relation between transcription factors and such regionalized gene expression has been established. Abnormal cardiac electrical function and arrhythmias in the postnatal heart may stem from a developmental changes in gene regulation. Genome-wide association studies have provided strong evidence that common genetic variation at developmental gene loci modulates electrocardiographic indices of conduction and repolarization and susceptibility to arrhythmia. Functional aspects are illustrated by description of selected prenatally occurring arrhythmias and their possible mechanisms. We also discuss recent findings and provide background insight into these complex mechanisms.
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Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghant. Disorders of plasma calcium. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0175.
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The extracellular calcium ion concentration is tightly regulated through the actions of parathyroid hormone (PTH) and vitamin D (1,25-dihydroxyvitamin D) on bone, kidney, and intestines. Abnormalities in these homeostatic mechanisms may lead to increased or decreased serum calcium concentrations, resulting in hypercalcaemia or hypocalcaemia, respectively. Hypercalcaemic disorders may be further divided into those associated with a high/high-normal serum PTH level, and those associated with a low serum PTH concentration. Hypocalcaemia occurs when abnormalities in the physiological regulation of PTH and vitamin D results in calcium levels lower than the desired normal range. Failure of release of calcium from bone, and increased binding of calcium in the circulation, are other factors causing hypocalcaemia. This chapter discusses hypercalcaemia and hypocalcaemia, exploring definitions of the diseases, their etiologies, typical and uncommon symptoms, demographics, natural history, complications, diagnostic approaches, other diagnoses that should be considered, prognosis, and treatment.
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Neligan, Patrick J., and Clifford S. Deutschman. Pathophysiology and causes of metabolic acidosis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0255.
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Critical illness is typically characterized by changes in the balance of water and electrolytes in the extracellular space, resulting in the accumulation of anionic compounds that manifests as metabolic acidosis. Metabolic acidosis manifests with tachypnoea, tachycardia, vasodilatation, headache and a variety of other non-specific symptoms and signs. It is caused by a reduction in the strong ion difference (SID) or an increase in weak acid concentration (albumin or phosphate). Increased SID results from hyperchloraemia, haemodilution or accumulation of metabolic by-products. A reduction in SID results in a corresponding reduction is serum bicarbonate. There is a corresponding increase in alveolar ventilation and reduced PaCO2. Lactic acidosis results from increased lactate production or reduced clearance. Ketoacidosis is associated with reduced intracellular glucose availability for metabolism, and is associated with insulin deficiency and starvation. Hyperchloraemic acidosis is associated with excessive administration of isotonic saline solution, renal tubular acidosis and ureteric re-implantation. Renal acidosis is associated with hyperchloraemia, hyperphosphataemia, and the accumulation of medley nitrogenous waste products.
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Kerr, Bradley J. The link between an Nav1.7 mutation and erythromelalgia. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0081.
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The landmark paper discussed in this chapter is ‘Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons’, published by Dib-Hajj et al. in 2005. The voltage-dependent sodium channels Nav1.7, Nav1.8, and Nav1.9 have a restricted pattern of expression in sensory neurons in the periphery and are concentrated in small nociceptive neurons of the dorsal root ganglion, the trigeminal ganglion, and the nodose ganglion. In this paper, Dib-Hajj and colleagues studied a family with erythromelalgia (Weir Mitchell disease), an autosomal-dominant, inherited pain disorder in which burning pain in the extremities can be triggered by warming of the skin or moderate exertion. By identifying a novel mutation in SCN9A, which encodes Nav1.7, they established the critical role of this specific ion channel in this patient population. These findings represent an important first step towards developing isoform-specific channel blockers for the treatment of an inherited chronic pain condition.
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Langer, Thomas, and Pietro Caironi. Pathophysiology and therapeutic strategy of respiratory alkalosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0114.
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Respiratory alkalosis is a condition characterized by low partial pressure of carbon dioxide and an associated elevation in arterial pH caused by an imbalance between CO2 production and removal, in favour of the latter. Conditions that cause increased alveolar ventilation, without having a reduction in pH as input stimulus, will cause hypocapnia associated with a variable degree of alkalosis. The major effect of hypocapnia is the increase in pH (alkalosis) and the consequent shift of electrolytes that occurs in relation to it. As a general law, in plasma, anions will increase, while cations will decrease. The acute reduction in ionized calcium, due to the change in extracellular pH, may cause neuromuscular symptoms ranging from paraesthesias, to tetany and seizures. The effect on urine is an increase in urinary strong ion difference/urinary anion gap and a consequent increase in urinary pH. Finally, acute hypocapnic alkalosis causes a constriction of cerebral arteries that can lead to a reduction of cerebral blood flow. The clinical approach to respiratory alkalosis is usually directed toward the diagnosis and treatment of the underlying clinical disorder.
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Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Disorders of acid–base balance. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0178.
Full textAbstract:
Normal metabolism results in a net acid production of approximately 1 mmol/kg day−1. Physiological pH is regulated by excretion of this acid load (as carbon dioxide) by the kidneys and the lungs. A series of buffers in the body reduces the effects of metabolic acids on body and urine pH. For acid–base disorders to occur, there must be excessive intake (or loss) of acid (or base) or, alternatively, an inability to excrete acid. For these changes to result in a substantially abnormal pH, the various buffer systems must been overwhelmed. The pH scale is logarithmic, so relatively small changes in pH signify large differences in hydrogen ion concentration. Most minor perturbations in acid–base balance are asymptomatic, as small changes in acid or base levels are rapidly controlled through consumption of buffers or through changes in respiratory rate. Alterations in renal acid excretion take some time to occur. Only when these compensatory mechanisms are overwhelmed do symptoms related to changes in pH develop. This chapter reviews the causes and consequences of acid–base disorders.
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Levitan, Irwin B., and Leonard K. Kaczmarek. The Neuron. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199773893.001.0001.
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The Fourth Edition of The Neuron provides a comprehensive first course in the cell and molecular biology of nerve cells. It begins with properties of the many newly discovered ion channels that have emerged through mapping of the genome and which shape the way a single neuron generates varied patterns of electrical activity. It also covers the molecular mechanisms that convert electrical activity into the secretion of neurotransmitter hormones at synaptic junctions between neurons. It discusses the biochemical pathways that are linked to the action of neurotransmitters and that can alter the cellular properties of neurons or sensory cells that transduce information from the outside world into the electrical code used by neurons, and the rapidly expanding knowledge of the molecular factors that induce an undifferentiated cell to become a neuron, and then guide it to form appropriate synaptic connections with its partners. Also addressed is the role of ongoing experience and activity in shaping these connections, and the mechanisms thought to underlie the phenomena of learning and memory.
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Blunn, Gordon. Bearing surfaces. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.007006.
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♦ Traditionally bearings were made from polyethylene and cobalt chrome. These bearings are still most commonly used for knee replacements. In hip replacements due to osteolysis caused by polyethylene wear alternative material combinations at the bearing surface are used♦ Highly cross linked plastics have been developed and have been shown to reduce wear. There are a number of different types available which differ in their performance♦ Metal on metal bearings first used in the 1960s have also been developed and show very low wear rates. These bearings are more susceptible to edge loading and the resulting metal ion release can result in adverse biological reactions leading to failure♦ Whilst ceramic on plastic surfaces have been used for a considerable amount of time the reduction in wear is not as great as with well functioning metal on metal bearings♦ Ceramic on ceramic bearings have been used for a considerable time and show even lower wear rates than metal on metal bearings. In the past there has been an incidence of catastrophic fracture of these bearings but developments in materials technology have considerably reduced these events.
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iPhone 6/6+ da ren jiao zhan! Shun jian shang shou + jin hua mi ji wan mei zhang wo! Xianggang: Chao mei ti chu ban, 2015.
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Ware, Lorraine B. Pathophysiology of acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0108.
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The acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure characterized by the acute onset of non-cardiogenic pulmonary oedema due to increased lung endothelial and alveolar epithelial permeability. Common predisposing clinical conditions include sepsis, pneumonia, severe traumatic injury, and aspiration of gastric contents. Environmental factors, such as alcohol abuse and cigarette smoke exposure may increase the risk of developing ARDS in those at risk. Pathologically, ARDS is characterized by diffuse alveolar damage with neutrophilic alveolitis, haemorrhage, hyaline membrane formation, and pulmonary oedema. A variety of cellular and molecular mechanisms contribute to the pathophysiology of ARDS, including exuberant inflammation, neutrophil recruitment and activation, oxidant injury, endothelial activation and injury, lung epithelial injury and/or necrosis, and activation of coagulation in the airspace. Mechanical ventilation can exacerbate lung inflammation and injury, particularly if delivered with high tidal volumes and/or pressures. Resolution of ARDS is complex and requires coordinated activation of multiple resolution pathways that include alveolar epithelial repair, clearance of pulmonary oedema through active ion transport, apoptosis, and clearance of intra-alveolar neutrophils, resolution of inflammation and fibrinolysis of fibrin-rich hyaline membranes. In some patients, activation of profibrotic pathways leads to significant lung fibrosis with resultant prolonged respiratory failure and failure of resolution.
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Bockenhauer, Detlef, and Robert Kleta. Approach to the patient with salt-wasting tubulopathies. Edited by Robert Unwin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0031_update_001.
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Sodium is the main ion of the extracellular compartments, and it is through control of sodium reabsorption that the kidneys maintain volume homoeostasis and systemic blood pressure. The amount of sodium that is first filtered by the glomerulus and then reabsorbed in the tubule is quite staggering: assuming a glomerular filtration rate of 100 mL/min and a serum sodium concentration of 140 mmol/L, an average-sized person filters about 20,000 mmol of sodium per day, equivalent to the amount in 1.2 kg of cooking salt. In the steady state, the amount of sodium excreted is equal to the amount ingested. An average Western diet contains about 8–10 g of salt per day; a low-salt diet may be around 2 g per day. Under physiological conditions, the tubules reabsorb about 99% of filtered sodium. This enormous task is accomplished by a combination of distinct and sequentially oriented sodium or sodium-coupled transport systems along the nephron and the concerted and parallel action of some of these systems within the kidney. These are described, along with the consequences of disorders of the processes. A diagnostic approach to salt-losing states such as Fanconi, Bartter Gitelman and other syndromes, and hypoaldosteronism, is described.
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Benarroch, Eduardo E. Neuroscience for Clinicians. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.001.0001.
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The aim of this book is to provide the clinician with a comprehensive and clinical relevant survey of emerging concepts on the organization and function of the nervous system and neurologic disease mechanisms, at the molecular, cellular, and system levels. The content of is based on the review of information obtained from recent advances in genetic, molecular, and cell biology techniques; electrophysiological recordings; brain mapping; and mouse models, emphasizing the clinical and possible therapeutic implications. Many chapters of this book contain information that will be relevant not only to clinical neurologists but also to psychiatrists and physical therapists. The scope includes the mechanisms and abnormalities of DNA/RNA metabolism, proteostasis, vesicular biogenesis, and axonal transport and mechanisms of neurodegeneration; the role of the mitochondria in cell function and death mechanisms; ion channels, neurotransmission and mechanisms of channelopathies and synaptopathies; the functions of astrocytes, oligodendrocytes, and microglia and their involvement in disease; the local circuits and synaptic interactions at the level of the cerebral cortex, thalamus, basal ganglia, cerebellum, brainstem, and spinal cord transmission regulating sensory processing, behavioral state, and motor functions; the peripheral and central mechanisms of pain and homeostasis; and networks involved in emotion, memory, language, and executive function.
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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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Masino, PHD, Susan A., ed. Ketogenic Diet and Metabolic Therapies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.001.0001.
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Ketogenic diets have been used to treat epilepsy for nearly a century. Alongside enduring clinical success with a ketogenic diet, metabolism’s critical role in health and in diseases in the central nervous system and throughout the body is increasingly appreciated. Furthermore, metabolism-based strategies have been proven equal or even superior to pharmacological treatments in specific cases and for specific diseases. Rather than causing unwanted off-target pharmacological side effects, addressing metabolic dysfunction can improve overall health simultaneously. Enduring interest in the ketogenic diet’s proven efficacy in stopping seizures and emerging efficacy in other disorders has fueled renewed efforts to determine key mechanisms and diverse applications of metabolic therapies. In parallel, multiple strategies are being developed to mobilize similar metabolic benefits without reliance on such a strict diet. Research interest in metabolic therapies has spread into laboratories and clinics of every discipline, and could yield entirely new classes of drugs and treatment regimens. This work is the first comprehensive scientific resource on the ketogenic diet, covering the latest research into the mechanisms, established and emerging applications, metabolic alternatives, and implications for health and disease. Experts in clinical and basic research share their research into mechanisms spanning from ion channels to epigenetics, their insights based on decades of experience with the ketogenic diet in epilepsy, and their evidence for emerging applications ranging from autism to Alzheimer’s disease to brain cancer.
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Eyre, Janet. Neurodevelopmental disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0189.
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Remarkable advances in the neurosciences, particularly in the fields of genetics, molecular biology, metabolism, and nutrition, have greatly advanced our understanding of how the brain develops and responds to environmental influences. Neurodevelopmental disorders arise from perturbation of these normal developmental processes, by insults from heterogeneous aetiological factors. These factors trigger a sequence of molecular, biochemical, and morphological alterations of the brain, resulting in a morphologically and/ or functionally abnormal brain. Rapidly advancing understanding of basic neurodevelopmental processes has direct relevance to understanding human neurodevelopmental disorders, providing insights into pathogenic mechanisms and revealing new pathways that can be exploited in diagnosis and treatment. Conversely the identification of the molecular bases of several neurodevelopmental disorders has also provided invaluable insights into the mechanisms of normal brain development. Technical advances have also improved methods for identifying brain regions involved in developmental disorders, for tracing connections between parts of the brain, for visualizing individual neurons in living brain preparations, for recording the activities of neurons, and for studying the activity of single-ion channels and the receptors for various neurotransmitters. During the past 10 years the genetic basis of an ever increasing number of neurodevelopmental disorders has been discovered and has led to better understanding of the neurobiological basis of even common disorders such as global developmental delay, cerebral palsy, and autism. Current research should reveal their underlying molecular biology and eventually the possibility of targeted chemotherapy and the prevention of many neurodevelopmental disorders.
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Raghunathan, Karthik, and Andrew Shaw. Crystalloids in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0057.
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‘Crystalloid’ refers to solutions of crystalline substances that can pass through a semipermeable membrane and are distributed widely in body fluid compartments. The conventional Starling model predicts transvascular exchange based on the net balance of opposing hydrostatic and oncotic forces. Based on this model, colloids might be considered superior resuscitative fluids. However, observations of fluid behaviour during critical illness are not consistent with such predictions. Large randomized controlled studies have consistently found that colloids offer no survival advantage relative to crystalloids in critically-ill patients. A revised Starling model describes a central role for the endothelial glycocalyx in determining fluid disposition. This model supports crystalloid utilization in most critical care settings where the endothelial surface layer is disrupted and lower capillary pressures (hypovolaemia) make volume expansion with crystalloids effective, since transvascular filtration decreases, intravascular retention increases and clearance is significantly reduced. There are important negative consequences of both inadequate and excessive crystalloid resuscitation. Precise dosing may be titrated based on functional measures of preload responsiveness like pulse pressure variation or responses to manoeuvres such as passive leg raising. Crystalloids have variable electrolyte concentrations, volumes of distribution, and, consequently variable effects on plasma pH. Choosing balanced crystalloid solutions for resuscitation may be potentially advantageous versus ‘normal’ (isotonic, 0.9%) saline solutions. When used as the primary fluid for resuscitation, saline solutions may have adverse effects in critically-ill patients secondary to a reduction in the strong ion difference and hyperchloraemic, metabolic acidosis. Significant negative effects on immune and renal function may result as well.
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Lambert, David G. Mechanisms and determinants of anaesthetic drug action. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0013.
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This chapter is broken into two main sections: a general description of the principles of ligand receptor interaction and a discussion of the main groups of ‘targets’; and explanation of some common pharmacological interactions in anaesthesia, critical care, and pain management. Agonists bind to and activate receptors while antagonists bind to receptors and block the effects of agonists. Antagonists can be competitive (most common) or non-competitive/irreversible. The main classes of drug target are enzymes, carriers, ion channels, and receptors with examples of anaesthetic relevance interacting with all classes. There are many examples in anaesthesia where multiple interacting drugs are co-administered—polypharmacology. To give an example: neuromuscular blockade. Rocuronium is a non-depolarizing neuromuscular blocker acting as a competitive antagonist at the nicotinic acetylcholine receptor. Rocuronium competes with endogenous acetylcholine to shift the concentration–response curve for contraction to the right. The degree of contractility is less for a given concentration of acetylcholine (agonist) in the presence of rocuronium. Using the same principle, the rightward shift can be compensated by increasing the amount of acetylcholine (as long as the amount of rocuronium presented to the receptor as an antagonist remains unchanged, its action can be overcome by increased agonist). Acetylcholine at the effect site is increased by acetylcholinesterase inhibition with neostigmine. One of the side-effects of neostigmine is that it acts as an indirect parasympathomimetic. In the cardiovascular system this would lead to muscarinic receptor-mediated bradycardia; these effects are routinely reversed by the competitive muscarinic antagonist glycopyrrolate.
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Schaible, Hans-Georg, and Rainer H. Straub. Pain neurophysiology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0059.
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Physiological pain is evoked by intense (noxious) stimuli acting on healthy tissue functioning as a warning signal to avoid damage of the tissue. In contrast, pathophysiological pain is present in the course of disease, and it is often elicited by low-intensity stimulation or occurs even as resting pain. Causes of pathophysiological pain are either inflammation or injury causing pathophysiological nociceptive pain or damage to nerve cells evoking neuropathic pain. The major peripheral neuronal mechanism of pathophysiological nociceptive pain is the sensitization of peripheral nociceptors for mechanical, thermal and chemical stimuli; the major peripheral mechanism of neuropathic pain is the generation of ectopic discharges in injured nerve fibres. These phenomena are created by changes of ion channels in the neurons, e.g. by the influence of inflammatory mediators or growth factors. Both peripheral sensitization and ectopic discharges can evoke the development of hyperexcitability of central nociceptive pathways, called central sensitization, which amplifies the nociceptive processing. Central sensitization is caused by changes of the synaptic processing, in which glial cell activation also plays an important role. Endogenous inhibitory neuronal systems may reduce pain but some types of pain are characterized by the loss of inhibitory neural function. In addition to their role in pain generation, nociceptive afferents and the spinal cord can further enhance the inflammatory process by the release of neuropeptides into the innervated tissue and by activation of sympathetic efferent fibres. However, in inflamed tissue the innervation is remodelled by repellent factors, in particular with a loss of sympathetic nerve fibres.