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Epilepsy poses unique problems and opportunities for cerebral imaging with positron emission tomography (PET). After reviewing PET methods in epilepsy applications, this chapter addresses the extensive applications of 2-[¹⁸F]fluoro-2-deoxyglucose (FDG) mapping of glucose metabolism in temporal lobe epilepsy (TLE). The widespread zone of interictal metabolic dysfunction is highly associated with sites of ictal onset and propagation in TLE. Interictal FDG PET is used in correlation with ictal electrophysiologic and structural magnetic resonance findings for the purposes of: 1) increasing certainty that the ictal onset zone has been accurately determined by noninvasive studies prior to therapeutic temporal lobe ablation, 2) optimizing selection of intracranial electrode placement sites for ictal monitoring, and 3) prognostication for epilepsy surgery with regard to seizure control.

The advent of positron emission tomography (PET) scanning using 2-deoxy-2-[¹⁸F] fluoro-D-glucose (FDG) has significantly improved our understanding of the pathomechanisms of different pediatric epilepsy syndromes. Furthermore, it has dramatically altered our management approach of certain intractable epilepsy syndromes, such as infantile spasms. Glucose metabolism PET scanning has assumed an important role not only in the identification and localization of epileptogenic cortex, but also in assessing the functional integrity of the entire cerebral hemisphere, thereby providing useful diagnostic and prognostic information, including the suggestion of underlying neurometabolic or neurogenetic disorders which may preclude epilepsy surgery. In certain progressive epilepsy syndromes like Rasmussen encephalitis and Sturge-Weber syndrome, PET scanning also may be used to assess disease progression. In this chapter, we discuss the relevant role of brain glucose metabolism PET in understanding the pathogenesis of pediatric epilepsy syndromes with regard to diagnosis and treatment.

This chapter points to a view of free will as a complex form of action control that is used (sometimes) by humans to achieve self-control and rational, intelligence decision-making, as well as making and following ad hoc plans. Research suggests that these activities deplete a common but limited energy resource, so the capacity for free will is limited and biologically expensive. Blood glucose (brain fuel) maybe a major part of the common resource. Rational choice, self-control, and planful behavior are more useful forms of free will than random action. Psychologists may profitably focus more on how this mechanism works than on debating whether it fits various philosophical or theological definitions of free will. The broader context is that free will can be understood as an evolutionary adaptation to enable humans to function in the increasingly complex social world afforded by culture.

Assessment of regional cerebral glucose metabolism by FDG-PET at the resting state is a standard functional technique to assess cerebral function. An increasing body of evidence indicates that substantial impairment of FDG uptake in temporo-parietal association cortices is a reliable predictor of rapid progression to dementia in patients with mild cognitive impairment (MCI). The definition of affected and reference regions, the methods for quantitative analysis, and other methodological issues that are relevant for use of the method in clinical studies are being addressed. Effects of aging, the selection of normal controls, and interaction with age and genetic risk factors are important factors that also need to be considered in designing and interpreting studies.

The current technology for self-monitoring of blood glucose (SMBG) levels has been well established since the 1980s. This practice is beneficial to patients with diabetes from both a clinical and an economic standpoint. Knowledge of their blood glucose levels can allow patients to select appropriate doses of insulin to regulate these levels. This chapter analyzes the technology, benefits, economic aspects, problems, and controversies associated with SMBG, continuous glucose monitoring, and the artificial pancreas as well as telemonitoring technology for diabetes management.

This chapter discusses enzymes of carbohydrate and energy metabolism in glial cells. These include enzymes of glucose metabolism, enzymes of glycogen metabolism, carbonic anhydrases, and enzymes of cellular energization.

Trace metals are required in small quantities for a wide array of metabolic functions in the body. In terms of obesity, they can enhance insulin action through activating insulin receptor sites, serve as cofactors or components for enzyme systems involved in glucose metabolism, increase insulin sensitivity, and act as antioxidants to prevent tissue oxidation. Chronic hyperglycemia causes significant alterations in the status of many trace metals in the body and consequently increases the oxidative stress which can contribute to the pathogenesis of infectious diseases. Whether obese individuals with trace metal deficiency (or toxicity) are at increased risk for infection is a matter of concern in many developing countries, where a growing segment of the population (exposed to traditional health risks) has embraced Western dietary habits. A better understanding of the roles of different trace metals will undoubtedly facilitate the development of new treatment and prevention strategies that can more effectively reduce the silent burden of comorbid obesity and infectious diseases.

The epidemics of obesity and diabetes are increasing rapidly world-wide. Due to the potentially devastating consequences of these metabolic diseases, it is imperative that modifiable causes of both diabetes and obesity be identified as potential areas of intervention. Although changes in diet and exercise have played an important role, another possible explanation for the epidemic is reduced sleep duration and quality. Sleep loss may be the result of either a voluntary restriction of time spent in bed or as a result of a sleep disorder. This chapter presents potential pathways leading from insufficient or disturbed sleep to diabetes and obesity, including impaired glucose metabolism, increases in appetite, and reduction in energy expenditure following reductions in sleep duration and/or quality. It explores the evidence for an association between metabolic diseases and sleep duration and quality.

This chapter covers interventional studies aimed at lowering the incidence of cardiovascular disease (CVD), nephropathy, retinopathy, blindness, lower-extremity amputation (LEA), peripheral sensory neuropathy, and autonomic neuropathy; and at prolonging life. It includes studies that address clinical endpoints. It shows that individuals with diabetes and their providers of care can reduce the occurrence of diabetic complications by lowering glucose, blood pressure, and LDL, either alone or in combination. Nonpharmacologic interventions, chiefly those related to retinopathy and obesity, also improve outcomes. To date evidence for lowering blood glucose and blood pressure does not support the use of specific agents except possibly metformin and blockade of the angiotensin system. For LDL, statins remain the intervention of choice.

Following an outline of the transmission electron microscope (TEM) and its working principles, this chapter starts with a description of specimen preparation methods for EM imaging, including negative staining, glucose embedment and ice embedment. The principle of image formation in the TEM is described as it pertains to biological weak phase objects, and in the process, the contrast transfer function (CTF) is introduced. It shows that EM images are effectively projections of the Coulomb potential distribution of the biological object, convoluted with that function. The chapter closes by describing methods for the determination and computational correction of the CTF.

Self-regulation refers to control over one's emotions, thoughts, and behaviors. Failure of self-regulation contributes to many important individual and societal problems, including problems with eating, spending, interpersonal violence, sexual promiscuity, and alcohol and drug use. Evidence points to a general pool of self-regulatory capacity. This chapter suggests that this capacity depends on, is reflected in, and affects physiology. That is, self-regulation is literally embodied. This assertion seems obvious with regard to the central nervous system, but less so with regard to peripheral physiology. Nonetheless, there is evidence that peripheral regulation of physiological parameters such as blood glucose and heart rate is intertwined with central regulation of the self. The chapter presents a brief overview of physiological systems involved in self-regulation, reviews the empirical links between self-regulation and physiology in several domains, and then suggests directions for future research.

This main focus of this chapter is on genetic disorders of the structure or synthesis of haemoglobin — especially sickle cell disease and the thalassaemias, which are common enough in many populations to justify antenatal and neonatal screening. Glucose-6-phosphate dehydrogenase deficiency also merits screening in certain populations where it commonly causes neonatal jaundice and kernicterus; and screening for hereditary bleeding diseases is indicated if there is a history of a previously affected child.

The pathophysiological process of atherosclerosis, which ultimately leads to cardiovascular disease, begins in childhood and young adulthood. This chapter describes the life course trajectories in blood pressure, lipids, glucose, insulin, and non-invasive assessments of vascular structure and function and, explores differences between males and females and by ethnic group. It reviews evidence regarding the associations of pre-adult risk factors with these trajectories, explores whether puberty, pregnancy, and the perimenopause are key periods when the trajectories show distinct changes, and describes how changes in the trajectories relate to cardiovascular disease. Higher blood pressure, low density lipoprotein cholesterol, and fasting glucose in adolescence and early adulthood are associated with adverse cardiometabolic events in older age. Despite cohort studies in children and adults often repeatedly measuring cardiometabolic markers, few have appropriately modelled change with age in relation to risk factors, or explored how different patterns of change relate to future disease risk.

This chapter integrates and organizes pharmacological studies of memory by searching for generalizations or “rules” about the roles of hormonal and neurotransmitter systems in the regulation of learning and memory processes. In doing so, it is important to examine carefully the extent to which these generalizations are similar and different for results obtained with systemic injections and those obtained with direct brain injections. Consistently, systemic injections of epinephrine or of glucose, which may contribute to epinephrine effects on memory, enhance memory when administered near the time of training. Similarly, systemically administered drugs that promote the functions of central cholinergic, glutaminergic, or noradrenergic systems enhance memory on later tests. Moreover, diminished release of the neurotransmitters or pharmacological blockade of their receptors can impair memory. There also appear to be some neurochemical systems, for example, opioid and GABA, for which activation impairs, and inactivation enhances, learning and memory.

Many animal and human studies have explored biochemical concomitants of aggressive and self-destructive behaviours. A small number of these studies have used pharmacological manipulations to provoke or reduce such behaviours. A common factor in these investigations is central nervous system (CNS) serotonin (5hydroxytryptamine, 5-HT); decreasing serotonergic functioning is conducive of aggressive and impulsive behaviours, increasing it reduces such behaviours. Another factor associated with impulsive, violent offences in some humans is a tendency to become mildly hypoglycaemic after an oral glucose load. Such mild hypoglycaemia is a state associated with irritability and impulsivity. This review develops the arguments that CNS serotonin metabolism may, to some extent, control glucose metabolism and that reduced central serotonin turnover may be causally linked to hypoglycaemic tendency in impulsive violent offenders and fire-setters.

This chapter begins with detailing the author's final results following her three-day grueling tests for glucose tolerance, psychological screening, kidney function, EKG, and a chest X-ray. The author found out that there was an issue with her blood pressure. It then outlines the four available choices she could take: to end the process, to lose some weight and reduce salt intake and retest in a few months, to start on a very low dose of antihypertensive medication and retest in two weeks, and finally, to take her current results to the Transplant Selection Committee and hope for the best. Ultimately, the chapter presents an alternative plan, to become part of the Kidney Paired Donation program, if the new blood tests ruled the author unable to donate directly to the intended recipient.

This chapter focuses on the bottom-up approach used to understand the nature of natural selection, and begins by discussing a bottom-up analysis of the lactose system. The study of lactose metabolism by Escherichia coli provides a tractable experimental system where mechanistic predictions about the direction and intensity of selection can be tested decisively. The chapter also illustrates other ways in which bottom-up experiments in evolution can be done. They can be used to study glucose metabolism in Drosophila and the genotype-phenotype map for single genes. The bottom-up approach can also be used to examine the similarities and differences in vision for organisms in different environments.

This chapter covers core curriculum topics related to diabetes and lipid metabolism. The diagnosis, investigation, classification, and pathophysiology of Type 1 and Type 2 diabetes mellitus is discussed in detail. A table has been used to sum up the clinical characteristics of monogenic diabetes subtypes in a concise though comprehensive manner. The MCQs have been updated to reflect current clinical practice guidelines of the National Institute for Health and Care Excellence and Joint British Diabetes Societies. MCQs have been added which evaluate a trainee’s knowledge on the management of diabetes in special circumstances (e.g. pregnancy, elderly age group, adolescence) and on the use of technology (e.g. continuous glucose monitoring). The positioning of novel therapeutic agents such as glucagon-like peptide 1 receptor agonist and sodium-glucose cotransporter-2 inhibitor in the management of Type 2 diabetes mellius has been updated based on the current evidence base. This chapter includes questions on the diagnosis and management of diabetic emergencies such as diabetic ketoacidosis and hyperosmolar hyperglycaemic syndrome. MCQs have been added and updated to cover current guidelines for the management of dyslipidaemia.

The original claims of cognitive neuroscience, an offshoot of computer science and psychology, were of a logical brain in which mental concepts could be identified and localized. Reviews of the imaging studies of two popular cognitive neuroscience concepts, “working memory” and “willed action,” show that these expectations are not fulfilled, while in a Pragmatist understanding of such generalizations they cannot be found. Instead, neuroimages are shown to determine the values of cerebral blood flow and energy consumption, which can create a neurophysiological, bottom-up basis of brain function.