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1
Pugliese, Peter T. Devour disease with shark liver oil: Breakthrough discovery can help boost your immune system. Green Bay, WI: IMPAKT Communications, 1999.
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2
Lane, I. William. Sharks still don't get cancer. Garden City Park, N.Y: Avery Pub. Group, 1996.
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3
Brazeau, Stéphanie, and Nicholas H. Ogden, eds. Earth observation, public health and one health: activities, challenges and opportunities. Wallingford: CABI, 2022. http://dx.doi.org/10.1079/9781800621183.0000.
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Abstract This book contains 4 chapters that discuss in the context of both the One Health concept and the SDG initiative, remote sensing can provide solutions to the priority of assessing and monitoring public health risks, and it can play an important role in supporting decision making to reduce health risks within our shared ecosystems. The growing awareness of complex but causal interactions among these realms has motivated professionals in a wide range of sectors to adopt the One Health approach, which promotes intersectoral collaboration to address health issues at the human-animal-environment interface. In its 2030 Agenda for Sustainable Development, the United Nations specifically identifies "strengthening the capacity of all countries, in particular developing countries, for early warning, risk reduction and management of national and global health risks" as part of their Good Health and Well-being Sustainable Development Goal (SDG). As examples presented in this book reveal, the risk of infectious disease emergence increases with a wide range of conditions and variables, including those associated with humans, animals, climate, and the environment. This book examines several priority themes to which EO and geomatics can make important contributions: mosquito-borne and tick-borne diseases; water-borne diseases; air quality and extreme heat effects; geospatial indicators of vulnerable human populations.
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Nurses, International Council of. Reducing the impact of HIV/AIDS on nursing and midwifery personnel. Geneva, Switzerland: ICN, International Council of Nurses, 2006.
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5
Nurses, International Council of. Reducing the impact of HIV/AIDS on nursing and midwifery personnel. Geneva, Switzerland: ICN, International Council of Nurses, 2000.
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6
Cummings, Jeffrey L., and Jagan A. Pillai. Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0001.
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Neurodegenerative diseases (NDDs) are growing in frequency and represent a major threat to public health. Advances in scientific progress have made it clear that NDDs share many underlying processes, including shared intracellular mechanisms such as protein misfolding and aggregation, cell-to-cell prion-like spread, growth factor signaling abnormalities, RNA and DNA disturbances, glial cell changes, and neuronal loss. Transmitter deficits are shared across many types of disorders. Means of studying NDDs with human iPS cells and transgenic models are similar. The progression of NDDs through asymptomatic, prodromal, and manifest stages is shared across disorders. Clinical features of NDDs, including cognitive impairment, disease progression, age-related effects, terminal stages, neuropsychiatric manifestations, and functional disorders and disability, have many common elements. Clinical trials, biomarkers, brain imaging, and regulatory aspects of NDD can share information across NDDs. Disease-modifying and transmitter-based therapeutic interventions, clinical trials, and regulatory approaches to treatments for NDDs are also similar.
7
Sharks Still Don't Get Cancer: The Continuing Story of Shark Cartilage Therapy. Avery, 1996.
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8
Baby Shark: The Shark Tooth Fairy. HarperCollins Publishers Limited, 2020.
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9
Hamilton, Sue L. Eaten by a Shark. ABDO Publishing Company, 2021.
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10
Baby Shark: Baby Shark and the Balloons. HarperCollins Publishers, 2019.
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11
Wash Your Fins, Baby Shark. Scholastic, Incorporated, 2020.
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12
Bajet, John John. Wash Your Fins, Baby Shark. Scholastic, Incorporated, 2020.
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13
Baby Shark: 5-Minute Stories. HarperCollins, 2021.
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14
Baby Shark: Wash Your Hands! HarperCollins Publishers Limited, 2020.
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15
Burton, Robert, Jerzy Leowski, and Maximilian de Courten. Integrating cancer control with control of other non-communicable diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199550173.003.0021.
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Chapter 21 discusses the integration of cancer control with control of other non-communicable diseases, including shared modifiable social, environmental, and behavioural determinants, systems that improve health, health sector responses to non-communicable diseases, and how a comprehensive view of chronic disease prevention and control also has implications for workforce and infrastructure planning.
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Kreit, John W. Severe Obstructive Lung Disease. Edited by John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0013.
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Although chronic obstructive lung disease, asthma, bronchiectasis, and bronchiolitis have very different causes, clinical features, and therapies, they share the same underlying pathophysiology. They are referred to as obstructive lung diseases because airway narrowing causes increased resistance and slowing of expiratory gas flow. Mechanical ventilation of patients with severe obstructive lung disease often produces two problems that must be recognized and effectively managed: over-ventilation and dynamic hyperinflation. Severe Obstructive Lung Disease reviews these two major adverse consequences of mechanical ventilation in patients with severe air flow obstruction. The chapter explains how to detect and correct both of these problems and provides guidelines for managing patients with respiratory failure caused by severe obstructive lung disease.
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Miller, Michelle A. Sleep, inflammation, and disease. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198778240.003.0012.
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Sleep is a fundamental requirement for living individuals. Sleep disturbances and sleep disorders have extensive effects on the immune system, affecting one’s susceptibility to, and ability to fight off, infections—both bacterial and viral—and the subsequent development of different diseases. This is mediated by the increase in pro-inflammatory cytokines associated with sleep loss and disruption. A number of common conditions, such as obesity, cardiovascular disease, metabolic syndrome, obstructive sleep apnoea syndrome, rheumatoid arthritis, and systemic lupus erythematosus, all share pro-inflammatory mechanisms and the presence of sleep disturbances. Early identification of sleep disorders, and the associated adverse inflammatory and metabolic risk factors, in affected individuals would have a clear clinical benefit.
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Baby Shark: Ultimate Sticker and Activity Book. BuzzPop, 2019.
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19
Banerjee, Amitava, and Kaleab Asrress. Screening for cardiovascular disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0351.
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Screening involves testing asymptomatic individuals who have risk factors, or individuals who are in the early stages of a disease, in order to decide whether further investigation, clinical intervention, or treatment is warranted. Therefore, screening is classically a primary prevention strategy which aims to capture disease early in its course, but it can also involve secondary prevention in individuals with established disease. In the words of Geoffrey Rose, screening is a ‘population’ strategy. Examples of screening programmes are blood pressure monitoring in primary care to screen for hypertension, and ultrasound examination to screen for abdominal aortic aneurysm. The effectiveness and feasibility of screening are influenced by several factors. First, the diagnostic accuracy of the screening test in question is crucial. For example, exercise ECG testing, although widely used, is not recommended in investigation of chest pain in current National Institute for Health and Care Excellence guidelines, due to its low sensitivity and specificity in the detection of coronary artery disease. Moreover, exercise ECG testing has even lower diagnostic accuracy in asymptomatic patients with coronary artery disease. Second, physical and financial resources influence the decision to screen. For example, the cost and the effectiveness of CT coronary angiography and other new imaging modalities to assess coronary vasculature must be weighed against the cost of existing investigations (e.g. coronary angiography) and the need for new equipment and staff training and recruitment. Finally, the safety of the investigation is an important factor, and patient preferences and physician preferences should be taken into consideration. However, while non-invasive screening examinations are preferable from the point of view of patients and clinicians, sometimes invasive screening tests may be required at a later stage in order to give a definitive diagnosis (e.g. pressure wire studies to measure fractional flow reserve in a coronary artery). The WHO’s principles of screening, first formulated in 1968, are still very relevant today. Decision analysis has led to ‘pathways’ which guide investigation and treatment within screening programmes. There is increasing recognition that there are shared risk factors and shared preventive and treatment strategies for vascular disease, regardless of arterial territory. The concept of ‘vascular medicine’ has gained credence, leading to opportunistic screening in other vascular territories if an individual presents with disease in one territory. For example, post-myocardial infarction patients have higher incidence of cerebrovascular and peripheral arterial disease, so carotid duplex scanning and measurement of the ankle–brachial pressure index may be valid screening approaches for arterial disease in other territories.
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Newman, Chris, and Andrew Byrne. Musteloid diseases: implications for conservation and species management. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198759805.003.0009.
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The role of disease in population regulation is often overlooked in ecology and conservation. Due to their diversity, the musteloids host a wide range of pathogens. These include diseases of commercial importance, such Aleutian mink disease virus which impacts mink ranching, or bovine tuberculosis leading to interventions to manage European badgers. Skunks and raccoons are major rabies hosts in North America, and because these small carnivores insinuate themselves into close proximity with people, they can pose substantial zoonotic risks. Musteloids also share diseases between species, such as mustelid herpes virus, canine distemper and infectious hepatitis viruses, along with a range of nematodes and protozoans; presenting a contagion risk when vulnerable musteloids are being conserved or reintroduced. Managing host density, vaccination and host isolation are thus the best tools for managing disease, where we advocate the UN-led ‘One Health approach, aimed at reducing risks of infectious diseases at the Animal-Human-Ecosystem interface
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Turk, Bela R., and Ali Fatemi. Diagnosis and Therapy for Lewy Body Dementia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0019.
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Almost undistinguished some 30 years ago, dementia with Lewy bodies is now shown to be the second most common neurodegenerative cause of dementia in the elderly. A host of neuroinflammatory mechanisms are attributed to Lewy bodies and their component alpha synuclein, a common pathology shared by Parkinson disease and Parkinson disease with dementia. Accurate diagnosis of patients is essential, as they show unique impairment patterns, which differ from other forms of dementia and show severe adverse reaction to neuroleptic medication, a common treatment in other degenerative diseases.
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Leirisalo-Repo, Marjatta, and John D. Carter. Infection and spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0009.
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Spondyloarthritis (SpA) is the designation encompassing a group of inflammatory diseases with several features in common. The patients have mono- or oligoarthritis with or without inflammatory back symptoms. Distinctive extra-articular inflammatory symptoms also characterize the diseases. The diagnostic subgroups in the SpA family include reactive arthritis (ReA), ankylosing spondylitis (AS), arthritis associated with inflammatory bowel disease (IBD), psoriasis arthritis (PsA), and some forms of juvenile-onset arthritis. These diseases share a strong association with a genetic marker, HLA-B27, absence of rheumatoid factor, tendency to family aggregation, and frequently occurring extra-articular manifestations. This chapter discusses the role of infections, either as triggering of the disease, most evident in the case of ReA, or as possibly contributing factors in the development of chronic forms of SpA and AS.
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Padilla, Claudia R., and Mario F. Mendez. Neuropsychiatric Features Across Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0006.
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Neuropsychiatric symptoms (NPS) are a major manifestation of neurodegenerative diseases(NDDs) including Alzheimer’s disease (AD), Dementia with Lewy Bodies (DLB) and frontotemporal dementia (FTD). NPS symptoms are a determining factor impacting economic and psychological costs for both the patient and their caregivers in these devastating illness. Recent developments in neuroscience have clarified the relationship of NPS with changes in brain structures, alterations in neural circuits and networks, and their neurotransmitter systems. It is increasingly recognized that NPS shared across different NDDs might have shared alterations in neural circuits and networks, and their neurotransmitter systems and ways to modulate them theraputcally. This chapter focuses on the more common NPS and their links to causative neurodegenerative processes that transcend specific diseases.
24
Baby Shark: The Big Sea Seek and Find. Little Bee Books Inc., 2021.
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25
Baby Shark: My First Big Book of Halloween. Little Bee Books Inc., 2021.
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26
Rogler, Gerhard. Gastrointestinal system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0021.
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Rheumatic diseases and diseases of the gastrointestinal (GI) tract are connected in two ways. The extraintestinal manifestations of inflammatory GI diseases such as inflammatory bowel disease affect joints in up to one-third of patients. On the other hand, several rheumatic diseases such as vasculitis or systemic lupus erythematosus (SLE) induce a wide spectrum of gastrointestinal manifestations. The GI tract constitutes a huge area in contact with the environment. It is exposed to billions of food antigens, commensal bacteria, and potential pathogens. Some of those antigens are thought to play a role in the pathogenesis of rheumatic diseases. The intestinal barrier function and the gut immune system are tightly regulated, as on one hand tolerance for food antigens and the resident commensal flora needs to be maintained, and on the other hand pathogens need to be rapidly and effectively eliminated. Non-infectious, chronic inflammatory diseases of the small and large intestine with rheumatic manifestations have been well known for decades. Among the susceptibility genes for Crohn's disease and ulcerative colitis are some that also cause susceptibility to rheumatoid arthritis or SLE, indicating a shared susceptibility and overlapping pathological mechanisms. Subsequently, similar therapeutic principles have successfully been applied in autoimmune GI and rheumatological diseases such as steroids, immunosuppressants, and anti-TNF (tumour necrosis factor) antibodies.
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Brown, Matthew A., and John Reveille. Genetics of spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0005.
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In addition to sharing clinical, histopathological, and immunological features, spondyloarthritis (SpA) encompasses a group of diseases that are genetically linked through shared associations with HLA-B27, as well as other genes of the IL-23R and aminopeptidase groups. Great progress has been made since the development of the genome-wide association study approach, with better dissection of the HLA associations of this group of diseases, as well as the discovery of multiple genetic loci found outside of the major histocompatibility complex, in ankylosing spondylitis (AS) in particular. These genetic data shed light on the related pathogenesis of AS and psoriatic arthritis (PsA), inflammatory bowel disease (IBD)-related arthritis, and reactive arthritis (ReA). Genetic associations also strengthen the suggestive data that Behçet’s disease (BD) and Familial Mediterranean Fever (FMF) are related to the more classical forms of SpA.
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Elewaut, Dirk, Heleen Cypers, Matthew L. Stoll, and Charles O. Elson. Extra-articular manifestations: inflammatory bowel disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0017.
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A significant overlap exists between spondyloarthritis (SpA) and inflammatory bowel disease (IBD), particularly in the IL-23/IL-17 pathway. Shared immunologic mechanisms include aberrant innate immune responses, an excess of Th1/Th17-mediated immunity, and inadequate immune regulation. Many genetic factors associated with IBD are involved in host–pathogen interactions and intestinal barrier function, and the intestinal microbiota do appear to play an important role in disease development. Hence the current hypothesis for IBD pathogenesis is that it stems from a dysregulated immune response to intestinal microbiota in a genetically susceptible host. In SpA, evidence for a role of intestinal microbiota is less abundant, but given the overlap with IBD, it is plausible that gut microbiota are important players in SpA pathogenesis as well. However, there are significant genetic differences between these two conditions, as well as differing responses to biologic therapy.
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Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0074_update_001.
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Individuals appear to be predisposed to antiglomerular basement membrane (anti-GBM) disease by carrying a predisposing human leucocyte antigen type, DRB1*1501 being identified as the highest risk factor, and there are likely to be other predisposing genes or influences on top of which a relatively rare ‘second hit’ leads to the development of autoimmunity. In anti-GBM disease this appears to have a self-perpetuating, accelerating component, that may be to do with antibodies and altered antigen presentation. Lymphocyte depletion may also predispose to the disease. A number of second hits have been identified and they seem to share a theme of damage to the glomerulus. There may be a prolonged (months to years) and usually subclinical phase in anti-GBM disease in which usually relatively low level antibody titres are associated with variable haematuria, sometimes minor pulmonary haemorrhage, but often no symptoms. Damage to the lung seems to determine whether there is a pulmonary component to the disease. Without pulmonary damage caused typically by smoking, inhalation of other fumes, and potentially infection or oxygen toxicity, the disease remains an isolated kidney disease. Antibodies appear to be an important component of the disease, but cell-mediated immunity is also critical to the clinical picture. In animal models, cell-mediated immunity triggered by the GBM antigen can cause severe renal damage in the absence of pathogenic antibody. The development of specific antibody also requires T-cell sensitization and help, and suppressing the response is likely to require suppressing both antibody and cell-mediated immunity. Antibodies recognize one major and some other epitopes, which are now well described. T-cell epitopes are becoming better understood. Evidence from animal models also suggests that the damage in anti-GBM disease is dependent on complement, macrophages, and neutrophils.
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Fye, W. Bruce. Surgeons Begin Trying to Treat Heart Disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199982356.003.0009.
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The development of heart surgery lagged behind operations on other organs. In the 1920s surgeons in Boston and in Europe attempted to open mitral valves that had become obstructed as a complication of rheumatic fever. Most of their patients died, and the operation was abandoned until after World War II. Operations to treat children with specific types of congenital heart disease were developed between 1938 and 1944. But these procedures involved the blood vessels outside the heart rather than structures within it. After the war, surgeons in Boston, Philadelphia, and London showed that it was safe to operate on patients with severe mitral stenosis. Without surgery, these individuals would die of heart failure. Mid-century optimism about the potential of treating patients with heart disease was fueled by the discovery of so-called miracle drugs, such as penicillin and cortisone (for which two Mayo staff members shared the Nobel Prize in 1950).
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Owen, Jennifer C., Dana M. Hawley, and Kathryn P. Huyvaert, eds. Infectious Disease Ecology of Wild Birds. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780198746249.001.0001.
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Disease ecology is an interdisciplinary field that recognizes that the host–parasite interaction is shaped by the environment and can affect and be affected by the processes that occur across all levels of ecological organization. This book focuses on the dynamics of infectious diseases for wild avian hosts across different scales of biological organization—from within-host processes to landscape-level patterns. Parasite–bird interactions are both influenced by and have consequences for every level of ecological hierarchy, from the physiology, behavior, and evolution of individual hosts up to the complex biotic and abiotic interactions occurring within biological communities and ecosystems. As the most diverse group of extant vertebrates, birds have evolved to utilize every ecological niche on earth, giving them the capacity to serve as a host of pathogens in every part of the world. The diversity of birds is outmatched only by the diversity of the parasite fauna infecting them. Given the overwhelming diversity of both avian hosts and their parasites, we have only scratched the surface regarding the role that pathogens play in avian biology and the role that birds play in the maintenance and spread of zoonotic pathogens. In addition to this understudied diversity, parasite–bird interactions are increasingly occurring in rapidly changing global environments—thus, their ecology is changing—and this shapes the complex ways by which parasites influence the interconnected health of birds, humans, and shared ecosystems. The chapters in this book illustrate that the understanding of these complex and multiscale interactions requires an inherently integrative approach.
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Kühn, Wolfgang, and Gerd Walz. The molecular basis of ciliopathies and cyst formation. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0303.
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Abnormalities of the cilium, termed ‘ciliopathies’, are the prime suspect in the pathogenesis of renal cyst formation because the gene products of cystic disease-causing genes localize to them, or near them. However, we only partially understand how cilia maintain the geometry of kidney tubules, and how abnormal cilia lead to renal cysts, and the diverse range of diseases attributed to them. Some non-cystic diseases share pathology of the same structures. Although still incompletely understood, cilia appear to orient cells in response to extracellular cues to maintain the overall geometry of a tissue, thereby intersecting with the planar cell polarity (PCP) pathway and the actin cytoskeleton. The PCP pathway controls two morphogenetic programmes, oriented cell division (OCD) and convergent extension (CE) through cell intercalation that both seem to play a critical role in cyst formation. The two-hit theory of cystogenesis, by which loss of the second normal allele causes tubular epithelial cells to form kidney cysts, has been largely borne out. Additional hits and influences may better explain the rate of cyst formation and inter-individual differences in disease progression. Ciliary defects appear to converge on overlapping signalling modules, including mammalian target of rapamycin and cAMP pathways, which can be targeted to treat human cystic kidney disease irrespective of the underlying gene mutation.
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Russi, Mark. Biological Hazards. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190662677.003.0016.
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This chapter describes various biological hazards and their impact on workers and others. A major focus of the chapter is biological hazards in healthcare and laboratory settings, including exposure to bloodborne pathogens and prevention of diseases related to them. Sections deal with sharps injuries, HIV/AIDS, hepatitis B virus, hepatitis C virus, tuberculosis, and other infectious diseases that can be acquired in the work environment via direct contact, droplet or airborne spread, or fecal-oral transmission. In addition, infectious agents spread by animal contact or arthropod vectors in a broad range of settings will be addressed. Newly emerging infectious or re-emerging infections, such as those due to H5N1 and novel H1N1 influenza, Middle Eastern respiratory syndrome (MERS), and Ebola Virus Disease (EVD) as well as agents associated with bioterrorism are discussed.
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Blacksher, Erika. Public Health and Social Justice: An Argument Against Stigma as a Tool of Health Promotion and Disease Prevention. Edited by Brenda Major, John F. Dovidio, and Bruce G. Link. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190243470.013.24.
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This chapter argues against the use of stigma-inducing measures as tools of public health on grounds of social justice. The value of social justice in public health includes both a distributive demand for a fair share of health and the social determinants thereof and a recognitional demand to be treated as a peer in public life. The use of stigma-inducing measures violates the first demand by thwarting people’s access to important intra- and interpersonal, communal, and institutional resources that confer a health advantage; it violates the second by denying people’s shared humanity and ignoring complex non-dominant identities. The position taken in this chapter does not preclude public health measures that regulate and ban health-harming substances or try to move people toward healthier behaviors. It does require that public health partner with people to identify their communities’ health challenges and opportunities and to treat people as resourceful agents of change.
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Rapoff, Michael, and Ron Freche. Hope and Children’s Health. Edited by Matthew W. Gallagher and Shane J. Lopez. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780199399314.013.16.
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Childhood is a critical time to develop hopeful thinking that can help children cope with challenges in general and those related to maintaining or improving their health. The purpose of this chapter is to (a) define hope as it applies to children and the growth of hope across developmental stages; (b) describe the way family members, teachers, and other significant adults can foster hope in children; (c) review studies on the relationship between hope and pediatric health and illness, including studies on health promotion, adherence to chronic pediatric diseases, and coping with a chronic pediatric disease; and (d) share knowledge related to patients with chronic pediatric diseases and how they maintain hope given the additional challenges they face in their lives.
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Macdougall, Iain C. Erythropoiesis-stimulating agents in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0124.
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The advent of recombinant human erythropoietin (epoetin) in the late 1980s transformed the management of renal anaemia, liberating many dialysis patients from lifelong regular blood transfusions, in turn causing severe iron overload and human leucocyte antigen sensitization. Epoetin can be administered either intravenously or subcutaneously, but the half-life of the drug is fairly short at around 6–8 hours, necessitating frequent injections. To circumvent this problem, two manipulations to the erythropoietin molecule were engineered. The first of these was to attach an extra two carbohydrate chains to the therapeutic protein hormone (to make darbepoetin alfa), and the second was to attach a large pegylation chain to make continuous erythropoietin receptor activator. Both of these strategies prolonged the circulating half-life of the erythropoietin analogue. The next erythropoietic agent to be produced was peginesatide, a peptide-based agent which had no structural homology with native or recombinant erythropoietin, but shared the same biological and functional characteristics. Future strategies include stabilization of hypoxia-inducible factor, by orally active inhibitors of the prolyl hydroxylase enzyme, and advanced clinical trials are underway. In the meantime, several large randomized controlled trials have highlighted the potential harm in targeting a near normal haemoglobin of 13–14 g/dL (with an increased risk of cardiovascular complications), and sub-normal correction of anaemia is now advised. Some patients may show mild or severe resistance to erythropoiesis-stimulating agent (ESA) therapy, and common causes include iron insufficiency, infection, and underlying inflammation. Very rarely, patients may produce antibodies against their ESA, which neutralize not only the ESA, but also endogenous erythropoietin, causing pure red cell aplasia.
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Keil, Geert, and Ralf Stoecker. Disease as a vague and thick cluster concept. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198722373.003.0003.
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This chapter relates the problem of demarcating the pathological from the non-pathological in psychiatry to the general problem of defining ‘disease’ in the philosophy of medicine. Section 2 revisits three prominent debates in medical nosology: naturalism versus normativism, the three dimensions of illness, sickness, and disease, and the demarcation problem. Sections 3–5 reformulate the demarcation problem in terms of semantic vagueness. ‘Disease’ exhibits vagueness of degree by drawing no sharp line in a continuum and is combinatorially vague because there are several criteria for the term’s use that might fall apart. Combinatorial vagueness explains why the other two debates appear hopeless: Should we construe ‘disease’ in a naturalistic or in a normative way? Neither answer is satisfactory. How should we balance the three dimensions of pathology? We do not have to, because illness, sickness and disease (narrowly conceived) are non-competing criteria for the application of the cluster term ‘disease’.
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Clair, Alicia. Music Therapy for People Who Have Alzheimer’s Disease. Edited by Jane Edwards. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780199639755.013.39.
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A description of the current state of music therapy research with those who have dementia and the future of music therapy in dementia care is provided in this chapter. The contents stem from many years of experience as a board-certified music therapist with those who have dementia and their care givers, and it culminates learning from clinical practice and research in the development of a theoretical framework and practice knowledge. Deep appreciation is expressed for all care receivers, and their care givers, who allowed music therapy to become part of their lives and who consented to participate in the development of knowledge to share with others. This chapter provides: (a) A review of selected clinical research studies in music therapy and dementia care, (b) updated dementia information that has implications for current music therapy practice, (c) a theoretical framework for music therapy, and (d) the theoretical principles that guide clinical music therapy practice with care receivers and caregivers.
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Hawker, Gillian, Anne Lyddiatt, Linda Li, Dawn Stacey, Susan Jaglal, Sarah Munce, and Esther Waugh. Patient information strategies for decision-making and management of osteoarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0021.
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Osteoarthritis (OA) is a chronic, disabling disease that warrants care that aligns with the principles of ‘chronic disease management’. Central to the success of chronic disease management is the ‘informed, activated patient’. Patient information strategies, including the use of patient decision aids, are essential to enabling patients with OA to self-manage their disease and engage in informed, shared decision-making. Such strategies are best delivered by a multidisciplinary team of healthcare providers and adapted to the characteristics, preferences, and values of the individual OA patient. Patients actively involved in their own disease management, that is, ‘self-management’, including shared goal-setting and decision-making about treatment interventions, are, on average, more adherent to treatment recommendations, have enhanced self-efficacy and, ultimately, experience better health outcomes.
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Haskard-Zolnierek, Kelly B., Tricia A. Miller, and M. Robin DiMatteo. Promoting treatment adherence. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198736134.003.0037.
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Empirical evidence demonstrates that quality healthcare outcomes depend greatly upon patients’ adherence to their recommended treatments. Patient adherence is a patient’s ability to follow his or her treatment recommendations given by a healthcare provider. Rates of adherence, however, can be as poor as 50% or less among patients with certain chronic diseases. For cancer patients, non-adherence can have serious consequences, including increased disease morbidity and mortality. Factors associated with non-adherence in cancer patients include treatment complexity, illness severity, patients’ beliefs and attitudes, lack of social support, and depression. Improving adherence depends upon effective provider–patient communication, trust in the therapeutic relationship, shared decision-making, and a realistic assessment of patients’ knowledge and understanding of their treatment. To assist cancer patients in acquiring appropriate disease and treatment information, to build commitment and motivation, and to assist in the development of strategies to overcome treatment barriers, healthcare professionals can use the Information-Motivation-Strategy model.
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Bending, David, Kiran Nistala, and Lucy R. Wedderburn. Pathogenesis of juvenile idiopathic arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0060.
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Although the term juvenile idiopathic arthritis (JIA) encompasses a heterogeneous group of diseases, they all share a common pathological hallmark: inflammation of the synovium. Highly activated T cells, monocytes, and neutrophils are attracted to the joint and secrete mediators that not only perpetuate inflammation but also may attenuate immune regulation. In the oligoarticular and polyarticular forms of JIA, which are thought to be autoimmune conditions, dysregulated adaptive immunity is a likely factor in disease pathogenesis; the nature of the interactions between T effector (Teff) cells and T regulatory cells (Treg) is probably a key factor in controlling disease progression. Factors that affect the frequency and function of Tregs and/or the sensitivity of Teffs to mechanisms of immune suppression will therefore impact on the disease course. In the systemic form of JIA, however, dysregulation of innate immune pathways appears more central to disease pathogenesis resulting in augmented levels of interleukins IL-1β, IL-6, and IL-18. In the end, a final, common pathological pathway in JIA is the activation of monocytes and neutrophils, which are the principal mediators of joint inflammation and damage. This is supported by the fact that the therapies that have targeted innate cytokine pathways have shown greater success in the treatment of JIA.
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Knott, Andrew B., and Ella Bossy-Wetzel. Mitochondrial Changes and Bioenergetics in Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0012.
Full textAbstract:
Mitochondria are dynamic organelles that are of critical importance for cellular survival and health. Because mitochondria play central roles in energy production and synaptic maintenance, neurons are believed to be particularly vulnerable to mitochondrial dysfunction. The discovery that genetic mutations in genes coding for mitochondrial proteins cause neurodegenerative conditions further hinted at the likelihood that mitochondrial dysfunction is a key pathway of neurodegeneration. Indeed, a wealth of research has identified mitochondrial dysfunction as an early and shared event of all common neurodegenerative diseases, both genetic and sporadic in origin. Specific types of mitochondrial dysfunction that have been observed in most neurodegenerative diseases include bioenergetic failure, increased oxidative stress, mitochondrial DNA mutations, defective calcium handling, impaired mitochondrial dynamics, defective mitophagy, and decreased mitochondrial biogenesis. The search for drugs that successfully target these pathways of mitochondrial dysfunction in neurodegeneration is ongoing.
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Goodyer, Paul. Kidney/ear syndromes. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0170.
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Malformations of the external ear may signal renal disease, but it is actually the disorders of the inner ear which reflect molecular pathways that are also crucial for kidney development. In a number of monogenic renal diseases, renal dysplasia is associated with deafness. Disorders of the kidney and inner ear are also linked in complex syndromes such as the human ciliopathies. In some cases, the loss of specific genes affects shared transport physiology, basement membrane assembly, or energy metabolism.The kidney and cochlea have a common susceptibility to toxins that are selectively concentrated by comparable uptake mechanisms in the two tissues.This chapter provides an overview of the many ways in which pathologies of the two organs are linked.
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Jardine, Alan G., and Rajan K. Patel. Lipid disorders of patients with chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0102.
Full textAbstract:
The risk of developing cardiovascular (CV) disease is increased in patients with chronic kidney disease (CKD) and although dyslipidaemia is a major contributory factor to the development of premature CV disease, the relationship is complex. Changes in lipid fractions are related to glomerular filtration rate and the presence and severity of proteinuria, diabetes, and other confounding factors. The spectrum of CV disease changes from lipid-dependent, atheromatous coronary disease in early CKD to lipid-independent, non-coronary disease, manifesting as heart failure, and sudden cardiac death in advanced and end-stage renal disease. Statin-based lipid-lowering therapy is proven to reduce coronary events across the spectrum of CKD. The relative reduction in overall CV events, however, diminishes as CKD progresses and the proportion of lipid-dependent coronary events declines. There is nevertheless a strong argument for the use of statin-based therapy across the spectrum of CKD. The argument is particularly strong for those patients with progressive renal disease who will eventually require transplantation, in whom preventive therapy should start as early as possible. The SHARP study established the benefits and endorses the use of lipid-lowering therapy in CKD 3-4 but uncertainty about the value of initiation of statin therapy in CKD 5 remains. There is, however, no rationale for stopping agents started earlier in the course of the illness for compelling indications, particularly in those who will ultimately be transplanted. The place of high-density lipoprotein-cholesterol raising and triglyceride lowering therapy needs to be assessed in trials. Modifying dyslipidaemia in CKD has demonstrated that lipid-dependent atheromatous cardiovascular disease is only one component of the burden of CV disease in CKD patients, that this is proportionately less in advanced CKD, and that modification of lipid profiles is only one part of CV risk management.
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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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Cummings, Jeffrey L., and Kate Zhong. Clinical Trials and Drug Development in Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0018.
Full textAbstract:
This chapter describes the common therapeutic targets, approaches to clinical trial design, biomarkers, and therapeutic interventions across neurodegenerative disorders (NDDs). Each unique NDD-Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), etc.-has a unique phenotype associated with the regional cell population most affected. Each disease, however, is associated with protein misfolding, oxidation, inflammation, apoptosis, and cell death. If vulnerable cell populations include transmitter source nuclei, transmitter deficits also emerge (e.g. cholinergic abnormalities in AD and dopaminergic deficits in PD). Biomarkers show regionally appropriate brain atrophy or process-related cerebrospinal deficits. Clinical trial designs share features for symptomatic interventions (e.g. cholinesterase inhibitors in AD and dopamine agents in PD) and disease-modifying therapies. Biomarkers play similar roles in trials for NDD, including demonstrating target engagement and supporting disease modification. No disease-modifying therapies have been approved for any NDDs; all programs face similar pharmacokinetic, pharmacodynamic, and regulatory challenges in therapeutic development.
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Safar, Jiri G. Prion Paradigm of Human Neurodegenerative Diseases Caused by Protein Misfolding. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0005.
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Data accumulated from different laboratories argue that a growing number of proteins causing neurodegeneration share certain characteristics with prions. Prion-like particles were produced from synthetic amyloid beta (Aβ) peptides of Alzheimer’s disease (AD), from recombinant α-synuclein linked to Parkinson’s disease (PD), and from recombinant tau associated with frontotemporal dementias (FTD). Evidence from human prions reveals that variable disease phenotypes, rates of propagation, and targeting of different brain structures are determined by distinct conformers (strains) of pathogenic prion protein. Recent progress in the development of advanced biophysical tools identified the structural characteristics of Aβ in the brain cortex of phenotypically diverse AD patients and thus allowed an investigation of the prion paradigm of AD. The findings of distinctly structured strains of human brain Aβ, forming a unique spectrum of oligomeric particles in the cortex of rapidly progressive cases, implicates these structures in variable rates of propagation in the brain.
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Staid, Rashna K. Key Nutrients for Normal Brain Health. Edited by Anthony J. Bazzan and Daniel A. Monti. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190690557.003.0002.
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Over the past several decades, there has been a sharp increase in psychiatric diseases but relatively little attention to improving poor nutritional patterns that affect mental health conditions. Long-term nutrient deprivation results in neuroinflammation, which contributes to causing mental illnesses such as depression, anxiety disorder, and schizophrenia. A growing body of research substantiates the benefits of supplementing many essential nutrients such as omega-3 fatty acids, vitamin D, the B complex vitamins, vitamin E, and the minerals magnesium, iron, zinc, choline, calcium, and selenium to help prevent and treat many mental illnesses. These nutrients are often limited in the standard Western diet. Importantly, it is not just one single nutrient that is important to optimizing brain health but all the nutrients working in concert in a healthy, well-balanced approach that helps to optimize brain function and prevent disease. This chapter reviews the various nutrients involved in maintaining optimal brain health.
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Prunty, Helen, Jamie L. Fraser, Charles P. Venditti, and Robin H. Lachmann. Branched Chain Amino Acids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0016.
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This chapter describes the four most common disorders affecting the degradation of branched chain amino acids: maple syrup urine disease, methylmalonic acidemia, propionic acidemia and isovaleric acidemia. These conditions most commonly present with encephalopathy in the newborn period, although cases with later onset have also been described. Although adult patients are less prone to acute metabolic decompensations, they do develop a number of long-term complications, both neurological and visceral. Management shares features with other disorders of protein metabolism and centers on a low-protein diet and the use of disease-specific amino acid supplements.
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Weiner, Marli F., and Mazie Hough. Placed Bodies. University of Illinois Press, 2017. http://dx.doi.org/10.5406/illinois/9780252036996.003.0004.
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This chapter examines how physicians developed the concept of place to reconcile the complexities of race and sex when defining bodies and their health and sicknesses. In the increasingly contested political arena of the antebellum years, southern physicians knew that their work would most likely be received favorably if it reinforced the region's distinctiveness. Awareness that some places were inherently unhealthy and that some people were more likely to get sick in them was part of the anecdotal medical lore that informed physicians' thinking about bodies as placed. Doctors were well aware that southerners fell victim to different diseases and had to be treated differently from people elsewhere in the nation. Thus, doctors argued that a specifically southern medical theory and practice was necessary. This chapter explores how nineteenth-century physicians seeking to understand the consequences of placed bodies invoked the South's climate and the concept of acclimation to explain disease. It shows that laypeople shared physicians' convictions that medicine was specific to place and that bodies were shaped by their environment.