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1
Davie, Michael B. Winning ways: Innovative leaders discuss their success strategies. [Ancaster, Ont.]: Manor House Pub., 2002.
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2
How They Achieved. New York: John Wiley & Sons, Ltd., 2001.
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3
What is a Gospel?: The genre of the canonical Gospels. Macon, Ga: Mercer University Press, 1985.
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4
Wyatt, Tristram D. 3. How behaviour develops. Oxford University Press, 2017. http://dx.doi.org/10.1093/actrade/9780198712152.003.0003.
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Behaviours evolve by natural selection. As genes influence how behaviours develop, selection on behaviour will alter gene frequencies in subsequent generations: genes that lead to successful behaviours in foraging, parental care, or mate choice, for example, will be represented in more individuals in future generations. If conditions change, then mutations of the genes that give rise to advantageous behaviours will be favoured by selection. ‘How behaviour develops’ explains that the environment is equally important: both genes and environment are intimately and interactively involved in behaviour development. Behavioural imprinting is also discussed along with co-opting genes, gene regulation, social influences on brain gene expression, phenotypic plasticity, and play.
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Switch: Activating Your Genes for a Leaner, Longer, Healthier Life. Simon & Schuster, Limited, 2020.
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6
Shane, Scott. Born Entrepreneurs, Born Leaders: How Your Genes Affect Your Work Life. Oxford University Press, 2010.
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7
Business Leader Profiles for Students. 2nd ed. Thomson Gale, 2002.
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8
Business Leaders: Steve Jobs (Korean Edition). Myeongjin Chulpansa/Tsai Fong Books, 2009.
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9
Gorman, Jack M. Life Events Shape Us. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850128.003.0003.
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Psychiatry downplayed the importance of life events in causing mental illness from the 1960s on, favoring a view that all disorders except one are the result of abnormal genes affecting chemical processes in the brain. Studying the exception, posttraumatic stress disorder (PTSD), when it was defined in 1980 helped lead to renewed recognition that early life adversity is central to all psychiatric conditions. At the same time, neuroscientists showed that early life experiences are capable of changing life-long behavior and brain function in laboratory animals. One mechanism by which this occurs is through the epigenetic regulation of gene expression. Epigenetics is the way that the expression levels of genes are controlled without changing the underlying genetic code. Epigenetics is an attractive way of understanding how individual life experiences are translated in the brain into each person’s unique set of emotions, behaviors, abilities, and risks for psychiatric abnormalities.
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Biloshytsky, Vadym, and Roman Cregg. Pioneering use of gene therapy for pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0083.
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The landmark paper discussed in this chapter is ‘Gene therapy for pain: Results of a Phase I clinical trial’, published by Fink et al. in 2011. In this study, the first of its kind, researchers studied the efficacy and safety of a modified herpes simplex virus (HSV) vector used to deliver PENK, which encodes proenkephalin, which is cleaved into the enkephalin peptides Met-enkephalin and Leu-enkephalin, which induce analgesia by acting on opioid receptors. The development of the HSV vector was based in part on results studies in which adenovirus, adeno-associated virus, or non-viral vectors were used to overexpress genes. Overexpression of a variety of large molecules leads to a reduction in pain-related behaviour in animals. Gene therapy in the treatment of chronic pain seems to offer a promising alternative to systemic or highly invasive therapies. However, additional research is needed to determine the safety, effectiveness, and cost-efficiency of this approach.
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Prasad, Supritha, and Edwin H. Cook. Novel Approaches for Treating Pediatric Psychiatric Disorders. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0067.
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Multifactorial mechanisms, including varying degrees of polygenic risk, contribute to most child onset psychiatric disorders. Methods to better understand the biological impact of inherited low-risk variation are emerging, and these studies may be useful to develop novel treatments for childhood onset psychiatric disorders. In some neurodevelopmental disorders, specifically autism spectrum disorder (ASD) and intellectual disability (ID), recurrent spontaneously mutated genes have been identified. This leads to the current focus on individual, high-risk targets (e.g., SHANK3, FMR1, MECP2, CHD8) for development of novel treatments. This chapter summarizes and begins to compare neurobiological data from several distinct single gene disorders as a means to guide further therapeutic development based on overlapping pathways of interest.
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Canli, Turhan, ed. The Oxford Handbook of Molecular Psychology. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199753888.001.0001.
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Determining the biological bases for behavior—and the extent to which we can observe and explain their neural underpinnings—requires a bold, broadly defined research methodology. The interdisciplinary entries in this handbook are organized around the principle of “molecular psychology,” which unites cutting-edge research from such wide-ranging disciplines as clinical neuroscience and genetics, psychology, behavioral neuroscience, and neuroethology. For the first time in a single volume, leaders from diverse research areas present their work in which they use molecular approaches to investigate social behavior, psychopathology, emotion, cognition, and stress in healthy volunteers, patient populations, and an array of nonhuman species including nonhuman primates, rodents, insects, and fish. Chapters draw on molecular methods covering candidate genes, genome-wide association studies, copy number variations, gene expression studies, and epigenetics while addressing the ethical, legal, and social issues to emerge from this new and exciting research approach.
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Hastie, Nick, and Eve Miller-Hodges. WT1 and its disorders. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0329_update_001.
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Mutations in the Wilms tumour suppressor gene, WT1, are associated with Wilms tumour in childhood. However, in addition WT1 has a key role in renal development, emerging roles in podocyte function, and a potential role in tissue regeneration. An understanding of WT1 is of increasing importance to clinical practice. WT1 is a complex gene with multiple isoforms. It is crucial for normal embryonic development, especially kidney development, where it is necessary for mesenchymal-to-epithelial transition to form the nephron. WT1 mutations lead to abnormalities in renal and genitourinary development, causing diseases such as Denys–Drash syndrome and Frasier syndrome as well as Wilms tumour. Recently, WT1 mutations have been recognized as a significant cause of isolated steroid-resistant nephrotic syndrome in children and young adults, without other associated syndromic features. WT1 continues to be expressed in adult podocytes, where it acts as a transcriptional activator of many podocyte genes. However, the specific role of WT1 in adult podocyte function remains poorly understood.
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Kanno, Hiroshi, and Joachim P. Steinbach. Familial tumour syndromes: von Hippel–Lindau disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0016.
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Von Hippel–Lindau (VHL) disease, an autosomal dominant familial tumour syndrome, is often associated with haemangioblastoma of the central nervous system. In the presence of oxygen, VHL protein serves to prevent the accumulation of hypoxia-inducible factor (HIF) protein by targeting it to the proteasomal pathway, while biallelic inactivation of the VHL gene blocks degradation of HIF and leads to constitutive activation of the HIF pathway although oxygen is present. HIF-target genes are involved in angiogenesis, proliferation, and metabolism enabling tumour growth. Haemangioblastoma is a highly vascularized, begin tumour commonly associated with a cyst, but it is linked with neurological morbidity and mortality based on its location and multiplicity. Haemangioblastoma in VHL is diagnosed according to symptoms and signs, past and family histories, laboratory data, neuroradiological findings, pathological findings, and genetic testing. Surgical treatment is usually the most recommended therapy for haemangioblastomas, and using well-defined microsurgical techniques, the majority can be resected safely.
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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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Raju, Raghavan, and Irshad H. Chaudry. The host response to hypoxia in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0305.
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The hypoxic response of the host is complex. While the oxygen-sensing intracellular machinery attempts to restore cellular homeostasis by augmenting respiration and blood flow, events such as severe haemorrhage lead to whole body hypoxia and decreased mitochondrial function. Immunological perturbations following severe haemorrhage may result in multiple organ dysfunction and sepsis, while impaired perfusion may lead to microvascular injury and local hypoxia. Trauma-haemorrhage or hypoxic exposure in animals causes a systemic inflammatory response, decreased antigen presentation by peritoneal macrophages, hypoxaemia and initiation of endoplasmic reticulum stress. In response, the protein level of the oxygen-sensing transcription factor, hypoxia inducible factor (HIF)-1 increases; this leads to the regulation of expression of a number of genes resulting in decreased mitochondrial ATP production, but enhanced glycolytic processes, thus shifting the energy balance. In addition, sustained tissue hypoxia leads to increased free radical production and cellular apoptosis. Though the initial host response to hypoxia may be protective, sustained hypoxia becomes detrimental to the tissues and the organism as a whole.
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Thomson, Jennifer. GM Crops and the Global Divide. CSIRO Publishing, 2021. http://dx.doi.org/10.1071/9781486312665.
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Attitudes to GM crops continue to generate tension, even though they have been grown commercially for over 20 years. Negative sentiment towards their development limits their adoption in Western countries, despite there being no evidence of harm to human health. These unfounded concerns about genetically modified crops have also inhibited uptake in many countries throughout Africa and Asia, having a major impact on agricultural productivity and preventing the widespread cultivation of potentially life-saving crops.
GM Crops and the Global Divide traces the historical importance that European attitudes to past colonial influences, aid, trade and educational involvement have had on African leaders and their people. The detrimental impact that these attitudes have on agricultural productivity and food security continues to be of growing importance, especially in light of climate change, drought and the potential rise in sea levels – the effects of which could be mitigated by the cultivation of GM and gene-edited crops.
Following on from her previous books Genes for Africa, GM Crops: The Impact and the Potential and Food for Africa, Jennifer Thomson unravels the reasons behind these negative attitudes towards GM crop production. By addressing the detrimental effects that anti-GM opinions have on nutrition security in developing countries and providing a clear account of the science to counter these attitudes, she hopes to highlight and ultimately bridge this global divide.
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Elliott, Perry, Kristina H. Haugaa, Pio Caso, and Maja Cikes. Restrictive cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0044.
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Restrictive cardiomyopathy is a heart muscle disorder characterized by increased myocardial stiffness that results in an abnormally steep rise in intraventricular pressure with small increases in volume in the presence of normal or decreased diastolic left ventricular volumes and normal ventricular wall thickness. The disease may be caused by mutations in a number of genes or myocardial infiltration. Arrhythmogenic right ventricular cardiomyopathy is an inherited cardiac muscle disease associated with sudden cardiac death, ventricular arrhythmias, and cardiac failure. It is most frequently caused by mutations in desmosomal protein genes that lead to fibrofatty replacement of cardiomyocytes, right ventricular dilatation, and aneurysm formation.
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Wu, David J., and Carolyn Schanen. Chromosome 15q11.2q13.3 Aneusomies and Autism Spectrum Disorders. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199744312.003.0017.
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Chapter 17 discusses Chromosome 15, which is a small, satellited acrocentric chromosome that shows remarkable structural complexity in the proximal long arm, and which leads to a host of rearrangements that have been implicated in human genetic disorders. Interpretation of potential genotype–phenotype relationships for the unique and overlapping deletions and duplications that have been identified must consider key structural and functional elements that impact the complement of genes that are ultimately misexpressed.
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Servais, Aude, and Bertrand Knebelmann. Cystinuria. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0024.
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Cystinuria (OMIM #220100) is an autosomal recessive disorder of a dibasic amino acid transport in the apical membrane of epithelial cells of the renal proximal tubule and small intestine. It leads to increased urinary cystine excretion and recurrent urolithiasis. The cystine transporter is an heterodimeric transporter which is composed of a heavy subunit, rBAT, linked to a light subunit, b0,+AT. Two genes, SLC3A1 (solute carrier family 3 member 1) and SLC7A9, coding for rBAT and b0,+AT, account for the genetic basis of cystinuria. Cystinuria may lead to obstruction, infections, and ultimately to renal insufficiency. The diagnosis of cystinuria mainly relies on stone analysis, urinary cystine measurement, or urinary cystine crystal identification. Medical treatment is based upon a stepwise strategy using hydration and alkalinization as basic measures, with the addition of thiol derivatives in refractory cases. Urological interventions are often indicated for the management of cystine stones >5 mm in diameter.
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Parens, Erik, and Josephine Johnston, eds. Human Flourishing in an Age of Gene Editing. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780190940362.001.0001.
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The potential use of CRISPR-Cas9 and other new gene editing technologies to alter the DNA of human beings raises a host of questions. Some questions are about safety: Can these technologies be deployed without posing an unreasonable risk of physical harm to current and future generations? Can all physical risks be adequately assessed and responsibly managed? Gene editing technologies also raise other, equally if not more difficult, questions that touch on deeply held, personal, cultural, and societal values: Might such technologies redefine what it means to be healthy, normal, or cherished? Might they undermine relationships between parents and children or exacerbate the gap between the haves and have-nots? The broadest form of this second kind of question about the impact of gene editing on values is the focus of this book: What might gene editing—and related technologies—mean for human flourishing? An interdisciplinary group of scholars asks age-old questions about the nature and well-being of humans in the context of revolutionary new biotechnology that has the potential to change the genetic makeup of both existing people and future generations. These authors aim to help readers engage in a conversation about the ethics of gene editing. It is through this conversation that citizens can influence laws and the distribution of funding for science and medicine; that professional leaders can shape understanding and use of gene editing and related technologies by scientists, patients, and practitioners; and that individuals can make decisions about their own lives and the lives of their families.
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Watson, Lucinda. How They Achieved: Stories of Personal Achievement and Business Success. Wiley, 2001.
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23
Grant, Warren, and Martin Scott-Brown. Principles of oncogenesis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0322.
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It is obvious that the process of developing cancer—oncogenesis—is a multistep process. We know that smoking, obesity, and a family history are strong independent predictors of developing malignancy; yet, in clinics, we often see that some heavy smokers live into their nineties and that some people with close relatives affected by cancer spend many years worrying about a disease that, in the end, they never contract. For many centuries scientists have struggled to understand the process that make cancer cells different from normal cells. There were those in ancient times who believed that tumours were attributable to acts of the gods. Hippocrates suggested that cancer resulted from an imbalance between the black humour that came from the spleen, and the other three humours: blood, phlegm, and bile. It is only in the last 100 years that biologists have been able to characterize some of the pathways that lead to the uncontrolled replication seen in cancer, and subsequently examine exactly how these pathways evolve. The rampant nature by which cancer invades local and distant tissues, as well its apparent ability to spread between related individuals led some, such as Peyton Rous in 1910, to suggest that cancer was an infectious condition. He was awarded a Nobel Prize in 1966 for the 50 years of work into investigating a link between sarcoma in chickens and a retrovirus that became known as Rous sarcoma virus. He had shown how retroviruses are able to integrate sequences of DNA coding for errors in cellular replication control (oncogenes) by introducing into the human cell viral RNA together with a reverse transcriptase. Viruses are now implicated in many cancers, and in countries where viruses such as HIV and EBV are endemic, the high incidence of malignancies such as Kaposi’s sarcoma and Burkitt’s lymphoma is likely to be directly related. There are several families of viruses associated with cancer, broadly classed into DNA viruses, which mutate human genes using their own DNA, and retroviruses, like Rous sarcoma virus, which insert viral RNA into the cell, where it is then transcribed into genes. This link with viruses has not only led to an understanding that cancer originates from genetic mutations, but has also become a key focus in the design of new anticancer therapies. Traditional chemotherapies either alter DNA structure (as with cisplatin) or inhibit production of its component parts (as with 5-fluorouracil.) These broad-spectrum agents have many and varied side effects, largely due to their non-specific activity on replicating DNA throughout the body, not just in tumour cells. New vaccine therapies utilizing gene-coding viruses aim to restore deficient biological pathways or inhibit mutated ones specific to tumour cells. The hope is that these gene therapies will be effective and easily tolerated by patients, but development is currently progressing with caution. In a trial in France of ten children suffering from X-linked severe combined immunodeficiency and who were injected with a vector that coded for the gene product they lacked, two of the children subsequently died from leukaemia. Further analysis confirmed that the DNA from the viral vector had become integrated into an existing, but normally inactive, proto-oncogene, LM02, triggering its conversion into an active oncogene, and the development of life-threatening malignancy. To understand how a tiny change in genetic structure could lead to such tragic consequences, we need to understand the molecular biology of the cell and, in particular, to pay attention to the pathways of growth regulation that are necessary in all mammalian cell populations. Errors in six key regulatory pathways are known as the ‘hallmarks of cancer’ and will be discussed in the rest of this chapter.
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Newman, Judith H. Conclusion. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190212216.003.0006.
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Although by no means offering a complete taxonomy of scripture formation, the book considers a wide range of literary genres and practices across the diverse population of Judeans throughout the region. The conclusion draws out some of the implications for understanding the fluid nature of scriptures in the Hellenistic-Roman era. The search for the “original text” of the Bible is a vain one; rather, scriptures were formed through a traditioning process that involved sacralization through the entwinement of prayer practices and textual interpretation. These texts were mediated by learned teachers and leaders in textual communities.
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Nielsen, David A., Dmitri Proudnikov, and Mary Jeanne Kreek. The Genetics of Impulsivity. Edited by Jon E. Grant and Marc N. Potenza. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195389715.013.0080.
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Impulsivity is a complex trait that varies across healthy individuals, although when excessive, it is generally regarded as dysfunctional. Impulsive behavior may lead to initiation of drug addiction that interferes with inhibitory controls, which may in turn result in facilitation of the individual’s impulsive acts. Although environmental factors play a considerable role in impulsive behavior, a body of evidence collected in twin studies suggests that about 45% of the variance in impulsivity is accounted for by genetic factors. Genetic variants studied in association with impulsivity include those fortryptophan hydroxylase 1 and 2 (TPH1 and TPH2), the serotonintransporter (SERT), serotonin receptors, and genes of the monoamine metabolism pathway (e.g., monoamine oxidase A, MAOA). Other systems may also play a role in these behaviors, such as the dopaminergic system (the dopamine receptors DRD2, DRD3, and DRD4, and the dopamine transporter, DAT), the catecholaminergic system (catechol-O-methyltransferase, COMT), and the GABAergic system (GABAreceptor subunit alpha-1, GABRA1; GABA receptor subunit alpha-6, GABRA6; and GABA receptor subunit beta-1, GABRB1). Taking into account involvement of the hypothalamic-pituitary-adrenal (HPA) axis, the number of candidate genes implicated in impulsivity may be increased significantly and, therefore, may go far beyond those of serotonergic and dopaminergic systems. For a number of years, our group has conducted studies of the association of genes involved in the modulation of the stress-responsive HPA axis and several neurotransmitter systems, all involved in the pathophysiology of anxiety and depressive disorders, impulse control and compulsive disorders, with drug addiction. These genes include those of the opioid system: the mu- and kappa-opioid receptors (OPRM1 and OPRK1) and the nociceptin/orphaninFQ receptor (OPRL1); the serotonergic system: TPH1 and TPH2 and the serotonin receptor 1B (5THR1B); the catecholamine system: COMT; the HPA axis: themelanocortin receptor type 2 (MC2R or adrenocorticotropic hormone, ACTHR); and the cannabinoid system: the cannabinoid receptor type 1 (CNR1). In this chapter we will focus on these findings.
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Fenno, Lief E., and Karl Deisseroth. Optogenetics and Related Technologies for Psychiatric Disease Research. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0006.
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Studying intact systems with simultaneous local precision and global scope is a fundamental challenge in biology. This familiar trade-off leads to important conceptual and experimental difficulties in psychiatric disease research and throughout the study of complex biological systems. Part of a solution may arise from optogenetics: the combination of genetic and optical methods to achieve gain- or loss-of-function of temporally defined events in specific cells embedded within intact living tissue or organisms. Such precise causal control within the functioning intact system can be achieved via introduction of genes that confer to cells both light-detection capability and specific effector function. A broad array of optogenetic tools and neuroscience applications have driven the wide adoption of optogenetics as a standard approach in neuroscience.
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Hodgkins, Christopher. Settlers in New Worlds. Edited by Andrew Hiscock and Helen Wilcox. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780199672806.013.31.
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Early modern colonial survival meant that imaginative writings about settlers in new worlds outnumbered imaginative writings by those settlers; yet new world settlers did leave literary artefacts of their interpretive communities. Writing about new worlds tended to fire the fancy, either in fantastic exploration narratives, fabulous colonial prospecti, reflective essays, or in the more outright fictions of dramatic and utopian literature, and of lyric and epic poetry. Writing in and from new worlds was often more quotidian, with nonfiction prose genres like ships’ logs, company reports, personal letters, spiritual diaries, and sermons predominating with a sprinkling of original poetry, proverb, and song. Old genres were modified, and new ones born, by necessity and invention: not only the traveller’s tale and ‘utopian’ fiction, but also the conquest story, the atrocity exposé, the settlers’ covenant, the captivity and conversion narrative, and the extended Eucharistic meditation and puritan jeremiad—and the novel.
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Miller, Michelle A. The genetics of sleep. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198778240.003.0006.
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The genetic regulation of normal sleep and sleep disorders is complex and often shows strong environmental interactions. This is a relatively new, and rapidly expanding, area of research, and the number of sleep conditions with established, underlying genetic components is growing. The genetic basis regulating the sleep–wake cycle has identified the Period genes. Their polymorphisms appear to determine the morning/night preferences of individuals. At present, the public health benefits are limited, but will increase as the identification and understanding of genetic causes for sleep conditions improve. This may lead to new diagnostic and treatment options including genetic counselling, improved therapeutic regimes, and new drug treatments.
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Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. The pancreas. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0046.
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Congenital anomalies 326Pancreatitis 328Pancreatic insufficiency 335These are rare. Most anomalies are sporadic. Only the gene coding for the homeodomain protein PDX1 is clearly demonstrated to be causal of pancreatic agenesis. Inactivation or inhibition of signalling molecule sonic hedgehog (Shh) could potentially lead to annular pancreas, pancreatic divisum, and pancreatic ectopia....
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Uller, Tobias, and Heikki Helanterä. Heredity and Evolutionary Theory. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780199377176.003.0010.
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Heredity is a central concept in biology and one of the core principles needed for adaptive evolution. For most of the past 100 years, heredity has been defined and conceptualized in terms of transmission of genes. This is heuristically useful but imposes a certain structure on evolutionary theory and leaves out aspects of heredity that may be important to understand evolution. Emerging developmental perspectives on evolution suggests that alternative ways to represent heredity may prove useful. To this end, this chapter explains how evolutionary biologists treat heredity, conceptually and mathematically. It argues that treating heredity as an outcome of developmental processes not only makes it clearer how different mechanisms of inheritance contribute to evolution but also shows that inheritance cannot be treated as a static channel of transmission of information because it evolves as part of the process of adaptation.
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James, Philip. What is the urban environment and what is biology? Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198827238.003.0001.
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The two main themes contained within the title The Biology of Urban Environments are explored. The initial focus is on urban environments. A discussion of the origins of cities and the global spread of urbanization leads on to a consideration of urban environments in the twenty-first century. In the second section, the focus switches to biology. The scope of the discipline is set out in terms of both the range of sub-disciplines and of biological scales. It is established from this discussion that in this book the topics considered span from genes to ecosystems and will be illustrated by examples of the biology of micro-organisms, plants, and animals. Importantly humans will be included within this consideration: our biology is affected by urban environments. The final part presents the structure of the book.
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Eisen, Tim. The patient with renal cell cancer. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0172.
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Renal cancer is the commonest malignancy of the kidney and worldwide, accounts for between 2% and 3% of the total cancer burden. The mainstay of curative treatment remains surgery. There have been significant advances in surgical technique, the most important ones being nephron-sparing surgery and laparoscopic nephrectomy. The medical treatment of advanced renal cell cancer has only improved markedly in the last decade with the development of antiangiogenic tyrosine-kinase inhibitors, inhibitors of mammalian target of rapamycin, and a diminished role for immunotherapy.Tyrosine-kinase inhibitor therapy results in reduction of tumour volume in around three-quarters of patients and doubles progression-free survival, but treatment is not curative. The management of side effects in patients on maintenance tyrosine-kinase inhibitors has improved in the last 3 years, although still presents difficulties which have to be actively considered.The molecular biology of renal cell carcinoma is better understood than for the majority of solid tumours. The commonest form of renal cancer, clear-cell carcinoma of the kidney, is strongly associated with mutations in the von Hippel–Lindau gene and more recently with chromatin-remodelling genes such as PBRM1. These genetic abnormalities lead to a loss of control of angiogenesis and uncontrolled proliferation of tumour cells. There is a very wide spectrum of tumour behaviour from the extremely indolent to the terribly aggressive. It is not currently known what accounts for this disparity in tumour behaviour.A number of outstanding questions are being addressed in scientific and clinical studies such as a clearer understanding of prognostic and predictive molecular biomarkers, the role of adjuvant therapy, the role of surgery in the presence of metastatic disease, how best to use our existing agents, and investigation of novel targets and therapeutic agents, especially novel immunotherapies.
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Vester, Udo, and Stefanie Weber. Branchio-oto-renal syndrome. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0358.
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Branchio-oto-renal (BOR) syndrome involves branchial arch fistulas or cysts, ear malformations with hearing loss, and anomalies of the kidney. BOR syndrome is inherited in an autosomal dominant trait and is caused in most cases by mutations in the EYA1 gene. A few families with gene mutations in SIX1 or SIX5 have also been described. The variability of clinical symptoms is wide. Renal involvement is observed in the majority of cases ranging from mild anomalies (e.g. dilation or duplication of the urinary tract) to severe hypodysplasia of the kidneys which eventually lead to renal failure. Branchio-otic syndrome (BOS) is characterized by branchial arch and ear anomalies without detectable renal pathology. BOR and BOS can be seen within the same family.
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Adkins, Daniel E., Kelli M. Rasmussen, and Anna R. Docherty. Social Epigenetics of Human Behavior. Edited by Rosemary L. Hopcroft. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780190299323.013.40.
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It is well established that extreme social adversity can lead to negative health outcomes decades after the resolution of the precipitating environmental insult. Although the underlying mechanisms through which such adversity gets “under the skin” to become biologically embedded have long been considered a black box, recent research has indicated an important mediating role for epigenetic mechanisms—molecular modifications that regulate gene activity without changing the DNA sequence. With technical and scientific developments now enabling genome-wide epigenetic studies in humans, behavioral researchers have an unprecedented opportunity to empirically map the ways in which social dynamics become epigenetically embedded, influencing downstream gene expression, health, and behavior. This chapter examines the current state of social epigenetics research and discusses the opportunities and challenges facing this emerging field.
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Harding, Sian E. The Exquisite Machine. The MIT Press, 2022. http://dx.doi.org/10.7551/mitpress/12836.001.0001.
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How science is opening up the mysteries of the heart, revealing the poetry in motion within the machine. Your heart is a miracle in motion, a marvel of construction unsurpassed by any human-made creation. It beats 100,000 times every day—if you were to live to 100, that would be more than 3 billion beats across your lifespan. Despite decades of effort in labs all over the world, we have not yet been able to replicate the heart's perfect engineering. But, as Sian Harding shows us in The Exquisite Machine, new scientific developments are opening up the mysteries of the heart. And this explosion of new science—ultrafast imaging, gene editing, stem cells, artificial intelligence, and advanced sub-light microscopy—has crucial, real-world consequences for health and well-being. Harding—a world leader in cardiac research—explores the relation between the emotions and heart function, reporting that the heart not only responds to our emotions, but it also creates them. The condition known as Broken Heart Syndrome, for example, is a real disorder that can follow bereavement or stress. The Exquisite Machine describes the evolutionary forces that have shaped the heart's response to damage, the astonishing rejuvenating power of stem cells, how we can avoid heart disease, and why it can be so hard to repair a damaged heart. It tells the stories of patients who have had the devastating experiences of a heart attack, chaotic heart rhythms, or stress-induced acute heart failure. And it describes how cutting-edge technologies are enabling experiments and clinical trials that will lead us to new solutions to the worldwide scourge of heart disease.
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Arnold, Paul. Genetics of OCD. Edited by Christopher Pittenger. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228163.003.0019.
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Obsessive-compulsive disorder (OCD) often runs in families and has been shown to have significant heritability. It is genetically complex, and two decades of genetic work have not converged on a clear understanding of genetic risk factors. However, accelerating progress in recent years has begun to generate some insights into the genetic architecture of the disorder, and greater clarity is likely to emerge in the coming decade. This chapter summarizes several lines of genetic work, including genome-wide genetic and linkage studies; candidate gene studies; and investigations of gene-environment interactions and of pharmacogenetics. One developing theme is that genetic variance in components of the brain’s glutamate signaling system may contribute to the development of OCD. Advancing understanding of the genetics of OCD may lead to new insights into pathobiology and to new tools to optimize individual treatment.
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Millie, Julian. The Unique Voice … and Its Travails. Cornell University Press, 2018. http://dx.doi.org/10.7591/cornell/9781501713118.003.0003.
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Chapter Three is the first in a bracket of two which compares orations by two skilled preachers, and which provides contextual background to the evaluations of preaching explored in later chapters. Kyai Al-Jauhari (b. 1971) is the most popular preacher amongst village audiences in West Java. His success is premised on his bold and shocking exercise of virtuoso skills in a number of performance genres. These skills are in great demand by mosque committees intent on attracting large audiences to community celebrations. At the same time, his unique voice leads to negative evaluations from outside the environment in which his preaching is valued so highly.
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Maj, Dorota. Modyfikujący wpływ roślinnych dodatków paszowych na użytkowość mięsną i ekspresję wybranych genów u królików w zależności od wieku i płci. Publishing House of the University of Agriculture in Krakow, 2017. http://dx.doi.org/10.15576/978-83-66602-29-8.
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The aim of the study was to determine the effect of feed additives (algae, soybean, and sunflower oil) used in the rabbit feed on: growth indices and slaughter traits, pH, colour, texture, chemical composition, fatty acid profile and oxidative stability (TBARS) of the meat as well as FTO and FABP4 genes expression in the meat’s intramuscular fat (m. longissimus lumborum), depending on the age and sex. The experimental material consisted of Termond White rabbits (n = 160, 80 females and 80 males). Animals were weaned on the 35th day of life, and housed in metal cages arranged in batteries (4 rabbits of the same sex in a cage). From weaning to 12 or 18 weeks of age, the rabbits were fed pellets ad libitum. Animals in the control group (C) received non-supplemented pellets throughout the experiment. In the other groups, the pellet contained 1% algae (A), 3% sunflower oil (OS), and 3% soybean oil(SO).The experimental diets were formulated to have similar protein and energy content. Diets were balanced by lowering the proportion of other feed components. The total share of all components remained at 100%. The results indicate that 3% vegetable oils (soybean or sunflower) supplementation of diets for growing rabbits leads to an increase of body weight and improvement of some of the slaughter traits, while 1% addition of algae to the feed causes deterioration of body weight and slaughter traits. The effect of oil additive depends on the animals’ age. Supplementation of the rabbits’ diet with algae (1%) or sunflower and soybean oils (3%) led to an increase in the dressing percentage of rabbits slaughtered at 18 weeks of age (approx. 3%), but had no effect on the dressing percentage of rabbits slaughtered at 12 weeks of age. Feeding pellets with either 3% vegetable oils or 1% algae additive to the rabbits did not significantly change the chemical composition of the meat. Protein content increased and intramuscular fat content decreased with age, while ash and water content were similar. The feed additives significantly differentiated meat acidity without deteriorating meat quality. Diet modification has not affected negatively meat colour. 24 h after the slaughter, the colour of rabbit meat was similar across the studied feeding groups. Correlation between diet and rabbits’ age was found. Meat texture (hardness, springiness and chewiness) of all rabbit groups slaughtered at 12 weeks of age was similar, and the shear for cewas greater in rabbits fed pellets with algae and soybean oil. At 18 weeks of age, rabbit meat from experimental groups had lower hardness and chewiness, compared to meat of the animals from the control group. Meat shear force was higher in the control group, and from algae-supplemented group. The correlation between diet and age was also found. The use of 3% vegetable oils or 1% algae as feed additives significantly reduced meat oxidative stability. Soybean or sunflower oil (3%) usedas feed additives favourably modified the fatty acid composition of intramuscular fat. Polyunsaturated fatty acids (PUFA) content was increased, including linoleic acid, and PUFA/MUFA ratio was improved. The content of these acids decreased with age. The use of algae (1%) as a feed additive resulted in positive effect on the increase of n-3 fatty acid content (EPA and DHA) in meat intramuscular fat. Algae supplementation improved pro-health properties of meat, with low n-6/n-3 acid ratio (2.5), indicating that diet modification may affect the fatty acid composition of rabbit meat. The influence of diet and age on FTO and FABP4 gene expression in meat intramuscular fat (m. longissimus lumborum) was found. FTO and FABP4 gene expression increased with age and was the highest in the group of rabbits with 1% algae supplementation in the diet. The effect of rabbits’ gender on growth, slaughter traits, meat quality and gene expression in rabbits was not observed. In conclusion, the use of natural feed additives, such as sunflower, soybean oil or algae, can improve the nutritional value of rabbit meat, without changing its chemical or physical properties, and therefore the meat can serve as functional food, with properties beneficial to human health. The results obtained in this study also indicate that the expression of FTO and FABP4 genes in rabbit muscles is regulated by dietary factors and age, which, in addition to cognitive significance, has practical implications for improving technological and dietary quality of rabbit meat.
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Bates, Catherine, and Patrick Cheney, eds. The Oxford History of Poetry in English. Oxford University Press, 2022. http://dx.doi.org/10.1093/oso/9780198830696.001.0001.
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Volume 4 of The Oxford History of Poetry in English aims to feature a history of the birth moment of modern ‘English’ poetry in greater detail than previous studies. To accomplish its aim, Sixteenth-Century British Poetry examines the literary transitions, institutional contexts, artistic practices, and literary genres within which poets compose their works. Each chapter combines an orientation to its topic and a contribution to the field. Specifically, the volume introduces a narrative about the advent of modern English poetry from Skelton to Spenser, attending to the events that underwrite the poets’ achievements: Humanism, Reformation, monarchism and republicanism, colonisation, print and manuscript, theatre, science, and companionate marriage. Featured are metre and form, figuration and allusiveness, and literary career, as well as a wide range of poets, from Wyatt, Surrey, and Isabella Whitney to Ralegh, Drayton, and Mary Herbert. Major works discussed include Sidney’s Astrophil and Stella, Spenser’s Faerie Queene, Marlowe’s Hero and Leander, and Shakespeare’s Sonnets.
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Winchester, Robert, Darren D. O’Rielly, and Proton Rahman. Genetics of psoriatic arthritis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0006.
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The psoriatic phenotype is clinically heterogeneous with psoriatic arthritis (PsA) itself being heterogeneous. Studies have consistently demonstrated that PsA has a strong genetic component and disease pathogenesis encompasses a complex interplay between genetic, immunological, and environmental factors. In this chapter, we will review the genetics of PsA including the major histocompatibility complex (MHC) region and non-MHC loci. We will detail how susceptibility genes can be grouped into barrier integrity, innate immune response, and adaptive immune response (particularly Th-17 lymphocyte signalling). We will articulate how these studies strongly support PsA as genetically different from PsV and that the genetic heterogeneity is likely attributed to different HLA susceptibility alleles within the MHC region that an individual carries. Furthermore, we will highlight new emerging technologies, in particular, next-generation sequencing, which may lead to new genetic discoveries in PsA.
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Valdes, Ana M. Genetics. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0009.
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Epidemiological studies have demonstrated that osteoarthritis (OA) is a complex trait with numerous environmental and genetic risk factors. A great deal of effort has been spent elucidating these risk factors and progress has been made. It is clear however that the causes behind OA development and progression continue to remain largely elusive. Identification of those genes that, in conjunction with environmental factors, predispose to OA severity will lead to a better understanding of the mechanisms underlying disease development and thus promote improved health strategies for prevention. An understanding of the molecular signalling pathways involved in the initiation and progression of the disease will improve clinical diagnosis and help identify improved, tailored treatment regimens. This chapter focuses on these issues, exploring the heritability of OA, known genetic risk factors, and specific traits and outcomes studied in the genetics of OA.
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Quin, Edel, Sonia Rafferty, and Charlotte Tomlinson. Safe Dance Practice. Human Kinetics, 2015. http://dx.doi.org/10.5040/9781718212886.
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Every dancer of every age, ability, and style should be able to engage fully in the act of dancing and be encouraged to achieve their potential without risk of harm to the body or mind. Practical information on all aspects of safe practice that is not too simplistic or complex has not always been easy to find. Enter Safe Dance Practice, by Edel Quin, Sonia Rafferty, and Charlotte Tomlinson. With nearly 60 years of collective experience in the dance profession as creative artists, teachers, and researchers, the authors translate extensive research and evidence-based practice in order to present the principles of safe practice that are essential to any dance experience. Guidelines in Implementing Principles The authors offer evidence-based guidelines on implementing diverse principles in practice, informing and supporting dance practitioners in an ever-growing pool of styles and genres. These guidelines and principles are of use not only to dancers and dance educators but also to choreographers, rehearsal and company directors, and studio managers. The information is underpinned by research in dance science and applied with contextual delivery in mind, ensuring an engaging experience for those accessing the book. Bridging the Gap Between Science and Practice Safe Dance Practice bridges the gap between academic research and its application for dancers and educators in all levels and genres. It illuminates the principles of working safely in dance so as to support best practice and encourages all dance practitioners and leaders to better understand, communicate, and apply principles of safe dance practice.
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Hinks, Anne, and Wendy Thomson. Genetics of juvenile rheumatic diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0043.
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Juvenile rheumatic diseases are heterogeneous, complex genetic diseases; to date only juvenile idiopathic arthritis (JIA) has been extensively studied in terms of identifying genetic risk factors. The MHC region is a well-established risk factor but in the last few years candidate gene and genome-wide association studies have been utilized in the search for non-HLA risk factors. There are now an additional 12 JIA susceptibility loci with evidence for association in more than one study. In addition, some subtype-specific associations are emerging. These risk loci now need to be investigated further using fine-mapping strategies and then appropriate functional studies to show how the variant alters the gene function. This knowledge will not only lead to a better understanding of disease pathogenesis for juvenile rheumatic diseases but may also aid in the classification of these heterogeneous diseases. It may identify new pathways for potential therapeutic targets and help in the prediction of disease outcome and response to treatment.
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Gropman, Andrea L., Belen Pappa, and Nicholas Ah Mew. The Urea Cycle Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0063.
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The urea cycle is the primary nitrogen disposal pathway in humans. The urea cycle requires the coordinated function of six enzymes and two mitochondrial transporters to catalyze the conversion of a molecule of ammonia, the α-nitrogen of aspartate and bicarbonate into urea. Whereas ammonia is toxic, urea is relatively inert, soluble in water, and readily excreted by the kidney in the urine. The accumulation of ammonia and other toxic intermediates of the cycle lead to predominantly neurological sequelae. All of the genes have been identified. The disorders may present at any age from the neonatal period to adulthood, with the more severe patients presenting earlier in life. Patients are at risk for metabolic decompensation throughout life, often triggered by illness, fasting, surgery and postoperative states, peripartum, stress, and increased exogenous protein load. This chapter addresses common somatic and neurological presentation, differential diagnosis, laboratory testing, and treatments.
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Parsonson, Ian. Australian Ark. CSIRO Publishing, 1998. http://dx.doi.org/10.1071/9780643100688.
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This definitive work on the introduction of domestic animals to Australia begins with the first white settlement at Botany Bay. It explores the foundations of our wool and beef industries, examining the role of early leaders like Phillip, King, Macarthur and Bligh.The book considers the successful introduction of the horse, Australia's first live animal export, and goes on to explore the role of the acclimatisation societies, the development of the veterinary profession and the control and eradication of some of the major exotic and introduced diseases of sheep and cattle.
The author, Dr Ian Parsonson, retired as Assistant Chief of the Australian Animal Health Laboratory at Geelong, Victoria, after a long career in veterinary practice and research. His areas of expertise include bacterial and viral diseases, pathology and microbiological laboratory safety. He is a committee member of the International Embryo Transfer Society and the Animal Gene Storage and Resource Centre of Australia.
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Costanzo, William V. When the World Laughs. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780190924997.001.0001.
Full textAbstract:
This is a book about the intersection of humor, history, and culture. It explores how film comedy, one of the world’s most popular movie genres, reflects the values and beliefs of those who enjoy its many forms, its most enduring characters and stories, its most entertaining routines and funniest jokes. What people laugh at in Europe, Africa, or the Far East reveals important truths about their differences and common bonds. By investigating their traditions of humor, by paying close attention to the kinds of comedy that cross national boundaries and what gets lost in translation, this study leads us to a deeper understanding of each other and ourselves. Section One begins with a survey of the theories and research that best explain how humor works. It clarifies the varieties of comic forms and styles, identifies the world’s most archetypal figures of fun, and traces the history of mirth from earliest times to today. It also examines the techniques and aesthetics of film comedy: how movies use the world’s rich repertoire of amusing stories, gags, and wit to make us laugh and think. Section Two offers a close look at national and regional trends. It applies the concepts set forth earlier to specific films across a broad spectrum of sub-genres, historical eras, and cultural contexts, providing an insightful comparative study of the world’s great traditions of film comedy.
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Hinks, Anne, and Wendy Thomson. Genetics of juvenile rheumatic diseases. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0043_update_002.
Full textAbstract:
Juvenile rheumatic diseases are heterogeneous, complex genetic diseases; to date only juvenile idiopathic arthritis (JIA) has been extensively studied in terms of identifying genetic risk factors. The MHC region is a well-established risk factor but in the last few years candidate gene and large-scale genome-wide association studies have been utilized in the search for non-HLA risk factors. There are now 17 JIA susceptibility loci which reach the genome-wide significance threshold for association and a further 7 regions with evidence for association in more than one study. In addition, some subtype-specific associations are emerging. These risk loci now need to be investigated further using fine-mapping strategies and then appropriate functional studies to show how the variant alters the gene function. This knowledge will not only lead to a better understanding of disease pathogenesis for juvenile rheumatic diseases but may also aid in the classification of these heterogeneous diseases. It may identify new pathways for potential therapeutic targets and help in the prediction of disease outcome and response to treatment.
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Hinks, Anne, and Wendy Thomson. Genetics of juvenile rheumatic diseases. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0043_update_003.
Full textAbstract:
Juvenile rheumatic diseases are heterogeneous, complex genetic diseases; to date only juvenile idiopathic arthritis (JIA) has been extensively studied in terms of identifying genetic risk factors. The MHC region is a well-established risk factor but in the last few years candidate gene and large-scale genome-wide association studies have been utilized in the search for non-HLA risk factors. There are now 17 JIA susceptibility loci which reach the genome-wide significance threshold for association and a further 7 regions with evidence for association in more than one study. In addition, some subtype-specific associations are emerging. These risk loci now need to be investigated further using fine-mapping strategies and then appropriate functional studies to show how the variant alters the gene function. This knowledge will not only lead to a better understanding of disease pathogenesis for juvenile rheumatic diseases but may also aid in the classification of these heterogeneous diseases. It may identify new pathways for potential therapeutic targets and help in the prediction of disease outcome and response to treatment.
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Hughes, Alis, and Lesley Jones. Pathogenic Mechanisms. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0013.
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Huntington’s disease (HD) pathogenesis is complex. In the two decades since the gene and its mutation were discovered, there has been extensive exploration of how the expanded CAG repeat in HTT leads to neurodegeneration in HD. This chapter focuses on the mechanisms that potentially contribute to the dysfunction and death of cells in HD. These include repeat instability and RNA toxicity and the production, processing, modification, and degradation of mutant huntingtin. The effects of mutant HTT on cellular processes such as transcription, transport, neurotransmission, and protein clearance are also described. The interdependence and individual importance of these mechanisms in disease etiology remains to be clarified; however, consideration of each could be important for the development of therapeutic interventions in HD.
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Kim, Kyung Hyun. Hegemonic Mimicry. Duke University Press, 2021. http://dx.doi.org/10.1215/9781478021803.
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In Hegemonic Mimicry, Kyung Hyun Kim considers the recent global success of Korean popular culture—the Korean wave of pop music, cinema, and television, which is also known as hallyu—from a transnational and transcultural perspective. Using the concept of mimicry to think through hallyu's adaptation of American sensibilities and genres, he shows how the commercialization of Korean popular culture has upended the familiar dynamic of major-to-minor cultural influence, enabling hallyu to become a dominant global cultural phenomenon. At the same time, its worldwide popularity has rendered its Koreanness opaque. Kim argues that Korean cultural subjectivity over the past two decades is one steeped in ethnic rather than national identity. Explaining how South Korea leaped over the linguistic and cultural walls surrounding a supposedly “minor” culture to achieve global ascendance, Kim positions K-pop, Korean cinema and television serials, and even electronics as transformative acts of reappropriation that have created a hegemonic global ethnic identity.