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Books on the topic 'Critic genetics'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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1

Bellino, Raffaello Maria. Critica della ragione predittiva: L'etica tra scienza e nescienza. Bari: Levante, 2004.

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2

Understanding genetics. 4th ed. New York: Oxford University Press, 1988.

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3

1883-1945, Mussolini Benito, ed. I discorsi del Duce: Un approccio critico-genetico. Ariccia (RM): Aracne editrice int.le S.r.l., 2015.

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4

Rothwell, Norman V. Understanding genetics: A molecular approach. New York: Wiley-Liss, 1993.

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5

Eugenics, human genetics, and human failings: The Eugenics Society, its sources and its critics in Britain. London: Routledge, 1992.

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6

Mazumdar, Pauline M. H. Eugenics, human genetics and human failings: The Eugenics Society, its source and its critics in Britain. London: Routledge, 1991.

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7

Comment c'est =: How it is ; and / et L'image : a critical-genetic edition = une édition critico-génétique. New York: Routledge, 2001.

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8

Filologia d'autore e critica genetica: Terzo quaderno del Dottorato in letterature straniere e scienze della letteratura, Università di Verona. Verona: Fiorini, 2009.

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9

Gattico, Emilio. Logica e psicologia nella cultura italiana del XIX secolo: Un tema di epistemologia genetica : analisi storico-critica della letteratura filosofica minore. Firenze: La nuova Italia, 1995.

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10

Viruses vs. superbugs: A solution to the antibiotics crisis? London: Macmillan, 2006.

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11

Fedoroff, Nina V. Shushi no kiki: GM nōsakubutsu to sekai no shokuryō anzen hoshō no kiki =: Seeds of a perfect storm: GM crops and the global food security crisis. Tōkyō: Monbu Kagakushō Kagaku Gijutsu Seisaku Kenkyūjo Kikakuka, 2009.

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12

Vincent, Jansen, ed. Population biology and criticality: From critical birth-death processes to self-organized criticality in mutation pathogen systems. London: Imperial College Press, 2011.

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13

Tani, Irene. Le Rime di Bernardo Cappello. Venice: Edizioni Ca' Foscari, 2018. http://dx.doi.org/10.30687/978-88-6969-257-4.

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Bernardo Cappello (Venezia 1498 ca.-Roma 1560), member of one of the oldest patrician families of Venice, played an active role in the politics of the Venetian Republic, until his exile in 1540. After that, he became a collaborator and a protégé of cardinal Alessandro Farnese, who is one of the most significant figures of the century. Then he took refuge in Rome, where over the years he held varied appointments. Since his youth and in parallel with his political career, Cappello constantly devoted himself to humanistic studies and to rhymes production: pupil of Pietro Bembo, interlocutor of Giovanni Della Casa and close friend to Bernardo Tasso, the author is among the greatest exponents of the sixteenth-century Petrarchism. For the first time the critical edition of Rime by Bernardo Cappello is here given, namely the book of 353 compositions that the author elaborated on the pattern of Bembo’s directives, over a large period of time. In his book of poetry (canzoniere), through lyrical pieces, the author creates his own existential and biographical path. Regarding the evolution of the architecture of Cappello’s collection, four witnesses survived, in which we distinguish different phases: the first one is genetic and manuscript (Roma, Biblioteca Casanatense, 277), with addition of corrections that generally are close to the textual variants of the princeps; the second is the print of 1560 for the press of the Guerra brothers; finally, a further evolutionary stage is represented by two postillated prints. To these witnesses a rich miscellaneous tradition is added, which, for a large number of rhymes, restores the elaborative complexity through multiple genetic forms. Poems ousted from the ancient print, but part of the canzoniere in other phases of composition, are included in this critical edition.
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14

Sumner, Jennifer A., Angela C. Bustamante, Karestan C. Koenen, and Monica Uddin. Genetics of PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0011.

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Trauma exposure and PTSD are heritable. However, the mechanisms of risk and resilience following trauma exposure are not yet well understood, suggesting that investigations into the genetic architecture of PTSD have much to contribute. This chapter reviews the rapidly growing literature on molecular genetic risk factors for PTSD, including findings from candidate gene and genome-wide association studies. Given the critical role of trauma exposure in the onset of PTSD, it also discusses gene-environment interplay, and highlights some recent findings from epigenetic studies. The chapter concludes by summarizing considerations for the field as it continues to move forward, and discusses exciting new developments in the search for genetic markers for PTSD.
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15

M, Rothkopf Michael, and Askanazi Jeffrey, eds. Intensive homecare. Baltimore: Williams & Wilkins, 1992.

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16

Yende, Sachin, and Derek C. Angus. Genetic Determinants of Sepsis Outcomes. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0027.

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Bone and joint processes take second stage to life-threatening organ failure in the setting of critical illness. However, bone and joint disorders can cause significant impairment in survivors of critical illness. Return to pre-admission function is often limited by acquired complications such as joint contractures, heterotopic ossification, and altered bone metabolism. Critical care physicians should maintain a high index of suspicion for joint contractures, as they are often asymptomatic but the source of enduring disability once the critical illness had receded. Research is needed to document the effectiveness of alternate positioning, stretching, and bracing which are the current standard practice for prevention of contractures. Heterotopic ossification should be considered in the context of a swollen, warm, painful musculoskeletal site. Early detection with triple phase bone scan and, in some cases, prophylaxis with non-steroidal anti-inflammatory medication or radiation may be warranted. Bone hyperresorption in ICU patients can be caused by immobility, heightened inflammatory status, medication, hormonal changes, and vitamin D deficiency. Laboratory biomarkers can guide treatment, which is important to prevent long-term osteoporosis and stress fractures. Systematic physical examination and early patient mobilization may represent important steps to detect and prevent joint contractures and heterotopic ossification.
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17

Wade, Tracey D., and Cynthia Bulik. Genetic Influences on Eating Disorders. Edited by W. Stewart Agras and Athena Robinson. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190620998.013.5.

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The current chapter reviews our progress in understanding how genes influence eating disorders by addressing the following areas: (1) how recognition of genetic influences on eating disorders emerged; (2) the complexities of gene environment interplay; (3) what twin studies can tell us about gene environment interplay, and (4) the current state of molecular genetic studies. It is concluded that both genes and nonshared environment play a critical role in the explanatory framework for the etiology of eating disorders. Shared environment is likely to contribute to the development of cognition and attitudes that may initiate disordered eating practices. Researchers are on the cusp of identifying specific genes that are implicated, and explication of the manner in which genes and the environment work together to increase risk for eating disorders hinges on the collection of larger samples.
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18

Genesis de Escritura y Estudios Culturales: Introduccion a la Critica Genetica (Coleccion Edicial Universidad). Edicial, 2000.

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19

Suffredini, Anthony F., and J. Perren Cobb. Genetic and molecular expression patterns in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0031.

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Investigators who study RNA, proteins, or metabolites use analytic platforms that simultaneously measure changes in the relative abundance of thousands of molecules in a single biological sample. Over the last decade, the application of these high-throughput, genome-wide platforms to study critical illness and injury has generated huge quantities of data that require specialized computational skills for analysis. These investigations hold promise for improving our understanding of the host response, thereby transforming the practice of intensive care. This chapter summarizes recent technological and computational approaches used in genomics, proteomics, and metabolomics. While major advances have been made with these approaches when applied to chronic diseases, the acute nature of critical illness and injury has unique challenges. The rapidity of initiating events, the trajectory of inflammation that follows injury or infection and the interplay of host responses to a replicating infection, all have major effects on changes in gene and molecular expression. This complexity is further accentuated by measurement that may vary with the timing and type of tissue sampled after the critical event. In addition, the hunt for novel molecular markers holds promise for identifying patients at risk for severe illness and for enabling more individualized therapy.
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20

Fly, Jones Beau, Scherpelz Martha S, and Thelen Judith N, eds. Cells and genes and me? Columbus, Ohio: Zaner-Bloser, 1992.

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21

Samuel, Beckett. Samuel Beckett Comment C'est How It Is And / et L'image: A Critical-Genetic Edition Une Edition Critic-Genetique. Routledge, 2001.

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22

Samuel, Beckett. Samuel Beckett Comment C'est How It Is And / et L'image: A Critical-Genetic Edition Une Edition Critic-Genetique. Routledge, 2016.

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23

Challenge of Plant and Agriculutral Sciences to the Crisis of Biosphere on the Earth in the 21st Century. Landes Bioscience, 2000.

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24

Van Herwegen, Jo, and Annette Karmiloff-Smith. Genetic Developmental Disorders and Numerical Competence across the Lifespan. Edited by Roi Cohen Kadosh and Ann Dowker. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199642342.013.031.

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Due to their frequent uneven cognitive profiles, genetic developmental disorders allow researchers to investigate which numerical sub-system of those present in typically developing infants best predicts subsequent numerical abilities. More importantly, they can provide evidence of which other cognitive abilities outside number are necessary for the successful development of these numerical sub-systems. We discuss evidence from cross-syndrome comparisons of adults, adolescents, children, and infants with Williams syndrome and those with Down syndrome to show that the approximate magnitude sub-system is crucial for later number development. In addition, we show that specific problems outside the number domain, and within basic-level visual and attention systems contribute to an explanation of the difficulties and proficiencies observed within each genetic disorder. Finally, we argue that a truly developmental approach is critical when using the cross-syndrome design in order to reveal subtle differences that impact over time on the development of cognitive abilities.
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25

Hallinan, Dara. Protecting Genetic Privacy in Biobanking through Data Protection Law. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780192896476.001.0001.

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Biobanks are critical infrastructure for medical research. Biobanks, however, are also the subject of considerable ethical and legal uncertainty. Given that biobanks process large quantities of genomic data, questions have emerged as to how genetic privacy should be protected. What types of genetic privacy rights and rights holders should be protected and to what extent? Since 25 May 2018, the General Data Protection Regulation (GDPR) has applied and now occupies a key position in the European legal framework for the regulation of biobanking. This book takes an in-depth look at the function, problems, and opportunities presented by European data protection law under the GDPR as a framework for the protection of genetic privacy in biobanking. It argues that the substantive framework presented by the GDPR already offers an admirable baseline level of protection for the range of genetic privacy rights engaged by biobanking. The book further contends that while numerous problems with this standard of protection are indeed identifiable, the GDPR offers the flexibility to accommodate solutions to these problems, as well as the procedural mechanisms to realise these solutions.
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26

McCuen, Marnie J. Redesigning Creation: Debating the Biotech Revolution. Gem Pubns, 2000.

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27

Buckholtz, Joshua W., and Andreas Meyer-Lindenberg. Genetic Perspectives on the Neurochemistry of Human Aggression and Violence. Edited by Turhan Canli. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.009.

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Violence is a devastating social phenomenon that is costly both to affected individuals and to society at large. Pathological aggression, especially reactive/impulsive aggression, is a cardinal symptom common to several psychiatric disorders—including antisocial personality disorder, borderline personality disorder, and psychopathy—that are associated with risk for violence. Thus, understanding the factors that predispose people to impulsive violence represents a crucial goal for psychology, neuroscience, and psychiatry. Although we are far from a full understanding of the etiopathophysiology of violence, impulsive aggression is heritable, suggesting that genetic mechanisms may be important for determining individual variation in susceptibility. This chapter synthesizes available preclinical and human data to propose a compelling neurogenetic mechanism for violence, specifically arguing that a genetically determined excess in serotonin signaling during a critical developmental period leads to dysregulation within a key corticolimbic circuit for emotional arousal and regulation, inhibitory control, and social cognition.
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28

Hausler, Thomas. Viruses vs. Superbugs: A Solution to the Antibiotics Crisis? Macmillan, 2006.

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29

Hausler, Thomas. Viruses vs. Superbugs: A Solution to the Antibiotics Crisis? Macmillan, 2007.

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30

Chung, Melissa, and Warren Lo. Pediatric Stroke. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0106.

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A variety of congenital and genetic disorders not seen frequently in adults may be responsible for stroke in infants and children. Stroke in newborn infants is as common as stroke in elderly individuals due to risk factor such as congenital heart disease, thrombophilia associated with polycythemia in neonates and genetic disorders, high estrogen impact from the mother during pregnancy, and inflammation due to infections. Stroke can also be caused by genetic disorders such as Ehleers-Danlos syndrome, Sturge-Weber syndrome, and vasculopathies such as lupus and fibromuscular dysplasia. Arterial dissection may be related to trauma and athletic injuries. Some drugs used to treat cancer such as asparaginase can also cause strokes, and infants and children can also present with venous sinus thrombosis associated with critical illness and dehydration.
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31

Geddes, John R., Nancy C. Andreasen, and Guy M. Goodwin, eds. New Oxford Textbook of Psychiatry. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198713005.001.0001.

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The third edition of the textbook presents psychiatry as a medical specialty. The application of science has transformed much of medicine by providing an understanding of the mechanisms of pathology. The genetic basis of psychiatry guarantees a future for explanation by neuroscience. The book sets the scene for such development by explaining the key issues relating to the patient’s perspective, stigma, the global challenge of mental disorder, practical ethics, and the foundations of psychiatry as phenomenology and a medical discipline. It further explains current controversies around diagnosis, psychopathology, evidence, and drug terminology. The scientific basis of psychiatric aetiology and treatment provide simple introductions to the relevant disciplines that underpin our scientific understanding. Individual disorders are covered in sections that follow the structure of the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5). Thus, it follows a clinically led summary of how patients present with psychiatric disorder. There is no denying the current utility of symptom-based diagnoses and the consensus that created the current categories. However, the project of applying neuroscience to psychiatry has not failed, as has sometimes been implied by criticism of DSM-5. For these reasons, chapters have been included on genetics, neurobiological targets, and imaging in the sections of the book focused on specific disorders. Sections have also been included on service provision and forensic psychiatry because these are critical to the context in which psychiatric disorder is managed.
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32

McDermott, Rose, and Peter K. Hatemi. DNA Is Not Destiny. Edited by Rosemary L. Hopcroft. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780190299323.013.41.

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Genetic influences are often misinterpreted to mean that an individual with a particular genotype is inevitably predisposed to engage in a given behavior or that genetic influences operate outside of human agency and social context. This chapter undertakes a qualitative investigation of a genetically informed (MAOA) sample to illustrate the critical differences between population estimates and individual accountability. The sample includes those whose lives have revolved around violence (e.g., gang members) and those whose lives are committed to peace (e.g., Buddhist monks). It is found that genotype alone cannot predict any one individual’s social behaviors, and it is argued that any decisions or legal precedents targeted toward predicting how a specific individual may act based on his or her DNA sequence require a more nuanced appreciation of how social factors, genetic dispositions, and personal experience intertwine in the context of human agency.
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33

Schmeink, Lars. Conclusion. Liverpool University Press, 2017. http://dx.doi.org/10.5949/liverpool/9781781383766.003.0008.

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Chapter 8 finally revisits the analyzed biopunk artifacts by introducing the concept of genohype as a liquid modern technique of applying a sort of individualistic genetic determinism. Biopunk, as dystopian warning about the liquid modern present, thus becomes a valid tool to renegotiate genohype and through critical posthumanist subjectivities to subvert the ideas implied in it.
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34

Messer, Neil. Contributions from Biology. Edited by Adrian Thatcher. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199664153.013.026.

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This chapter surveys biological research on selected topics in human sexuality and reproduction. It begins with a brief introduction to the approaches of evolutionary biology and behavioural genetics. Subsequent sections survey insights offered by these disciplines into the evolutionary origins of sex, sexual selection theory and human mating strategies, sexual diversity (particularly same-sex attraction and sexual behaviour), and sexual dimorphism and intersex. Critical perspectives on these topics from biologists and others are discussed, and a concluding section outlines some issues of concern to theologians engaging with this material.
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35

Stevens, Robert D. Introduction: Biological Mechanisms of Injury and Repair. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0026.

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Chapter 26 is an introduction to devoted to biological mechanisms underpinning organ dysfunction and repair in critical illness, and how research has generated fundamental insights into the biology of conditions, such as sepsis and ARDS, and has suggested important new therapeutic paradigms. It also specifically addresses issues surrounding genetic susceptibility, cognitive deficiency, frailty, myocardial ischaemia, muscle wasting, sepsis-associated encephalopathy (SAE), CIP, and structural muscle alterations.
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36

Ferrari, Lynne R. Sickle Cell Disease. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0051.

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Sickle cell anemia is a disease that combines molecular biology, clinical features, biochemistry, pathology, natural selection, population genetics, gene expression, and genomics and is the world’s most common life-threatening monogenic disorder. Clinical features include anemia; painful crisis especially in fingers, chest, and long bones; hemolysis; splenic infarction resulting in functional asplenia; and microinfarction leading to neurologic and renal impairment. The maintenance of adequate body temperature with active warming devices and warmed intravenous fluids, monitoring hydration and urine output, providing supplemental oxygen, and limiting surgical and anesthesia times to reduce pulmonary complications constitute the best management for patients with sickle cell disease.
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37

Singh, Marvin M., and Gerard E. Mullin. Diet, Environmental Chemicals, and the Gut Microbiome. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190490911.003.0006.

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This chapter reviews the latest research on gut health and addresses the nutritional and environmental effects on the gut microbiome, a key player in pathogenesis of diseases such as inflammation, intestinal permeability, obesity, metabolic syndrome, diabetes, cardiovascular disease, and neurologic conditions. The 100 trillion microorganisms that cohabit within each of us play a critical role in maintaining health and preventing disease. Many factors can alter and interact with the microbiome, including nutrition, genetics, and environmental exposures. Clinicians need to understand these relationships to help patients make the informed decisions that can impact their daily lives and the health of subsequent generations.
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38

de Melo-Martin, Inmaculada. Rethinking Reprogenetics. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190460204.001.0001.

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Reprogenetic technologies, which combine the power of reproductive techniques with the tools of genetic science and technology, promise prospective parents a remarkable degree of control to pick and choose the likely characteristics of their offspring. Prominent authors such as Agar, Buchanan, DeGrazia, Green, Harris, Robertson, Savulescu, and Silver have flocked to the banner of reprogenetics. For them, increased reproductive choice and reduced suffering through the elimination of genetic disease and disability are just the first step. They advocate use of these technologies to create beings who enjoy longer and healthier lives, possess greater intellectual capacities, and are capable of more refined emotional experiences. Indeed, Harris and Savulescu take reprogenetic technologies to be so valuable that their use is not only morally permissible but morally obligatory. Rethinking Reprogenetics challenges this mainstream view with a contextualized, gender-attentive philosophical perspective. It shows that one need not be a Luddite, a social conservative, or a religious zealot to be critical of reprogenetics. Pointing out the flawed nature of the arguments put forward by the technologies’ proponents, Rethinking Reprogenetics reveals the problematic nature of the assumptions underpinning current evaluations of these technologies and offers a framework for a more critical and skeptical assessment.
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39

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.

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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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40

Japan) Toyota Conference 1998 Shizuoka-Shi, Kazuo N. Watanabe, and Atsushi Komamine. Proceedings of the 12th Toyota Conference: Challenge of Plant and Agricultural Sciences to the Crisis of Biosphere on the Earth in the 21st Century (Environmental Intelligence Unit). R. G. Landes, 1999.

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41

Hopkins, Ramona O., Maria E. Carlo, and James C. Jackson. Critical Illness and Long-Term Cognitive Impairment. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199398690.003.0003.

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Evidence from dozens of studies of thousands of individuals suggest that as many as half of critical illness survivors experience significant deficits in memory, executive functioning, attention, and processing speed that persist years after discharge from the intensive care unit (ICU). This chapter reviews the prevalence, characteristics, possible mechanisms, and risk factors for long-term cognitive impairment after critical illness. Some key risks factors—notably, delirium—may be modifiable, whereas others, such as genetic markers, are not. Cognitive impairments are associated with psychiatric disorders, including depression, anxiety, and posttraumatic stress disorder. The impact of critical illness–related cognitive impairment on individuals and society includes financial costs, inability to return to work, impairments in instrumental activities of daily living (financial management, medication management, shopping, home care), reduced quality of life, and caregiver burden. Efforts need to be directed not only at modifying risk factors but also at attempting to prevent, treat, and remediate deficits.
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42

Cortina, Lilia, and Anna Kirkland. Looking Forward. Edited by Adrienne J. Colella and Eden B. King. Oxford University Press, 2016. http://dx.doi.org/10.1093/oxfordhb/9780199363643.013.34.

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Many questions remain unanswered within research on employment discrimination. This chapter focuses on three broad topics that seem especially important for future inquiry: (1) theories of intersectionality and double jeopardy that can complicate our understanding of employment discrimination but also bring greater ecological validity to this field of study; (2) contested categories and identities appearing in recently enacted laws, particularly around health, genetics, family responsibility, and lifestyle discrimination; and (3) expanded understanding of the “life cycle” of employment disputes beyond that addressed by the law, including attention to life before, during, and after perceived discrimination. More broadly, this chapter also highlights (4) newer, interdisciplinary fields that offer boundary-spanning vantage points, promising to move discrimination research in new directions; such fields include feminist studies, sociolegal studies, disability studies, queer studies, and critical race studies.
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43

Scodari, Christine. Alternate Roots. University Press of Mississippi, 2018. http://dx.doi.org/10.14325/mississippi/9781496817785.001.0001.

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For over two decades, the media have chronicled escalating participation in family history prompted by, among other things, the aging of Baby Boomers and Generation Xers, the growing availability of digital genealogy sites and archives, and a burgeoning interest in racial and ethnic history and culture of the sort inspired by the airing of the historical drama miniseries Roots forty years ago. Alternate Roots is the first book to critically address a wide array of media-related institutions, texts, technologies, and practices of family history readily encountered in the new millennium, including genealogy-themed television series, books, documentaries, websites, family photos and civil records, social media interactions, genealogical institutions, “roots” tourism, and genetic ancestry testing services capitalizing on the 2003 mapping of the human genome. These objects of inquiry present unique and pressing issues for critical investigation in terms of economic and privacy concerns as well as ethnicity, race, and hybrid identities. Judiciously interweaving her own genealogical journey involving ethnic, racial, classed, and gendered identities pertinent to her southern Italian and Italian American family history throughout the multifaceted examination of critical objects, Christine Scodari unearths pivot points of thought and action in the performance and representation of family history that can be adapted by others and facilitated by digital media. This alternate roots strategy, an expansive approach to family history, enables practitioners to venture beyond genetic definitions of kinship, their own ancestral history, and the struggles of those sharing their affiliations, and to interrogate genealogical media and related commodities and activities accordingly.
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44

Armstrong, Neil, and Willem van Mechelen, eds. Oxford Textbook of Children's Sport and Exercise Medicine. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.001.0001.

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Comprehensive and up to date, this textbook on children’s sport and exercise medicine features research and practical experience of internationally recognized scientists and clinicians that informs and challenges readers. Four sections—Exercise Science, Exercise Medicine, Sport Science, and Sport Medicine—provide a critical, balanced, and thorough examination of each subject, and each chapter provides cross-references, bulleted summaries, and extensive reference lists. Exercise Science covers growth, biological maturation and development, and examines physiological responses to exercise in relation to chronological age, biological maturation, and sex. It analyses kinetic responses at exercise onset, scrutinizes responses to exercise during thermal stress, and evaluates how the sensations arising from exercise are detected and interpreted during youth. Exercise Medicine explores physical activity and fitness and critically reviews their role in young people’s health. It discusses assessment, promotion, and genetics of physical activity, and physical activity in relation to cardiovascular health, bone health, health behaviours, diabetes, asthma, congenital conditions, and physical/mental disability. Sport Science analyses youth sport, identifies challenges facing the young athlete, and discusses the physiological monitoring of the elite young athlete. It explores molecular exercise physiology and the potential role of genetics. It examines the evidence underpinning aerobic, high-intensity, resistance, speed, and agility training programmes, as well as effects of intensive or over-training during growth and maturation. Sport Medicine reviews the epidemiology, prevention, diagnosis, and management of injuries in physical education, contact sports, and non-contact sports. It also covers disordered eating, eating disorders, dietary supplementation, performance-enhancing drugs, and the protection of young athletes.
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45

Breban, Maxime, and Hill Gaston. Immune mechanisms: adaptive immunity. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0008.

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The role of adaptive immunity (i.e. the involvement of B and T lymphocytes) in the pathogenesis of axial spondyloarthritis has been investigated in both human disease and relevant animal models. Studies of B cell responses have not generally implicated an autoantibody in the disease, but there are abnormalities of antibody responses, particularly increased titres of antibodies to various gut bacteria. T cells are critical to the disease in animal models other than those where overexpression of a cytokine is engineered, suggesting that they are the drivers of the inflammatory response. There is convergent evidence from animal models, genetics in humans, and direct observation of human peripheral blood and joints to implicate T cells producing IL-17 under the influence of IL-23. These in turn may be responding to bacteria either in the gut or on the skin.
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46

Christopher, Evans J., Brigitte L. Kieffer, David Jentsch, and Rafael J. Maldonado. Animal Models of Addiction. 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/9780190681425.003.0043.

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Drug addiction, now officially diagnosed as substance use disorder (SUD), is a chronic brain syndrome characterized by the compulsive use of drugs, loss of control over drug taking in spite of its adverse consequences, and relapse even after long periods of drug abstinence. Animal models have played a critical role in our understanding of the molecules, circuits, and behaviors associated with substance use disorders. This chapter reviews animal models that have been widely used to assess all stages of the addiction cycle: from drug initiation, through drug seeking, to withdrawal and relapse. We discuss the power of genetics, especially in generating rodent models for the discovery of essential proteins and pathways regulating behaviors exhibited during the different stages of the addiction cycle. Preclinical research in animal models will undoubtedly continue to reveal therapeutic strategies for substance use disorders.
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47

Weiss, Elizabeth, and James W. Springer. Repatriation and Erasing the Past. University Press of Florida, 2020. http://dx.doi.org/10.5744/florida/9781683401575.001.0001.

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Engaging a longstanding controversy important to archaeologists and indigenous communities, Repatriation and Erasing the Past takes a critical look at laws that mandate the return of human remains from museums and laboratories to ancestral burial grounds. Anthropologist Elizabeth Weiss and attorney James Springer offer scientific and legal perspectives on the way repatriation laws impact research. Weiss discusses how anthropologists draw conclusions about past peoples through their study of skeletons and mummies and argues that continued curation of human remains is important. Springer reviews American Indian law and how it helped to shape laws such as NAGPRA (the Native American Graves Protection and Repatriation Act). He provides detailed analyses of cases including the Kennewick Man and the Havasupai genetics lawsuits. Together, Weiss and Springer critique repatriation laws and support the view that anthropologists should prioritize scientific research over other perspectives.
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Trocello, Jean-Marc, and France Woimant. Disorders of Copper and Iron Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0044.

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Both copper and iron are essential metals that have a critical function in a series of biochemical pathways. This chapter describes the disorders associated with genetic abnormalities in copper and iron metabolic pathways and their manifestations in adult patients. Mutations in the genes of the copper transporting P-type ATPases, ATP7A and ATP7B are associated with Wilson disease, Menkes disease, occipital horn syndrome and ATP7A-related distal motor neuropathy. Neurodegeneration with brain iron accumulation (NBIA) is a group of disorders characterized by excess iron deposition in globus pallidus, substantia nigra pars reticulata, striata and cerebellar dentate nuclei. Several genes associated with NBIA have been identified.
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Fox, Susan H. Seizures and Shakes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0017.

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Wilson’s disease is an autosomal recessive, treatable heredodegenerative disorder characterized by excessive deposition of copper in the liver, brain, and other tissues including the kidneys, pancreas, and joints. Early recognition of the disorder, which can present with a variety of movement disorders and neuropsychiatric phenomena, is critical to avoid irreversible end organ damage through the initiation of copper chelating agents. Diagnosis relies first on demonstrating evidence of brain iron deposition on magnetic resonance imaging of brain and elevated urinary copper excretion in the appropriate clinical context. Genetic testing for mutations in the ATP7B gene will identify a mutation in up to 90% of cases.
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West-Eberhard, Mary Jane. Developmental Plasticity and Evolution. Oxford University Press, 2003. http://dx.doi.org/10.1093/oso/9780195122343.001.0001.

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The first comprehensive synthesis on development and evolution: it applies to all aspects of development, at all levels of organization and in all organisms, taking advantage of modern findings on behavior, genetics, endocrinology, molecular biology, evolutionary theory and phylogenetics to show the connections between developmental mechanisms and evolutionary change. This book solves key problems that have impeded a definitive synthesis in the past. It uses new concepts and specific examples to show how to relate environmentally sensitive development to the genetic theory of adaptive evolution and to explain major patterns of change. In this book development includes not only embryology and the ontogeny of morphology, sometimes portrayed inadequately as governed by "regulatory genes," but also behavioral development and physiological adaptation, where plasticity is mediated by genetically complex mechanisms like hormones and learning. The book shows how the universal qualities of phenotypes--modular organization and plasticity--facilitate both integration and change. Here you will learn why it is wrong to describe organisms as genetically programmed; why environmental induction is likely to be more important in evolution than random mutation; and why it is crucial to consider both selection and developmental mechanism in explanations of adaptive evolution. This book satisfies the need for a truly general book on development, plasticity and evolution that applies to living organisms in all of their life stages and environments. Using an immense compendium of examples on many kinds of organisms, from viruses and bacteria to higher plants and animals, it shows how the phenotype is reorganized during evolution to produce novelties, and how alternative phenotypes occupy a pivotal role as a phase of evolution that fosters diversification and speeds change. The arguments of this book call for a new view of the major themes of evolutionary biology, as shown in chapters on gradualism, homology, environmental induction, speciation, radiation, macroevolution, punctuation, and the maintenance of sex. No other treatment of development and evolution since Darwin's offers such a comprehensive and critical discussion of the relevant issues. Developmental Plasticity and Evolution is designed for biologists interested in the development and evolution of behavior, life-history patterns, ecology, physiology, morphology and speciation. It will also appeal to evolutionary paleontologists, anthropologists, psychologists, and teachers of general biology.
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