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Books on the topic 'Epigentic control'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Grafi, Gideon, and Nir Ohad, eds. Epigenetic Memory and Control in Plants. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-35227-0.

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2

Mukesh, Verma, Dunn Barbara K, Umar Asad, and National Cancer Institute (U.S.). Division of Cancer Prevention., eds. Epigenetics in cancer prevention: Early detection and risk assessment. New York: New York Academy of Sciences, 2003.

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3

Epigenetic Memory And Control In Plants. Springer-Verlag Berlin and Heidelberg GmbH &, 2013.

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4

Grafi, Gideon, and Nir Ohad. Epigenetic Memory and Control in Plants. Springer, 2013.

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5

Grafi, Gideon, and Nir Ohad. Epigenetic Memory and Control in Plants. Springer, 2015.

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6

Wolffe, Alan P., and Fyodor Urnov. Epigenetics: Principles of Eukaryotic Genome Control. Wiley-Liss, 2008.

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7

Qiu, Xuan. Epigenetic Control of Tumor Suppressor Genes in Lung Cancer. INTECH Open Access Publisher, 2012.

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8

Cabej, Nelson R. Neural Control of Development: The Epigenetic Theory of Heredity. Albanet, 2005.

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9

Cabej, Nelson R. Neural Control of Development: The Epigenetic Theory of Heredity. 2nd ed. Albanet, 2005.

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10

Yang, Jin, Pei Han, Wei Li, and Ching-Pin Chang. Epigenetics and post-transcriptional regulation of cardiovascular development. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0032.

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Cardiac organogenesis requires the control of gene expression at distinct developmental windows in order to organize morphogenetic steps in the correct sequence for heart development. This is facilitated by concerted regulation at three levels: chromatin, transcription, and post-transcriptional modifications. Epigenetic regulation at the chromatin level changes the chromatin scaffold of DNA to regulate accessibility of the DNA sequence to transcription factors for genetic activation or repression. At the genome, long non-coding RNAs work with epigenetic factors to alter the chromatin scaffold or form DNA-RNA complexes at specific genomic loci to control the transcription of genetic information. After RNA transcription, the expression of genetic information can be further modified by microRNAs. Each layer of gene regulation requires the participation of many factors, with their combinatorial interactions providing variations of genetic expression at distinct pathophysiological phases of the heart. The major functions of chromatin remodellers and non-coding RNAs are discussed.

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11

Liu, Liang. Epigenetic Control of Mammalian Development: Studies on an Imprinting Control Region (Comprehensive Summaries of Uppsala Dissertations from the Faculty Science and Technology, 722). Uppsala Universitet, 2002.

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12

Aparicio, Oscar Martin. Telomeric position effect in S. cerevisiae: A model for the establishment of alternative transcriptional states under epigenetic control. 1993.

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13

Maruniak, Joel A. Environmental Chemicals and their Effects on Human Physiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190490911.003.0003.

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Environmental chemicals interact with the normal processes occurring in human bodies in many detrimental ways. Chapter 3 discusses the basic mechanisms by which exposures to environmental chemicals perturb normal homeostasis; interfere with the communication systems that coordinate proper functioning of cells, tissues, and organs; and modify gene expression by inducing epigenetic changes. Environmental chemicals disrupt homeostasis in adults, but fetuses, infants, children, and adolescents, whose homeostatic control systems are continuing to develop, are at the greatest risk for long-term adverse health outcomes due to even brief exposures during vulnerable periods in development.

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14

Bateson, Patrick. Evolutionary Theory Evolving. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780199377176.003.0004.

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The formation of new species was thought to result from a slow process of Darwinian evolution, but evidence indicates it can occur suddenly. The organism was thought to be passive, playing no role in evolution, but it can affect the evolution of its descendants because of its mobility, choices, control of the environment, and adaptability. Developmental processes were thought to be irrelevant to an understanding of evolution, but the enormous growth of epigenetics suggests that these processes can play an important role in evolutionary change. Acquired information can be passed to progeny without changing DNA sequences, and information can be inherited for a period in the absence of the initial environmental trigger. All this evidence suggests that evolutionary theory is evolving.

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15

Prescott, Tony J., and Leah Krubitzer. Evo-devo. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780199674923.003.0008.

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This chapter explores how principles underlying natural evo-devo (evolution and development) continue to inspire the design of artificial systems from models of cell growth through to simulated three-dimensional evolved creatures. Research on biological evolvability shows that phenotypic outcomes depend on multiple interactions across different organizational levels—the adult organism is the outcome of a series of genetic cascades modulated in time and space by the wider embryological, bodily, and environmental context. This chapter reviews evo-devo principles discovered in biology and explores their potential for improving the evolvability of artificial systems. Biological topics covered include adaptive, selective, and generative mechanisms, and the role of epigenetic processes in creating phenotypic diversity. Modeling approaches include L-systems, Boolean networks, reaction-diffusion processes, genetic algorithms, and artificial embryogeny. A particular focus is on the evolution and development of the mammalian brain and the possibility of designing, using synthetic evo-devo approaches, brain-like control architectures for biomimetic robots.

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16

Anderson, Michael, and Corinne Roughley. Social and Economic Differences in Mortality. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198805830.003.0019.

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Nineteenth-century male death rates were more influenced by occupation than by social class. This was because major variations in exposure, depending on where someone lived and the hazards which he faced at work, were more important than income or status. Over time the risk rankings of many occupations changed markedly. By the mid-twentieth century class gradients in mortality were clear, especially at the top and bottom of the hierarchy. However, it remains the case that even after controlling for social class, significant differences in mortality remain. Research since the 1980s has shown that including controls for area deprivation still does not wholly account for what is observed. In particular, a ‘Glasgow effect’ of enhanced mortality remains unexplained. A range of possible reasons have been offered for Glasgow’s enhanced mortality, including recent research on epigenetic effects.

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17

Umar, Asad, M.D.) Epigenetics in Cancer Prevention: Early Detection and Risk Assessment Workshop (2001 : Bethesda, and Barbara K. Dunn. Epigenetics in Cancer Prevention: Early Detection and Risk Assessment (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2003.

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18

Dean, Michael, and Karobi Moitra. Biology of Neoplasia. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0002.

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The term “cancer” encompasses a large heterogeneous group of diseases that involve uncontrolled cell growth, division, and survival, culminating in local invasion and/or distant metastases. Cancer is fundamentally a genetic disease at the cellular level. Tumors occur because clones of abnormal cells acquire multiple lesions in DNA, nearly always involving mutations, chromosomal rearrangements, and extensive alteration of the epigenome. Up to 10% of cancers also involve inherited germline mutations that are moderately to highly penetrant. Cancers begin as localized growths or premalignant lesions that may regress or disappear spontaneously, or progress to a malignant primary tumor. The somatic changes that drive abnormal growth involve activating mutations of specific oncogenes, inactivation of tumor suppressor genes, and/or disruption of epigenetic controls. The latter can result from methylation or the modification of histones and other proteins that affect the remodeling of chromosomes. Numerous non-inherited factors can cause cancer by accelerating these events.

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19

Umar, Asad, M.D.) Epigenetics in Cancer Prevention: Early Detection and Risk Assessment Workshop (2001 : Bethesda, Barbara K. Dunn, and Mukesh Verma. Epigenetics in Cancer Prevention: Early Detection and Risk Assessment (Annals of the New York Academy of Sciences, V. 983). New York Academy of Sciences, 2003.

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20

Thun, Michael J., Martha S. Linet, James R. Cerhan, Christopher A. Haiman, and David Schottenfeld. Introduction. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0001.

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This Introduction provides a broad overview of the scientific advances and crosscutting developments that increasingly influence epidemiologic research on the causes and prevention of cancer. High-throughput technologies have identified the molecular “driver” events in tumor tissue that underlie the multistage development of many types of cancer. These somatic (largely acquired) alterations disrupt normal genetic and epigenetic control over cell maintenance, division and survival. Tumor classification is also changing to reflect the genetic and molecular alterations in tumor tissue, as well as the anatomic, morphologic, and histologic phenotype of the cancer. Genome-wide association studies (GWAS) have identified more than 700 germline (inherited) genetic loci associated with susceptibility to various forms of cancer, although the risk estimates for almost all of these are small to modest and their exact location and function remain to identified. Advances in genomic and other “OMIC” technologies are identifying biomarkers that reflect internal exposures, biological processes and intermediate outcomes in large population studies. While research in many of these areas is still in its infancy, mechanistic and molecular assays are increasingly incorporated into etiologic studies and inferences about causation. Other sections of the book discuss the global public health impact of cancer, the growing list of exposures known to affect cancer risk, the epidemiology of over 30 types of cancer by tissue of origin, and preventive interventions that have dramatically reduced the incidence rates of several major cancers.

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21

Miu, Andrei C., Judith R. Homberg, and Klaus-Peter Lesch, eds. Genes, brain, and emotions. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198793014.001.0001.

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With the advent of methods from behavioral genetics, molecular biology, and cognitive neuroscience, affective science has recently started to approach genetic influences on emotion, and the underlying intermediate neural mechanisms through which genes and experience shape emotion. The aim of this volume is to offer a comprehensive account of current research in the genetics of emotion, written by leading researchers, with extensive sections focused on methods, intermediate phenotypes, and clinical and translational work. Major methodological approaches are reviewed in the first section, including the two traditional “workhorses” in the field, twin studies and gene–environment interaction studies, and the more recently developed epigenetic modification assays, genome-wide association studies, and optogenetic methods. Parts 2 and 3 focus on a variety of psychological (e.g. fear conditioning, emotional action control, emotion regulation, emotional memory, decision-making) and biological (e.g. neural activity assessed using functional neuroimaging, electroencephalography, and psychophysiological methods; telomere length) mechanisms, respectively, that may be viewed as intermediate phenotypes in the pathways between genes and emotional experience. Part 4 concentrates on the genetics of emotional dysregulation in neuropsychiatric disorders (e.g. post-traumatic stress disorder, eating disorders, obsessive–compulsive disorder, Tourette’s syndrome), including factors contributing to the risk and persistence of these disorders (e.g. child maltreatment, personality, emotional resilience, impulsivity). In addition, two chapters in Part 4 review genetic influences on the response to psychotherapy (i.e. therapygenetics) and pharmacological interventions (i.e. pharmacogenetics) in anxiety and affective disorders.

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22

Peixe, Tiago Severo, Luciane Maria Ribeiro Neto, Sergio Graff, and Carlos Eduardo Matos dos Santos. Toxicologia: Tópicos aplicados. Brazil Publishing, 2020. http://dx.doi.org/10.31012/978-65-5861-195-0.

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O livro Toxicologia: Tópicos Aplicados é dedicado a múltiplos segmentos além do universo acadêmico, pois coloca o tema toxicologia em diferentes cenários práticos, no contexto dos profissionais que precisam do uso dessa ciência para executar suas atividades e principalmente para dar suporte e embasamento aos relatórios e laudos que envolvem medicamentos, drogas e produtos químicos presentes no dia a dia e seus riscos e perigos para a saúde humana e ambiental. Escrito por toxicologistas formados em diferentes áreas da toxicologia, desde professores acadêmicos, médicos, peritos, biológicos, biomédicos, farmacêuticos e químicos, o livro cobre aspectos básicos em seus primeiros capítulos, estendendo-se a questões importantes em áreas como reprodução, embriologia e teratogenese, desreguladores endócrinos, epigenética e imunologia. Além disso, os autores também abordam temas relevantes na área ambiental e de avaliação de risco, considerando também a toxicologia de alimentos e perspectivas no âmbito forense, em toxicologia analítica e no registro e regulação legislatória de produtos químicos e farmacêuticos de acordo com as agências de controle brasileiras. Com linguagem de fácil compreensão e aplicada, é de leitura indicada a qualquer profissional que precisa do uso de toxicologia em suas funções e também para estudantes de graduação que estão à procura de conceitos e exemplos de como a toxicologia é utilizada e considerada para a liberação de medicamentos e produtos químicos, em doping e drogas de abuso, em alimentos e também no ambiente.

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