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Published: 10 December 2022
Last updated: 28 January 2023

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1

service), ScienceDirect (Online, ed. Computational methods for genetics of complex traits. London: Academic Press, 2010.

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2

1960-, Paterson Andrew H., ed. Molecular dissection of complex traits. Boca Raton, Fla: CRC Press, 1998.

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3

Genes, chromosomes, and disease: From simple traits, to complex traits, to personalized medicine. Upper Saddle River, New Jersey: FT Press Science, 2011.

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4

Fontanesi, Luca, ed. The genetics and genomics of the rabbit. Wallingford: CABI, 2021. http://dx.doi.org/10.1079/9781780643342.0000.

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Abstract The purpose of the book is to present in one location a comprehensive overview of the progress of genetics in the rabbit, with a modern vision that integrates genomics to obtain a complete picture of the state of the art and of the applications in this species, defined according to the multiple uses and multi-faceted places that this species has in applied and fundamental biology. The 18 chapters cover several fields of genetics and genomics: Chapters 1 and 2 present the rabbit within the evolutionary framework, including the systematics, its domestication and an overview of the genetic resources (breeds and lines) that have been developed after domestication. Chapters 3-5 cover the rabbit genome, cytogenetics and genetic maps and immunogenetics in this species. Chapters 6-8 present the genetics and molecular genetics of coat colours, fibre traits and other morphological traits and defects. Chapters 9-13 cover the genetics of complex traits (disease resistance, growth and meat production traits, reproduction traits), reproduction technologies and genetic improvement in the meat rabbits. Chapters 14-18 present the omics vision, the biotech and biomodelling perspectives and applications of the rabbit. This book is addressed to a broad audience, including students, teachers, researchers, veterinarians and rabbit breeders.
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5

C, Rao D., and Province Michael Arthur, eds. Genetic dissection of complex traits. San Diego: Academic Press, 2001.

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6

1947-, Fischer Ernst Peter, Hood Leroy E, and Möller Gerald, eds. Complex traits. München: Piper, 1997.

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7

Genetic Dissection of Complex Traits, Volume 60. 2nd ed. Academic Press, 2008.

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8

C, Rao D., and Gu C. Charles, eds. Genetic dissection of complex traits. 2nd ed. London: Academic Press, 2008.

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9

Rao, D. C. Genetic Dissection of Complex Traits. Elsevier Science & Technology Books, 2000.

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10

Rao, D. C., and C. Charles Gu. Genetic Dissection of Complex Traits. Elsevier Science & Technology Books, 2008.

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11

Dunlap, Jay C., and Jason H. Moore. Computational Methods for Genetics of Complex Traits. Elsevier Science & Technology Books, 2010.

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12

Paterson, Andrew H. Molecular Dissection of Complex Traits. Taylor & Francis Group, 2019.

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13

Paterson, Andrew H. Molecular Dissection of Complex Traits. Taylor & Francis Group, 2019.

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14

Paterson, Andrew H. Molecular Dissection of Complex Traits. Taylor & Francis Group, 2019.

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15

Paterson, Andrew H. Molecular Dissection of Complex Traits. Taylor & Francis Group, 2019.

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16

Rice, John. Genetic Analysis of Complex Traits: Affective Disorders. John Wiley & Sons Inc, 2000.

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17

Beier. Genetics of Complex Traits in Model Systems. John Wiley & Sons Inc, 2009.

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18

Computational Methods for Genetics of Complex Traits. Elsevier, 2010. http://dx.doi.org/10.1016/c2009-0-62092-4.

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19

Rao, D. C. Genetic Dissection of Complex Traits (Advances in Genetics, Volume 42) (Advances in Genetics). Academic Press, 2000.

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20

Rao, D. C. Genetic Dissection of Complex Traits (Advances in Genetics, Volume 42) (Advances in Genetics). Academic Press, 2000.

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21

1955-, Saxton Arnold Myron, and SAS Institute, eds. Genetic analysis of complex traits using SAS. Cary, N.C: SAS Institute, 2004.

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22

Gelernter, Joel. Complex Trait Genetics and Population Genetics in Psychiatry. Edited by Turhan Canli. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.016.

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Nearly all behavioral traits, ranging from personality traits such as neuroticism to schizophrenia and autism, are genetically influenced. With only minor exceptions, all are genetically complex—meaning that inheritance is not simply dominant or recessive or sex-linked, but follows more complex patterns indicative of more complex mechanisms. Most risk variants identified to date have only small effects on risk, and, in most cases, many risk variants at many risk loci interact with environmental factors to produce the phenotype. Such complexity has led to great challenges in increasing our knowledge of the inheritance of behavioral traits. Recent methodological advances have provided an improved set of tools that has led to advances in our understanding of the genetic influences on a range of behavioral traits. This chapter examines some of the issues involved that tend to make this a difficult problem and some of the solutions now being employed to approach those problems.
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23

Fatumo, Segun, Tinashe Chikowore, and Karoline Kuchenbaecker, eds. Genetics of Complex Traits & Diseases from Under-Represented Populations. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-464-0.

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24

Morris, Andrew, and Eleftheria Zeggini. Assessing Rare Variation in Complex Traits: Design and Analysis of Genetic Studies. Springer, 2015.

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25

Morris, Andrew, and Eleftheria Zeggini. Assessing Rare Variation in Complex Traits: Design and Analysis of Genetic Studies. Springer, 2016.

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26

Morris, Andrew, and Eleftheria Zeggini. Assessing Rare Variation in Complex Traits: Design and Analysis of Genetic Studies. Springer, 2015.

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27

Pontarotti, Pierre. Evolutionary Biology: Convergent Evolution, Evolution of Complex Traits, Concepts and Methods. Springer, 2016.

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28

Pontarotti, Pierre. Evolutionary Biology: Convergent Evolution, Evolution of Complex Traits, Concepts and Methods. Springer London, Limited, 2016.

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29

Pontarotti, Pierre. Evolutionary Biology: Convergent Evolution, Evolution of Complex Traits, Concepts and Methods. Springer, 2018.

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30

Pontarotti, Pierre. Evolutionary Biology: Self/Nonself Evolution, Species and Complex Traits Evolution, Methods and Concepts. Springer, 2017.

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31

Pontarotti, Pierre. Evolutionary Biology: Self/Nonself Evolution, Species and Complex Traits Evolution, Methods and Concepts. Springer, 2018.

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32

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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33

Walsh, Bruce, and Michael Lynch. Evolution and Selection of Quantitative Traits. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198830870.001.0001.

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Quantitative traits—be they morphological or physiological characters, aspects of behavior, or genome-level features such as the amount of RNA or protein expression for a specific gene—usually show considerable variation within and among populations. Quantitative genetics, also referred to as the genetics of complex traits, is the study of such characters and is based on mathematical models of evolution in which many genes influence the trait and in which non-genetic factors may also be important. Evolution and Selection of Quantitative Traits presents a holistic treatment of the subject, showing the interplay between theory and data with extensive discussions on statistical issues relating to the estimation of the biologically relevant parameters for these models. Quantitative genetics is viewed as the bridge between complex mathematical models of trait evolution and real-world data, and the authors have clearly framed their treatment as such. This is the second volume in a planned trilogy that summarizes the modern field of quantitative genetics, informed by empirical observations from wide-ranging fields (agriculture, evolution, ecology, and human biology) as well as population genetics, statistical theory, mathematical modeling, genetics, and genomics. Whilst volume 1 (1998) dealt with the genetics of such traits, the main focus of volume 2 is on their evolution, with a special emphasis on detecting selection (ranging from the use of genomic and historical data through to ecological field data) and examining its consequences. This extensive work of reference is suitable for graduate level students as well as professional researchers (both empiricists and theoreticians) in the fields of evolutionary biology, genetics, and genomics. It will also be of particular relevance and use to plant and animal breeders, human geneticists, and statisticians.
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34

Kan, Carol, and Ma-Li Wong. Genetics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0004.

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An association between type 2 diabetes mellitus (T2DM) and depression has been reported in epidemiological studies. Finding a genetic overlap between T2DM and depression will provide evidence to support a common biological pathway to both disorders. Genetic correlations observed from twin studies indicate that a small magnitude of the variance in liability can be attributed to genetic factors. However, no genetic overlap has been observed between T2DM and depression in genome-wide association studies using both the polygenic score and the linkage disequilibrium score regression approaches. Clarifying the shared heritability between these two complex traits is an important next step towards better therapy and treatment. Another area that needs to be explored is gene–environment interaction, since genotypes can affect an individual’s responses to the environment and environment can differentially affect genotypes expression.
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35

Genetic analysis of complex traits: Proceedings of Genetic Analysis Workshop 5, held at Chantilly, France, September 2-5, 1987. Liss, 1989.

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36

Hunt, John, James Rapkin, and Clarissa House. The genetics of reproductive behavior. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198797500.003.0002.

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Genes play a fundamental role in the regulation and evolution of most phenotypic traits, including behavior. This chapter focuses on the genetics of reproductive behavior in insects.More specifically, the distribution of genetic effects for reproductive behavior in insects (many genes of small effect or few genes of large effect) is examined, as well as how these genes interact with each other, with genes for other important traits, and with the abiotic and social environments. The chapter concludes by discussing the wider implications of this complex genetic architecture to the evolution of reproductive behaviors in insects and outline some key directions for future research on this topic.
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37

Rosell, Daniel R., and Larry J. Siever. The Neurobiology and Genetics of Schizotypal Personality Disorder. Edited by Christian Schmahl, K. Luan Phan, Robert O. Friedel, and Larry J. Siever. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199362318.003.0012.

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This chapter focuses on the neurobiology of schizotypal personality disorder (SPD) as well as schizotypy or attenuated schizophrenia-spectrum traits present among the general population, as opposed to clinical cohorts. It can be assumed that a better understanding of the neurobiology of SPD will hopefully lead to enhancements of the diagnosis and treatment of this complex, impairing, yet understudied, condition and the assessment of novel therapeutics. The chapter first characterizes the SPD construct, then turns to the genetics and development of SPD, followed by a review of studies employing nonimaging, laboratory measures. Then anatomical, functional, and neurochemical imaging findings are discussed.
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38

Hartl, Daniel L. A Primer of Population Genetics and Genomics. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780198862291.001.0001.

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A Primer of Population Genetics and Genomics, 4th edition, has been completely revised and updated to provide a concise but comprehensive introduction to the basic concepts of population genetics and genomics. Recent textbooks have tended to focus on such specialized topics as the coalescent, molecular evolution, human population genetics, or genomics. This primer bucks that trend by encouraging a broader familiarity with, and understanding of, population genetics and genomics as a whole. The overview ranges from mating systems through the causes of evolution, molecular population genetics, and the genomics of complex traits. Interwoven are discussions of ancient DNA, gene drive, landscape genetics, identifying risk factors for complex diseases, the genomics of adaptation and speciation, and other active areas of research. The principles are illuminated by numerous examples from a wide variety of animals, plants, microbes, and human populations. The approach also emphasizes learning by doing, which in this case means solving numerical or conceptual problems. The rationale behind this is that the use of concepts in problem-solving lead to deeper understanding and longer knowledge retention. This accessible, introductory textbook is aimed principally at students of various levels and abilities (from senior undergraduate to postgraduate) as well as practising scientists in the fields of population genetics, ecology, evolutionary biology, computational biology, bioinformatics, biostatistics, physics, and mathematics.
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39

Naumova, Anna K., and Celia M. T. Greenwood. Epigenetics and Complex Traits. Springer, 2013.

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40

Naumova, Anna K., and Celia M. T. Greenwood. Epigenetics and Complex Traits. Springer, 2016.

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41

Greenwood, Celia M. T., and Anna K. Naumova. Epigenetics and Complex Traits. Springer London, Limited, 2013.

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42

Sexton, Arnold M. Genetic Analysis of Complex Traits Using SAS. Books by Users Press, 2004.

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43

Spielman, Richard S. Genetic Analysis of Complex Traits: Insulin-Dependent Diabetes Mellitus. John Wiley & Sons Inc, 2000.

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44

Sohail, Mashaal, Jeremy Berg, and Diego Ortega-Del Vecchyo, eds. Genetic Architecture and Evolution of Complex Traits and Diseases in Diverse Human Populations. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-871-6.

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45

Genetic analysis of complex traits: Proceedings of Genetic Analysis Workshop 5, held at Chantilly, France, September 2-5, 1987. Liss, 1989.

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46

Zhang, Yuan-Ming, Zhenyu Jia, and Jim M. Dunwell, eds. The Applications of New Multi-Locus GWAS Methodologies in the Genetic Dissection of Complex Traits. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88945-834-9.

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47

Levinson, Douglas F., and Walter E. Nichols. Genetics of Depression. 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/9780190681425.003.0024.

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Major depressive disorder (MDD) is a common and heterogeneous complex trait. Twin heritability is 35%–40%, perhaps higher in severe/recurrent cases. Adverse life events (particularly during childhood) increase risk. Current evidence suggests some overlap in genetic factors among MDD, bipolar disorder, and schizophrenia. Large genome-wide association studies (GWAS) are now proving successful. Polygenic effects of common SNPs are substantial. Findings implicate genes with effects on synaptic development and function, including two obesity-associated genes (NEGR1 and OLFM4), but not previous “candidate genes.” It can now be expected that larger GWAS samples will produce additional associations that shed new light on MDD genetics.
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48

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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49

Srinivas, Krishna Ravi. Intellectual Property Rights and the Politics of Food. Edited by Ronald J. Herring. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780195397772.013.34.

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The legal status of plant genetic resources has been subject to numerous international agreements and laws over the centuries. The “common heritage of mankind” approach enabled free access but proved unworkable because of conflicts over intellectual property rights. The Convention on Biological Diversity (1992) recognized sovereign rights of nations over genetic resources within their territory. The Trade Related Intellectual Property Rights Agreement under auspices of the World Trade Organization mandated intellectual property protection for plant varieties, but synchronizing such rights has proved problematic. Many developing countries have enacted sui generis regimes to comply with TRIPS requirements. The International Union for the Protection of New Varieties of Plants Convention provides models that have changed over time. With the advent of agricultural biotechnology and availability of intellectual property rights for plant components, patents relating to plant genetic resources have increased. As plant genetic resources are subject to many overlapping treaties, the regime governing them is becoming more complex, resulting in inconsistencies and disputes. While the rights of plant breeders and the private seed industry are well protected in formal agreements, the rights of farmers, who have nurtured diversity in plant genetic resources, developed varieties of crops with different traits, and contributed to exchange and conservation of plant genetic resources, are left to the discretion of nation-states. Farmers’ rights are mentioned in many international legal instruments, but no binding treaty or convention mandates protecting and promoting the rights of working farmers.
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50

Troisi, Alfonso. Detachment. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199393404.003.0003.

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Most of us find social encounters rewarding, especially when we encounter those with whom we are familiar and have built up a relationship. From an evolutionary point of view, this is not surprising; human beings are fundamentally social organisms, and human development and functioning occur within a social context. The origin of individual differences in the capacity to experience social reward is likely to involve a complex interplay of genetic and environmental variables, including genetic variation, early experience and current situational factors. A few individuals seem to lie at the lower extreme of this continuum, experiencing little or no positive feelings during affiliative interactions. This chapter deals with the psychological and behavioral traits that characterize these uncommon individuals and reviews the mechanisms likely to cause their emotional detachment. The chapter then discusses the importance of aversive early experience in promoting an avoidant style of adult attachment and the role of the brain opioid system and genetic polymorphisms in mediating diminished hedonic response to affiliative interactions.
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