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1

Nawrot, Tim. Genetic Variation & Environmental Factors in Biological & Arterial Ageing. Leuven Univ Pr, 2005.

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2

Sharpe, Cameron Saunders. Genetic and environmental variation in stress physiology among steelhead trout (Oncorhynchus mykiss). 1992.

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3

Balduman, Lisa M. Variation in adaptive traits of coastal Douglas-fir: Genetic and environmental components. 1995.

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4

Bhopal, Raj S. Variation in disease by time, place, and person: Background and a framework for analysis of genetic and environmental effects. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198739685.003.0003.

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Diseases wax and wane in their population frequency. The underlying reasons are often difficult to detect and may remain a mystery. The principles behind the investigation of clusters, outbreaks, epidemics, and inequalities in both of communicable and non-communicable diseases, are similar. On those occasions when the mystery is solved we tend to gain huge insights, both scientific and practical to help in disease control. Disease variations are often, however, artefactual, and arise from data errors. A systematic approach to the analysis of variation in disease begins by differentiating artef
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5

Human Genetic Variation in Response to Medical and Environmental Agents : Pharmacogenetics and Ecogenetics: International Titisee Conference, ... of Germany, October 13th - 15th, 1977. Springer, 2012.

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6

Samuels, Jack, Marco A. Grados, Elizabeth Planalp, and O. Joseph Bienvenu. Genetic Understanding of OCD and Spectrum Disorders. Edited by Gail Steketee. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195376210.013.0025.

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This chapter reviews the evidence for the genetic etiology of OCD and spectrum conditions. A genetic basis is supported by the familial aggregation of OCD; evidence for involvement of genes of major effect in segregation analyses; and higher concordance for OCD in identical than non-identical twins. Recent studies also support linkage of OCD to specific chromosomal regions and association of OCD with specific genetic polymorphisms. However, specific genes causing OCD have not yet been firmly established. The search for genes is complicated by the clinical and etiologic heterogeneity of OCD, as
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7

New research at the National Institute of Environmental Health Sciences, part of the National Institutes of Health, found that a common genetic variation makes some people more susceptible to coronary heart disease (CHD). National Institutes of Health, 2006.

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8

Trucco, Elisa M., Gabriel L. Schlomer, and Brian M. Hicks. A Developmental Perspective on the Genetic Basis of Alcohol Use Disorder. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676001.003.0004.

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Approximately 48–66% of the variation in alcohol use disorders is heritable. This chapter provides an overview of the genetic influences that contribute to alcohol use disorder within a developmental perspective. Namely, risk for problematic alcohol use is framed as a function of age-related changes in the relative contribution of genetic and environmental factors and an end state of developmental processes. This chapter discusses the role of development in the association between genes and the environment on risk for alcohol use disorder. Designs used to identify genetic factors relevant to p
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9

Walsh, Bruce, and Michael Lynch. Short-term Changes in the Variance: 2. Changes in the Environmental Variance. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198830870.003.0017.

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While classical quantitative genetics usually assumes that all genotypes have the same environmental variance (the assumption of homoscedasticity), in reality, genotypes can show heteroscedasticity in the environmental variance. When such variation is heritable (i.e., has an additive variance in an outbred population), then the environmental variance can change under selection. This can either be due to an indirect response (such as during directional selection on a trait), or through direct selection to increase the homogeneity of a trait (such as for increased uniformity during harvesting).
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10

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 s
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11

James, Philip. Spatial patterns. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198827238.003.0008.

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In this chapter, the discussion focuses on the spatial variation of species within urban environment. Studies on urban–rural gradients are discussed. These are studies along gradients of disturbance and environmental stress. The extreme heterogeneity of urban environments, where contrasting urban forms are juxtaposed, is recognized as an issue in drawing generalities. Despite this, some limited generalities in the patterns of species richness and density can be detected. The intermediate disturbance hypothesis is discussed and its limitations identified. Examples are presented from a number of
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12

Tackett, Jennifer L., Avantè J. Smack, and Kathleen W. Reardon. Examining Relational Aggression in an Individual Differences Context. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190491826.003.0010.

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Individual differences, such as normal-range personality, personality pathology, and genetics (specifically behavioral genetics), are variables or constructs that can be used to distinguish people. Individual differences have also been used to understand differences in antisocial behavior, including relational aggression, and can help inform the scientific conceptualization of this behavior. This chapter summarizes evidence for individual differences in relational aggression in three dimensions: normal-range personality, personality pathology, and behavioral genetics. Relationally aggressive b
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13

Tangen, Catherine M., Marian L. Neuhouser, and Janet L. Stanford. Prostate Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0053.

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Prostate cancer is the most common solid tumor and the second leading cause of cancer-related mortality in American men. Worldwide, prostate cancer ranks second and fifth as a cause of cancer and cancer deaths, respectively. Despite the international burden of disease due to prostate cancer, its etiology is unclear in most cases. Established risk factors include age, race/ancestry, and family history of the disease. Prostate cancer has a strong heritable component, and genome-wide association studies have identified over 110 common risk-associated genetic variants. Family-based sequencing stud
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14

Barr, Christina S. Gene-by-Environment Interactions in Primates. Edited by Turhan Canli. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.006.

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Because of their complex social structures, behaviors, and genetic similarities to humans, nonhuman primates are useful for studying how genetic factors influence alcohol consumption. The neurobiological systems that influence addiction vulnerability may do so by acting on alcohol response, reward pathways, behavioral dyscontrol, and vulnerability to stress and anxiety. Rhesus macaques show individual differences in alcohol response and temperament, and such differences are influenced by genetic variants that are similar functionally to those present in humans. Genes in which variation moderat
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15

DeRubeis, Robert J., and Daniel R. Strunk, eds. The Oxford Handbook of Mood Disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780199973965.001.0001.

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Mood disorders are a pressing societal problem, with depression alone now constituting a leading cause of disability in Western Europe and the United States. In the most comprehensive volume of its kind, the Oxford Handbook of Mood Disorders provides detailed coverage of the characterization, understanding, and treatment of mood disorders. Chapters are written by the world’s leading experts in their respective areas. The Handbook provides coverage of unipolar depression, bipolar disorder, and variants of these disorders. Current approaches to classifying the mood disorders are reviewed, and co
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16

Divan, Aysha, and Janice A. Royds. 7. Molecular biology in the clinic. Oxford University Press, 2016. http://dx.doi.org/10.1093/actrade/9780198723882.003.0007.

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Environmental agents can cause genetic and epigenetic changes to DNA, the consequences of which lead to deregulation of cellular processes and pathways that cause disease. Genetic variation can either be inherited if acquired through the germline or non-heritable when the DNA changes occur in somatic (body) cells. ‘Molecular biology in the clinic’ discusses two key contemporary areas of clinical research that have benefited from an improved knowledge of their molecular basis: ageing and cancer. It shows that we are now better able to predict disease risk and design drugs that have higher clini
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17

Barton, Anne. Basics of genetics. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0037.

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Genetic factors are important in predisposing to nearly all of the conditions managed by rheumatologists; indeed, musculoskeletal diseases, like other complex diseases, are thought to be caused by environmental triggers in genetically susceptible individuals. Studying genetic susceptibility factors is more straightforward than environmental factors because, first, genetic changes are stable and do not vary throughout life; second, genetic changes exist before disease onset and so could be causative rather than occurring as a result of disease; and, third, genetic variation is easy to measure r
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18

Schutte, Nienke M., Meike Bartels, and Eco JC de Geus. Genetics of physical activity and physical fitness. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0020.

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Regular physical activity and fitness are key contributors to children’s health. It is important to understand sources of variation in phenotypes seen among children and adolescents. It is important to calculate the relative importance of genetic and environmental factors to observed individual differences. Heritability estimates of physical activity vary, depending on sample size and measurement instrument, but the overall importance of environmental factors seems to decrease in adolescence, whereas genetic effects become more prominent. Twin and family studies show that individual difference
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19

Sonuga-Barke, Edmund J. S. Attention-Deficit/Hyperactivity Disorder. Edited by Philip David Zelazo. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199958474.013.0022.

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In this chapter I review the literature on attention-deficit/hyperactivity disorder (ADHD) with the aim of providing a developmental synthesis. In the first section I ask: What is ADHD? I conclude that it is a relatively broad construct that, although having validity as a mental disorder dimension and utility as diagnostic category, is frequently comorbid with, but can be distinguished from, other disorders, and is highly heterogeneous. In the second section I ask: What causes ADHD? I conclude that ADHD has a complex set of causes implicating multiple genetic and environmental risks (and their
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20

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 lowe
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21

Husni, Elaine, and Madonna Michael. Epidemiology of psoriatic arthritis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0003.

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The epidemiological studies of psoriatic arthritis (PsA) is quite challenging as our understanding of the disease is evolving. A wide range of incidence and prevalence is reported among different countries suggesting genetic and environmental factors influencing the epidemiology of PsA. Other contributing factors accounting for the wide range and variation of PsA epidemiology include age and gender variations, ethnicity, lack of precise case definition, and small sample size. A high level of suspicion in patients with pre-existing psoriasis, and collaborative efforts shared between primary car
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22

Williams, Elizabeth A., and Tyler J. Carrier, eds. An -omics Perspective on Marine Invertebrate Larvae. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198786962.003.0019.

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The diverse phenotypes exhibited by marine invertebrate larvae are the result of complex gene-environment interactions. Recently, technological advances in molecular biology have enabled large-scale -omics approaches, which can provide a global overview of the molecular mechanisms that shape the larval genotype-phenotype landscape. -omics approaches are facilitating our understanding of larval development and life history evolution, larval response to environmental stress, the larval microbiome, larval physiology and feeding, and larval behavior. These large-scale molecular approaches are even
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23

Doherty, Michael, Johannes Bijlsma, Nigel Arden, David J. Hunter, and Nicola Dalbeth. Introduction: what is osteoarthritis? Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0001.

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This brief introductory chapter summarizes some of the key clinical and structural features of osteoarthritis (OA) and highlights some general observations and concepts concerning the nature of OA. General observations include the preservation of OA throughout human evolution; the occurrence of OA in many other animals; the dynamic, metabolically active nature of OA pathophysiology; the fact that most OA never associates with symptoms or functional impairment; and the good outcome in many cases of symptomatic OA. Such observations support the concept of OA as the inherent repair process of syn
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24

Holroyd, Christopher R., Nicholas C. Harvey, Mark H. Edwards, and Cyrus Cooper. Environment. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0038.

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Musculoskeletal disease covers a broad spectrum of conditions whose aetiology comprises variable genetic and environmental contributions. More recently it has become clear that, particularly early in life, the interaction of gene and environment is critical to the development of later disease. Additionally, only a small proportion of the variation in adult traits such as bone mineral density has been explained by specific genes in genome-wide association studies, suggesting that gene-environment interaction may explain a much larger part of the inheritance of disease risk than previously thoug
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25

Holroyd, Christopher R., Nicholas C. Harvey, Mark H. Edwards, and Cyrus Cooper. Environment. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0038_update_001.

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Musculoskeletal disease covers a broad spectrum of conditions whose aetiology comprises variable genetic and environmental contributions. More recently it has become clear that, particularly early in life, the interaction of gene and environment is critical to the development of later disease. Additionally, only a small proportion of the variation in adult traits such as bone mineral density has been explained by specific genes in genome-wide association studies, suggesting that gene-environment interaction may explain a much larger part of the inheritance of disease risk than previously thoug
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