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Books on the topic 'Gene polymorphisms'

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Published: 4 June 2021
Last updated: 10 March 2023

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1

Koen, Vandenbroeck, ed. Cytokine gene polymorphisms in multifactorial conditions. Boca Raton, FL: CRC Taylor & Francis, 2006.

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2

Masatoshi, Nei, ed. Humanpolymorphic genes. New York: Oxford University Press, 1988.

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3

Roychoudhury, Arun K. Human polymorphic genes: World distribution. New York: Oxford University Press, 1988.

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4

Green, Elaine. Apolipoproteins E and (a) gene polymorphisms and susceptibility to coronary heart disease. Birmingham: University of Birmingham, 1994.

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5

George, Stamatoyannopoulos, and Nienhuis Arthur W, eds. Experimental approaches for the study of hemoglobin switching: Proceedings of the Fourth Conference on Hemoglobin Switching, October 1-3, 1984. New York: A.R. Liss, 1985.

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6

de, Vienne D., ed. Molecular markers in plant genetics and biotechnology. Enfield, NH: Science Publishers, 2003.

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7

J, Henry Robert, ed. Plant genotyping II: SNP technology. Wallingford, UK: CABI, 2008.

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8

George, Stamatoyannopoulos, Nienhuis Arthur W, and Conference on Hemoglobin Switching (7th : 1990 : Airlie, Va.), eds. The Regulation of hemoglobin switching. Baltimore: Johns Hopkins University Press, 1991.

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9

George, Stamatoyannopoulos, and Nienhuis Arthur W, eds. Hemoglobin switching: Proceedings of the Sixth Conference on Hemoglobin Switching, held in Airlie, Virginia, September 24-27, 1988. New York: A.R. Liss, 1989.

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10

Farhan, Ayar Jawi. T cell receptor gene polymorphism and usage in rheumatoid arthritis. Manchester: University of Manchester, 1997.

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11

Ellegren, Hans. Genome analysis with microsatellite markers. Uppsala: Dept. of Animal Breeding and Genetics, Swedish University of Agricultural Sciences, 1993.

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12

Kiaris, Hippokratis. Genes, polymorphisms, and the making of societies: How genetic behavioral traits influence human cultures. Boca Raton: Universal-Publishers, 2012.

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13

Bieber, Heidi. Traces of antiquity in genes: Comparative study of serum protein polymorphisms between populations of Africa, Europe and Amerindians of Central America. Aachen: Shaker Verlag, 1997.

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14

Liu, Zhanjiang. Next generation sequencing and whole genome selection in aquaculture. Ames, Iowa: Wiley-Blackwell, 2011.

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15

Berkowitz, Noah C. Functional importance of polymorphic subregions in the C3H anti I-Ab alloresponse. [New York]: [Columbia University], 1993.

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16

Oelbaum, Raymond Stuart. An analysis of four candidate genes for non-insulin-dependent diabetes using restriction fragment length polymorphism markers. Manchester: University of Manchester, 1994.

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17

Vandenbroeck, Koen. Cytokine Gene Polymorphisms in Multifactorial Conditions. CRC, 2006.

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18

Vandenbroeck, Koen. Cytokine Gene Polymorphisms in Multifactorial Conditions. Taylor & Francis Group, 2006.

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19

Vandenbroeck, Koen. Cytokine Gene Polymorphisms in Multifactorial Conditions. Taylor & Francis Group, 2006.

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20

Ordovas, Jose M., and Laurence Parnell. Nutrigenetics and Nutrigenomics. Wiley-Liss, 2006.

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21

Visentainer, Jeane. Importance of Non-HLA Gene Polymorphisms in Hematopoietic Stem Cell Transplantation. INTECH Open Access Publisher, 2012.

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22

Egwuekwe, Ejike R. Vitamin d Receptor Gene Polymorphisms and the Risks of Breast Cancer. iUniverse, Incorporated, 2020.

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23

Cleary, Sean P. Association of missense polymorphisms in the Adenomatous polyposis coli gene and colorectal cancer. 2004.

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24

(Editor), Dominique De Vienne, and Dominique De Vienne (Editor), eds. Molecular Markers in Plant Genetics and Biotechnology. Science Publishers, 2003.

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25

Hwang, Rudi. Pharmacogenetic analysis of dopamine receptor gene polymorphisms and clinical response to clozapine in patients with schizophrenia. 2006.

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26

Experimental approaches for the study of hemoglobin switching: Proceedings of the Fourth Conference on Hemoglobin Switching, October 1-3, 1984 (Progress in clinical and biological research). A.R. Liss, 1985.

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27

Tahir, Muhammad. Use of isozyme polymorphisms in lentil (LENS· culinaris Medik.) for gene mapping and detection of quantitative trait loci. 1990.

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28

Yan, Lu. Polymorphisms in the catechol-O-methyltransferase gene ( COMT) affect the risk for chronic post-mastectomy pain syndrome (PMPS). 2006.

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29

Morell-Ducos, Fausto. COMT and morphine use in cancer pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0082.

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The landmark paper discussed in this chapter is ‘Genetic variation in the catechol-O-methyltransferase (COMT) gene and morphine requirements in cancer patients with pain’, published by Rakvåg et al. in 2008. Genetic variation contributes to differences in pain sensitivity and response to analgesics. Catecholamines are involved in the modulation of pain and are metabolized by catchol-O-methyltransferase (COMT). Genetic variability in the COMT gene may therefore contribute to differences in pain sensitivity and response to analgesics. It has been shown that a polymorphism in the COMT gene, Rs4680 (val158met), influences pain sensitivity and efficacy for morphine in cancer pain treatment. This study investigated whether the variability in other regions in the COMT gene also contributes to the inter-individual variability of morphine efficacy by mapping 11 single nucleotide polymorphisms, constructing haplotypes from them, and then comparing genotypes and haplotypes against pharmacological, demographic, and patient symptom measurements in patients receiving morphine for cancer pain.
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30

X.M. Yin, M.M. Yuan, L. Chen, F.X. Chen, and J.Y. Wang*. Polymorphisms of the Myf6 gene exon 1 and their relationship with growth and reproductive traits in Jinghai Yellow Chicken. Verlag Eugen Ulmer, 2019. http://dx.doi.org/10.1399/eps.2019.271.

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31

Westberg, Lars, and Hasse Walum. Oxytocin and Vasopressin Gene Variation and the Neural Basis of Social Behaviors. Edited by Turhan Canli. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.011.

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Experimental studies in rodents and humans show that the neuropeptides oxytocin and vasopressin are important regulators of behaviors related to social interactions. Evidence for positive effects of oxytocin treatment on symptoms of psychiatric disorders characterized by impaired social functioning has emerged. Numerous studies report associations between various social behaviors, the risk of autism, and polymorphisms inOXTRandAVPR1A. This chapter provides an overview of these genetic association studies. Although many of the published findings are inconclusive and need replication in independent samples, the chapter concludes that variants ofOXTRandAVPR1Aseem to moderate individual variation in different aspects of social behavior. The challenges for future studies include replication of current findings, identification of the functional variants, and characterization of the neural mechanisms mediating the gene-behavior associations, as well as exploration of the pharmacogenetic potential ofOXTRandAVPR1Ain future clinical trials.
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32

Stomatoyannopoulos, George, and Arthur W. Nienhuis. Hemoglobin Switching, Part A: Transcriptional Regulation: Proceedings of the Sixth Conference on Hemoglobin Switching Held in Airlie, Virginia, sept. Wiley-Liss, 1989.

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33

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 well as the possibility of gene–gene and gene–environmental interactions. Despite this complexity, developments in molecular and statistical genetics, and further refinement of the phenotype hold promise for further deepening our genetic understanding of OCD and spectrum disorders in the coming decade.
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34

Nienhuis, Arthur W., and George Stomatoyannpoulos. Hemoglobin Switching, Part B: Cellular and Molecular Mechanisms (Progress in Clinical and Biological Research, Vol 316B). Wiley-Liss, 1989.

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35

Hemoglobin switching: Proceedings of the Sixth Conference on Hemoglobin Switching, held in Airlie, Virginia, September 24-27, 1988 (Progress in clinical and biological research). A.R. Liss, 1989.

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36

Fabbri, Chiara, and Alessandro Serretti. The treatment of bipolar disorder in the era of personalized medicine: myth or promise? Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0031.

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Bipolar disorder (BD) is a chronic disease associated with high personal and socio-economic burden. Genetics accounts for 20–95% of variability in central nervous system drug disposition and pharmacodynamics, thus genetic markers are considered a promising way to develop tailored treatments and improve the prognosis of the disease. Among mood stabilizers, lithium response was the most investigated phenotype and the most replicated genes are involved in synaptic plasticity (BDNF), serotonergic (SLC6A4) and dopaminergic (DRD1) neurotransmission, and second messenger cascades (GSK3B). Relevant pharmacogenetic findings regarding other mood stabilizers are hyperammonaemia (CPS1 gene) and hepatic dysfunction (POLG gene) induced by valproate and immune-mediated cutaneous hypersensitivity reactions (HLA-B*1502) induced by lamotrigine or carbamazepine. Polymorphisms in cytochrome (CYP) P450 genes are expected to provide useful information particularly in case of polypharmacy. Despite few pharmacogenetic tests are currently recommended, the development of pharmacogenetics in other fields of medicine provides an encouraging perspective.
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37

Divan, Aysha, and Janice A. Royds. 2. DNA. Oxford University Press, 2016. http://dx.doi.org/10.1093/actrade/9780198723882.003.0002.

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Another significant milestone was the publication in 2003 of the complete sequence of the human genome—the entire DNA contained within the forty-six chromosomes located in the nucleus of each human somatic (body) cell. Once this was published, further worldwide projects were launched to work out what the functions of these genes and other regions of the genome actually were. ‘DNA’ outlines the components of the human genome and their organization; DNA replication; mutations and correction mechanisms; polymorphisms; and new DNA technologies, including gene cloning, the polymerase chain reaction, and sequencing methods. Finally, bioinformatics and the subsequent issues of privacy and how this information could be used are discussed.
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38

Turner, Neil, Teena Tandon, and Rajiv Agarwal. APOL1 and renal disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0341_update_001.

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Although apolipoprotein L1 (APOL1) is not known to be a direct cause of renal disease, it has emerged as a powerful cofactor in several important conditions. APOL1 gene polymorphisms account for the restriction of HIV-associated collapsing focal segmental glomerulosclerosis (FSGS) to those with African ancestry. In Africa, the disease-predisposing alleles seem to have been selected for because they convey resistance to some strains of trypanosomiasis. The same alleles are associated with increased susceptibility to primary FSGS, and are probably able to fully account for the excess of FSGS in black races. Two high-risk alleles have been labelled G1 and G2. To have increased susceptibility, individuals must usually have two copies, that is, it is recessive, but the gene frequency is high in West and Southern Africa and in those descended from those regions. The same alleles convey susceptibility to other more common renal diseases. Numerically the most significant association is with nephropathy previously attributed to hypertension. Recent evidence suggests that the gene may increase rate of progression in renal disease of various types, including diabetes. The mechanism is not known.
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39

Troisi, Alfonso. Infidelity. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199393404.003.0005.

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This chapter reviews recent data on the evolution of sexual strategies in humans and shows how, in the natural environment, the adaptive functions of sexual infidelity were substantially different in males and females. The meaning of technical terms used by evolutionary biologists to describe different behavioral strategies related to maximization of reproductive success are explained, including the Coolidge effect, good-gene sexual strategy, and serial monogamy. Biological analysis of motivations for sexual infidelity integrate evolutionary hypotheses with recent data from molecular genetic studies of personality showing that carriers of some genetic polymorphisms related to novelty seeking are more prone to sexual promiscuity. Finally, the chapter reports a clinical case showing how cultural prejudice can distort individual expectations about what is normal sexual desire.
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40

Hope, James, and Mark P. Dagleish. Prion-protein-related diseases of animals and man. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0041.

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Scrapie, bovine spongiform encephalopathy (BSE), Creutzfeldt–Jakob disease (CJD), and related diseases of mink (transmissible mink encephalopathy), mule deer and elk (chronic wasting disease) are the founder members of a group of diseases called the transmissible degenerative (or spongiform) encephalopathies (TSE). These diseases can be transmitted by prions from affected to healthy animals by inoculation or by feeding diseased tissues. Prions are cellular proteins that can transfer metabolic and pathological phenotypes vertically from parent to progeny or horizontally between cells and animals. TSEs are characterised by the accumulation of the prion form of the mammalian prion protein (PrPC) in the central nervous system or peripheral tissues of animals and humans. Mutations of the human PrP gene are linked to rare, familial forms of disease and prion-protein gene polymorphisms in humans and other species are linked to survival time and disease characteristics in affected individuals. Iatrogenic transmission of CJD in man has occurred, and a variant form of CJD (vCJD) is due to cross-species transmission of BSE from cattle to humans. Atypical forms of scrapie and BSE have been identified during large-scale monitoring for TSEs worldwide. This chapter outlines our current understanding of scrapie, BSE, CJD and other TSEs and highlights recent progress in defining the role in disease of the prion protein, PrP.
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41

Han, Shihui. Gene-culture interaction on human behavior and the brain. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780198743194.003.0007.

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Chapter 7 reviews empirical findings that allow consideration of biological and environmental influences on human behavior from an evolutionary perspective (e.g., gene-culture coevolution) and from a perspective of individual development (e.g., gene-culture interaction). It also reviews imaging genetic studies that link genes with brain functional organization. It introduces a cultural neuroscience paradigm for investigating genetic influences on the coupling of brain activity and culture by presenting two studies that examined how serotonin transporter functional polymorphism and oxytocin receptor gene moderate the association between interdependence and brain activities involved in self-reflection and empathy. These studies illustrate a new approach to understanding the manner with which culture interacts with gene to shape human brain activity.
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42

Anand, Angeline, and Jose Heavena Fernando. Diabetes Mellitus: Gene Polymorphism and Total Antioxidant Status in Type 2 Diabetes. Independently Published, 2019.

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43

Malheiro, Adriana, David Courtin, Eduardo Antonio Donadi, and Rajendranath Ramasawmy, eds. The Role of Gene Polymorphism in Modulating the Immune Responses against Tropical Infectious Diseases. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-382-0.

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44

Wani, Dr Ab Ahad, ed. Polymorphism of MSTN Gene in Boer and Bakerwal Goats and its Association with Growth Traits. AkiNik Publications, 2021. http://dx.doi.org/10.22271/ed.book.1077.

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45

Chan, Florance. TBI and depression: The role of the serotonin transporter gene promoter region (5-HTTLPR) polymorphism. 2005.

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46

Whitworth, Caroline, and Stewart Fleming. Malignant hypertension. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0216.

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Malignant hypertension (MH) is recognized clinically by elevated blood pressure together with retinal haemorrhages or exudates with or without papilloedema (grades III or IV hypertensive retinopathy); and may constitute a hypertensive emergency or crisis when complicated by evidence of end-organ damage including microangiopathic haemolysis, encephalopathy, left ventricular failure, and renal failure. Though reversible, it remains a significant cause of end-stage renal failure, and of cardiovascular and cerebrovascular morbidity and mortality in developing countries.MH can complicate pre-existing hypertension arising from diverse aetiologies, but most commonly develops from essential hypertension. The absolute level of blood pressure appears not to be critical to the development of MH, but the rate of rise of blood pressure may well be relevant in the pathogenesis. The pathogenesis of this transformation remains unclear.The pathological hallmark of MH is the presence of fibrinoid necrosis (medial vascular smooth muscle cell necrosis and fibrin deposition within the intima) involving the resistance arterioles in many organs. Fibrinoid necrosis is not specific to MH and this appearance is seen in other conditions causing a thrombotic microangiopathy such as haemolytic uraemic syndrome, scleroderma renal crisis, antiphospholipid syndrome, and acute vascular rejection post transplant. MH can both cause a thrombotic microangiopathy (TMA) but can also complicate underlying conditions associated with TMA.The pathophysiological factors that interact to generate and sustain this condition remain poorly understood. Risk factors include Afro-Caribbean race, smoking history, younger age of onset of hypertension, previous pregnancy, and untreated hypertension associated with non-compliance or cessation of antihypertensive therapy.Evidence from clinical studies and animal models point to a central role for the intrarenal renin–angiotensin system (RAS) in MH; there is good evidence for renal vasoconstriction and activation of the renal paracrine RAS potentiating MH once established; however, there may also be a role in the predisposition of MH suggested by presence of increased risk conferred by an ACE gene polymorphism in humans and polymorphisms for both ACE and AT1 receptor in an animal model of spontaneous MH. Other vasoactive mediators such as the endothelin and the inflammatory response may be important contributing to and increasing endothelial damage. There have been no randomized controlled trials to define the best treatment approach, but progressive lowering of pressures over days is considered safest unless made more urgent by critical clinical state. It seems logical to introduce ACE inhibition cautiously and early, but in view of the risk of rapid pressure lowering some recommend delay.
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47

Saab, Yolande. Renin-angiotensin-associated gene polymorphism frequencies in the Lebanese population and their association with depressive disorders. 2004.

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48

Walsh, Bruce, and Michael Lynch. Using Molecular Data to Detect Selection: Signatures from Multiple Historical Events. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198830870.003.0010.

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This chapter examines the search for a pattern of repetitive adaptive substitutions over evolutionary time. In contrast with the previous chapter, only a modest number of tests toward this aim have been proposed. The HKA and McDonald-Kreitman tests contrast the polymorphism to divergence ratio between different genomic classes (such as different genes or silent versus replacement sites within the same gene). These approaches can detect an excess of substitutions, which allows one to estimate the fraction of adaptive sites. This chapter reviews the empirical data on estimates of this fraction and discusses some of the sources of bias it its estimation. Over an even longer time scale, one can contrast the rate of change of sites in a sequence over a phylogeny. These tests require a rather special type of selection, wherein the same specific site (usually a codon) experiences multiple adaptive substitutions over a phylogeny, such as might occur in arms-race genes.
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49

A Functional Polymorphism in the Epidermal Growth Factor Gene Independently Predicts Clinical Decompensation in HCV-Related Cirrhosis. 2014.

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50

(Editor), Graham R. Taylor, and Ian N. Day (Editor), eds. Guide to Mutation Detection. Wiley, 2005.

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