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Books on the topic 'Polymorphism of the TLR4 gene'

Author: Grafiati

Published: 28 May 2022

Last updated: 30 July 2025

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1

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

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2

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

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3

Masatoshi, Nei, ed. Humanpolymorphic genes. Oxford University Press, 1988.

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4

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

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5

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

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6

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

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7

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. A.R. Liss, 1985.

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8

de Luis Roman, Daniel-Antonio, and Ana B. Crujeiras, eds. Gene Polymorphism and Nutrition: Relationships with Chronic Disease. MDPI, 2023. http://dx.doi.org/10.3390/books978-3-0365-7771-5.

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9

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

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10

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

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11

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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12

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

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13

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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14

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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15

Osman, Marwa. In Silico Analysis and Modeling of Deleterious Single Nucleotide Polymorphism (Snps) in Human Gata4 Gene. GRIN Verlag GmbH, 2016.

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16

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

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17

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

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18

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

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19

A Primer of Genome Science. Sinauer Associates, 2001.

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20

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 rec

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21

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

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22

Garrib, Alam. Insertion/deletion polymorphism of the angiotensin-converting enzyme gene in patients who misuse alcohol or in patientswith renal artery stenosis. 1995.

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23

Kiel, Universität, ed. Variant detection and single nucleotide polymorphism typing of lipopolysaccharide-induced transcritpion factor regulating tumor necrosis factor [alpha] gene and caspase recruitment domain 15 gene: Association with inflammatory bowel disease and response to infliximab treatment. 2004.

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24

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, Rs468

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25

Hamilton, Matthew Lloyd. COMT genotypes in pain responses. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0080.

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The landmark study discussed in this chapter is ‘COMT val158met genotype affects μ‎-opioid neurotransmitter responses to a pain stressor’, published by Zubieta et al. in 2003. Catechol-O-methyl-transferase (COMT) is a key modulator of dopaminergic and noradrenergic neurotransmission. This study focused on a single nucleotide polymorphism of the COMT gene encoding the substitution of valine (val) by methionine (met) at Codon 158 (val158met), resulting in a three- to fourfold reduction in its activity. Individuals with the val/val genotype have the highest activity of COMT, val/met genotypes hav

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26

Minelli, Alessandro. Evolvability and Its Evolvability. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780199377176.003.0007.

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No universally accepted notion of evolvability is available, focus being alternatively put onto either genetic or phenotypic change. The heuristic power of this concept is best found when considering the intricacies of the genotype→phenotype map, which is not necessarily predictable, expression of variation depending on the structure of gene networks and especially on the modularity and robustness of developmental systems. We can hardly ignore evolvability whenever studying the role of cryptic variation in evolution, the often pervious boundary between phenotypic plasticity and the expression

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27

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 a

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28

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-existi

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