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Książki na temat „Single nucleotide polymorphisms”

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Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 6 września 2023

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1

Kwok, Pui-Yan. Single Nucleotide Polymorphisms. New Jersey: Humana Press, 2002. http://dx.doi.org/10.1385/1592593275.

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2

Sauna, Zuben E., i Chava Kimchi-Sarfaty, red. Single Nucleotide Polymorphisms. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-05616-1.

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3

Komar, Anton A., red. Single Nucleotide Polymorphisms. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-411-1.

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4

Single nucleotide polymorphisms: Methods and protocols. Wyd. 2. New York: Humana, 2009.

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5

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

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6

1955-, Carracedo Ángel, red. Forensic DNA typing protocols. Totowa, N.J: Humana Press, 2005.

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7

1956-, Kwok Pui-Yan, red. Single nucleotide polymorphisms: Methods and protocols. Totowa, N.J: Humana Press, 2003.

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8

Komar, Anton A. Single Nucleotide Polymorphisms: Methods and Protocols. Humana Press, 2012.

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9

Kwok, Pui-Yan. Single Nucleotide Polymorphisms: Methods and Protocols (Methods in Molecular Biology). Humana Press, 2002.

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10

Sauna, Zuben E., i Chava Kimchi-Sarfaty. Single Nucleotide Polymorphisms: Human Variation and a Coming Revolution in Biology and Medicine. Springer International Publishing AG, 2022.

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11

Charney, Alexander, i Pamela Sklar. Genetics of Schizophrenia and Bipolar Disorder. Redaktorzy Dennis S. Charney, Eric J. Nestler, Pamela Sklar i Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0013.

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Schizophrenia and bipolar disorder are the classic psychotic disorders. Both diseases are strongly familial, but have proven recalcitrant to genetic methodologies for identifying the etiology until recently. There is now convincing genetic evidence that indicates a contribution of many DNA changes to the risk of becoming ill. For schizophrenia, there are large contributions of rare copy number variants and common single nucleotide variants, with an overall highly polygenic genetic architecture. For bipolar disorder, the role of copy number variation appears to be much less pronounced. Specific common single nucleotide polymorphisms are associated, and there is evidence for polygenicity. Several surprises have emerged from the genetic data that indicate there is significantly more molecular overlap in copy number variants between autism and schizophrenia, and in common variants between schizophrenia and bipolar disorder.
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12

Morell-Ducos, Fausto. COMT and morphine use in cancer pain. Redaktorzy Paul Farquhar-Smith, Pierre Beaulieu i 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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13

Eyre, Steve, i Jane Worthington. Genetics of rheumatoid arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0040.

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A range of epidemiological studies have clearly established that susceptibility to rheumatoid arthritis (RA) is determined by both genetic and environmental factors. Studies over the last five decades have used a variety of approaches to identify the genetic variants associated with disease. HLA DRB1 was the first RA susceptibility locus to be discovered and has the largest effect size. We describe current understanding of the complexities of HLA association for RA. Linkage and small-scale association studies prior to 2007 provided convincing evidence for only one more RA susceptibility locus, PTPN22. Major breakthroughs in high-throughput genotyping and systematic discovery and mapping of hundreds of thousands of single nucleotide polymorphisms (SNPs) led to large-scale genome-wide association studies used for the first time for RA in 2007. This approach has had a dramatic impact on our knowledge of the susceptibility loci for RA, such that over 60 risk variants have now been robustly identified. We present an overview of these studies and the loci that have been identified. We consider how this knowledge is contributing to a greater understanding of the aetiology and pathology of the disease and in turn how this can influence management of patients presenting with an inflammatory arthritis. We consider some of the unanswered questions and the approaches that will need to be taken to address them.
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14

Eyre, Steve, Jane Worthington i Sebastien Viatte. Genetics of rheumatoid arthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0040_update_003.

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A range of epidemiological studies have clearly established that susceptibility to rheumatoid arthritis (RA) is determined by both genetic and environmental factors. Studies over the last five decades have used a variety of approaches to identify the genetic variants associated with disease. HLA DRB1 was the first RA susceptibility locus to be discovered and has the largest effect size. We describe current understanding of the complexities of HLA association for RA. Linkage and small-scale association studies prior to 2007 provided convincing evidence for only one more RA susceptibility locus, PTPN22. Major breakthroughs in high-throughput genotyping, and systematic discovery and mapping of hundreds of thousands of single nucleotide polymorphisms (SNPs) led to large-scale genome-wide association studies used for the first time for RA in 2007. Widespread utilization of this approach has had a dramatic impact on our knowledge of the susceptibility loci for RA, such that over 100 risk variants have now been robustly identified. We present an overview of these studies and the loci that have been identified. We consider how this knowledge is contributing to a greater understanding of the aetiology and pathology of the disease, and in turn how this can influence management of patients presenting with an inflammatory arthritis. We consider some of the unanswered questions and the approaches that will need to be taken to address them.
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15

Lewis, Myles, i Tim Vyse. Genetics of connective tissue diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0042.

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The advent of genome-wide association studies (GWAS) has been an exciting breakthrough in our understanding of the genetic aetiology of autoimmune diseases. Substantial overlap has been found in susceptibility genes across multiple diseases, from connective tissue diseases and rheumatoid arthritis (RA) to inflammatory bowel disease, coeliac disease, and psoriasis. Major technological advances now permit genotyping of millions of single nucleotide polymorphisms (SNPs). Group analysis of SNPs by haplotypes, aided by completion of the Hapmap project, has improved our ability to pinpoint causal genetic variants. International collaboration to pool large-scale cohorts of patients has enabled GWAS in systemic lupus erythematosus (SLE), systemic sclerosis and Behçet's disease, with studies in progress for ANCA-associated vasculitis. These 'hypothesis-free' studies have revealed many novel disease-associated genes. In both SLE and systemic sclerosis, identified genes map to known pathways including antigen presentation (MHC, TNFSF4), autoreactivity of B and T lymphocytes (BLK, BANK1), type I interferon production (STAT4, IRF5) and the NFκ‎B pathway (TNIP1). In SLE alone, additional genes appear to be involved in dysregulated apoptotic cell clearance (ITGAM, TREX1, C1q, C4) and recognition of immune complexes (FCGR2A, FCGR3B). Future developments include whole-genome sequencing to identify rare variants, and efforts to understand functional consequences of susceptibility genes. Putative environmental triggers for connective tissue diseases include infectious agents, especially Epstein-Barr virus; cigarette smoking; occupational exposure to toxins including silica; and low vitamin D, due to its immunomodulatory effects. Despite numerous studies looking at toxin exposure and connective tissue diseases, conclusive evidence is lacking, due to either rarity of exposure or rarity of disease.
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16

Carracedo, Angel. Forensic DNA Typing Protocols. Humana Press, 2004.

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17

Forensic DNA typing protocols. Totowa, NJ: Humana Press, 2004.

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18

Bayer, Christina. Bedeutung Von Single Nucleotid Polymorphismen Im Nod2/Card15-Gen Fur Das Uberleben Nach Allogener Stammzelltransplantation Im Kindes- Und Jugendalter. Logos Verlag Berlin, 2015.

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19

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

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20

Hamilton, Matthew Lloyd. COMT genotypes in pain responses. Redaktorzy Paul Farquhar-Smith, Pierre Beaulieu i 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 have intermediate activity, and met/met genotypes have the lowest activity of COMT. Using a mixture of PET imaging of the binding of μ‎-opioid receptors and correlation with clinical outcomes, this groundbreaking study provided evidence that confirmed their hypothesis and established the COMT val158met SNP as one of the first gene modifications with direct ramifications on human pain.
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21

Forensic DNA Typing Protocols. Humana Press Inc.,U.S., 2005.

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