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Books on the topic 'Gens candidats'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Bennett, Philip. Parkinson's disease: A molecular investigation of potential candidate genes. University of Birmingham, 1995.

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2

Ramsden, James Daniel. Angiopoietins in goitre: Candidates for anti-angiogenic gene therapy? University of Birmingham, 2002.

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3

Shieh, Jia-Ching. Isolation and characterisation of candida albicans cell cycle genes. University of Manchester, 1994.

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4

Nolan, Tania. Molecular analysis of cell cycle genes in Candida albicans. University of Manchester, 1996.

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5

Nicholl, David J. A study of candidate genes in Parkinson's disease and related neurodegenerative disorders. University of Birmingham, 1998.

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6

Stoldt, Volker R. Morphogenese des humanpathogenen Pilzes Candida albicans: Isolierung und Charakterisierung der Gene EFGI und RFGI. J. Cramer, 1995.

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7

Dyer, Philip Henry. Investigation of the genetics of nephropathy in type 1 diabetes mellitus: Candidate gene studies. University of Birmingham, 2000.

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8

Thompson, Miles. Mutation screening of dopamine and serotonin candidate genes in Tourette's syndrome and alcohol-dependent patients. National Library of Canada = Bibliothèque nationale du Canada, 1999.

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9

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

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10

Crowley, J. Isolation of candida albican genes involved in cAMP metabolism by the rescue of caffeine sensitive saccharomyces cerevisiae mutants. UMIST, 1996.

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11

Crosby, Andrew Harry. Genetic and physical mapping of the dentinogenesis imperfecta type II locus: The exclusion of three candidate genes from a causative role in the pathogenesis of this disorder. University of Manchester, 1995.

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12

Petit, Frédéric. Traité d\'astronomie pour les gens du monde, avec des notes complémentaires: Pour les candidats au baccalauréat, aux Écoles spéciales et à la licence ès sciences mathématiques. Tome 1. Adamant Media Corporation, 2001.

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13

Petit, Frédéric. Traité d\'astronomie pour les gens du monde, avec des notes complémentaires: Pour les candidats au baccalauréat, aux Écoles spéciales et à la licence ès sciences mathématiques. Tome 2. Adamant Media Corporation, 2001.

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14

Goldman, David, Zhifeng Zhou, and Colin Hodgkinson. The Genetic Basis of Addictive Disorders. 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/9780190681425.003.0042.

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Addictive disorders are moderately to highly heritable, indicating that alleles transmitted from parents are protective, or enhance risk by whatever mechanisms. However, the inheritance of addictive disorders is complex, involving hundreds of genes and variants that are both common and rare, and that vary in effect size and context of action. Genes altering risk for addictions have been identified by pathway and candidate gene studies in humans and model organisms, and genomic approaches including genome-wide association, meiotic linkage, and sequencing. Genes responsible for shared liability

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15

Clemas, Joseph A. The isolation of the LYS1, LYS5, and LYS7 genes of Candida albicans: The characterization of the LYS7 gene of Candida albicans. 1991.

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16

Bonetta, Laura Paola. Molecular cloning of candidate Wilms tumour genes on chromosome 11p13. 1992.

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17

Tülümen, Erol, and Martin Borggrefe. Monogenic and oligogenic cardiovascular diseases: genetics of arrhythmias—short QT syndrome. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0150.

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Short QT syndrome (SQTS) is a very rare, sporadic or autosomal dominant inherited channelopathy characterized by abnormally short QT intervals on the electrocardiogram and increased propensity to atrial and ventricular tachyarrhythmias and/or sudden cardiac death. Since its recognition as a distinct clinical entity in 2000, significant progress has been made in defining the clinical, molecular, and genetic basis of SQTS. To date, several causative gain-of-function mutations in potassium channel genes and loss-of-function mutations in calcium channel genes have been identified. The physiologica

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18

MacGregor, Alex, Ana Valdes, and Frances M. K. Williams. Genetics of osteoarthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0044.

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In this chapter we outline the approaches which have been adopted to identify genetic variants predisposing to osteoarthritis (OA), a condition long recognized as having a heritable component. Such routes to their identification include examining mendelian traits in which OA is a feature, candidate gene studies based on knowledge of OA pathobiology, linkage analysis in related individuals, and, more recently, genome-wide association studies in large samples of unrelated individuals. It is increasingly evident that the main symptom deriving from OA—notably joint pain—also has a genetic basis bu

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19

Distel, Marijn A., and Marleen H. M. de Moor. Genetic Influences on Borderline Personality Disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199997510.003.0007.

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Borderline personality disorder (BPD) tends to “run in families.” Twin and twin family studies show that BPD is moderately heritable, with some evidence for nonadditive gene action. BPD co-occurs with Axis I and other Axis II disorders, as well as with a certain profile of normal personality traits. Multivariate twin (family) studies have shown that these phenotypic associations are partly due to genetic associations, and this is observed most strongly for BPD and neuroticism. Candidate gene-finding studies for BPD suggest the possible role of genes in the serotonergic and dopaminergic system,

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20

Zai, Gwyneth Ching Mung. Candidate genes on chromosome 6p in obsessive-compulsive disorder and schizophrenia. 2004.

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21

Seah, Linden. Characterization of the cloned LYS2 gene of Candida albicans. 1994.

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22

Guthrie, Deanne M. Isolation and characterization of the LYS16 gene of Candida albicans. 1990.

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23

Haiman, Christopher, and David J. Hunter. Genetic Epidemiology of Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676827.003.0004.

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This chapter explores the genetic epidemiology of cancer: the identification and quantification of inherited genetic factors, and their potential interaction with the environment, in the etiology of cancer in human populations. It also describes the techniques used to identify genetic variants that contribute to cancer susceptibility. It describes the older research methods for identifying the chromosomal localization of high-risk predisposing genes, such as linkage analysis within pedigrees and allele-sharing methods, as it is important to understand the foundations of the field. It also revi

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24

Hoornaert, Inge. Identification & Evaluation of Candidate Tumour Suppressor Genes on Chromosome Region 12P12-13. Leuven Univ Pr, 2002.

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25

1947-, Lusis Aldons J., Rotter Jerome I, and Sparkes Robert S. 1930-, eds. Molecular genetics of coronary artery disease: Candidate genes and processes in atherosclerosis. Karger, 1992.

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26

Otowa, Takeshi, Roxann Roberson-Nay, Mandakh Bekhbat, Gretchen N. Neigh, and John M. Hettema. Genetics of Anxiety Disorders. 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/9780190681425.003.0033.

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This chapter provides a broad overview of the state of research in the genetics of the major anxiety disorders (ADs). They exhibit moderate familial aggregation and heritability due to genetic risk factors that are shared between them as well as those that are disorder-specific. Many candidate gene association studies have been published, with a small set of genes that have been consisted validated for their role in one or more anxiety phenotypes. Genome-wide association studies of ADs are in their infancy, with a handful of published studies for each disorder so far and more to come conducted

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27

Evaluation of candidate genes in family studies: Generalized estimating equations and bootstrap approaches. National Library of Canada, 1998.

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28

The Genetics of Sjogren's Syndrom: Candidate Gene Analyses and Genome-wide Linkage Studies. University of Bergen, 2002.

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29

Canli, Turhan, ed. The Oxford Handbook of Molecular Psychology. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199753888.001.0001.

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Determining the biological bases for behavior—and the extent to which we can observe and explain their neural underpinnings—requires a bold, broadly defined research methodology. The interdisciplinary entries in this handbook are organized around the principle of “molecular psychology,” which unites cutting-edge research from such wide-ranging disciplines as clinical neuroscience and genetics, psychology, behavioral neuroscience, and neuroethology. For the first time in a single volume, leaders from diverse research areas present their work in which they use molecular approaches to investigate

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30

Klempan, Timothy Arthur. Transmission analysis of presynaptic and neurodevelopmental candidate gene variants in schizophrenia and bipolar affective disorder. 2004.

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31

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 “can

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32

Holliday, Kate L., Wendy Thomson, and John McBeth. Genetics of chronic musculoskeletal pain. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0045.

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Chronic pain disorders are prevalent and a large burden on health care resources. Around 10% of the general population report chronic widespread pain, which is the defining feature of fibromyalgia. Fibromyalgia is a poorly understood idiopathic disorder which is also characterized by widespread tenderness and commonly occurs with comorbid mood disorders, fatigue, sleep disturbance, and cognitive dysfunction. A role for genetics in chronic pain disorders has been identified by twin studies, with heritability estimates of around 50%. Susceptibility genes for chronic pain are likely to be involve

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33

Holliday, Kate L., Wendy Thomson, John McBeth, and Nisha Nair. Genetics of chronic musculoskeletal pain. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0045_update_001.

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Chronic pain disorders are prevalent and a large burden on health care resources. Around 10% of the general population report chronic widespread pain, which is the defining feature of fibromyalgia. Fibromyalgia is a poorly understood idiopathic disorder which is also characterized by widespread tenderness and commonly occurs with comorbid mood disorders, fatigue, sleep disturbance, and cognitive dysfunction. A role for genetics in chronic pain disorders has been identified by twin studies, with heritability estimates of around 50%. Susceptibility genes for chronic pain are likely to be involve

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34

Yoon, Il-Sang. Molecular analysis of altered calcium homeostasis in bipolar disorder using differential display and candidate gene approaches. 2002.

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35

Gedil, Melaku Ayele. Marker development, genome mapping, and cloning of candidate disease resistance genes in sunflower, Helianthus annuus L. 1999.

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36

Garrad, Richard C. The molecular and functional analysis of the LYS1 gene of Candida albicans and characterization of lysine auxotrophs of Candida spp. 1993.

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37

Wong, Albert Hung Choy. Identification and analysis of candidate genes for schizophrenia based on the neonatal ventral-hippocampal lesioned rat model. 2001.

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38

Lusis, Aldons J., and Jerome I. Rotter. Molecular Genetics of Coronary Artery Disease: Candidate Genes and Processes in Atherosclerosis (Key Issues in Human Genetics). S. Karger Publishers (USA), 1992.

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39

Sumner, Jennifer A., Angela C. Bustamante, Karestan C. Koenen, and Monica Uddin. Genetics of PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0011.

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Trauma exposure and PTSD are heritable. However, the mechanisms of risk and resilience following trauma exposure are not yet well understood, suggesting that investigations into the genetic architecture of PTSD have much to contribute. This chapter reviews the rapidly growing literature on molecular genetic risk factors for PTSD, including findings from candidate gene and genome-wide association studies. Given the critical role of trauma exposure in the onset of PTSD, it also discusses gene-environment interplay, and highlights some recent findings from epigenetic studies. The chapter conclude

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40

Arthur, Brown. Molecular analysis of an insertional mutation at the mouse dt locus: the identification of a candidate dt gene. 1993.

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41

Hongtrakul, Vipa. The development and analysis of sequence-based DNA markers in sunflower for DNA fingerprinting and candidate gene analysis. 1997.

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42

Morphogene Des Humanpathogenen Pilzes Candida Albicans: Isolierung Und Charakterisierung Der Gene Efg1 Und Rfg1 (Bibliotheca Mycologica). Gebruder Borntraeger Verlagsbuchhandlung, 1995.

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43

Arnold, Paul. Genetics of OCD. Edited by Christopher Pittenger. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228163.003.0019.

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Obsessive-compulsive disorder (OCD) often runs in families and has been shown to have significant heritability. It is genetically complex, and two decades of genetic work have not converged on a clear understanding of genetic risk factors. However, accelerating progress in recent years has begun to generate some insights into the genetic architecture of the disorder, and greater clarity is likely to emerge in the coming decade. This chapter summarizes several lines of genetic work, including genome-wide genetic and linkage studies; candidate gene studies; and investigations of gene-environment

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44

Bentham, James R. The genetics of congenital heart disease. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, et al. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0022.

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Congenital heart disease (CHD) is defined as a structural cardiac malformation resulting from an abnormality of development; 8% of CHD is inherited in a Mendelian fashion and 12% results from chromosomal imbalance. Recurrence risk and new research suggest that even the remaining 80% of patients without an identifiable familial or syndromic basis for disease may have an identifiable genetic cause. The potential to understand these mechanisms is increasing with the advent of new sequencing techniques which have identified multiple or single rare variants and/or copy number variants clustering in

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45

Hinks, Anne, and Wendy Thomson. Genetics of juvenile rheumatic diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0043.

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Juvenile rheumatic diseases are heterogeneous, complex genetic diseases; to date only juvenile idiopathic arthritis (JIA) has been extensively studied in terms of identifying genetic risk factors. The MHC region is a well-established risk factor but in the last few years candidate gene and genome-wide association studies have been utilized in the search for non-HLA risk factors. There are now an additional 12 JIA susceptibility loci with evidence for association in more than one study. In addition, some subtype-specific associations are emerging. These risk loci now need to be investigated fur

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46

Hinks, Anne, and Wendy Thomson. Genetics of juvenile rheumatic diseases. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0043_update_002.

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Juvenile rheumatic diseases are heterogeneous, complex genetic diseases; to date only juvenile idiopathic arthritis (JIA) has been extensively studied in terms of identifying genetic risk factors. The MHC region is a well-established risk factor but in the last few years candidate gene and large-scale genome-wide association studies have been utilized in the search for non-HLA risk factors. There are now 17 JIA susceptibility loci which reach the genome-wide significance threshold for association and a further 7 regions with evidence for association in more than one study. In addition, some su

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47

Hinks, Anne, and Wendy Thomson. Genetics of juvenile rheumatic diseases. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0043_update_003.

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Juvenile rheumatic diseases are heterogeneous, complex genetic diseases; to date only juvenile idiopathic arthritis (JIA) has been extensively studied in terms of identifying genetic risk factors. The MHC region is a well-established risk factor but in the last few years candidate gene and large-scale genome-wide association studies have been utilized in the search for non-HLA risk factors. There are now 17 JIA susceptibility loci which reach the genome-wide significance threshold for association and a further 7 regions with evidence for association in more than one study. In addition, some su

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48

Mitchell, Colter. The Genetics of Human Behavior. Edited by Rosemary L. Hopcroft. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780190299323.013.43.

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This chapter examines the recent massive expansion of genetic research into human behavior. Based on decades of twin research, there were high expectations of strong genetic effects for almost all behavior. Further work on candidate genes from animal research proved initially exciting. Although that research continues, it now currently receives much less attention, in contrast to whole-genome examinations. This chapter provides insight into the whole-genome era of behavioral research and the extent to which it may or may not be a profitable endeavor. Sociologists are generally unaware of this

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49

Stoddard, Frederick J., and Robert L. Sheridan. Wound Healing and Depression. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0009.

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Depression and wound healing are bidirectional processes for adults and children consistent with the conception of depression as systemic. This systemic interaction is similar to the “bidirectional impact of mood disorder on risk for development, progression, treatment, and outcomes of medical illness” generally. And, evidence is growing that the bidirectional impact of mood disorder may be true for injuries and for trauma surgery. Animal models have provided some support that treatment of depression may improve wound healing. An established biological model for a mechanism delaying wound heal

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50

Studies of Wnt Signalling in Drosophila:: Screens for Candidate Transcripts of a New Gene Involved in Transduction and Genetic and Molecular Analysis of a Potential Target. University of Antwerp, 1999.

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