Thematische Bibliographien / Alleles / Bücher
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Bücher zum Thema „Alleles“

Autor: Grafiati
Veröffentlicht am 4. Juni 2021
Zuletzt aktualisiert am 25. Juli 2025

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1

Meksem, Khalid. The handbook of plant mutation screening: Mining of natural and induced alleles. Wiley-VCH, 2010.

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2

Logan, Angela Berti. Characterization of new alleles of PHO85, a cyclin-dependent kinase of Saccharomyces cerevisiae. National Library of Canada = Bibliothèque nationale du Canada, 1999.

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3

Currie, Krista Ann. PCR amplification of alleles at D1S80 locus: Comparative study of two Northern Ontario populations. Laurentian University, Department of Biology, 2000.

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4

Walker, Elizabeth Ann. Cloning, characterization and expression in Escherichia coli of S-(self-incompatibility) alleles from Papaver rhoeas L. University of Birmingham, 1994.

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5

Kauffmann, Jean-Paul. 31, allées Damour. Berg international, 2004.

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6

Comment, Bernard. Allées et venues. C. Bourgois, 1992.

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7

Chaudron, Roger. Les allées du Phnom. Éditions des écrivains, 1998.

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8

Tamer, Ulkü. Alleben öyküleri. Can, 1991.

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9

O'Sullivan, Donna. Alleged affections. Primary Press, 1986.

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10

Baudouin, Denis. Dans les allées du pouvoir. J.C. Lattès, 1990.

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11

Bellet, Maurice. Les allées du Luxembourg: Roman. Desclée de Brouwer, 1996.

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12

Peil, Andreas. Identifizierung und Klassifizierung von S-allelen in Solanum und vergleichende Analysen von Solanaceae-S-allelen. [s.n.], 1995.

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13

Besand, Anja, Mark Arenhövel, and Olaf Sanders, eds. Väter allerlei Geschlechts. Springer Fachmedien Wiesbaden, 2017. http://dx.doi.org/10.1007/978-3-658-16424-9.

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14

Cox, Arthur N., ed. Allen’s Astrophysical Quantities. Springer New York, 2002. http://dx.doi.org/10.1007/978-1-4612-1186-0.

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15

Lovette, Teichert, ed. Allerlei zum Lesen. D.C. Heath, 1992.

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16

N, Cox Arthur, ed. Allen's astrophysical quantities. 4th ed. AIP Press, 2000.

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17

Allen, Jeffrey G. Jeff Allen's best. Wiley, 1990.

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18

Tushinski, Jim. Van Allen's ecstasy. Lethe Press, 2010.

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19

Tushinski, Jim. Van Allen's ecstasy. Lethe Press, 2010.

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20

Office, General Accounting. Alleged materiel disposal. The Office, 1993.

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21

Office, General Accounting. Alleged materiel disposal. The Office, 1993.

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22

Saint-Paul, Gilles. Equilibrium allele distribution in trading populations. IZA, 2006.

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23

Williams, Richelle. Compensating alleles in acyclovir-resistant herpes simplex virus type 1. 2007.

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24

Meksem, Khalid, and Guenter Kahl. Handbook of Plant Mutation Screening: Mining of Natural and Induced Alleles. Wiley & Sons, Incorporated, John, 2009.

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25

Meksem, Khalid, and Guenter Kahl. Handbook of Plant Mutation Screening: Mining of Natural and Induced Alleles. Wiley & Sons, Limited, John, 2010.

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26

Walsh, Bruce, and Michael Lynch. Short-term Changes in the Variance: 1. Changes in the Additive Variance. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198830870.003.0016.

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Selection changes the additive-genetic variance (and hence the response in the mean) by both changing allele frequencies and by generating correlations among alleles at different loci (linkage disequilibrium). Such selection-induced correlations can be generated even between unlinked loci, and (generally) are negative, such that alleles increasing trait values tend to become increasingly negative correlated under direction or stabilizing selection, and positively correlated under disruptive selection. Such changes in the additive-genetic variance from disequilibrium is called the Bulmer effect
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27

Walsh, Bruce, and Michael Lynch. Neutral Evolution in One- and Two-Locus Systems. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198830870.003.0002.

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This chapter reviews the population-genetic theory of neutral alleles in finite populations, examining the probabilities and times to loss or fixation, summary statistics for molecular variation, coalescent theory (the distribution of times back to common ancestry for a sample of alleles), and both mutation-drift and mutation-drift-migration equilibrium models.
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28

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
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29

Walsh, Bruce, and Michael Lynch. Interaction of Selection, Mutation, and Drift. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198830870.003.0007.

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This chapter examines the joint impact of selection, mutation, and drift on the allele frequencies at a locus. One key finding is that if the strength of selection is sufficiently weak relative to drift, alleles behave as if they are effectively neutral. Hence, as a population attempts to evolve toward some ideal (optimal) value, the beneficial increment from new mutations eventually becomes sufficiently weak (relative to drift) they are efficiently neutral, implying that perfect adaptation is never possible. This is the notion of the drift barrier. Another key ideal is Haldane's principle: th
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30

Frankham, Richard, Jonathan D. Ballou, Katherine Ralls, et al. Inbreeding reduces reproductive fitness. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198783398.003.0003.

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The harmful impacts of inbreeding are generally greater in species that naturally outbreed compared to those in inbreeding species, greater in stressful than benign environments, greater for fitness than peripheral traits, and greater for total fitness compared to its individual components. Inbreeding reduces survival and reproduction (i.e., it causes inbreeding depression), and thereby increases the risk of extinction. Inbreeding depression is due to increased homozygosity for harmful alleles and at loci exhibiting heterozygote advantage. Natural selection may remove (purge) the alleles that
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31

Parham, Peter, Linda D. Barber, and Steven G. E. Marsh. HLA FactsBook. Elsevier Science & Technology Books, 1999.

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32

Marsh, Steven G. E., Peter Parham, and Linda D. Barber. The HLA FactsBook (Factsbook). Academic Press, 2000.

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33

Bärtsch, Stephan. Development of transgenic Drosophila melanogaster models for studying in vivio and in vitro homologous recombination between duplicated alleles. 1997.

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34

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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35

Harms, Matthew B., and Timothy M. Miller. Amyotrophic Lateral Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0027.

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Recent advances in sequencing technologies have dramatically expanded the number of genes associated with amyotrophic lateral sclerosis, including rare but highly penetrant causative mutations as well as common risk alleles. This chapter discusses these gene discoveries and how they have implicated a diverse array of biological pathways essential for motor neuron health and have begun to inform our understanding of ALS pathogenesis as a heterogeneous and multistep process. Insights from these discoveries are leading to a new generation of targeted therapies directed at specific genes and are p
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36

Burghes, Arthur H. M., and Vicki L. McGovern. Spinal Muscular Atrophy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0034.

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Spinal muscular atrophies affect the lower motor neuron. The most common SMA maps to 5q is an autosomal recessive disorder. SMA is caused by loss or mutation of the SMN1 gene and retention of the SMN2 gene, and these genes lie in a complex area of the genome. Mild missense alleles of SMN1 work to complement SMN2 to give function and therapeutics that restore SMN levels are in clinical testing. Modifiers that lie outside the SMN gene locus and influence severity clearly exist, but what they are remains unknown as do the critical genes affected by SMN deficiency.
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37

Ng, Dominic S. Tangier Disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0035.

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Tangier disease is characterized by profound high-density lipoprotein (HDL) deficiency in association with accumulation of cholesterol esters in tissues, especially those of the reticuloendothelial system. Clinical signs include hyperplastic, yellow-orange colored tonsils, peripheral neuropathies, and hepatosplenomegaly. The disease is caused by two mutant alleles of the ABCA1 gene encoding ATP-binding cassette subfamily A member 1. Despite severe HDL deficiency, predisposition to accelerated coronary heart disease is highly variable in affected individuals. With the exception of tonsillectomy
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38

Renton, Alan E., and Alison M. Goate. Genetics of Dementia. 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/9780190681425.003.0051.

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The genetic architecture of dementia is polygenic and complex, with risk alleles spanning frequency–effect size space. Despite significant progress, most genes influencing these disorders await discovery. Known risk loci implicate perturbed pathways that coalesce around recurring mechanistic themes, notably the autophagosome-lysosome system, the cytoskeleton, endocytosis, innate immunity, lipid metabolism, mitochondria, and the ubiquitin-proteasome system. Phenotypic and pathophysiological pleiotropy suggests some conditions form continuous clinicopathogenetic disease spectra blurring classica
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39

Coles, Alasdair, and Alastair Compston. Multiple sclerosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0016.

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The papers in this chapter illustrate the picture that has emerged of multiple sclerosis as an inflammatory disorder of the central nervous system, caused by a complex interplay of multiple genetic susceptibility alleles and unknown environmental triggers. Multiple sclerosis is a disease in which there is first demyelination of nerves, followed by axonal degeneration. Demyelination is caused by inflammation, as shown by the synthesis of immunoglobulins within the CNS, and magnetic resonance imaging has shown that only the minority of inflammatory lesions cause symptoms. All of these discoverie
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40

Cazeneuve, Cécile, and Alexandra Durr. Genetic and Molecular Studies. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0006.

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Huntington’s disease (HD) is a rare inherited neurologic disorder due to a single mutational mechanism in a large gene (HTT). The mutation is an abnormal CAG repeat expansion, which is translated to a polyglutamine stretch in the huntingtin protein. The growing field of repeat expansion disorders benefits greatly from the lessons learned from the role of the CAG repeat expansion in HD and its resulting phenotype–genotype correlations. The molecular diagnosis can be difficult, and there are some pitfalls for accurate sizing of the CAG repeat, especially in juvenile HD and for intermediate allel
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41

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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42

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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43

Chang, Ellen T., and Hans-Olov Adami. Nasopharyngeal Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676827.003.0008.

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The distinctive global incidence patterns and risk factors for nasopharyngeal carcinoma (NPC) make this a unique malignancy that represents an epidemiologic challenge. NPC is rare throughout most of the world but relatively common in southern China, Southeast Asia, the Arctic, North Africa, and the Middle East. This pattern is determined in part by the geographic and ethnic distribution of established risk factors for NPC, which include early/aberrant Epstein Barr virus infection, Chinese-style salted fish consumption, family history, certain human leukocyte antigen alleles, and tobacco smokin
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44

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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45

Westfall, Nils C., and Charles B. Nemeroff. Child Abuse and Neglect as Risk Factors for Post-Traumatic Stress Disorder. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0025.

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Child abuse and neglect confer substantially increased risks of developing post-traumatic stress disorder (PTSD) for the victims and possibly even their offspring. Furthermore, they are associated with more severe and treatment-resistant PTSD and common comorbid conditions, such as major depressive disorder. This chapter begins by discussing the epidemiology of child abuse, neglect, and maltreatment-associated PTSD to provide a sense of the nature and scope of these major public health problems, then describes the major ways in which child abuse and neglect may contribute to increased liabilit
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46

Simonton, Dean Keith. Spontaneity in Evolution, Learning, Creativity, and Free Will. Edited by Kalina Christoff and Kieran C. R. Fox. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780190464745.013.21.

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This chapter proposes that spontaneous variation has a central role in biological evolution, operant conditioning, creative thinking, and personal agency. But to support these advantageous outcomes, this spontaneity must be joined with some selection process or procedure that decides which alleles, behaviors, ideas, or choices are most adaptive or useful. The argument begins with spontaneous variations in evolutionary theory, and then turns to operant conditioning, with emphasis on the origins of spontaneous behaviors. That analysis leads directly to a discussion that introduces a three-parame
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47

Krause, N., M. Ogasawara, H. Ohno, et al. Cumulenes and Allenes. Georg Thieme Verlag KG, 2008. http://dx.doi.org/10.1055/sos-sd-044-00000.

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48

Glenn, Emmanuel. Alley's World: Let's Go Alley's. blackcomicsstudios llc, 2023.

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49

Les allées du pouvoir. Libre expression, 1985.

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50

Heide, Kurt von der, and Kurt Von Der Heide. Lippisches Allerlei. Books on Demand GmbH, 2014.

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