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Libros sobre el tema "Alleles"

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Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 5 de marzo de 2023

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1

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

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2

Logan, Angela Berti. Characterization of new alleles of PHO85, a cyclin-dependent kinase of Saccharomyces cerevisiae. Ottawa: 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. Sudbury, Ont: 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. Birmingham: University of Birmingham, 1994.

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5

Comment, Bernard. Allées et venues. [Paris]: C. Bourgois, 1992.

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6

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

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7

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

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8

Baudouin, Denis. Dans les allées du pouvoir. [Paris]: J.C. Lattès, 1990.

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9

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

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10

Tamer, Ulkü. Alleben öyküleri. Istanbul: Can, 1991.

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11

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

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12

Les allées du bois de Boulogne. Paris: Presses de la Cité, 1985.

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13

Sŏul, kolmokkil pʻunggyŏng. Kyŏnggi-do Pʻaju-si: Buk Hausŭ, 2006.

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14

Taber, A. M. Allenovye uglevodorody: Poluchenie, svoĭstva, primenenie. Moskva: "Nauka", 1987.

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15

Van Allen's ecstasy. Maple Shade, N.J: Lethe Press, 2010.

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16

Allen, Jeffrey G. Jeff Allen's best. New York: J. Wiley, 1990.

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17

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

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18

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

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19

Van Allen's ecstasy. New York: Southern Tier Editions, Harrington Park Press, 2004.

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20

Office, General Accounting. Alleged materiel disposal. Washington, D.C: The Office, 1993.

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21

Office, General Accounting. Alleged materiel disposal. Washington, D.C: The Office, 1993.

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22

N, Cox Arthur, ed. Allen's astrophysical quantities. 4a ed. New York: AIP Press, 2000.

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23

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

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24

Tushinski, Jim. Van Allen's ecstasy. Maple Shade, N.J: Lethe Press, 2010.

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25

Allen, Jeffrey G. Jeff Allen's best. New York: Wiley, 1990.

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26

Tushinski, Jim. Van Allen's ecstasy. Maple Shade, N.J: Lethe Press, 2010.

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27

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

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28

Claude, Masset, Soulier Philippe, Musée archéologique départemental du Val-d'Oise. y Musée de préhistoire d'Ile-de-France, eds. Allées couvertes et autres monuments funéraires du néolithique dans la France du Nord-Ouest: Allées sans retour. Paris: Errance, 1995.

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29

Balbachan, Eduardo Luis. Los ignorados pasajes de Buenos Aires. Bs. As. [i. e. Buenos Aires]: Corregidor, 2010.

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30

Liu, Yue. Beijing hu tong 66. 8a ed. Beijing Shi: Zhong gong dang shi chu ban she, 2009.

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31

Bei jing hu tong. Beijing Shi: Dang dai Zhongguo chu ban she, 2008.

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32

Ma, Ling. Beijing hu tong. Beijing Shi: Shi jie zhi shi chu ban she, 2011.

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33

Beijing Shi gui hua wei yuan hui. Beijing jiu cheng hu tong shi lu. 8a ed. Beijing: Zhongguo jian zhu gong ye chu ban she, 2008.

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34

Beijing hu tong: Hutong in Beijing. Hefei: Huang shan shu she, 2011.

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35

Qingdao lao cheng de jie dao yu sheng huo. Nanjing Shi: Dong nan da xue chu ban she, 2012.

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36

Zhang, Xichang. Shuo nong. 8a ed. Jinan Shi: Shandong hua bao chu ban she, 2005.

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37

1838-1927, Allebé August, Loos Wiepke, Tuyll van Serooskerken, Carel van., Teylers Museum, Dordrechts Museum y Provinciaal Museum van Drenthe, eds. Waarde heer Allebé: Leven en werk van August Allebé, 1838-1927. Zwolle: Waanders, 1988.

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38

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

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39

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

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40

Walsh, Bruce y 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 effects. For a large number of loci, the amount of change can be predicted from the Bulmer equation, the analog of the breeder's equation, but now for the change in the variance. Upon cessation of selection, any disequilibrium decays away, and the variances revert back to their additive-genic variances (the additive variance in the absence of disequilibrium). Assortative mating also generates such disequilibrium.
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41

Walsh, Bruce y 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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42

Turner, Neil, Teena Tandon y Rajiv Agarwal. APOL1 and renal disease. Editado por 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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43

Walsh, Bruce y 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: the decline in mean population fitness generated by deleterious mutations is largely independent of their selective effects, but instead is simply a function of their mutation rate.
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44

Frankham, Richard, Jonathan D. Ballou, Katherine Ralls, Mark D. B. Eldridge, Michele R. Dudash, Charles B. Fenster, Robert C. Lacy y Paul Sunnucks. 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 cause inbreeding depression, especially following inbreeding or population bottlenecks, but it has limited effects in small populations and usually does not completely eliminate inbreeding depression. Inbreeding depression is nearly universal in sexually reproducing organisms that are diploid or have higher ploidies.
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45

Haiman, Christopher y 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 reviews the epidemiologic study designs that can be helpful in identifying low-risk alleles in candidate gene and genome-wide association studies, as well as gene–environment interactions. Finally, it describes some of the genotyping and sequencing platforms commonly employed for high-throughput genome analysis, and the concept of Mendelian randomization and how it may be useful in the study of biomarkers and environmental causes of cancer.
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46

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

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47

The HLA FactsBook (Factsbook). Academic Press, 2000.

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48

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

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49

Harms, Matthew B. y 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 poised to inform how patients with amyotrophic lateral sclerosis are evaluated and treated in the clinic.
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50

Burghes, Arthur H. M. y 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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