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Libri sul tema "Locusts Genetics"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 6 febbraio 2022

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1

Edwards, Sara Joanne. Genetic analysis of the Treacher Collins syndrome locus. Manchester: University of Manchester, 1995.

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2

Gladwin, Amanda Jane. The molecular genetic analysis of the Treacher Collins syndrome locus. Manchester: University of Manchester, 1996.

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3

Perveen, Rahat. Genetic and physical mapping around the Treacher Collins syndrome locus. Manchester: University of Manchester, 1994.

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4

Heather, Lisa Jane. Physical and genetic mapping around a candidate locus for orofacial clefting. Manchester: University of Manchester, 1994.

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5

Plätke, Rosemarie. Die Entstehung von Supergenen in unterteilten Populationen: Ein theoretischer Ansatz anhand eines Zwei-Locus-Modells. Krefeld: Marchal und Matzenbacher, 1986.

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6

Miller, Carey S. Molecular genetic studies of the cytochrome f locus in Vicia faba L. Ottawa: National Library of Canada, 1990.

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7

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. Manchester: University of Manchester, 1995.

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8

O'Brien, Stephen J. Genetic Maps: Locus Maps of Complex Genomes (Genetic Maps) (Genetic Maps). 5th ed. Cold Spring Harbor Laboratory Press, 1990.

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9

Walsh, Bruce, and Michael Lynch. The Population Genetics of Selection. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198830870.003.0005.

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Abstract (sommario):

This chapter examines models of one- and two-locus selection in the absence of drift and mutation. Expressions for the per-generation rate of allele-frequency change and the expected time for a specified amount of change are developed for single-locus models, and their equilibrium structure is examined for those settings where selection retains more than one allele. The presence of selection-generated linkage disequilibrium greatly complicates the extension of single-locus results to two loci, and the chapter examines some of the resulting complications. Finally, it examines the nature of sele

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10

Iyamabo, Odianosen E. Effects of selection, recombination and plot type on phenotypic and quantitative trait locus analyses in barley (Hordeum vulgare L.). 1993.

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11

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

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Abstract (sommario):

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,

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12

Eyre, Steve, Jane Worthington, and 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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Abstract (sommario):

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,

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13

J, O'Brien Stephen, ed. Genetic maps: Locus maps of complex genomes. 5th ed. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory, 1990.

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14

Genetic maps: Locus maps of complex genomes. 6th ed. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 1993.

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15

O'Brien, Stephen J. Genetic Maps: Locus Maps of Complex Genomes. 6th ed. Cold Spring Harbor Laboratory Press, 1993.

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16

J, O'Brien Stephen, and Cold Spring Harbor Laboratory, eds. Genetic maps: Locus maps of complex genomes. 5th ed. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 1990.

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17

Jeter, John Mark. Molecular analysis of the nar1 locus in barley. 1987.

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18

O'Brien, Stephen J. Genetic Maps: Locus Maps of Complex Genomes : Book 6 : Plants (Genetic Maps Book 6) (Genetic Maps Book 6). 6th ed. Cold Spring Harbor Laboratory Pr, 1993.

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19

Blech-Hermoni, Yotam N. Studies on a conserved genetic locus for chronic pain. 2006.

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20

O'Brien, Stephen J. Genetic Maps: Locus Maps of Complex Genomes : Book 4 Nonhuman Vertebrates (Genetic Maps Book 4) (Genetic Maps Book 4). 6th ed. Cold Spring Harbor Laboratory Pr, 1993.

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21

O'Brien, Stephen J. Genetic Maps: Locus Maps of Complex Genomes : Book 3 : Lower Eukaryotes (Genetic Maps Book 3) (Genetic Maps Book 3). 6th ed. Cold Spring Harbor Laboratory Pr, 1993.

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22

O'Brien, Stephen J. Genetic Maps: Locus Maps of Complex Genomes : Book 2 : Bacteria, Algae, and Protozoa (Genetic Maps Book 2) (Genetic Maps Book 2). 6th ed. Cold Spring Harbor Laboratory Pr, 1993.

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23

O'Brien, Stephen J. Genetic Maps: Locus Maps of Complex Genomes : Bacteria, Algae, and Protozoa, Book 2 (Genetic Maps Book 2) (Genetic Maps Book 2). 5th ed. Cold Spring Harbor Laboratory Press, 1990.

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24

Traore, Abdoulaye. Quantitative trait locus mapping of yield and yield components in barley (Hordeum vulgare L.). 1993.

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25

Pavlus, Janice Elaine. Characterization of two lethal mutations induced by chromosomal rearrangements involving the 4f-rnp locus of Drosophila melanogaster. 1996.

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26

Price, Susan. Genetic bone and joint disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0276.

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Abstract (sommario):

Genetic conditions affecting the skeleton and supporting structures are individually rare and heterogeneous. This chapter presents an approach to assessing patients with suspected skeletal dysplasia, osteogenesis imperfecta, Marfan syndrome, and Ehlers–Danlos syndrome. Skeletal dysplasias are caused by abnormalities of bone growth and modelling; the commonest non-lethal type is achondroplasia, with an incidence of 1/10 000 to 1/30 000. The typical presentation of osteogenesis imperfecta is with multiple fractures, sometimes prenatally. There may be associated short stature, bone deformity, den

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27

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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Abstract (sommario):

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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28

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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Abstract (sommario):

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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29

Serres, F. J. De. Utilization of Mammalian Specific Locus Studies in Hazard Evaluation and Estimation of Genetic Risk. Springer, 2011.

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30

Ivakine, Evgueni. Genetic and molecular analysis of the insulin dependent diabetes 4 locus in the NOD mouse. 2004.

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31

Zhang, Yuan-Ming, Zhenyu Jia, and Jim M. Dunwell, eds. The Applications of New Multi-Locus GWAS Methodologies in the Genetic Dissection of Complex Traits. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88945-834-9.

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32

Popovic, Maja. Genetic and physical mapping of the Shwachman-Diamond syndrome locus at the pericentromeric region of chromosome 7. 2003.

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33

A Review of the Genetics of Alcoholism and a Confirmatory Study of an Acute Alcohol Withdrawal Quantitative Trait Locus in Mice. Storming Media, 1999.

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34

Poel, Sheryl Ziemin Van der. Identification of a tumor suppressor gene locus by recognition of interferon gene deletions within human chromosome band 9P22 in human leukemias and identification and isolation of sequences which recognize a previously undiscovered gene MLL, whose transcripts span the human chromosome band 11Q23 translocation breakpoint junctions in human leukemia and whose sequences share homology with the Drosophila trithorax regulatory gene. 1993.

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35

Grams, Morgan E., and Josef Coresh. Chronic kidney disease in the developed world. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0095.

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Abstract (sommario):

Chronic kidney disease is common, increasing in prevalence, and associated with significant morbidity and mortality. A disease of multiple and complex aetiologies, chronic kidney disease is more prevalent among elderly, hypertensive, and diabetic persons—all growing segments of the developed world. This chapter discusses trends in and determinants of chronic kidney disease prevalence, incidence, and prognosis. In addition, advances in chronic kidney disease staging and reporting as well as the discovery of a major genetic locus for hypertensive kidney disease in populations of African ancestry

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36

Aikhenvald, Alexandra Y. Polysynthetic Structures of Lowland Amazonia. Edited by Michael Fortescue, Marianne Mithun, and Nicholas Evans. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780199683208.013.18.

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Abstract (sommario):

Lowland Amazonia is the locus of substantial linguistic diversity in terms of genetic affiliation, language structure, and numbers of languages. This chapter will focus on the distribution of types of polysynthetic patterns within Lowland Amazonia, with special attention to the spread, and the types, of noun incorporation. The highest concentration of polysynthetic languages in Amazonia is the region south of the Amazon River, spanning adjacent regions of Peru, Brazil, and Bolivia. Polysynthetic patterns can be reconstructed for the protolanguages of some families, such as Panoan, Harakmbet, a

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37

Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0064_update_001.

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Abstract (sommario):

It has been clear for several decades from comparison with the rodent model disease Heymann nephritis that membranous glomerulonephritis (MGN) is an immune condition in which antibodies, usually autoantibodies, bind to targets on the surface of podocytes. However, the antigen in Heymann nephritis, megalin, is not present on human podocytes. The first potential antigen was identified by studying rare examples of maternal alloimmunization, leading to congenital membranous nephropathy in the infant caused by antibodies to neutral endopeptidase. More recently, the target of autoantibody formation

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38

Budimirovic, Dejan B., and Megha Subramanian. Neurobiology of Autism and Intellectual Disability. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0052.

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Abstract (sommario):

Fragile X syndrome (FXS) is a neurodevelopmental disorder that manifests with a range of cognitive, behavioral, and social impairments. It is a monogenetic disease caused by silencing of the FMR1 gene, in contrast to autism spectrum disorder (ASD) that is a behaviorally-defined set of complex disorders. Because ASD is a major and growing public health concern, current research is focused on identifying common therapeutic targets among patients with different molecular etiologies. Due to the prevalence of ASD in FXS and its shared neurophysiology with ASD, FXS has been extensively studied as a

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39

(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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40

Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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