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Books on the topic 'Genomic search'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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1

Ahmed, Tariq. Search for RAS-like genes in the C.albicans genome. Manchester: UMIST, 1995.

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2

Dr. B.P. Pal Birth Centenary Symposium (2006 National Academy of Agricultural Sciences). Search for new genes. Edited by Pal B. P. 1906-1989, Chopra V. L, and National Academy of Agricultural Sciences. New Delhi: Academic Foundation in association with National Academy of Agricultural Sciences, 2007.

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3

Dr. B.P. Pal Birth Centenary Symposium (2006 National Academy of Agricultural Sciences). Search for new genes. Edited by Chopra V. L, Pal B. P. 1906-1989, and National Academy of Agricultural Sciences. New Delhi: Academic Foundation in association with National Academy of Agricultural Sciences, 2007.

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4

Tanzi, Rudolph E. Decoding darkness: The search for the genetic causes of Alzheimer's disease. Cambridge, Mass: Perseus Publishing, 2000.

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5

Tanzi, Rudolph E. Decoding darkness: The search for the genetic causes of Alzheimer's disease. Cambridge, Mass: Perseus Pub., 2000.

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6

B, Parson Ann, ed. Decoding darkness: The search for the genetic causes of Alzheimer's disease. Cambridge, Mass: Perseus Publ., 2000.

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7

Neanderthal Man In Search Of Lost Genomes. Basic Books, 2013.

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8

Pääbo, Svante. Neanderthal Man: In Search of Lost Genomes. 2016.

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9

Walsh, Bruce, and Michael Lynch. Using Molecular Data to Detect Selection: Signatures from Multiple Historical Events. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198830870.003.0010.

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This chapter examines the search for a pattern of repetitive adaptive substitutions over evolutionary time. In contrast with the previous chapter, only a modest number of tests toward this aim have been proposed. The HKA and McDonald-Kreitman tests contrast the polymorphism to divergence ratio between different genomic classes (such as different genes or silent versus replacement sites within the same gene). These approaches can detect an excess of substitutions, which allows one to estimate the fraction of adaptive sites. This chapter reviews the empirical data on estimates of this fraction and discusses some of the sources of bias it its estimation. Over an even longer time scale, one can contrast the rate of change of sites in a sequence over a phylogeny. These tests require a rather special type of selection, wherein the same specific site (usually a codon) experiences multiple adaptive substitutions over a phylogeny, such as might occur in arms-race genes.
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10

(Editor), V. L. Chopra, R. P. Sharma (Editor), S. R. Bhat (Editor), and B. M. Prasanna (Editor), eds. Search for New Genes. Academic Foundation, 2007.

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11

Wang, Jason T. L., Bruce A. Shapiro, and Dennis Shasha, eds. Pattern Discovery in Biomolecular Data. Oxford University Press, 1999. http://dx.doi.org/10.1093/oso/9780195119404.001.0001.

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Finding patterns in biomolecular data, particularly in DNA and RNA, is at the center of modern biological research. These data are complex and growing rapidly, so the search for patterns requires increasingly sophisticated computer methods. Pattern Discovery in Biomolecular Data provides a clear, up-to-date summary of the principal techniques. Each chapter is self-contained, and the techniques are drawn from many fields, including graph theory, information theory, statistics, genetic algorithms, computer visualization, and vision. Since pattern searches often benefit from multiple approaches, the book presents methods in their purest form so that readers can best choose the method or combination that fits their needs. The chapters focus on finding patterns in DNA, RNA, and protein sequences, finding patterns in 2D and 3D structures, and choosing system components. This volume will be invaluable for all workers in genomics and genetic analysis, and others whose research requires biocomputing.
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12

FUQUA, JAKOB. IN SEARCH OF THE SPIRITUAL GENOME: THE COMPLETE BLUEPRINT OF MAN. 1st Books Library, 2004.

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13

Sex Itself: The Search for Male and Female in the Human Genome. University of Chicago Press, 2013.

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14

Richardson, Sarah S. Sex Itself: The Search for Male and Female in the Human Genome. University of Chicago Press, 2015.

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15

Canli, Turhan. Is Depression an Infectious Disease? Edited by Turhan Canli. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.28.

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In molecular psychology, the tools of molecular biology and genomics are applied to study and better understand behavior. In this chapter, the author applies this approach to present a novel perspective on major depressive disorder (MDD). The treatment approach for MDD has not changed much in half a century, and—in general—today’s treatments are not more effective than earlier ones. The author suggests a new approach, one that conceptualizes MDD as an infectious disease. The author presents a set of four clues that are consistent with such a claim and lays out a molecular approach to how a search for a disease-causing agent could be conducted.
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16

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 subtype-specific associations are emerging. These risk loci now need to be investigated further using fine-mapping strategies and then appropriate functional studies to show how the variant alters the gene function. This knowledge will not only lead to a better understanding of disease pathogenesis for juvenile rheumatic diseases but may also aid in the classification of these heterogeneous diseases. It may identify new pathways for potential therapeutic targets and help in the prediction of disease outcome and response to treatment.
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17

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 subtype-specific associations are emerging. These risk loci now need to be investigated further using fine-mapping strategies and then appropriate functional studies to show how the variant alters the gene function. This knowledge will not only lead to a better understanding of disease pathogenesis for juvenile rheumatic diseases but may also aid in the classification of these heterogeneous diseases. It may identify new pathways for potential therapeutic targets and help in the prediction of disease outcome and response to treatment.
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18

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 concludes by summarizing considerations for the field as it continues to move forward, and discusses exciting new developments in the search for genetic markers for PTSD.
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19

Comfort, Nathaniel C. The Tangled Field: Barbara McClintock's Search for the Patterns of Genetic Control. Harvard University Press, 2003.

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20

The Tangled Field : Barbara McClintock's Search for the Patterns of Genetic Control. Harvard University Press, 2001.

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21

Tanzi, Rudolph E., Rudolph Tanzi, and Ann B. Parson. Decoding Darkness: The Search for the Genetic Causes of Alzheimer's Disease. Basic Books, 2001.

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22

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 further using fine-mapping strategies and then appropriate functional studies to show how the variant alters the gene function. This knowledge will not only lead to a better understanding of disease pathogenesis for juvenile rheumatic diseases but may also aid in the classification of these heterogeneous diseases. It may identify new pathways for potential therapeutic targets and help in the prediction of disease outcome and response to treatment.
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23

Molecular Diagnostics and Biological Safety 2021. COVID-19: Epidemiology, Diagnosis and Prophylaxis: Conference Abstracts. Central Research Institute for Epidemiology, 2021. http://dx.doi.org/10.36233/978-5-6045286-2-4.

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The pandemic of the new coronavirus infection has spread to more than 200 countries. To date, over 130 million people have been affected and over 2.8 million have died. COVID-19 infection has a number of specific epidemiological and clinical features. In severe cases of the disease, acute respiratory distress syndrome develops, which is often fatal. The SARS-CoV-2 virus is susceptible to mutations, which alarms the scientific community all over the world. Therefore, scientific research in the field of COVID-19, the search for new diagnostic tools, methods for nonspecific and specific prevention and treatment are central topics today.This collection contains abstracts submitted by leading experts in the field of epidemiology, clinics of infectious diseases, molecular diagnostics, young researchers and medical practitioners. Published materials contain data on the methods of molecular diagnostics of COVID-19, se-quencing of the SARS-CoV-2 genome, epidemiology of new coronavirus infection, immuno-pathogenesis of COVID-19, clinical features of infection and treatment options, as well as the study of post-infectious and post-vaccination immunity and examples of complex measures for nonspecific prevention of COVID-19.The materials of the Congress are of interest to doctors and researchers of all specialties, teachers of secondary and higher educational institutions.
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