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Books on the topic 'Diseases - genetic mapping'

Author: Grafiati
Published: 4 June 2021
Last updated: 17 February 2022

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1

S, Rajadhyaksha Medha, ed. New biology and genetic diseases. New Delhi: Oxford University Press, 1999.

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2

1939-, Read Andrew P., ed. Molecular basis of inherited disease. 2nd ed. Oxford: IRL Press at Oxford University Press, 1992.

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3

Davies, K. E. Molecular basis of inherited disease. Oxford: IRL Press, 1988.

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4

Mastro, Richard Giulio Del. The human genome: Mapping the X-chromosome and the molecular analysis of selected genetic diseases. Birmingham: University of Birmingham, 1991.

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5

E, Lindsten Jan, Pettersson Ulf, Nobelstiftelsen, and Alfred Nobel's Björkborn Foundation, eds. Etiology of human disease at the DNA level. New York: Raven Press, 1991.

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6

1950-, Waldholz Michael, ed. Genome: The story of the most astonishing scientific adventure of our time--the attempt to map all the genes in the human body. New York, N.Y: Simon and Schuster, 1990.

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7

Bishop, Jerry E. Genome: The story of the most astonishing scientific adventure of our time--the attempt to map all the genes in the human body. New York, N.Y: Simon and Schuster, 1990.

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8

Bishop, Jerry E. Genome: The story of the most astonishing scientific adventure of our time, the attempt to map all the genes in the human body. New York: Open Road Integrated Media, 2014.

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9

Wexler, Alice. Mapping fate: A memoir of family, risk, and genetic research. Berkeley: University of California Press, 1995.

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10

Mapping fate: A memoir of family, risk, and genetic research. New York: Times Books, 1995.

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11

Baruah, Dhani Ram. It was a distant dream now it is the reality in the entire planet of diseased and unhealthy human genome. Sonapur, Assam: Dr. Dhani Ram Baruah Heart City & City of Human Genome, The Institute of Applied Human Genetic Engineering, 2010.

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12

Investigating the human genome: Insights into human variation and disease susceptibility. Upper Saddle River, N.J: Pearson Education, 2011.

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13

Ivar-Harry, Pawlowitzki, Edwards J. H, and Thompson E. A. 1949-, eds. Genetic mapping of disease genes. San Diego: Academic Press, 1997.

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14

1957-, Haines Jonathan L., and Pericak-Vance Margaret Ann, eds. Genetic analysis of complex diseases. 2nd ed. New York, NY: Wiley-Liss, 2006.

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15

1957-, Haines Jonathan L., and Pericak-Vance Margaret Ann, eds. Approaches to gene mapping in complex human diseases. New York: Wiley-Liss, 1998.

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16

Massoudi, Mojtaba. Genetic mapping of pepper, Capsicum annuum L., and identification of markers linked to Phytophthora root rot resistance (Phytophthora capsici). 1996.

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17

Massoudi, Mojtaba. Genetic mapping of pepper, Capsicum annuum L., and identification of markers linked to Phytophthora root rot resistance (Phytophthora capsici). 1996.

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18

Read, Andrew, and K. E. Davies. Molecular Basis of Inherited Disease: In Focus. Oxford University Press, USA, 1989.

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19

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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20

Multipoint Mapping & Linkage Based Upon Affect Pedigree Mem. John Wiley & Sons, 1990.

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21

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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22

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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23

Introduction to human biochemical and molecular genetics. New York: McGraw-Hill, Health Professions Division, 1990.

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24

Yang, Hai-Tao. Genetic Analysis of Autoimmune Diseases Using Animal Models: Mapping Susceptibility Genes for Multiple Sclerosis and Rheumatoid Arthritis (Comprehensive Summaries of Uppsala Dissertations, 927). Uppsala Universitet, 2001.

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25

Genome: The Story of the Most Astonishing Scientific Adventure of Our Time. iUniverse, 1999.

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26

Toojinda, Theeryut. Mapping and introgression of disease resistance genes in barley (Hordeum vulgare L.). 1998.

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27

Appasani, Krishnarao. Optogenetics: From Neuronal Function to Mapping and Disease Biology. Cambridge University Press, 2017.

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28

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

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29

Between the Lines of Genetic Code: Genetic Interactions in Understanding Disease and Complex Phenotypes. Elsevier Science & Technology Books, 2013.

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30

Mapping Fate: A Memoir of Family, Risk, and Genetic Research. University of California Press, 1996.

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31

Maya, Pines, and Howard Hughes Medical Institute, eds. The genes we share with yeast, flies, worms, and mice: New clues to human health and disease. Chevy Chase, Md: Howard Hughes Medical Institute, 2001.

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32

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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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, PTPN22. Major breakthroughs in high-throughput genotyping and systematic discovery and mapping of hundreds of thousands of single nucleotide polymorphisms (SNPs) led to large-scale genome-wide association studies used for the first time for RA in 2007. This approach has had a dramatic impact on our knowledge of the susceptibility loci for RA, such that over 60 risk variants have now been robustly identified. We present an overview of these studies and the loci that have been identified. We consider how this knowledge is contributing to a greater understanding of the aetiology and pathology of the disease and in turn how this can influence management of patients presenting with an inflammatory arthritis. We consider some of the unanswered questions and the approaches that will need to be taken to address them.
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33

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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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, PTPN22. Major breakthroughs in high-throughput genotyping, and systematic discovery and mapping of hundreds of thousands of single nucleotide polymorphisms (SNPs) led to large-scale genome-wide association studies used for the first time for RA in 2007. Widespread utilization of this approach has had a dramatic impact on our knowledge of the susceptibility loci for RA, such that over 100 risk variants have now been robustly identified. We present an overview of these studies and the loci that have been identified. We consider how this knowledge is contributing to a greater understanding of the aetiology and pathology of the disease, and in turn how this can influence management of patients presenting with an inflammatory arthritis. We consider some of the unanswered questions and the approaches that will need to be taken to address them.
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34

Editor), Jeffrey Hoone (Designer, and Gary Schneider (Photographer), eds. Genetic Self-Portrait. Light Work, 1999.

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35

Sakr, Bouazza. Inheritance and linkage of genetic markers and resistance to Ascochyta blight in lentil. 1994.

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36

1942-, Canter Charles R., ed. Biotechnology and human genetic predisposition to disease: Proceedings of a UCLA symposium held at Steamboat Springs, Colorado, March 27-April 3, 1989. New York: Wiley-Liss, 1990.

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37

News, PM Medical Health. 21st Century Complete Guide to Human Genome Research: Genetic Mapping, DNA Sequencing, Chromosomes, Bioethics, Tools and Techniques, Gene Variations and Disease. Progressive Management, 2002.

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38

Cantor, Charles R. Biotechnology and Human Genetic Predisposition to Disease: Proceedings of a UCLA Symposium Held at Steamboat Springs, Colorado, March 27-April 3, 19 (UCLA ... Molecular and Cellular Biology, New Series). Wiley-Liss, 1990.

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39

E, Davies K., and Tilghman Shirley M, eds. Genome maps and neurological disorders. Plainview, N.Y: Cold Spring Harbor Laboratory Press, 1993.

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40

Bass, Cristina, Barbara Bauce, and Gaetano Thiene. Arrhythmogenic right ventricular cardiomyopathy: diagnosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0360.

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Arrhythmogenic cardiomyopathy is a heart muscle disease clinically characterized by life-threatening ventricular arrhythmias and pathologically by an acquired and progressive dystrophy of the ventricular myocardium with fibrofatty replacement. The clinical manifestations of arrhythmogenic cardiomyopathy vary according to the ‘phenotypic’ stage of the underlying disease process. Since there is no ‘gold standard’ to reach the diagnosis of arrhythmogenic cardiomyopathy, multiple categories of diagnostic information have been combined. Different diagnostic categories include right ventricular morphofunctional abnormalities (by echocardiography and/or angiography and/or cardiovascular magnetic resonance imaging), histopathological features on endomyocardial biopsy, electrocardiogram, arrhythmias, and family history, including genetics. The diagnostic criteria were revised in 2010 to improve diagnostic sensitivity, but with the important prerequisite of maintaining diagnostic specificity. Quantitative parameters have been put forward and abnormalities are defined based on the comparison with normal subject data. A definite diagnosis of arrhythmogenic cardiomyopathy is achieved when two major, or one major and two minor, or four minor criteria from different categories are met. The main differential diagnoses are idiopathic right ventricular outflow tract tachycardia, myocarditis, sarcoidosis, dilated cardiomyopathy, right ventricular infarction, congenital heart diseases with right ventricular overload, and athlete’s heart. Among diagnostic tools, contrast-enhanced cardiovascular magnetic resonance is playing a major role in detecting subepicardial-midmural left ventricular free wall involvement, even preceding morphofunctional abnormalities. Moreover, electroanatomical mapping is an invasive tool able to detect early right ventricular free wall involvement in terms of low-voltage areas. Both techniques are increasingly used in the diagnostic work-up although are not yet part of diagnostic criteria.
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41

Benarroch, Eduardo E. Neuroscience for Clinicians. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.001.0001.

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The aim of this book is to provide the clinician with a comprehensive and clinical relevant survey of emerging concepts on the organization and function of the nervous system and neurologic disease mechanisms, at the molecular, cellular, and system levels. The content of is based on the review of information obtained from recent advances in genetic, molecular, and cell biology techniques; electrophysiological recordings; brain mapping; and mouse models, emphasizing the clinical and possible therapeutic implications. Many chapters of this book contain information that will be relevant not only to clinical neurologists but also to psychiatrists and physical therapists. The scope includes the mechanisms and abnormalities of DNA/RNA metabolism, proteostasis, vesicular biogenesis, and axonal transport and mechanisms of neurodegeneration; the role of the mitochondria in cell function and death mechanisms; ion channels, neurotransmission and mechanisms of channelopathies and synaptopathies; the functions of astrocytes, oligodendrocytes, and microglia and their involvement in disease; the local circuits and synaptic interactions at the level of the cerebral cortex, thalamus, basal ganglia, cerebellum, brainstem, and spinal cord transmission regulating sensory processing, behavioral state, and motor functions; the peripheral and central mechanisms of pain and homeostasis; and networks involved in emotion, memory, language, and executive function.
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42

Snyder, Michael. Genomics and Personalized Medicine. Oxford University Press, 2016. http://dx.doi.org/10.1093/wentk/9780190234775.001.0001.

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In 2001 the Human Genome Project succeeded in mapping the DNA of humans. This landmark accomplishment launched the field of genomics, the integrated study of all the genes in the human body and the related biomedical interventions that can be tailored to benefit a person's health. Today genomics, part of a larger movement toward personalized medicine, is poised to revolutionize health care. By cross-referencing an individual's genetic sequence -- their genome -- against known elements of "Big Data," elements of genomics are already being incorporated on a widespread basis, including prenatal disease screening and targeted cancer treatments. With more innovations soon to arrive at the bedside, the promise of the genomics revolution is limitless. This entry in the What Everyone Needs to Know series offers an authoritative resource on the prospects and realities of genomics and personalized medicine. As this science continues to alter traditional medical paradigms, consumers are faced with additional options and more complicated decisions regarding their health care. This book provides the essential information everyone needs.
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43

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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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 model for ASD. Studies in the animal models have provided breakthrough insights into the pathophysiology of FXS that have led to novel therapeutic targets for its core deficits (e.g., mGluR theory of fragile X). Yet recent clinical trials of both GABA-B agonist and mGluR5 antagonist revealed a lack of specific and sensitive outcome measures capturing the full range of improvements of patients with FXS. Recent research shows promise for the mapping of the multitude of genetic variants in ASD onto shared pathways with FXS. Nonetheless, in light of the huge level of locus heterogeneity in ASD, further effort in finding convergence in specific molecular pathways and reliable biomarkers is required in order to perform targeted treatment trials with sufficient sample size. This chapter focuses on the neurobehavioral phenotype caused by a full-mutation of the FMR1 gene, namely FXS, and the neurobiology of this disorder of relevance to the targeted molecular treatments of its core symptoms.
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44

1961-, Pujol Ernesto, Light Work (Organization : Syracuse, N.Y.), Robert B. Menschel Photography Gallery., and Visual AIDS (Organization), eds. Desire: Contemporary photography from the Visual AIDS Archive Project. Syracuse, N.Y: Light Work, 1999.

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