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Linkage disequilibrium maps and association mapping
Newton E. Morton
Newton E. Morton
Published June 1, 2005
Citation Information: J Clin Invest. 2005;115(6):1425-1430. https://doi.org/10.1172/JCI25032.
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Linkage disequilibrium maps and association mapping

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Abstract

The causal chain between a gene and its effect on disease susceptibility cannot be understood until the effect has been localized in the DNA sequence. Recently, polymorphisms incorporated in the HapMap Project have made linkage disequilibrium (LD) the most powerful tool for localization. The genetics of LD, the maps and databases that it provides, and their use for association mapping, as well as alternative methods for gene localization, are briefly described.

Authors

Newton E. Morton

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Genetic epidemiology of diabetes
M. Alan Permutt, … , Jonathon Wasson, Nancy Cox
M. Alan Permutt, … , Jonathon Wasson, Nancy Cox
Published June 1, 2005
Citation Information: J Clin Invest. 2005;115(6):1431-1439. https://doi.org/10.1172/JCI24758.
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Genetic epidemiology of diabetes

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Abstract

Conventional genetic analysis focuses on the genes that account for specific phenotypes, while traditional epidemiology is more concerned with the environmental causes and risk factors related to traits. Genetic epidemiology is an alliance of the 2 fields that focuses on both genetics, including allelic variants in different populations, and environment, in order to explain exactly how genes convey effects in different environmental contexts and to arrive at a more complete comprehension of the etiology of complex traits. In this review, we discuss the epidemiology of diabetes and the current understanding of the genetic bases of obesity and diabetes and provide suggestions for accelerated accumulation of clinically useful genetic information.

Authors

M. Alan Permutt, Jonathon Wasson, Nancy Cox

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Finding schizophrenia genes
George Kirov, … , Michael C. O’Donovan, Michael J. Owen
George Kirov, … , Michael C. O’Donovan, Michael J. Owen
Published June 1, 2005
Citation Information: J Clin Invest. 2005;115(6):1440-1448. https://doi.org/10.1172/JCI24759.
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Finding schizophrenia genes

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Abstract

Genetic epidemiological studies suggest that individual variation in susceptibility to schizophrenia is largely genetic, reflecting alleles of moderate to small effect in multiple genes. Molecular genetic studies have identified a number of potential regions of linkage and 2 associated chromosomal abnormalities, and accumulating evidence favors several positional candidate genes. These findings are grounds for optimism that insight into genetic factors associated with schizophrenia will help further our understanding of this disease and contribute to the development of new ways to treat it.

Authors

George Kirov, Michael C. O’Donovan, Michael J. Owen

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The genetic epidemiology of neurodegenerative disease
Lars Bertram, Rudolph E. Tanzi
Lars Bertram, Rudolph E. Tanzi
Published June 1, 2005
Citation Information: J Clin Invest. 2005;115(6):1449-1457. https://doi.org/10.1172/JCI24761.
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The genetic epidemiology of neurodegenerative disease

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Abstract

Gene defects play a major role in the pathogenesis of degenerative disorders of the nervous system. In fact, it has been the very knowledge gained from genetic studies that has allowed the elucidation of the molecular mechanisms underlying the etiology and pathogenesis of many neurodegenerative disorders. In this review, we discuss the current status of genetic epidemiology of the most common neurodegenerative diseases: Alzheimer disease, Parkinson disease, Lewy body dementia, frontotemporal dementia, amyotrophic lateral sclerosis, Huntington disease, and prion diseases, with a particular focus on similarities and differences among these syndromes.

Authors

Lars Bertram, Rudolph E. Tanzi

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Learning from failure: congestive heart failure in the postgenomic age
Ivor J. Benjamin, Michael D. Schneider
Ivor J. Benjamin, Michael D. Schneider
Published March 1, 2005
Citation Information: J Clin Invest. 2005;115(3):495-499. https://doi.org/10.1172/JCI24477.
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Learning from failure: congestive heart failure in the postgenomic age

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Abstract

The prognosis of heart failure is worse than that of most cancers, but new therapeutic interventions using stem and other cell-based therapies are succeeding in the fight against it, and old drugs, with new twists, are making a comeback. Genetically engineered animal models are driving insights into the molecular mechanisms that cause hearts to fail, accelerating drug discoveries, and inspiring cell-based therapeutic interventions for both acquired and inheritable cardiac diseases.

Authors

Ivor J. Benjamin, Michael D. Schneider

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Oxygen, oxidative stress, hypoxia, and heart failure
Frank J. Giordano
Frank J. Giordano
Published March 1, 2005
Citation Information: J Clin Invest. 2005;115(3):500-508. https://doi.org/10.1172/JCI24408.
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Oxygen, oxidative stress, hypoxia, and heart failure

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Abstract

A constant supply of oxygen is indispensable for cardiac viability and function. However, the role of oxygen and oxygen-associated processes in the heart is complex, and they and can be either beneficial or contribute to cardiac dysfunction and death. As oxygen is a major determinant of cardiac gene expression, and a critical participant in the formation of ROS and numerous other cellular processes, consideration of its role in the heart is essential in understanding the pathogenesis of cardiac dysfunction.

Authors

Frank J. Giordano

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NO/redox disequilibrium in the failing heart and cardiovascular system
Joshua M. Hare, Jonathan S. Stamler
Joshua M. Hare, Jonathan S. Stamler
Published March 1, 2005
Citation Information: J Clin Invest. 2005;115(3):509-517. https://doi.org/10.1172/JCI24459.
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NO/redox disequilibrium in the failing heart and cardiovascular system

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Abstract

There is growing evidence that the altered production and/or spatiotemporal distribution of reactive oxygen and nitrogen species creates oxidative and/or nitrosative stresses in the failing heart and vascular tree, which contribute to the abnormal cardiac and vascular phenotypes that characterize the failing cardiovascular system. These derangements at the integrated system level can be interpreted at the cellular and molecular levels in terms of adverse effects on signaling elements in the heart, vasculature, and blood that subserve cardiac and vascular homeostasis.

Authors

Joshua M. Hare, Jonathan S. Stamler

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Genetic causes of human heart failure
Hiroyuki Morita, … , Jonathan Seidman, Christine E. Seidman
Hiroyuki Morita, … , Jonathan Seidman, Christine E. Seidman
Published March 1, 2005
Citation Information: J Clin Invest. 2005;115(3):518-526. https://doi.org/10.1172/JCI24351.
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Genetic causes of human heart failure

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Abstract

Factors that render patients with cardiovascular disease at high risk for heart failure remain incompletely defined. Recent insights into molecular genetic causes of myocardial diseases have highlighted the importance of single-gene defects in the pathogenesis of heart failure. Through analyses of the mechanisms by which a mutation selectively perturbs one component of cardiac physiology and triggers cell and molecular responses, studies of human gene mutations provide a window into the complex processes of cardiac remodeling and heart failure. Knowledge gleaned from these studies shows promise for defining novel therapeutic targets for genetic and acquired causes of heart failure.

Authors

Hiroyuki Morita, Jonathan Seidman, Christine E. Seidman

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Protein kinase cascades in the regulation of cardiac hypertrophy
Gerald W. Dorn II, Thomas Force
Gerald W. Dorn II, Thomas Force
Published March 1, 2005
Citation Information: J Clin Invest. 2005;115(3):527-537. https://doi.org/10.1172/JCI24178.
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Protein kinase cascades in the regulation of cardiac hypertrophy

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Abstract

In broad terms, there are 3 types of cardiac hypertrophy: normal growth, growth induced by physical conditioning (i.e., physiologic hypertrophy), and growth induced by pathologic stimuli. Recent evidence suggests that normal and exercise-induced cardiac growth are regulated in large part by the growth hormone/IGF axis via signaling through the PI3K/Akt pathway. In contrast, pathological or reactive cardiac growth is triggered by autocrine and paracrine neurohormonal factors released during biomechanical stress that signal through the Gq/phospholipase C pathway, leading to an increase in cytosolic calcium and activation of PKC. Here we review recent developments in the area of these cardiotrophic kinases, highlighting the utility of animal models that are helping to identify molecular targets in the human condition.

Authors

Gerald W. Dorn II, Thomas Force

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Toward transcriptional therapies for the failing heart: chemical screens to modulate genes
Timothy A. McKinsey, Eric N. Olson
Timothy A. McKinsey, Eric N. Olson
Published March 1, 2005
Citation Information: J Clin Invest. 2005;115(3):538-546. https://doi.org/10.1172/JCI24144.
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Toward transcriptional therapies for the failing heart: chemical screens to modulate genes

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Abstract

In response to acute and chronic stresses, the heart frequently undergoes a remodeling process that is accompanied by myocyte hypertrophy, impaired contractility, and pump failure, often culminating in sudden death. The existence of redundant signaling pathways that trigger heart failure poses challenges for therapeutic intervention. Cardiac remodeling is associated with the activation of a pathological gene program that weakens cardiac performance. Thus, targeting the disease process at the level of gene expression represents a potentially powerful therapeutic approach. In this review, we describe strategies for normalizing gene expression in the failing heart with small molecules that control signal transduction pathways directed at transcription factors and associated chromatin-modifying enzymes.

Authors

Timothy A. McKinsey, Eric N. Olson

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