Research Topics
Species | TIMOTHY MARK OLSONSummaryAffiliation: Mayo Clinic Country: USA Publications
Research Grants
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Publications
Histoplasmosis infection in patients with rheumatoid arthritis, 1998-2009Timothy C Olson
Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
BMC Infect Dis 11:145. 2011..Patients with rheumatic diseases including rheumatoid arthritis (RA) are at increased risk for infections related to both the disease and its treatments. These include uncommonly reported infections due to histoplasmosis...- Human K(ATP) channelopathies: diseases of metabolic homeostasisTimothy M Olson
Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
Pflugers Arch 460:295-306. 2010..Thus, advances in molecular medicine in the emerging field of human KATP channelopathies offer new opportunities for targeted individualized screening, early diagnosis, and tailored therapy... - KATP channel mutation confers risk for vein of Marshall adrenergic atrial fibrillationTimothy M Olson
Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
Nat Clin Pract Cardiovasc Med 4:110-6. 2007..In the absence of traditional risk factors for disease, a genetic defect in electrical homeostasis underlying stress-induced AF was explored... 
What makes the heart fail? New insights from defective genesTimothy M Olson
Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
Acta Paediatr Suppl 95:17-21. 2006..CONCLUSION: Collectively, family-based studies of DCM provide the rationale for clinical screening in first-degree relatives, regardless of family history or age of the index case...- Sodium channel mutations and susceptibility to heart failure and atrial fibrillationTimothy M Olson
Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minn 55905, USA
JAMA 293:447-54. 2005..Recently, genetic defects in calcium and potassium regulation have been discovered in patients with DCM, implicating an alternative disease mechanism. The full spectrum of genetic defects in DCM, however, has not been established... - Inherited and de novo mutations in the cardiac actin gene cause hypertrophic cardiomyopathyT M Olson
Department of Pediatrics, Division of Pediatric Cardiology, Salt Lake City, UT 84113, USA
J Mol Cell Cardiol 32:1687-94. 2000..These findings support the hypothesis that a single amino acid substitution in actin causes either congestive heart failure or maladaptive cardiac hypertrophy, depending on its effect on actin structure and function... - Mutations that alter the surface charge of alpha-tropomyosin are associated with dilated cardiomyopathyT M Olson
Department of Pediatrics, Division of Cardiology and Biochemistry, University of Utah, Salt Lake City, UT 84113, USA
J Mol Cell Cardiol 33:723-32. 2001..Therefore, substitution of different amino acid residues in the same thin filament proteins is associated with the distinct phenotypes of cardiac hypertrophy or congestive heart failure... - Myosin light chain mutation causes autosomal recessive cardiomyopathy with mid-cavitary hypertrophy and restrictive physiologyTimothy M Olson
Department of Medicine, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN 55905, USA
Circulation 105:2337-40. 2002..Autosomal dominant hypertrophic cardiomyopathy (HCM) is caused by inherited defects of sarcomeric proteins. We tested the hypothesis that homozygosity for a sarcomeric protein defect can cause recessive HCM... - Metavinculin mutations alter actin interaction in dilated cardiomyopathyTimothy M Olson
Department of Pediatrics and the Division of Cardiology, University of Utah, Salt Lake City, Utah, USA
Circulation 105:431-7. 2002..We tested the hypothesis that heritable dysfunction of metavinculin may contribute to the pathogenesis of dilated cardiomyopathy (DCM)... - Mutations in ribonucleic acid binding protein gene cause familial dilated cardiomyopathyKatharine M Brauch
Cardiovascular Genetics Laboratory, College of Medicine, Mayo Clinic, Rochester, Minnesota, USA
J Am Coll Cardiol 54:930-41. 2009..We sought to identify a novel gene for dilated cardiomyopathy (DCM)... - The effect of the brain-type natriuretic peptide single-nucleotide polymorphism rs198389 on test characteristics of common assaysLisa C Costello-Boerrigter
Cardiorenal Research Laboratory, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN 55905, USA
Mayo Clin Proc 86:210-8. 2011.... - A human atrial natriuretic peptide gene mutation reveals a novel peptide with enhanced blood pressure-lowering, renal-enhancing, and aldosterone-suppressing actionsPaul M McKie
Cardiorenal Research Laboratory, Division of Cardiovascular Diseases, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA
J Am Coll Cardiol 54:1024-32. 2009..We sought to determine the physiologic actions and potential therapeutic applications of mutant atrial natriuretic peptide (mANP)... - Atrial natriuretic peptide frameshift mutation in familial atrial fibrillationDenice M Hodgson-Zingman
Department of Internal Medicine, University of Iowa, Carver College of Medicine, Iowa City, USA
N Engl J Med 359:158-65. 2008..This report implicates perturbation of the atrial natriuretic peptide-cyclic guanosine monophosphate (cGMP) pathway in cardiac electrical instability... - Familial atrial fibrillation is a genetically heterogeneous disorderDawood Darbar
Department of Medicine, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota 55905, USA
J Am Coll Cardiol 41:2185-92. 2003..In four families with AF, we have excluded linkage to chromosome 10q22-q24, establishing that at least two disease genes are responsible for this disorder... - ABCC9 mutations identified in human dilated cardiomyopathy disrupt catalytic KATP channel gatingMartin Bienengraeber
Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic College of Medicine, Mayo Foundation, Rochester, Minnesota 55905, USA
Nat Genet 36:382-7. 2004..Defective catalysis-mediated pore regulation is thus a mechanism for channel dysfunction and susceptibility to dilated cardiomyopathy... - Frequency of development of idiopathic dilated cardiomyopathy among relatives of patients with idiopathic dilated cardiomyopathyVirginia V Michels
Department of Medical Genetics, Mayo Foundation, 200 First Street SW, Rochester, MN 55905, USA
Am J Cardiol 91:1389-92. 2003 - Cardiac KATP channels in health and diseaseGarvan C Kane
Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
J Mol Cell Cardiol 38:937-43. 2005.... - Identification of a metavinculin missense mutation, R975W, associated with both hypertrophic and dilated cardiomyopathyVlad C Vasile
Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
Mol Genet Metab 87:169-74. 2006..However, this study demonstrates that the same fundamental mutation in humans can yield either cardiomyopathic phenotype, underscoring a critical role for modifier genes and/or environmental stressors in cardiac remodeling... - Kv1.5 channelopathy due to KCNA5 loss-of-function mutation causes human atrial fibrillationTimothy M Olson
Department of Medicine, Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
Hum Mol Genet 15:2185-91. 2006..This first report of Kv1.5 loss-of-function channelopathy establishes KCNA5 mutation as a novel risk factor for repolarization deficiency and atrial fibrillation... - Comprehensive mutation scanning of LMNA in 268 patients with lone atrial fibrillationKatharine M Brauch
Cardiovascular Genetics Laboratory, College of Medicine, Mayo Clinic, Rochester, Minnesota, USA
Am J Cardiol 103:1426-8. 2009..Comprehensive mutation scanning identified only 1 potentially pathogenic mutation. In conclusion, LMNA mutations rarely cause lone AF and routine genetic testing of LMNA in these patients does not appear warranted... - X-linked nonsyndromic sinus node dysfunction and atrial fibrillation caused by emerin mutationMargaret L Karst
Department of Medicine, Division of Cardiovascular Diseases, and Pediatric and Adolescent Medicine, College of Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA
J Cardiovasc Electrophysiol 19:510-5. 2008..This study sought to identify the genetic basis for male-restricted, nonsyndromic sinus node dysfunction and AF in a multigenerational family... - K(ATP) channel polymorphism is associated with left ventricular size in hypertensive individuals: a large-scale community-based studySantiago Reyes
Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN, USA
Hum Genet 123:665-7. 2008..These findings implicate Kir6.2 K23 as a risk factor for adverse subclinical myocardial remodeling, and underscore the significance of cardiac K(ATP) channels within the population... - Gene mutations in apical hypertrophic cardiomyopathyMichael Arad
Department of Genetics, Harvard Medical School, Boston, MA 02115, USA
Circulation 112:2805-11. 2005..Only a limited number of sarcomere gene defects (eg, cardiac actin Glu101Lys) consistently produce apical HCM... - Lone atrial fibrillation: influence of familial disease on gender predilectionLin Y Chen
Department of Medicine, Cardiovascular Division, National University of Singapore, Singapore
J Cardiovasc Electrophysiol 19:802-6. 2008..We sought to determine gender distribution in sporadic and familial LAF, gender-based differences, and phenotypic differences between sporadic and familial LAF... - Inherited arrhythmias: a National Heart, Lung, and Blood Institute and Office of Rare Diseases workshop consensus report about the diagnosis, phenotyping, molecular mechanisms, and therapeutic approaches for primary cardiomyopathies of gene mutations affeStephan E Lehnart
Department of Physiology and Cellular Biophysics, Clyde and Helen Wu Center for Molecular Cardiology, College of Physicians and Surgeons of Columbia University, P and S 9 401 box 22, 630 W 168 St, New York, NY 10032, USA
Circulation 116:2325-45. 2007....
Research Grants
- Identification of Disease Genes for Atrial FibrillationTimothy Olson; Fiscal Year: 2009..The long-term objectives of this work are to gain new insights into molecular mechanisms of arrhythmogenesis and to improve prediction, prevention, and treatment of AF. ..
- Mapping Novel Disease Genes for Dilated CardiomyopathyTimothy Olson; Fiscal Year: 2007..Discovering the genetic basis of DCM will lead to better ways to diagnose and prevent the progressive weakening of heart muscle that afflicts patients with this disorder. ..
- Identification of Disease Genes for Atrial FibrillationTimothy Olson; Fiscal Year: 2007..The long-term objectives of this work are to gain new insights into molecular mechanisms of arrhythmogenesis and to improve prediction, prevention, and treatment of AF. ..
- Mapping Novel Disease Genes for Dilated CardiomyopathyTimothy Olson; Fiscal Year: 2004..The long-term objectives of this work are to gain new insights into molecular mechanisms for heart failure and to improve prediction, prevention, and treatment of DCM. ..
- Mapping Novel Disease Genes for Dilated CardiomyopathyTIMOTHY MARK OLSON; Fiscal Year: 2010..Discovering the genetic basis of DCM will lead to better ways to diagnose and prevent the progressive weakening of heart muscle that afflicts patients with this disorder. ..