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30 results on '"London, Barry"'

10. Abstract 93: The Radiation Mitigator MMS350 Prevents Bradyarrhythmias in Irradiated Mice

Author

Morgan, Gina M, primary, Kutschke, William J, additional, Matasic, Daniel S, additional, Epperly, Michael W, additional, Greenberger, Joel S, additional, Kalen, Amanda L, additional, Waldron, Timothy J, additional, Schoenfield, Joshua D, additional, McCormick, Michael L, additional, Yoon, Jin-Young, additional, Wipf, Peter, additional, Spitz, Douglas R, additional, and London, Barry, additional

Published
2017
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14. Cardiac Na + Current Regulation by Pyridine Nucleotides

Author

Liu, Man, primary, Sanyal, Shamarendra, additional, Gao, Ge, additional, Gurung, Iman S., additional, Zhu, Xiaodong, additional, Gaconnet, Georgia, additional, Kerchner, Laurie J., additional, Shang, Lijuan L., additional, Huang, Christopher L.-H., additional, Grace, Andrew, additional, London, Barry, additional, and Dudley, Samuel C., additional

Published
2009
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23. Two Isoforms of the Mouse Ether-a-go-go –Related Gene Coassemble to Form Channels With Properties Similar to the Rapidly Activating Component of the Cardiac Delayed Rectifier K + Current

Author

London, Barry, primary, Trudeau, Matthew C., additional, Newton, Kimberly P., additional, Beyer, Anita K., additional, Copeland, Neal G., additional, Gilbert, Debra J., additional, enkins, Nancy A. J, additional, Satler, Carol A., additional, and Robertson, Gail A., additional

Published
1997
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24. Cardiac Na+ Current Regulation by Pyridine Nucleotides.

Author

Liu, Man, Sanyal, Shamarendra, Ge Gao, Gurung, Iman S., Xiaodong Zhu, Gaconnet, Georgia, Kerchner, Laurie J., Shang, Lijuan L., Huang, Christopher L.-H., Grace, Andrew, London, Barry, and Dudley, Jr., Samuel C.

Subjects
NAD (Coenzyme), SODIUM channels, GENETIC mutation, BRUGADA syndrome, HEART cells, ENERGY metabolism
Abstract

The article presents a study which examined the involvement of nicotinamide adenine dinucleotide (NADH) in the regulation of human cardiac sodium channels (NaV1.5). The study discussed the association of NaV1.5 mutations with Brugada syndrome (BrS.) The researchers used rate neonatal cardiomyocytes and HEK293 cells. The study revealed that pyridine nucleotides regulate NaV1.5, and suggested connection between NAD-dependent energy metabolism with sodium current.

Published
2009
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25. Homozygous Missense N629D hERG (KCNH2) Potassium Channel Mutation Causes Developmental Defects in the Right Ventricle and Its Outflow Tract and Embryonic Lethality.

Author

Guo Qi Teng, Xian Zhao, Lees-Miller, James P., Quinn, F. Russell, Pin Li, Rancourt, Derrick E., London, Barry, Cross, James C., and Duff, Henry J.

Subjects
ABNORMALITIES in animals, POTASSIUM channels, RIGHT heart ventricle, CARDIOVASCULAR diseases, EMBRYO anatomy, BRANCHIAL arch
Abstract

The article focuses on the role homozygous missense N629D human ERG (KNCH2) potassium channel mutation in embryo cardiac development. Altered looping architecture, poorly developed bulbus cordis, and distorted sac and branchial arc are some of the developmental defects because of the mutation. Results show that defects in cardiac ontogeny in the first branchial arch, outflow tract, and the right ventricle are caused by the loss of IKr function in N629D/N629D cardiovascular system.

Published
2008
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29. Cardiac Na+ current regulation by pyridine nucleotides.

Author

Liu M, Sanyal S, Gao G, Gurung IS, Zhu X, Gaconnet G, Kerchner LJ, Shang LL, Huang CL, Grace A, London B, and Dudley SC Jr

Subjects
Animals, Antineoplastic Agents pharmacology, Benzophenanthridines pharmacology, Brugada Syndrome genetics, Cell Line, Cyclic AMP-Dependent Protein Kinases antagonists & inhibitors, Cyclic AMP-Dependent Protein Kinases genetics, Cyclic AMP-Dependent Protein Kinases metabolism, Down-Regulation drug effects, Down-Regulation genetics, Enzyme Inhibitors pharmacology, Glycerolphosphate Dehydrogenase genetics, Humans, Mice, Muscle Proteins genetics, Myocardium metabolism, NAD genetics, NAV1.5 Voltage-Gated Sodium Channel, Oxidation-Reduction, Protein Kinase C antagonists & inhibitors, Protein Kinase C genetics, Protein Kinase C metabolism, Rats, Sodium Channels genetics, Superoxide Dismutase genetics, Superoxide Dismutase metabolism, Tachycardia, Ventricular genetics, Tachycardia, Ventricular metabolism, Brugada Syndrome metabolism, Glycerolphosphate Dehydrogenase metabolism, Muscle Proteins metabolism, Mutation, NAD metabolism, Sodium metabolism, Sodium Channels metabolism
Abstract

Rationale: Mutations in glycerol-3-phosphate dehydrogenase 1-like (GPD1-L) protein reduce cardiac Na+ current (I(Na)) and cause Brugada Syndrome (BrS). GPD1-L has >80% amino acid homology with glycerol-3-phosphate dehydrogenase, which is involved in NAD-dependent energy metabolism., Objective: Therefore, we tested whether NAD(H) could regulate human cardiac sodium channels (Na(v)1.5)., Methods and Results: HEK293 cells stably expressing Na(v)1.5 and rat neonatal cardiomyocytes were used. The influence of NADH/NAD+ on arrhythmic risk was evaluated in wild-type or SCN5A(+/-) mouse heart. A280V GPD1-L caused a 2.48+/-0.17-fold increase in intracellular NADH level (P<0.001). NADH application or cotransfection with A280V GPD1-L resulted in decreased I(Na) (0.48+/-0.09 or 0.19+/-0.04 of control group, respectively; P<0.01), which was reversed by NAD+, chelerythrine, or superoxide dismutase. NAD+ antagonism of the Na+ channel downregulation by A280V GPD1-L or NADH was prevented by a protein kinase (PK)A inhibitor, PKAI(6-22). The effects of NADH and NAD+ were mimicked by a phorbol ester and forskolin, respectively. Increasing intracellular NADH was associated with an increased risk of ventricular tachycardia in wild-type mouse hearts. Extracellular application of NAD+ to SCN5A(+/-) mouse hearts ameliorated the risk of ventricular tachycardia., Conclusions: Our results show that Na(v)1.5 is regulated by pyridine nucleotides, suggesting a link between metabolism and I(Na). This effect required protein kinase C activation and was mediated by oxidative stress. NAD+ could prevent this effect by activating PKA. Mutations of GPD1-L may downregulate Na(v)1.5 by altering the oxidized to reduced NAD(H) balance.

Published
2009
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30. CaM kinase inhibition: apply directly to the heart?

Author

London B

Subjects
Animals, Arrhythmias, Cardiac enzymology, Calcium metabolism, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Calcium-Calmodulin-Dependent Protein Kinases metabolism, Enzyme Activation, Humans, Mice, Mice, Transgenic, Potassium Channels metabolism, Ventricular Remodeling physiology, Calcium-Calmodulin-Dependent Protein Kinases antagonists & inhibitors, Cardiomyopathy, Dilated enzymology, Myocardium enzymology
Published
2006
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