55 research outputs found
From thermal rectifiers to thermoelectric devices
We discuss thermal rectification and thermoelectric energy conversion from
the perspective of nonequilibrium statistical mechanics and dynamical systems
theory. After preliminary considerations on the dynamical foundations of the
phenomenological Fourier law in classical and quantum mechanics, we illustrate
ways to control the phononic heat flow and design thermal diodes. Finally, we
consider the coupled transport of heat and charge and discuss several general
mechanisms for optimizing the figure of merit of thermoelectric efficiency.Comment: 42 pages, 22 figures, review paper, to appear in the Springer Lecture
Notes in Physics volume "Thermal transport in low dimensions: from
statistical physics to nanoscale heat transfer" (S. Lepri ed.
Frataxin deficiency promotes endothelial senescence in pulmonary hypertension
The dynamic regulation of endothelial pathophenotypes in pulmonary hypertension (PH) remains undefined. Cellular senescence is linked to PH with intracardiac shunts; however, its regulation across PH subtypes is unknown. Since endothelial deficiency of iron-sulfur (Fe-S) clusters is pathogenic in PH, we hypothesized that a Fe-S biogenesis protein, frataxin (FXN), controls endothelial senescence. An endothelial subpopulation in rodent and patient lungs across PH subtypes exhibited reduced FXN and elevated senescence. In vitro, hypoxic and inflammatory FXN deficiency abrogated activity of endothelial Fe-S–containing polymerases, promoting replication stress, DNA damage response, and senescence. This was also observed in stem cell–derived endothelial cells from Friedreich’s ataxia (FRDA), a genetic disease of FXN deficiency, ataxia, and cardiomyopathy, often with PH. In vivo, FXN deficiency–dependent senescence drove vessel inflammation, remodeling, and PH, whereas pharmacologic removal of senescent cells in Fxn-deficient rodents ameliorated PH. These data offer a model of endothelial biology in PH, where FXN deficiency generates a senescent endothelial subpopulation, promoting vascular inflammatory and proliferative signals in other cells to drive disease. These findings also establish an endothelial etiology for PH in FRDA and left heart disease and support therapeutic development of senolytic drugs, reversing effects of Fe-S deficiency across PH subtypes
Revisiting methods for assessing and comparing left ventricular diastolic stiffness: Impact of relaxation, external forces, hypertrophy, and comparators
American Journal of Physiology - Heart and Circulatory Physiology2935H2738-H274
Age-associated increases in pulmonary artery systolic pressure in the general population
Circulation119202663-267
Pulmonary Hypertension in Heart Failure With Preserved Ejection Fraction. A Community-Based Study
Journal of the American College of Cardiology53131119-112
Deranged myofilament phosphorylation and function in experimental heart failure with preserved ejection fraction
Alternate Circulating Pro-B-Type Natriuretic Peptide and B-Type Natriuretic Peptide Forms in the General Population
Journal of the American College of Cardiology49111193-120
Cardiac structure and ventricular-vascular function in persons with heart failure and preserved ejection fraction from Olmsted County, Minnesota
Circulation115151982-199
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