E
Edward G. Lakatta
Researcher at National Institutes of Health
Publications - 902
Citations - 95504
Edward G. Lakatta is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Blood pressure & Population. The author has an hindex of 146, co-authored 858 publications receiving 88637 citations. Previous affiliations of Edward G. Lakatta include University of Pittsburgh & University College London.
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Journal ArticleDOI
Resveratrol prevents high fat/sucrose diet-induced central arterial wall inflammation and stiffening in nonhuman primates.
Julie A. Mattison,Mingyi Wang,Michel Bernier,Jing Zhang,Sung-Soo Park,Stuart Maudsley,Steven S. An,Lakshmi Santhanam,Bronwen Martin,Shakeela Faulkner,Christopher H. Morrell,Christopher H. Morrell,Joseph A. Baur,Leonid Peshkin,Danuta Sosnowska,Anna Csiszar,Richard Herbert,Edward M. Tilmont,Zoltan Ungvari,Kevin J. Pearson,Edward G. Lakatta,Rafael de Cabo +21 more
TL;DR: In rhesus monkeys, a 2 year diet high in fat and sucrose increases not only body weight and cholesterol, but also induces prominent central arterial wall stiffening and increases PWV and inflammation, and dietary resveratrol prevented the HFS-inducedarterial wall inflammation and the accompanying increase in PWV.
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Age and gender affect ventricular-vascular coupling during aerobic exercise.
Samer S. Najjar,Steven P. Schulman,Gary Gerstenblith,Jerome L. Fleg,David A. Kass,Frances C. O'Connor,Lewis C. Becker,Edward G. Lakatta +7 more
TL;DR: Sub-optimal ventricular-vascular coupling helps to explain the age-associated blunting of maximal exercise EF, and its underlying mechanisms appear to differ between men and women.
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Termination of Ca2+ release by a local inactivation of ryanodine receptors in cardiac myocytes
James S.K. Sham,Long-Sheng Song,Yi Chen,Li Hua Deng,Michael D. Stern,Edward G. Lakatta,Heping Cheng +6 more
TL;DR: The results indicate that Ca2+ release is terminated primarily by a highly localized, use-dependent inactivation of RyRs but not by the stochastic closing or adaptation ofRyRs in intact ventricular myocytes.
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Arterial aging and subclinical arterial disease are fundamentally intertwined at macroscopic and molecular levels.
TL;DR: This review provides a landscape of central arterial aging and age-disease interactions, integrating perspectives that range from humans to molecules, with the goal that future therapies for cardiovascular diseases also will target the prevention or amelioration of unsuccessful arterial Aging.
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Cellular calcium fluctuations in mammalian heart: direct evidence from noise analysis of aequorin signals in Purkinje fibers
TL;DR: Noise analysis of the aequorin luminescence reveals prominent peaks of power density at frequencies of 1-4 Hz; these peaks become larger and shift to higher frequencies as the [Ca2+]i increases, suggesting that Ca2+ release and uptake by the sarcoplasmic reticulum generate these events.