Institution
University of Kentucky
Education•Lexington, Kentucky, United States•
About: University of Kentucky is a education organization based out in Lexington, Kentucky, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 43933 authors who have published 92195 publications receiving 3256087 citations. The organization is also known as: UK.
Topics: Population, Poison control, Health care, Oxidative stress, Cancer
Papers published on a yearly basis
Papers
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TL;DR: Accomplishments in improving the health impact of physical education and areas lacking progress are reviewed and an agenda for actualizing the promise of Health-Optimizing Physical Education is identified.
Abstract: The 1991 paper, “Physical Education's Role in Public Health” described the importance of physical education in addressing public health problems. On its 20th anniversary, this article reviews accomplishments in improving the health impact of physical education and identifies areas lacking progress. Major accomplishments include development of evidence-based programs, documentation of health and academic benefits of physical education, and acceptance of physical education as a public health resource. Additional work is needed to evaluate the uptake of evidence-based programs, improve national surveillance of physical education quantity and quality, establish stronger policies supporting active physical education, and achieve wide acceptance of public health goals within the physical education field. These opportunities constitute an agenda for actualizing the promise of Health-Optimizing Physical Education before the next 20-year anniversary.
432 citations
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TL;DR: During pathological neovascularization, VEGF164 selectively induces inflammation and cellular immunity, which provide positive and negative angiogenic regulation, respectively, and new therapeutic approaches for selectively targeting pathological, but not physiological, retinal neov vascularization are outlined.
Abstract: Hypoxia-induced VEGF governs both physiological retinal vascular development and pathological retinal neovascularization. In the current paper, the mechanisms of physiological and pathological neovascularization are compared and contrasted. During pathological neovascularization, both the absolute and relative expression levels for VEGF164 increased to a greater degree than during physiological neovascularization. Furthermore, extensive leukocyte adhesion was observed at the leading edge of pathological, but not physiological, neovascularization. When a VEGF164-specific neutralizing aptamer was administered, it potently suppressed the leukocyte adhesion and pathological neovascularization, whereas it had little or no effect on physiological neovascularization. In parallel experiments, genetically altered VEGF164-deficient (VEGF120/188) mice exhibited no difference in physiological neovascularization when compared with wild-type (VEGF+/+) controls. In contrast, administration of a VEGFR-1/Fc fusion protein, which blocks all VEGF isoforms, led to significant suppression of both pathological and physiological neovascularization. In addition, the targeted inactivation of monocyte lineage cells with clodronate-liposomes led to the suppression of pathological neovascularization. Conversely, the blockade of T lymphocyte–mediated immune responses with an anti-CD2 antibody exacerbated pathological neovascularization. These data highlight important molecular and cellular differences between physiological and pathological retinal neovascularization. During pathological neovascularization, VEGF164 selectively induces inflammation and cellular immunity. These processes provide positive and negative angiogenic regulation, respectively. Together, new therapeutic approaches for selectively targeting pathological, but not physiological, retinal neovascularization are outlined.
431 citations
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TL;DR: In this article, LiCoO(sub 2)-O(1.15) was found to be Li{sub 1.15}CoO{sub 2.16} or, within experimental uncertainty, LiCo(sub + 0.08)O(0.05 to 0.5 {micro}m thick.
Abstract: Thin-film rechargeable lithium batteries with amorphous and crystalline LiCoO{sub 2} cathodes were investigated. The lithium cobalt oxide films were deposited by radio-frequency (RF) magnetron sputtering of an LiCoO{sub 2} target in a 3:1 Ar/O{sub 2} mixture gas. From proton-induced {gamma}-ray emission analysis (PIGE) and Rutherford backscattering spectrometry (RBS), the average composition of these films was determined to be Li{sub 1.15}CoO{sub 2.16} or, within experimental uncertainty, LiCoO{sub 2} + 0.08 Li{sub 2}O. The X-ray powder diffraction patterns of films annealed in air at 500 to 700 C were consistent with the regular hexagonal structure observed for crystalline LiCoO{sub 2}. The discharge curves of the cells with amorphous LiCoO{sub 2} cathodes showed no obvious structural transition between 4.2 and 2.0 V, while the discharge curves of the cells with polycrystalline cathodes were consistent with a two-phase potential plateau at {approximately}3.9 V with a relatively large capacity. Two lower capacity plateaus were observed at {approximately} 4.2 and 4.1 V with the 600 and 700 C annealed cathodes; the {minus}dq/dV peaks were broader and weaker for the 600 C annealed cathodes and were not present at all with the 500 C annealed films. The chemical diffusion coefficients of Li{sup +} in the cathodes obtainedmore » from ac impedance measurements at cell potentials of {approximately} 4 V ranged from {approximately} 10{sup {minus}12} cm{sup 2}/s for the as-deposited amorphous cathodes to {approximately} 10{sup {minus}9} cm{sup 2}/s for the films annealed at 700 C. The capacity loss on extended cycling of the thin-film cells varied with the crystallinity and thickness of the cathodes and with temperature. With the highly crystalline, 700 C annealed material, losses on cycling between 4.2 and 3.8 V at 25 C ranged from 0.0001%/cycle (> 10{sup 4} cycles) to 0.002%/cycle for cells with cathodes form 0.05 to 0.5 {micro}m thick.« less
431 citations
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TL;DR: The loss of synapses in AD is widespread and significant in frontal cortex; there is observable compensation by enlargement of synaptic size.
431 citations
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TL;DR: The current rapid progress in elucidation of mechanisms of protein oxidation in neuronal loss should provide further insight into the importance of free radical oxidative stress in these neurodegenerative disorders.
431 citations
Authors
Showing all 44305 results
Name | H-index | Papers | Citations |
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Mark P. Mattson | 200 | 980 | 138033 |
Carlo M. Croce | 198 | 1135 | 189007 |
Charles A. Dinarello | 190 | 1058 | 139668 |
Richard A. Gibbs | 172 | 889 | 249708 |
Gang Chen | 167 | 3372 | 149819 |
David A. Bennett | 167 | 1142 | 109844 |
Carl W. Cotman | 165 | 809 | 105323 |
Rodney S. Ruoff | 164 | 666 | 194902 |
David Tilman | 158 | 340 | 149473 |
David Cella | 156 | 1258 | 106402 |
Richard E. Smalley | 153 | 494 | 111117 |
Deepak L. Bhatt | 149 | 1973 | 114652 |
Kevin Murphy | 146 | 728 | 120475 |
Jian Yang | 142 | 1818 | 111166 |
Thomas J. Smith | 140 | 1775 | 113919 |