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
More filters
••
International Agency for Research on Cancer1, University of Bristol2, University Hospitals Bristol NHS Foundation Trust3, Vanderbilt University Medical Center4, University of Kentucky5, University of Copenhagen6, Lund University7, Technische Universität München8, Fred Hutchinson Cancer Research Center9, Harvard University10, Dartmouth College11, University of Liverpool12, Umeå University13, National Institute of Occupational Health14, New Generation University College15, Radboud University Nijmegen16, BC Cancer Agency17, Washington State University18, University of Hawaii19, Ontario Institute for Cancer Research20, University of Southern California21, Technion – Israel Institute of Technology22, University of Salzburg23, Curie Institute24, Nofer Institute of Occupational Medicine25, University of Ostrava26, Charles University in Prague27, Nanjing Medical University28, University of Oviedo29, University of Sheffield30, University of Texas MD Anderson Cancer Center31, University of Pittsburgh32, Lunenfeld-Tanenbaum Research Institute33
TL;DR: The results are consistent with a causal role of fasting insulin and low-density lipoprotein cholesterol in lung cancer etiology, as well as for BMI in squamous cell and small cell carcinoma, and the latter relation may be mediated by a previously unrecognized effect of obesity on smoking behavior.
Abstract: Background: Assessing the relationship between lung cancer and metabolic conditions is challenging because of the confounding effect of tobacco. Mendelian randomization (MR), or the use of genetic ...
653 citations
••
TL;DR: Emerging evidences indicate that Snail causes a metabolic reprogramming, bestows tumor cells with cancer stem cell-like traits, and additionally, promotes drug resistance, tumor recurrence and metastasis.
Abstract: Epithelial-mesenchymal transition (EMT) is a highly conserved process in which polarized, immobile epithelial cells lose tight junctions, associated adherence, and become migratory mesenchymal cells. Several transcription factors, including the Snail/Slug family, Twist, δEF1/ZEB1, SIP1/ZEB2 and E12/E47 respond to microenvironmental stimuli and function as molecular switches for the EMT program. Snail is a zinc-finger transcriptional repressor controlling EMT during embryogenesis and tumor progression. Through its N-terminal SNAG domain, Snail interacts with several corepressors and epigenetic remodeling complexes to repress specific target genes, such as the E-cadherin gene (CDH1). An integrated and complex signaling network, including the RTKs, TGF-β, Notch, Wnt, TNF-α, and BMPs pathways, activates Snail, thereby inducing EMT. Snail expression correlates with the tumor grade, nodal metastasis of many types of tumor and predicts a poor outcome in patients with metastatic cancer. Emerging evidences indicate that Snail causes a metabolic reprogramming, bestows tumor cells with cancer stem cell-like traits, and additionally, promotes drug resistance, tumor recurrence and metastasis. Despite many new and exciting developments, several challenges remain to be addressed in order to understand more thoroughly the role of Snail in metastasis. Additional investigations are required to disclose the contribution of microenvironmental factors on tumor progression. This information will lead to a comprehensive understanding of Snail in cancer and will provide us with novel approaches for preventing and treating metastatic cancers.
651 citations
••
TL;DR: This study suggests that neuro-inflammatory reaction could contribute to AD pathology, and anti-inflammatory agent could be useful for the prevention of AD.
Abstract: Alzheimer's disease (AD) is characterized by extensive loss of neurons in the brain of AD patients. Intracellular accumulation of beta-amyloid peptide (Aβ) has also shown to occur in AD. Neuro-inflammation has been known to play a role in the pathogenesis of AD. In this study, we investigated neuro-inflammation and amyloidogenesis and memory impairment following the systemic inflammation generated by lipopolysaccharide (LPS) using immunohistochemistry, ELISA, behavioral tests and Western blotting. Intraperitoneal injection of LPS, (250 μg/kg) induced memory impairment determined by passive avoidance and water maze tests in mice. Repeated injection of LPS (250 μg/kg, 3 or 7 times) resulted in an accumulation of Aβ1–42 in the hippocampus and cerebralcortex of mice brains through increased β- and γ-secretase activities accompanied with the increased expression of amyloid precursor protein (APP), 99-residue carboxy-terminal fragment of APP (C99) and generation of Aβ1–42 as well as activation of astrocytes in vivo. 3 weeks of pretreatment of sulindac sulfide (3.75 and 7.5 mg/kg, orally), an anti-inflammatory agent, suppressed the LPS-induced amyloidogenesis, memory dysfunction as well as neuronal cell death in vivo. Sulindac sulfide (12.5–50 μM) also suppressed LPS (1 μg/ml)-induced amyloidogenesis in cultured neurons and astrocytes in vitro. This study suggests that neuro-inflammatory reaction could contribute to AD pathology, and anti-inflammatory agent could be useful for the prevention of AD.
650 citations
••
TL;DR: The concept of the proximity compatibility principle (PCP) is described and its relevance to display design is demonstrated: Displays relevant to a common task or mental operation should be rendered close together in perceptual space (close display proximity).
Abstract: In this report we describe the concept of the proximity compatibility principle (PCP) and demonstrate its relevance to display design: Displays relevant to a common task or mental operation (close task or mental proximity) should be rendered close together in perceptual space (close display proximity). Different forms of task proximity are discussed, as are the different information-processing mechanisms that underlie the effects of the several different design manipulations of display proximity. Experimental data that support this process-based elaboration of PCP are then reviewed in design contexts relating to aviation, graphs, display layout, and decision aiding.
650 citations
••
TL;DR: In this paper, a new structure (shell or plate) containing an integrated distributed piezoelectric sensor and actuator is proposed, where the distributed sensing layer monitors the structural oscillation due to the direct PDE and the distributed actuator layer suppresses the oscillation via the converse PDE.
642 citations
Authors
Showing all 44305 results
Name | H-index | Papers | Citations |
---|---|---|---|
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 |