Institution
University of Utah
Education•Salt Lake City, Utah, United States•
About: University of Utah is a education organization based out in Salt Lake City, Utah, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 52894 authors who have published 124076 publications receiving 5265834 citations. The organization is also known as: The U & The University of Utah.
Topics: Population, Poison control, Health care, Cancer, Transplantation
Papers published on a yearly basis
Papers
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01 Jul 2002TL;DR: The work presented in this paper leverages the time-tested techniques of photographic practice to develop a new tone reproduction operator and uses and extends the techniques developed by Ansel Adams to deal with digital images.
Abstract: A classic photographic task is the mapping of the potentially high dynamic range of real world luminances to the low dynamic range of the photographic print. This tone reproduction problem is also faced by computer graphics practitioners who map digital images to a low dynamic range print or screen. The work presented in this paper leverages the time-tested techniques of photographic practice to develop a new tone reproduction operator. In particular, we use and extend the techniques developed by Ansel Adams to deal with digital images. The resulting algorithm is simple and produces good results for a wide variety of images.
1,708 citations
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Heribert Schunkert1, Inke R. König1, Sekar Kathiresan2, Muredach P. Reilly3 +163 more•Institutions (59)
TL;DR: This paper performed a meta-analysis of 14 genome-wide association studies of coronary artery disease (CAD) comprising 22,233 individuals with CAD (cases) and 64,762 controls of European descent followed by genotyping of top association signals in 56,682 additional individuals.
Abstract: We performed a meta-analysis of 14 genome-wide association studies of coronary artery disease (CAD) comprising 22,233 individuals with CAD (cases) and 64,762 controls of European descent followed by genotyping of top association signals in 56,682 additional individuals. This analysis identified 13 loci newly associated with CAD at P < 5 - 10'8 and confirmed the association of 10 of 12 previously reported CAD loci. The 13 new loci showed risk allele frequencies ranging from 0.13 to 0.91 and were associated with a 6% to 17% increase in the risk of CAD per allele. Notably, only three of the new loci showed significant association with traditional CAD risk factors and the majority lie in gene regions not previously implicated in the pathogenesis of CAD. Finally, five of the new CAD risk loci appear to have pleiotropic effects, showing strong association with various other human diseases or traits.
1,705 citations
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TL;DR: The Tol2kit greatly facilitates zebrafish transgenesis, simplifies the sharing of clones, and enables large‐scale projects testing the functions of libraries of regulatory or coding sequences.
Abstract: Transgenesis is an important tool for assessing gene function. In zebrafish, transgenesis has suffered from three problems: the labor of building complex expression constructs using conventional subcloning; low transgenesis efficiency, leading to mosaicism in transient transgenics and infrequent germline incorporation; and difficulty in identifying germline integrations unless using a fluorescent marker transgene. The Tol2kit system uses site-specific recombination-based cloning (multisite Gateway technology) to allow quick, modular assembly of [promoter]-[coding sequence]-[3' tag] constructs in a Tol2 transposon backbone. It includes a destination vector with a cmlc2:EGFP (enhanced green fluorescent protein) transgenesis marker and a variety of widely useful entry clones, including hsp70 and beta-actin promoters; cytoplasmic, nuclear, and membrane-localized fluorescent proteins; and internal ribosome entry sequence-driven EGFP cassettes for bicistronic expression. The Tol2kit greatly facilitates zebrafish transgenesis, simplifies the sharing of clones, and enables large-scale projects testing the functions of libraries of regulatory or coding sequences.
1,704 citations
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TL;DR: KVLQT1 is the subunit that coassembles with minK to form IKS channels and IKS dysfunction is a cause of cardiac arrhythmia, and is shown to encode a K+ channel with biophysical properties unlike other known cardiac currents.
Abstract: THE slowly activating delayed-rectifier K+ current, IKS, modulates the repolarization of cardiac action potentials. The molecular structure of the IKS channel is not known, but physiological data indicate that one component of theIKSchannel is minK (refs 1–6), a 130-amino-acid protein with a single putative transmembrane domain7. The size and structure of this protein is such that it is unlikely that minK alone forms functional channels8,9. We have previously used positional cloning techniques to define a new putative K+-channel gene, KVLQT110. Mutations in this gene cause long-QT syndrome, an inherited disorder that increases the risk of sudden death from cardiac arrhythmias. Here we show that KVLQT1 encodes a K+ channel with biophysical properties unlike other known cardiac currents. We considered that KVLQT1 might coassemble with another subunit to form func-tional channels in cardiac myocytes. Coexpression of KVLQT1 with minK induced a current that was almost identical to cardiac IKS. Therefore, KVLQT1 is the subunit that coassembles with minK to form IKS channels and IKS dysfunction is a cause of cardiac arrhythmia.
1,680 citations
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University of Bologna1, University of Utah2, University of Jena3, Imperial College London4, University of Barcelona5, Royal Liverpool and Broadgreen University Hospital NHS Trust6, University of Texas MD Anderson Cancer Center7, University of Poitiers8, Norwegian University of Science and Technology9, University of Adelaide10, Catholic University of Korea11, University of Chicago12, University of Toronto13, University of Bordeaux14, Masaryk University15, Heidelberg University16, Leipzig University17, University of Naples Federico II18, Fred Hutchinson Cancer Research Center19, University of Turin20, Wayne State University21, Cornell University22, Uppsala University23
TL;DR: Optimal responders to chronic myeloid leukemia treatment should continue therapy indefinitely, with careful surveillance, or they can be enrolled in controlled studies of treatment discontinuation once a deeper molecular response is achieved.
1,679 citations
Authors
Showing all 53431 results
Name | H-index | Papers | Citations |
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Bert Vogelstein | 247 | 757 | 332094 |
George M. Whitesides | 240 | 1739 | 269833 |
Hongjie Dai | 197 | 570 | 182579 |
Robert M. Califf | 196 | 1561 | 167961 |
Frank E. Speizer | 193 | 636 | 135891 |
Yusuke Nakamura | 179 | 2076 | 160313 |
David L. Kaplan | 177 | 1944 | 146082 |
Marc G. Caron | 173 | 674 | 99802 |
George M. Church | 172 | 900 | 120514 |
Steven P. Gygi | 172 | 704 | 129173 |
Lily Yeh Jan | 162 | 467 | 73655 |
Tobin J. Marks | 159 | 1621 | 111604 |
David W. Bates | 159 | 1239 | 116698 |
Alfred L. Goldberg | 156 | 474 | 88296 |
Charles M. Perou | 156 | 573 | 202951 |