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Institution

University of California, Irvine

EducationIrvine, California, United States
About: University of California, Irvine is a education organization based out in Irvine, California, United States. It is known for research contribution in the topics: Population & Galaxy. The organization has 47031 authors who have published 113602 publications receiving 5521832 citations. The organization is also known as: UC Irvine & UCI.


Papers
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Proceedings ArticleDOI
08 May 2007
TL;DR: This work proposes a simple algorithm based on novel indexing and optimization strategies that solves the problem of finding all pairs of vectors whose similarity score is above a given threshold without relying on approximation methods or extensive parameter tuning.
Abstract: Given a large collection of sparse vector data in a high dimensional space, we investigate the problem of finding all pairs of vectors whose similarity score (as determined by a function such as cosine distance) is above a given threshold. We propose a simple algorithm based on novel indexing and optimization strategies that solves this problem without relying on approximation methods or extensive parameter tuning. We show the approach efficiently handles a variety of datasets across a wide setting of similarity thresholds, with large speedups over previous state-of-the-art approaches.

768 citations

Journal ArticleDOI
TL;DR: Functional studies indicate that this mutation leads to the simultaneous decrease in cytochrome oxidation, increase in reactive oxygen, and increased reactive nitrogen, which suggests that mitochondrial DNA mutations resulting in increased reactive oxygen and reactive nitrogen generation may be involved in prostate cancer biology.
Abstract: Mitochondrial DNA (mtDNA) mutations have been found in many cancers but the physiological derangements caused by such mutations have remained elusive. Prostate cancer is associated with both inherited and somatic mutations in the cytochrome c oxidase (COI) gene. We present a prostate cancer patient-derived rare heteroplasmic mutation of this gene, part of mitochondrial respiratory complex IV. Functional studies indicate that this mutation leads to the simultaneous decrease in cytochrome oxidation, increase in reactive oxygen, and increased reactive nitrogen. These data suggest that mitochondrial DNA mutations resulting in increased reactive oxygen and reactive nitrogen generation may be involved in prostate cancer biology.

768 citations

Journal ArticleDOI
TL;DR: In this article, the second-best optimal level of gasoline taxation taking into account unpriced pollution, congestion, and accident externalities, as well as interactions with the broader fiscal system is developed.
Abstract: This paper develops an analytical framework to assess the second-best optimal level of gasoline taxation taking into account unpriced pollution, congestion, and accident externalities, as well as interactions with the broader fiscal system. We provide calculations of the optimal taxes for the US and the UK under a variety of parameter scenarios. Under our central parameter values, the second-best optimal gasoline tax is $1.01/gal for the US and $1.34/gal for the UK. Current tax rates are much lower than this in the US and higher in the UK. The calculations are moderately sensitive to alternative parameter assumptions. The congestion externality is the largest component in both nations; revenue-raising needs also play a significant role, as do accident externalities and local air pollution. Potential welfare gains from reducing the current UK tax rate are estimated at nearly one-fourth the production cost of all gasoline used in the UK. Even larger gains could be achieved by switching to a tax on vehicle miles with equal revenue yield. For the US, the welfare gains from optimizing the gasoline tax are smaller, but those from switching to an optimal tax on vehicle miles are very large.

768 citations

Journal ArticleDOI
07 Aug 2006-Oncogene
TL;DR: The mtDNA mutations in tumors may fall into two main classes: (1) severe mutations that inhibit OXPHOS, increase reactive oxygen species (ROS) and promote tumor cell proliferation and (2) milder mutations that may permit tumors to adapt to new environments.
Abstract: The metabolism of solid tumors is associated with high lactate production while growing in oxygen (aerobic glycolysis) suggesting that tumors may have defects in mitochondrial function. The mitochondria produce cellular energy by oxidative phosphorylation (OXPHOS), generate reactive oxygen species (ROS) as a by-product, and regulate apoptosis via the mitochondrial permeability transition pore (mtPTP). The mitochondria are assembled from both nuclear DNA (nDNA) and mitochondrial DNA (mtDNA) genes. The mtDNA codes for 37 genes essential of OXPHOS, is present in thousands of copies per cell, and has a very high mutations rate. In humans, severe mtDNA mutations result in multisystem disease, while some functional population-specific polymorphisms appear to have permitted humans to adapt to new environments. Mutations in the nDNA-encoded mitochondrial genes for fumarate hydratase and succinate dehydrogenase have been linked to uterine leiomyomas and paragangliomas, and cancer cells have been shown to induce hexokinase II which harnesses OXPHOS adenosine triphosphate (ATP) production to drive glycolysis. Germline mtDNA mutations at nucleotides 10398 and 16189 have been associated with breast cancer and endometrial cancer. Tumor mtDNA somatic mutations range from severe insertion-deletion and chain termination mutations to mild missense mutations. Surprisingly, of the 190 tumor-specific somatic mtDNA mutations reported, 72% are also mtDNA sequence variants found in the general population. These include 52% of the tumor somatic mRNA missense mutations, 83% of the tRNA mutations, 38% of the rRNA mutations, and 85% of the control region mutations. Some associations might reflect mtDNA sequencing errors, but analysis of several of the tumor-specific somatic missense mutations with population counterparts appear legitimate. Therefore, mtDNA mutations in tumors may fall into two main classes: (1) severe mutations that inhibit OXPHOS, increase ROS production and promote tumor cell proliferation and (2) milder mutations that may permit tumors to adapt to new environments. The former may be lost during subsequent tumor oxygenation while the latter may become fixed. Hence, mitochondrial dysfunction does appear to be a factor in cancer etiology, an insight that may suggest new approaches for diagnosis and treatment.

765 citations

Journal ArticleDOI
TL;DR: The final results of the search for the lepton flavour violating decay were presented in this paper, based on the full dataset collected by the MEG experiment at the Paul Scherrer Institut in the period 2009-2013.
Abstract: The final results of the search for the lepton flavour violating decay $$\mathrm {\mu }^+ \rightarrow \mathrm {e}^+ \mathrm {\gamma }$$ based on the full dataset collected by the MEG experiment at the Paul Scherrer Institut in the period 2009–2013 and totalling $$7.5\times 10^{14}$$ stopped muons on target are presented. No significant excess of events is observed in the dataset with respect to the expected background and a new upper limit on the branching ratio of this decay of $$ \mathcal{B} (\mu ^+ \rightarrow \mathrm{e}^+ \gamma ) < 4.2 \times 10^{-13}$$ (90 % confidence level) is established, which represents the most stringent limit on the existence of this decay to date.

764 citations


Authors

Showing all 47751 results

NameH-indexPapersCitations
Daniel Levy212933194778
Rob Knight2011061253207
Lewis C. Cantley196748169037
Dennis W. Dickson1911243148488
Terrie E. Moffitt182594150609
Joseph Biederman1791012117440
John R. Yates1771036129029
John A. Rogers1771341127390
Avshalom Caspi170524113583
Yang Gao1682047146301
Carl W. Cotman165809105323
John H. Seinfeld165921114911
Gregg C. Fonarow1611676126516
Jerome I. Rotter1561071116296
David Cella1561258106402
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20242
2023252
20221,224
20216,519
20206,348
20195,610