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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.
Topics: Population, Galaxy, Poison control, Cancer, Gene


Papers
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Journal ArticleDOI
TL;DR: The roles of computer technologies in the workplace, in decision making, in altering power relationships, and in influencing personal privacy are examined and two broad perspectives are contrasted.
Abstract: Recent empirical studies of computing use in organizations and in public life are examined. The roles of computer technologies in the workplace, in decision making, in altering power relationships, and in influencing personal privacy are examined. In addition, studies that examine the social accountability of computing arrangements to broad publics are reviewed. All studies of computing in social life make important assumptions about the social world in which computing is embedded. Two broad perspectives are contrasted. Systems rationalism, a collection of approaches including management science, managerial rationalism, and the systems approach, is found to be most helpful in stable settings, when there is considerable consensus over important social values. Segmented-institutionalist analyses, which assume social conflict rather than consensus, are particularly powerful as the social world of computing use becomes more dynamic and as a wider variety of groups is involved.

814 citations

Journal ArticleDOI
TL;DR: It is suggested that inhibition of anandamide deactivation may contribute to the antipsychotic effects of cannabidiol potentially representing a completely new mechanism in the treatment of schizophrenia.
Abstract: Cannabidiol is a component of marijuana that does not activate cannabinoid receptors, but moderately inhibits the degradation of the endocannabinoid anandamide. We previously reported that an elevation of anandamide levels in cerebrospinal fluid inversely correlated to psychotic symptoms. Furthermore, enhanced anandamide signaling let to a lower transition rate from initial prodromal states into frank psychosis as well as postponed transition. In our translational approach, we performed a double-blind, randomized clinical trial of cannabidiol vs amisulpride, a potent antipsychotic, in acute schizophrenia to evaluate the clinical relevance of our initial findings. Either treatment was safe and led to significant clinical improvement, but cannabidiol displayed a markedly superior sideeffect profile. Moreover, cannabidiol treatment was accompanied by a significant increase in serum anandamide levels, which was significantly associated with clinical improvement. The results suggest that inhibition of anandamide deactivation may contribute to the antipsychotic effects of cannabidiol potentially representing a completely new mechanism in the treatment of schizophrenia. Translational Psychiatry (2012) 2, e94; doi:10.1038/tp.2012.15; published online 20 March 2012

812 citations

Journal ArticleDOI
TL;DR: The opportunity to move from a neighborhood with a highlevel of poverty to one with a lower level of poverty was associated with modest but potentially important reductions in the prevalence of extreme obesity and diabetes.
Abstract: ference of 4.61 percentage points (95% confidence interval (CI), −8.54 to −0.69), 3.38 percentage points (95% CI, −6.39 to −0.36), and 4.31 percentage points (95% CI, −7.82 to −0.80), respectively. The differences between the group receiving traditional vouchers and the control group were not significant. CONCLUSIONS The opportunity to move from a neighborhood with a high level of poverty to one with a lower level of poverty was associated with modest but potentially important reductions in the prevalence of extreme obesity and diabetes. The mechanisms under - lying these associations remain unclear but warrant further investigation, given their potential to guide the design of community-level interventions intended to improve health. (Funded by HUD and others.)

810 citations

Journal ArticleDOI
14 Sep 2006-Nature
TL;DR: By site-directed mutagenesis, it is shown that a point mutation from glutamate to aspartate at position 180 in the conserved S1–S2 loop of Orai transforms the ion selectivity properties of CRAC current from being Ca2+-selective with inward rectification to being selective for monovalent cations and outwardly rectifying.
Abstract: Recent RNA interference screens have identified several proteins that are essential for store-operated Ca2+ influx and Ca2+ release-activated Ca2+ (CRAC) channel activity in Drosophila and in mammals, including the transmembrane proteins Stim (stromal interaction molecule) and Orai. Stim probably functions as a sensor of luminal Ca2+ content and triggers activation of CRAC channels in the surface membrane after Ca2+ store depletion. Among three human homologues of Orai (also known as olf186-F), ORAI1 on chromosome 12 was found to be mutated in patients with severe combined immunodeficiency disease, and expression of wild-type Orai1 restored Ca2+ influx and CRAC channel activity in patient T cells. The overexpression of Stim and Orai together markedly increases CRAC current. However, it is not yet clear whether Stim or Orai actually forms the CRAC channel, or whether their expression simply limits CRAC channel activity mediated by a different channel-forming subunit. Here we show that interaction between wild-type Stim and Orai, assessed by co-immunoprecipitation, is greatly enhanced after treatment with thapsigargin to induce Ca2+ store depletion. By site-directed mutagenesis, we show that a point mutation from glutamate to aspartate at position 180 in the conserved S1-S2 loop of Orai transforms the ion selectivity properties of CRAC current from being Ca2+-selective with inward rectification to being selective for monovalent cations and outwardly rectifying. A charge-neutralizing mutation at the same position (glutamate to alanine) acts as a dominant-negative non-conducting subunit. Other charge-neutralizing mutants in the same loop express large inwardly rectifying CRAC current, and two of these exhibit reduced sensitivity to the channel blocker Gd3+. These results indicate that Orai itself forms the Ca2+-selectivity filter of the CRAC channel.

808 citations

Journal ArticleDOI
TL;DR: Findings indicate that PPAR-α mediates the anti-inflammatory effects of PEA and suggest that this fatty-acid ethanolamide may serve, like its analog OEA, as an endogenous ligand of PPar-α.
Abstract: Palmitoylethanolamide (PEA), the naturally occurring amide of palmitic acid and ethanolamine, reduces pain and inflammation through an as-yet-uncharacterized mechanism. Here, we identify the nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-alpha) as the molecular target responsible for the anti-inflammatory properties of PEA. PEA selectively activates PPAR-alpha in vitro with an EC(50) value of 3.1 +/- 0.4 microM and induces the expression of PPAR-alpha mRNA when applied topically to mouse skin. In two animal models, carrageenan-induced paw edema and phorbol ester-induced ear edema, PEA attenuates inflammation in wild-type mice but has no effect in mice deficient in PPAR-alpha. The natural PPAR-alpha agonist oleoylethanolamide (OEA) and the synthetic PPAR-alpha agonists GW7647 and Wy-14643 mimic these effects in a PPAR-alpha-dependent manner. These findings indicate that PPAR-alpha mediates the anti-inflammatory effects of PEA and suggest that this fatty-acid ethanolamide may serve, like its analog OEA, as an endogenous ligand of PPAR-alpha.

808 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
20216,518
20206,348
20195,610