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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: In the middle-aged and elderly, CHD risk increased with lower DBP at any level of SBP>/=120 mm Hg, suggesting that higher PP was an important component of risk.
Abstract: Background—Current definitions of hypertension are based on levels of systolic blood pressure (SBP) and diastolic blood pressure (DBP), but not on pulse pressure (PP). We examined whether PP adds useful information for predicting coronary heart disease (CHD) in the population-based Framingham Heart Study. Methods and Results—We studied 1924 men and women between 50 and 79 years of age at baseline with no clinical evidence of CHD and not taking antihypertensive drug therapy. Cox regression, adjusted for age, sex, and other risk factors, was used to assess the relations between blood pressure components and CHD risk over a 20-year follow-up. The association with CHD risk was positive for SBP, DBP, and PP, considering each pressure individually; of the 3, PP yielded the largest χ2 statistic. When SBP and DBP were jointly entered into the multivariable model, the association with CHD risk was positive for SBP (HR, 1.22; 95% CI, 1.15 to 1.30) and negative for DBP (HR, 0.86; 95% CI, 0.75 to 0.98). Four subgroup...

1,758 citations

Journal ArticleDOI
TL;DR: It is proposed that STIM1, a ubiquitously expressed protein that is conserved from Drosophila to mammalian cells, plays an essential role in SOC influx and may be a common component of SOC and CRAC channels.
Abstract: Store-operated Ca2+ (SOC) channels regulate many cellular processes, but the underlying molecular components are not well defined. Using an RNA interference (RNAi)-based screen to identify genes that alter thapsigargin (TG)-dependent Ca2+ entry, we discovered a required and conserved role of Stim in SOC influx. RNAi-mediated knockdown of Stim in Drosophila S2 cells significantly reduced TG-dependent Ca2+ entry. Patch-clamp recording revealed nearly complete suppression of the Drosophila Ca2+ release-activated Ca2+ (CRAC) current that has biophysical characteristics similar to CRAC current in human T cells. Similarly, knockdown of the human homologue STIM1 significantly reduced CRAC channel activity in Jurkat T cells. RNAi-mediated knockdown of STIM1 inhibited TG- or agonist-dependent Ca2+ entry in HEK293 or SH-SY5Y cells. Conversely, overexpression of STIM1 in HEK293 cells modestly enhanced TG-induced Ca2+ entry. We propose that STIM1, a ubiquitously expressed protein that is conserved from Drosophila to mammalian cells, plays an essential role in SOC influx and may be a common component of SOC and CRAC channels.

1,751 citations

Journal ArticleDOI
Adam C. Naj1, Gyungah Jun2, Gary W. Beecham1, Li-San Wang3  +153 moreInstitutions (38)
TL;DR: The Alzheimer Disease Genetics Consortium performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1), two replication stages (stages 2 and 3), and both joint analysis and meta-analysis approaches were used.
Abstract: The Alzheimer Disease Genetics Consortium (ADGC) performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1) and two replication stages (stages 2 and 3). Both joint analysis and meta-analysis approaches were used. We obtained genome-wide significant results at MS4A4A (rs4938933; stages 1 and 2, meta-analysis P (P(M)) = 1.7 × 10(-9), joint analysis P (P(J)) = 1.7 × 10(-9); stages 1, 2 and 3, P(M) = 8.2 × 10(-12)), CD2AP (rs9349407; stages 1, 2 and 3, P(M) = 8.6 × 10(-9)), EPHA1 (rs11767557; stages 1, 2 and 3, P(M) = 6.0 × 10(-10)) and CD33 (rs3865444; stages 1, 2 and 3, P(M) = 1.6 × 10(-9)). We also replicated previous associations at CR1 (rs6701713; P(M) = 4.6 × 10(-10), P(J) = 5.2 × 10(-11)), CLU (rs1532278; P(M) = 8.3 × 10(-8), P(J) = 1.9 × 10(-8)), BIN1 (rs7561528; P(M) = 4.0 × 10(-14), P(J) = 5.2 × 10(-14)) and PICALM (rs561655; P(M) = 7.0 × 10(-11), P(J) = 1.0 × 10(-10)), but not at EXOC3L2, to late-onset Alzheimer's disease susceptibility.

1,743 citations

Journal ArticleDOI
TL;DR: The 1993 Special Research Forum on Configurations as discussed by the authors was dedicated to the proposition that configurational theory and research can significantly advance understanding of people, groups, and organizations, and thus can be used to improve organizational analysis.
Abstract: The 1993 Special Research Forum on Configurations is dedicated to the proposition that configurational theory and research can significantly advance understanding of people, groups, and organizations. In this introductory essay, we define configurational approaches to organizational analysis, trace the history of configurational thinking, distinguish the contingency approach from the configurational approach, and highlight key contributions of the five empirical articles that make up the special research forum. Most of these articles report research conducted at the organizational level of analysis, but we argue that the configurational perspective has unrealized potential at other levels as well and suggest some configurational approaches to revitalizing theory and research at the individual and group levels.

1,729 citations

Journal ArticleDOI
TL;DR: CHD, CVD, and total mortality are significantly higher in US adults with than in those without MetS, and MetS more strongly predicts CHD,CVD,and total mortality than its individual components.
Abstract: Background— Mortality resulting from coronary heart disease (CHD), cardiovascular disease (CVD), and all causes in persons with diabetes and pre-existing CVD is high; however, these risks compared with those with metabolic syndrome (MetS) are unclear. We examined the impact of MetS on CHD, CVD, and overall mortality among US adults. Methods and Results— In a prospective cohort study, 6255 subjects 30 to 75 years of age (54% female) (representative of 64 million adults in the United States) from the Second National Health and Nutrition Examination Survey were followed for a mean±SD of 13.3±3.8 years. MetS was defined by modified National Cholesterol Education Program criteria. From sample-weighted multivariable Cox proportional-hazards regression, compared with those with neither MetS nor prior CVD, age-, gender-, and risk factor–adjusted hazard ratios (HRs) for CHD mortality were 2.02 (95% CI, 1.42 to 2.89) for those with MetS and 4.19 (95% CI, 3.04 to 5.79) for those with pre-existing CVD. For CVD mortal...

1,720 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