Institution
University of California, Irvine
Education•Irvine, 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 published on a yearly basis
Papers
More filters
••
University of Washington1, University of Tennessee Health Science Center2, University of Arizona3, Rutgers University4, University of Iowa5, Rush University Medical Center6, Fred Hutchinson Cancer Research Center7, Pfizer8, Brown University9, University of Nevada, Reno10, University of Texas at San Antonio11, Kaiser Permanente12, University of California, Los Angeles13, University of Cincinnati14, Baylor College of Medicine15, University of North Carolina at Chapel Hill16, Wayne State University17, Howard University18, George Washington University19, University of California, Irvine20, Ohio State University21, Medical College of Wisconsin22, University of Pittsburgh23, Stony Brook University24, University of California, San Diego25, University of Alabama at Birmingham26, Harvard University27, University of Minnesota28, Yeshiva University29, University of Massachusetts Medical School30, University of Miami31, University of Florida32, Emory University33, University of California, Davis34, National Institutes of Health35, University of Wisconsin-Madison36, Stanford University37, Northwestern University38, Wake Forest University39, University at Buffalo40
TL;DR: A low-fat dietary pattern intervention did not reduce the risk of colorectal cancer in postmenopausal women during 8.1 years of follow-up, and secondary analyses suggested potential interactions with baseline aspirin use and combined estrogen-progestin use status.
Abstract: ContextObservational studies and polyp recurrence trials are not conclusive regarding the effects of a low-fat dietary pattern on risk of colorectal cancer, necessitating a primary prevention trial.ObjectiveTo evaluate the effects of a low-fat eating pattern on risk of colorectal cancer in postmenopausal women.Design, Setting, and ParticipantsThe Women’s Health Initiative Dietary Modification Trial, a randomized controlled trial conducted in 48 835 postmenopausal women aged 50 to 79 years recruited between 1993 and 1998 from 40 clinical centers throughout the United States.InterventionsParticipants were randomly assigned to the dietary modification intervention (n = 19 541; 40%) or the comparison group (n = 29 294; 60%).The intensive behavioral modification program aimed to motivate and support reductions in dietary fat, to increase consumption of vegetables and fruits, and to increase grain servings by using group sessions, self-monitoring techniques, and other tailored and targeted strategies. Women in the comparison group continued their usual eating pattern.Main Outcome MeasureInvasive colorectal cancer incidence.ResultsA total of 480 incident cases of invasive colorectal cancer occurred during a mean follow-up of 8.1 (SD, 1.7) years. Intervention group participants significantly reduced their percentage of energy from fat by 10.7% more than did the comparison group at 1 year, and this difference between groups was mostly maintained (8.1% at year 6). Statistically significant increases in vegetable, fruit, and grain servings were also made. Despite these dietary changes, there was no evidence that the intervention reduced the risk of invasive colorectal cancer during the follow-up period. There were 201 women with invasive colorectal cancer (0.13% per year) in the intervention group and 279 (0.12% per year) in the comparison group (hazard ratio, 1.08; 95% confidence interval, 0.90-1.29). Secondary analyses suggested potential interactions with baseline aspirin use and combined estrogen-progestin use status (P = .01 for each). Colorectal examination rates, although not protocol defined, were comparable between the intervention and comparison groups. Similar results were seen in analyses adjusting for adherence to the intervention.ConclusionIn this study, a low-fat dietary pattern intervention did not reduce the risk of colorectal cancer in postmenopausal women during 8.1 years of follow-up.Clinical Trials RegistrationClinicalTrials.gov Identifier: NCT00000611
655 citations
••
TL;DR: iMGLs were used to examine the effects of Aβ fibrils and brain-derived tau oligomers on AD-related gene expression and to interrogate mechanisms involved in synaptic pruning, and whole-transcriptome analysis demonstrates that they are highly similar to cultured adult and fetal human microglia.
655 citations
••
TL;DR: The mechanical properties of the underlying ECM regulate Rho‐mediated contractility in SMCs by disrupting a presumptive cell‐ECM force balance, which in turn regulates cytoskeletal assembly and ultimately, cell migration.
Abstract: Increasing evidence suggests that mechanical cues inherent to the extracellular matrix (ECM) may be equally as critical as its chemical identity in regulating cell behavior. We hypothesized that the mechanical properties of the ECM directly regulate the motility of vascular smooth muscle cells (SMCs) and tested this hypothesis using polyacrylamide substrates with tunable mechanical properties. Quantification of the migration speed on uniformly compliant hydrogels spanning a range of stiffnesses (Young's moduli values from 1.0 to 308 kPa for acrylamide/bisacrylamide ratios between 5/0.1% and 15/1.2%, respectively) revealed a biphasic dependence on substrate compliance, suggesting the existence of an optimal substrate stiffness capable of supporting maximal migration. The value of this optimal stiffness shifted depending on the concentration of ECM protein covalently attached to the substrate. Specifically, on substrates presenting a theoretical density of 0.8 microg/cm(2) fibronectin, the maximum speed of 0.74 +/- 0.09 microm/min was achieved on a 51.9 kPa gel; on substrates presenting a theoretical density of 8.0 microg/cm(2) fibronectin, the maximum speed of 0.72 +/- 0.06 microm/min occurred on a softer 21.6 kPa gel. Pre-treatment of cells with Y27632, an inhibitor of the Rho/Rho-kinase (ROCK) pathway, reduced these observed maxima to values comparable to those on non-optimal stiffnesses. In parallel, quantification of TritonX-insoluble vinculin via Western blotting, coupled with qualitative fluorescent microscopy, revealed that the formation of focal adhesions and actin stress fibers also depends on ECM stiffness. Combined, these data suggest that the mechanical properties of the underlying ECM regulate Rho-mediated contractility in SMCs by disrupting a presumptive cell-ECM force balance, which in turn regulates cytoskeletal assembly and ultimately, cell migration.
655 citations
••
TL;DR: There is now convincing in vitro evidence that E( 2) can modulate the functions of neural and vascular cells via non-genomic actions, and the actions of discrete pools of E(2) receptors are likely to contribute to the overall effects of the sex steroids.
Abstract: Functional evidence for the existence of plasma membrane estrogen receptors in a variety of cell types continues to accumulate. Many of these functions originate from rapid signaling events, transduced in response to 17beta-estradiol (E(2)). It has been convincingly shown that E(2) activates phosphoinositol 3-kinase and protein kinase B/AKT, and stimulates ERK and p38 MAP kinases. In part, this stems from G-protein activation and the resulting calcium flux. As a result, the link between E(2) action at the cell membrane and discrete biological actions in the cell has been strengthened. There is now convincing in vitro evidence that E(2) can modulate the functions of neural and vascular cells via non-genomic actions. Thus, the actions of discrete pools of E(2) receptors are likely to contribute to the overall effects of the sex steroids.
654 citations
••
TL;DR: During the entire period, the mass loss concentrated in areas closest to warm, salty, subsurface, circumpolar deep water (CDW), consistent with enhanced polar westerlies pushing CDW toward Antarctica to melt its floating ice shelves, destabilize the glaciers, and raise sea level.
Abstract: We use updated drainage inventory, ice thickness, and ice velocity data to calculate the grounding line ice discharge of 176 basins draining the Antarctic Ice Sheet from 1979 to 2017. We compare the results with a surface mass balance model to deduce the ice sheet mass balance. The total mass loss increased from 40 ± 9 Gt/y in 1979–1990 to 50 ± 14 Gt/y in 1989–2000, 166 ± 18 Gt/y in 1999–2009, and 252 ± 26 Gt/y in 2009–2017. In 2009–2017, the mass loss was dominated by the Amundsen/Bellingshausen Sea sectors, in West Antarctica (159 ± 8 Gt/y), Wilkes Land, in East Antarctica (51 ± 13 Gt/y), and West and Northeast Peninsula (42 ± 5 Gt/y). The contribution to sea-level rise from Antarctica averaged 3.6 ± 0.5 mm per decade with a cumulative 14.0 ± 2.0 mm since 1979, including 6.9 ± 0.6 mm from West Antarctica, 4.4 ± 0.9 mm from East Antarctica, and 2.5 ± 0.4 mm from the Peninsula (i.e., East Antarctica is a major participant in the mass loss). During the entire period, the mass loss concentrated in areas closest to warm, salty, subsurface, circumpolar deep water (CDW), that is, consistent with enhanced polar westerlies pushing CDW toward Antarctica to melt its floating ice shelves, destabilize the glaciers, and raise sea level.
654 citations
Authors
Showing all 47751 results
Name | H-index | Papers | Citations |
---|---|---|---|
Daniel Levy | 212 | 933 | 194778 |
Rob Knight | 201 | 1061 | 253207 |
Lewis C. Cantley | 196 | 748 | 169037 |
Dennis W. Dickson | 191 | 1243 | 148488 |
Terrie E. Moffitt | 182 | 594 | 150609 |
Joseph Biederman | 179 | 1012 | 117440 |
John R. Yates | 177 | 1036 | 129029 |
John A. Rogers | 177 | 1341 | 127390 |
Avshalom Caspi | 170 | 524 | 113583 |
Yang Gao | 168 | 2047 | 146301 |
Carl W. Cotman | 165 | 809 | 105323 |
John H. Seinfeld | 165 | 921 | 114911 |
Gregg C. Fonarow | 161 | 1676 | 126516 |
Jerome I. Rotter | 156 | 1071 | 116296 |
David Cella | 156 | 1258 | 106402 |