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Institution

University of Colorado Boulder

EducationBoulder, Colorado, United States
About: University of Colorado Boulder is a education organization based out in Boulder, Colorado, United States. It is known for research contribution in the topics: Population & Galaxy. The organization has 48794 authors who have published 115151 publications receiving 5387328 citations. The organization is also known as: CU Boulder & UCB.
Topics: Population, Galaxy, Poison control, Solar wind, Stars


Papers
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Journal ArticleDOI
21 May 2014-JAMA
TL;DR: The Lung Cancer Mutation Consortium was formed to perform multiplexed assays testing adenocarcinomas of the lung for drivers in 10 genes to enable clinicians to select targeted treatments and enroll patients into clinical trials.
Abstract: Importance Targeting oncogenic drivers (genomic alterations critical to cancer development and maintenance) has transformed the care of patients with lung adenocarcinomas. The Lung Cancer Mutation Consortium was formed to perform multiplexed assays testing adenocarcinomas of the lung for drivers in 10 genes to enable clinicians to select targeted treatments and enroll patients into clinical trials. Objectives To determine the frequency of oncogenic drivers in patients with lung adenocarcinomas and to use the data to select treatments targeting the identified driver(s) and measure survival. Design, Setting, and Participants From 2009 through 2012, 14 sites in the United States enrolled patients with metastatic lung adenocarcinomas and a performance status of 0 through 2 and tested their tumors for 10 drivers. Information was collected on patients, therapies, and survival. Interventions Tumors were tested for 10 oncogenic drivers, and results were used to select matched targeted therapies. Main Outcomes and Measures Determination of the frequency of oncogenic drivers, the proportion of patients treated with genotype-directed therapy, and survival. Results From 2009 through 2012, tumors from 1007 patients were tested for at least 1 gene and 733 for 10 genes (patients with full genotyping). An oncogenic driver was found in 466 of 733 patients (64%). Among these 733 tumors, 182 tumors (25%) had the KRAS driver; sensitizing EGFR , 122 (17%); ALK rearrangements, 57 (8%); other EGFR , 29 (4%); 2 or more genes, 24 (3%); ERBB2 (formerly HER2 ), 19 (3%); BRAF , 16 (2%); PIK3CA , 6 ( MET amplification, 5 ( NRAS , 5 ( MEK1 , 1 ( AKT1 , 0. Results were used to select a targeted therapy or trial in 275 of 1007 patients (28%). The median survival was 3.5 years (interquartile range [IQR], 1.96-7.70) for the 260 patients with an oncogenic driver and genotype-directed therapy compared with 2.4 years (IQR, 0.88-6.20) for the 318 patients with any oncogenic driver(s) who did not receive genotype-directed therapy (propensity score–adjusted hazard ratio, 0.69 [95% CI, 0.53-0.9], P = .006). Conclusions and Relevance Actionable drivers were detected in 64% of lung adenocarcinomas. Multiplexed testing aided physicians in selecting therapies. Although individuals with drivers receiving a matched targeted agent lived longer, randomized trials are required to determine if targeting therapy based on oncogenic drivers improves survival. Trial Registration clinicaltrials.gov Identifier:NCT01014286.

1,356 citations

Journal ArticleDOI
TL;DR: A meta-analysis of 48 neuroimaging studies of reappraisal suggests that reappRAisal involves the use of cognitive control to modulate semantic representations of an emotional stimulus, and these altered representations in turn attenuate activity in the amygdala.
Abstract: In recent years, an explosion of neuroimaging studies has examined cognitive reappraisal, an emotion regulation strategy that involves changing the way one thinks about a stimulus in order to change its affective impact Existing models broadly agree that reappraisal recruits frontal and parietal control regions to modulate emotional responding in the amygdala, but they offer competing visions of how this is accomplished One view holds that control regions engage ventromedial prefrontal cortex (vmPFC), an area associated with fear extinction, that in turn modulates amygdala responses An alternative view is that control regions modulate semantic representations in lateral temporal cortex that indirectly influence emotion-related responses in the amygdala Furthermore, while previous work has emphasized the amygdala, whether reappraisal influences other regions implicated in emotional responding remains unknown To resolve these questions, we performed a meta-analysis of 48 neuroimaging studies of reappraisal, most involving downregulation of negative affect Reappraisal consistently 1) activated cognitive control regions and lateral temporal cortex, but not vmPFC, and 2) modulated the bilateral amygdala, but no other brain regions This suggests that reappraisal involves the use of cognitive control to modulate semantic representations of an emotional stimulus, and these altered representations in turn attenuate activity in the amygdala

1,354 citations

Journal ArticleDOI
TL;DR: An optical-digital system that delivers near-diffraction-limited imaging performance with a large depth of field that is the standard incoherent optical system modified by a phase mask with digital processing of the resulting intermediate image.
Abstract: We designed an optical‐digital system that delivers near-diffraction-limited imaging performance with a large depth of field. This system is the standard incoherent optical system modified by a phase mask with digital processing of the resulting intermediate image. The phase mask alters or codes the received incoherent wave front in such a way that the point-spread function and the optical transfer function do not change appreciably as a function of misfocus. Focus-independent digital filtering of the intermediate image is used to produce a combined optical‐digital system that has a nearly diffraction limited point-spread function. This high-resolution extended depth of field is obtained through the expense of an increased dynamic range of the incoherent system. We use both the ambiguity function and the stationary-phase method to design these phase masks.

1,344 citations

Journal ArticleDOI
10 Jul 1992-Science
TL;DR: The data considerably strengthen the contention that the synaptic changes exhibited in LTP are the basis for spatial memory.
Abstract: Although long-term potentiation (LTP) has been studied as the mechanism for hippocampus-dependent learning and memory, evidence for this hypothesis is still incomplete. The mice with a mutation in the alpha-calcium-calmodulin-dependent kinase II (alpha-CaMKII), a synaptic protein enriched in the hippocampus, are appropriate for addressing this issue because the hippocampus of these mice is deficient in LTP but maintains intact postsynaptic mechanisms. These mutant mice exhibit specific learning impairments, an indication that alpha-CaMKII has a prominent role in spatial learning, but that it is not essential for some types of non-spatial learning. The data considerably strengthen the contention that the synaptic changes exhibited in LTP are the basis for spatial memory.

1,341 citations

Journal ArticleDOI
31 May 1996-Science
TL;DR: A second gene for autosomal dominant polycystic kidney disease was identified by positional cloning and it has amino acid similarity with PKD1, the Caenorhabditis elegans homolog of PKD 1, and the family of voltage-activated calcium channels.
Abstract: A second gene for autosomal dominant polycystic kidney disease was identified by positional cloning. Nonsense mutations in this gene (PKD2) segregated with the disease in three PKD2 families. The predicted 968-amino acid sequence of the PKD2 gene product has six transmembrane spans with intracellular amino- and carboxyl-termini. The PKD2 protein has amino acid similarity with PKD1, the Caenorhabditis elegans homolog of PKD1, and the family of voltage-activated calcium (and sodium) channels, and it contains a potential calcium-binding domain.

1,336 citations


Authors

Showing all 49233 results

NameH-indexPapersCitations
Yi Chen2174342293080
Robert J. Lefkowitz214860147995
Rob Knight2011061253207
Charles A. Dinarello1901058139668
Jie Zhang1784857221720
David Haussler172488224960
Bradley Cox1692150156200
Gang Chen1673372149819
Rodney S. Ruoff164666194902
Menachem Elimelech15754795285
Jay Hauser1552145132683
Robert E. W. Hancock15277588481
Robert Plomin151110488588
Thomas E. Starzl150162591704
Rajesh Kumar1494439140830
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023164
2022779
20216,286
20206,493
20196,063
20185,522