Institution
University of Colorado Boulder
Education•Boulder, 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 published on a yearly basis
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Memorial Sloan Kettering Cancer Center1, Harvard University2, Vanderbilt University3, Brigham and Women's Hospital4, University of Texas MD Anderson Cancer Center5, University of Colorado Boulder6, Partners HealthCare7, Emory University8, University of California, Los Angeles9, Johns Hopkins University10, University of Texas Southwestern Medical Center11, University of Pittsburgh12, Medical University of South Carolina13, National Institutes of Health14, Georgetown University15
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
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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
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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
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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
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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
Name | H-index | Papers | Citations |
---|---|---|---|
Yi Chen | 217 | 4342 | 293080 |
Robert J. Lefkowitz | 214 | 860 | 147995 |
Rob Knight | 201 | 1061 | 253207 |
Charles A. Dinarello | 190 | 1058 | 139668 |
Jie Zhang | 178 | 4857 | 221720 |
David Haussler | 172 | 488 | 224960 |
Bradley Cox | 169 | 2150 | 156200 |
Gang Chen | 167 | 3372 | 149819 |
Rodney S. Ruoff | 164 | 666 | 194902 |
Menachem Elimelech | 157 | 547 | 95285 |
Jay Hauser | 155 | 2145 | 132683 |
Robert E. W. Hancock | 152 | 775 | 88481 |
Robert Plomin | 151 | 1104 | 88588 |
Thomas E. Starzl | 150 | 1625 | 91704 |
Rajesh Kumar | 149 | 4439 | 140830 |