Institution
Indiana University
Education•Bloomington, Indiana, United States•
About: Indiana University is a education organization based out in Bloomington, Indiana, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 64480 authors who have published 150058 publications receiving 6392902 citations. The organization is also known as: Indiana University system & indiana.edu.
Topics: Population, Poison control, Context (language use), Health care, Cancer
Papers published on a yearly basis
Papers
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TL;DR: In this paper, the authors present two cases where public officials play a major role in the process of coproduction, a process through which inputs from individuals who are not “in” the same organization are transformed into goods and services.
1,922 citations
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TL;DR: The genome-wide characteristics of rare (<1% frequency) copy number variation in ASD are analysed using dense genotyping arrays to reveal many new genetic and functional targets in ASD that may lead to final connected pathways.
Abstract: The autism spectrum disorders (ASDs) are a group of conditions characterized by impairments in reciprocal social interaction and communication, and the presence of restricted and repetitive behaviours. Individuals with an ASD vary greatly in cognitive development, which can range from above average to intellectual disability. Although ASDs are known to be highly heritable ( approximately 90%), the underlying genetic determinants are still largely unknown. Here we analysed the genome-wide characteristics of rare (<1% frequency) copy number variation in ASD using dense genotyping arrays. When comparing 996 ASD individuals of European ancestry to 1,287 matched controls, cases were found to carry a higher global burden of rare, genic copy number variants (CNVs) (1.19 fold, P = 0.012), especially so for loci previously implicated in either ASD and/or intellectual disability (1.69 fold, P = 3.4 x 10(-4)). Among the CNVs there were numerous de novo and inherited events, sometimes in combination in a given family, implicating many novel ASD genes such as SHANK2, SYNGAP1, DLGAP2 and the X-linked DDX53-PTCHD1 locus. We also discovered an enrichment of CNVs disrupting functional gene sets involved in cellular proliferation, projection and motility, and GTPase/Ras signalling. Our results reveal many new genetic and functional targets in ASD that may lead to final connected pathways.
1,919 citations
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TL;DR: In this article, the applicability of vegetation fraction derived from a spectral mixture model as an alternative indicator of vegetation abundance was investigated based on examination of a Landsat Enhanced Thematic Mapper Plus (ETM+) image of Indianapolis City, IN, USA, acquired on June 22, 2002.
1,917 citations
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TL;DR: TIR1 is an auxin receptor that mediates Aux/IAA degradation and auxin-regulated transcription and the loss of TIR1 and three related F-box proteins eliminates saturable auxin binding in plant extracts.
Abstract: The plant hormone auxin regulates diverse aspects of plant growth and development. Recent studies indicate that auxin acts by promoting the degradation of the Aux/IAA transcriptional repressors through the action of the ubiquitin protein ligase SCFTIR1. The nature of the signalling cascade that leads to this effect is not known. However, recent studies indicate that the auxin receptor and other signalling components involved in this response are soluble factors. Using an in vitro pull-down assay, we demonstrate that the interaction between transport inhibitor response 1 (TIR1) and Aux/IAA proteins does not require stable modification of either protein. Instead auxin promotes the Aux/IAA–SCFTIR1 interaction by binding directly to SCFTIR1. We further show that the loss of TIR1 and three related F-box proteins eliminates saturable auxin binding in plant extracts. Finally, TIR1 synthesized in insect cells binds Aux/IAA proteins in an auxin-dependent manner. Together, these results indicate that TIR1 is an auxin receptor that mediates Aux/IAA degradation and auxin-regulated transcription.
1,900 citations
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TL;DR: Findings from a cohort study show that being abused or neglected as a child increases one's risk for delinquency, adult criminal behavior, and violent criminal behavior; however, the majority of abused and neglected children do not become delinquent, criminal, or violent.
Abstract: Despite widespread belief that violence begets violence, methodological problems substantially restrict knowledge of the long-term consequences of childhood victimization. Empirical evidence for this cycle of violence has been examined. Findings from a cohort study show that being abused or neglected as a child increases one's risk for delinquency, adult criminal behavior, and violent criminal behavior. However, the majority of abused and neglected children do not become delinquent, criminal, or violent. Caveats in interpreting these findings and their implications are discussed in this article.
1,897 citations
Authors
Showing all 64884 results
Name | H-index | Papers | Citations |
---|---|---|---|
Frank B. Hu | 250 | 1675 | 253464 |
Stuart H. Orkin | 186 | 715 | 112182 |
Bruce M. Spiegelman | 179 | 434 | 158009 |
David R. Williams | 178 | 2034 | 138789 |
D. M. Strom | 176 | 3167 | 194314 |
Markus Antonietti | 176 | 1068 | 127235 |
Lei Jiang | 170 | 2244 | 135205 |
Brenda W.J.H. Penninx | 170 | 1139 | 119082 |
Nahum Sonenberg | 167 | 647 | 104053 |
Carl W. Cotman | 165 | 809 | 105323 |
Yang Yang | 164 | 2704 | 144071 |
Jaakko Kaprio | 163 | 1532 | 126320 |
Ralph A. DeFronzo | 160 | 759 | 132993 |
Gavin Davies | 159 | 2036 | 149835 |
Tyler Jacks | 158 | 463 | 115172 |