Institution
Yale University
Education•New Haven, Connecticut, United States•
About: Yale University is a education organization based out in New Haven, Connecticut, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 89824 authors who have published 220665 publications receiving 12834776 citations. The organization is also known as: Yale & Collegiate School.
Topics: Population, Poison control, Medicine, Cancer, Health care
Papers published on a yearly basis
Papers
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TL;DR: Providing specific definitions for compliance and persistence is important for sound quantitative expressions of patients' drug dosing histories and their explanatory power for clinical and economic events and adoption by health outcomes researchers will provide a consistent framework and lexicon for research.
1,920 citations
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TL;DR: A novel potential cell surface receptor of the tyrosine kinase gene family has been identified and characterized by molecular cloning and its primary sequence is very similar to that of the human epidermal growth factor receptor and the v-erbB oncogene product.
Abstract: A novel potential cell surface receptor of the tyrosine kinase gene family has been identified and characterized by molecular cloning. Its primary sequence is very similar to that of the human epidermal growth factor receptor and the v-erbB oncogene product; the chromosomal location of the gene for this protein is coincident with the neu oncogene, which suggests that the two genes may be identical.
1,919 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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Hobart Corporation1, University of Copenhagen2, Spanish National Research Council3, University of Évora4, Conservation International5, University of Wollongong6, University of Hong Kong7, National Cheng Kung University8, Umeå University9, James Cook University10, Commonwealth Scientific and Industrial Research Organisation11, University of Cape Town12, Stellenbosch University13, National Oceanic and Atmospheric Administration14, Monash University15, Yale University16, University of Tasmania17, University of Picardie Jules Verne18, Southern Cross University19, University of Western Australia20, University of Eastern Finland21, University of Queensland22, Zoological Society of London23, National Oceanography Centre24, University of Florida25, University of California, Irvine26, La Trobe University27, University of British Columbia28, Academia Sinica29, University of New South Wales30
TL;DR: The negative effects of climate change cannot be adequately anticipated or prepared for unless species responses are explicitly included in decision-making and global strategic frameworks, and feedbacks on climate itself are documented.
Abstract: Distributions of Earth’s species are changing at accelerating rates, increasingly driven by human-mediated climate change. Such changes are already altering the composition of ecological communities, but beyond conservation of natural systems, how and why does this matter? We review evidence that climate-driven species redistribution at regional to global scales affects ecosystem functioning, human well-being, and the dynamics of climate change itself. Production of natural resources required for food security, patterns of disease transmission, and processes of carbon sequestration are all altered by changes in species distribution. Consideration of these effects of biodiversity redistribution is critical yet lacking in most mitigation and adaptation strategies, including the United Nation’s Sustainable Development Goals.
1,917 citations
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TL;DR: Results indicate that survivin may counteract a default induction of apoptosis in G2/M phase of the cell cycle in a cycle-regulated manner and indicate that the overexpression of survivin in cancer may overcome this apoptotic checkpoint and favour aberrant progression of transformed cells through mitosis.
Abstract: Progression of the cell cycle and control of apoptosis (programmed cell death) are thought to be intimately linked processes, acting to preserve homeostasis and developmental morphogenesis. Although proteins that regulate apoptosis have been implicated in restraining cell-cycle entry and controlling ploidy (chromosome number), the effector molecules at the interface between cell proliferation and cell survival have remained elusive. Here we show that a new inhibitor of apoptosis (IAP) protein, survivin, is expressed in the G2/M phase of the cell cycle in a cycle-regulated manner. At the beginning of mitosis, survivin associates with microtubules of the mitotic spindle in a specific and saturable reaction that is regulated by microtubule dynamics. Disruption of survivin-microtubule interactions results in loss of survivin's anti-apoptosis function and increased caspase-3 activity, a mechanism involved in cell death, during mitosis. These results indicate that survivin may counteract a default induction of apoptosis in G2/M phase. The overexpression of survivin in cancer may overcome this apoptotic checkpoint and favour aberrant progression of transformed cells through mitosis.
1,915 citations
Authors
Showing all 91064 results
Name | H-index | Papers | Citations |
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Richard A. Flavell | 231 | 1328 | 205119 |
Eugene Braunwald | 230 | 1711 | 264576 |
Matthias Mann | 221 | 887 | 230213 |
Bruce S. McEwen | 215 | 1163 | 200638 |
Robert J. Lefkowitz | 214 | 860 | 147995 |
Edward Giovannucci | 206 | 1671 | 179875 |
Rakesh K. Jain | 200 | 1467 | 177727 |
Francis S. Collins | 196 | 743 | 250787 |
Lewis C. Cantley | 196 | 748 | 169037 |
Martin White | 196 | 2038 | 232387 |
Ronald Klein | 194 | 1305 | 149140 |
Thomas C. Südhof | 191 | 653 | 118007 |
Michael Rutter | 188 | 676 | 151592 |
David H. Weinberg | 183 | 700 | 171424 |
Douglas R. Green | 182 | 661 | 145944 |