Institution
University of Lisbon
Education•Lisbon, Lisboa, Portugal•
About: University of Lisbon is a education organization based out in Lisbon, Lisboa, Portugal. It is known for research contribution in the topics: Population & European union. The organization has 19122 authors who have published 48503 publications receiving 1102623 citations. The organization is also known as: Universidade de Lisboa & Lisbon University.
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TL;DR: In this article, the authors present some of the recent results already obtained as well as the ones that are being developed in their laboratory, showing that the combination of high channel mobility and transparency produced at room temperature makes these thin film transistors a very promising low cost device for the next generation of invisible and flexible electronics.
355 citations
Cardiovascular Institute of the South1, Alfred I. duPont Hospital for Children2, University of Texas Southwestern Medical Center3, Baylor College of Medicine4, Florida Atlantic University5, University of Lisbon6, University of Paris7, University of Pennsylvania8, Boston Children's Hospital9, University of Amsterdam10, Central European Institute of Technology11, Ohio State University12, Queen Mary University of London13, Vanderbilt University14, West Virginia University15, Copenhagen University Hospital16, University of São Paulo17, Erasmus University Rotterdam18, Washington University in St. Louis19, Osaka University20
TL;DR: The Expert Consensus Panel recommends that FH genetic testing become the standard of care for patients with definite or probable FH, as well as for their at-risk relatives, and more accurate risk stratification.
354 citations
Trinity College, Dublin1, University of Pittsburgh2, Icahn School of Medicine at Mount Sinai3, University of Toronto4, University of Bologna5, Guy's and St Thomas' NHS Foundation Trust6, Goethe University Frankfurt7, King's College London8, University of Paris9, Pasteur Institute10, University College Dublin11, University of Lisbon12, Instituto Gulbenkian de Ciência13, University of Michigan14, Vanderbilt University15, Utrecht University16, University of Washington17, University of Oxford18, Memorial University of Newfoundland19, University of Miami20, McGill University21, University of Gothenburg22, University of Pennsylvania23, University of Manchester24, University of Illinois at Chicago25, Newcastle University26, New York University27, Nathan Kline Institute for Psychiatric Research28, University of Manitoba29, Cornell University30, Stanford University31, University of Toulouse32, Harvard University33, Indiana University34, National and Kapodistrian University of Athens35, Carnegie Mellon University36, Medical Research Council37, University of Iowa38, McMaster University39, Yale University40, University of Alberta41, University of British Columbia42, University of California, Los Angeles43, University of Utah44, University of North Carolina at Chapel Hill45, Autism Speaks46, Veterans Health Administration47, German Cancer Research Center48, Tufts University49, Centre national de la recherche scientifique50, French Institute of Health and Medical Research51, Pierre-and-Marie-Curie University52, Ohio State University53
TL;DR: Stage 2 of the Autism Genome Project genome-wide association study is reported, adding 1301 ASD families and bringing the total to 2705 families analysed, and it is reasonable to conclude that common variants affect the risk for ASD but their individual effects are modest.
Abstract: While it is apparent that rare variation can play an important role in the genetic architecture of autism spectrum disorders (ASDs), the contribution of common variation to the risk of developing ASD is less clear. To produce a more comprehensive picture, we report Stage 2 of the Autism Genome Project genome-wide association study, adding 1301 ASD families and bringing the total to 2705 families analysed (Stages 1 and 2). In addition to evaluating the association of individual single nucleotide polymorphisms (SNPs), we also sought evidence that common variants, en masse, might affect the risk. Despite genotyping over a million SNPs covering the genome, no single SNP shows significant association with ASD or selected phenotypes at a genome-wide level. The SNP that achieves the smallest P-value from secondary analyses is rs1718101. It falls in CNTNAP2, a gene previously implicated in susceptibility for ASD. This SNP also shows modest association with age of word/phrase acquisition in ASD subjects, of interest because features of language development are also associated with other variation in CNTNAP2. In contrast, allele scores derived from the transmission of common alleles to Stage 1 cases significantly predict case status in the independent Stage 2 sample. Despite being significant, the variance explained by these allele scores was small (Vm< 1%). Based on results from individual SNPs and their en masse effect on risk, as inferred from the allele score results, it is reasonable to conclude that common variants affect the risk for ASD but their individual effects are modest.
353 citations
Commonwealth Scientific and Industrial Research Organisation1, University of Sydney2, Australian Astronomical Observatory3, University of Lisbon4, National Radio Astronomy Observatory5, University of Nottingham6, University of Hertfordshire7, University of the Western Cape8, Victoria University of Wellington9, Ruhr University Bochum10, European Southern Observatory11, INAF12, University of Minnesota13, University College London14, Universidad de Guanajuato15, Durham University16, California Institute of Technology17, Institute of Cosmology and Gravitation, University of Portsmouth18, Max Planck Society19, Monash University, Clayton campus20, Cardiff University21, University of Washington22, UK Astronomy Technology Centre23, University of Edinburgh24, University of Cambridge25, Space Telescope Science Institute26, Macquarie University27, University of Tasmania28, University of Sussex29, National Centre for Radio Astrophysics30, Mount Stromlo Observatory31, University of British Columbia32
TL;DR: The EMU project as discussed by the authors is a wide-field radio continuum survey planned for the new Australian Square Kilometre Array Pathfinder (ASKAP) telescope, with a resolution of 10 arcsec.
Abstract: EMU is a wide-field radio continuum survey planned for the new Australian Square Kilometre Array Pathfinder (ASKAP) telescope. The primary goal of EMU is to make a deep (rms ~10 μJy/beam) radio continuum survey of the entire Southern sky at 1.3 GHz, extending as far North as +30° declination, with a resolution of 10 arcsec. EMU is expected to detect and catalogue about 70 million galaxies, including typical star-forming galaxies up to z ~ 1, powerful starbursts to even greater redshifts, and active galactic nuclei to the edge of the visible Universe. It will undoubtedly discover new classes of object. This paper defines the science goals and parameters of the survey, and describes the development of techniques necessary to maximise the science return from EMU.
353 citations
TL;DR: Observations support a role for human‐like telomeres in allowing longer lifespans to evolve, demonstrate the need to include telomere length in the analysis of comparative studies of oxidative protection in the biology of aging, and identify which mammals can be used as appropriate model organisms for the study of the role of telomees in human cancer and aging.
Abstract: Progressive telomere shortening from cell division (replicative aging) provides a barrier for human tumor progression. This program is not conserved in laboratory mice, which have longer telomeres and constitutive telomerase. Wild species that do / do not use replicative aging have been reported, but the evolution of different phenotypes and a conceptual framework for understanding their uses of telomeres is lacking. We examined telomeres / telomerase in cultured cells from > 60 mammalian species to place different uses of telomeres in a broad mammalian context. Phylogeny-based statistical analysis reconstructed ancestral states. Our analysis suggested that the ancestral mammalian phenotype included short telomeres (< 20 kb, as we now see in humans) and repressed telomerase. We argue that the repressed telomerase was a response to a higher mutation load brought on by the evolution of homeothermy. With telomerase repressed, we then see the evolution of replicative aging. Telomere length inversely correlated with lifespan, while telomerase expression co-evolved with body size. Multiple independent times smaller, shorter-lived species changed to having longer telomeres and expressing telomerase. Trade-offs involving reducing the energetic / cellular costs of specific oxidative protection mechanisms (needed to protect < 20 kb telomeres in the absence of telomerase) could explain this abandonment of replicative aging. These observations provide a conceptual framework for understanding different uses of telomeres in mammals, support a role for human-like telomeres in allowing longer lifespans to evolve, demonstrate the need to include telomere length in the analysis of comparative studies of oxidative protection in the biology of aging, and identify which mammals can be used as appropriate model organisms for the study of the role of telomeres in human cancer and aging.
352 citations
Authors
Showing all 19716 results
| Name | H-index | Papers | Citations |
|---|---|---|---|
| Joao Seixas | 153 | 1538 | 115070 |
| A. Gomes | 150 | 1862 | 113951 |
| Marco Costa | 146 | 1458 | 105096 |
| António Amorim | 136 | 1477 | 96519 |
| Osamu Jinnouchi | 135 | 885 | 86104 |
| P. Verdier | 133 | 1111 | 83862 |
| Andy Haas | 132 | 1096 | 87742 |
| Wendy Taylor | 131 | 1252 | 89457 |
| Steve McMahon | 130 | 878 | 78763 |
| Timothy Andeen | 129 | 1069 | 77593 |
| Heather Gray | 129 | 966 | 80970 |
| Filipe Veloso | 128 | 887 | 75496 |
| Nuno Filipe Castro | 128 | 960 | 76945 |
| Oliver Stelzer-Chilton | 128 | 1141 | 79154 |
| Isabel Marian Trigger | 128 | 974 | 77594 |