Institution
University of São Paulo
Education•São Paulo, Brazil•
About: University of São Paulo is a education organization based out in São Paulo, Brazil. It is known for research contribution in the topics: Population & Context (language use). The organization has 136513 authors who have published 272320 publications receiving 5127869 citations. The organization is also known as: USP & Universidade de São Paulo.
Topics: Population, Context (language use), Medicine, Health care, Immune system
Papers published on a yearly basis
Papers
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TL;DR: Important improvements in health status and life expectancy are reported, which can be ascribed largely to progress in social determinants of health and to implementation of a comprehensive national health system with strong social participation.
471 citations
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Erasmus University Medical Center1, University of Ulsan2, Aarhus University Hospital3, University of Toronto4, Icahn School of Medicine at Mount Sinai5, Norfolk and Norwich University Hospital6, Stanford University7, University of São Paulo8, Veterans Health Administration9, Oulu University Hospital10, Leipzig University11, University Hospitals of Cleveland12, Columbia University Medical Center13, Imperial College London14
TL;DR: CABG had a mortality benefit over PCI in patients with multivessel disease, particularly those with diabetes and higher coronary complexity, and no benefit for CABG over PCI was seen in Patients with left main disease.
471 citations
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University of Oxford1, University of Birmingham2, University of São Paulo3, Oswaldo Cruz Foundation4, University of Washington5, Fred Hutchinson Cancer Research Center6, Evandro Chagas Institute7, Pasteur Institute8, Ontario Institute for Cancer Research9, University of Nottingham10, Scripps Research Institute11, University of California, San Francisco12, Mexican Social Security Institute13, National Autonomous University of Mexico14, Paul Ehrlich Institute15, Colorado State University16, University of Pittsburgh17, University Hospital Heidelberg18, State University of Feira de Santana19, Federal University of Amazonas20, Federal University of Tocantins21, University of Sydney22, University of Edinburgh23, National Institutes of Health24, University of Texas Medical Branch25
TL;DR: The origin and epidemic history of ZIKV in Brazil and the Americas remain poorly understood, despite the value of this information for interpreting observed trends in reported microcephaly and other birth defects as mentioned in this paper.
Abstract: Transmission of Zika virus (ZIKV) in the Americas was first confirmed in May 2015 in northeast Brazil. Brazil has had the highest number of reported ZIKV cases worldwide (more than 200,000 by 24 December 2016) and the most cases associated with microcephaly and other birth defects (2,366 confirmed by 31 December 2016). Since the initial detection of ZIKV in Brazil, more than 45 countries in the Americas have reported local ZIKV transmission, with 24 of these reporting severe ZIKV-associated disease. However, the origin and epidemic history of ZIKV in Brazil and the Americas remain poorly understood, despite the value of this information for interpreting observed trends in reported microcephaly. Here we address this issue by generating 54 complete or partial ZIKV genomes, mostly from Brazil, and reporting data generated by a mobile genomics laboratory that travelled across northeast Brazil in 2016. One sequence represents the earliest confirmed ZIKV infection in Brazil. Analyses of viral genomes with ecological and epidemiological data yield an estimate that ZIKV was present in northeast Brazil by February 2014 and is likely to have disseminated from there, nationally and internationally, before the first detection of ZIKV in the Americas. Estimated dates for the international spread of ZIKV from Brazil indicate the duration of pre-detection cryptic transmission in recipient regions. The role of northeast Brazil in the establishment of ZIKV in the Americas is further supported by geographic analysis of ZIKV transmission potential and by estimates of the basic reproduction number of the virus.
470 citations
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Manchester Academic Health Science Centre1, Boston Children's Hospital2, Harvard University3, University of Pavia4, Necker-Enfants Malades Hospital5, University of Liverpool6, University of Florence7, University of Colorado Denver8, NHS Ayrshire and Arran9, Children's Hospital at Westmead10, Royal Hospital for Sick Children11, Katholieke Universiteit Leuven12, University of Burgundy13, University of Brescia14, French Institute of Health and Medical Research15, McMaster Children's Hospital16, Paris Descartes University17, Leeds Teaching Hospitals NHS Trust18, University of São Paulo19, University of Glasgow20, University of Milan21, Great Ormond Street Hospital22, Pierre-and-Marie-Curie University23, University of Cape Town24, Southern General Hospital25, Children's National Medical Center26
TL;DR: It is demonstrated that aberrant sensing of nucleic acids can cause immune upregulation and heterozygous mutations in the cytosolic double-stranded RNA receptor gene IFIH1 (also called MDA5) cause a spectrum of neuroimmunological features consistently associated with an enhanced interferon state.
Abstract: The type I interferon system is integral to human antiviral immunity. However, inappropriate stimulation or defective negative regulation of this system can lead to inflammatory disease. We sought to determine the molecular basis of genetically uncharacterized cases of the type I interferonopathy Aicardi-Goutieres syndrome and of other undefined neurological and immunological phenotypes also demonstrating an upregulated type I interferon response. We found that heterozygous mutations in the cytosolic double-stranded RNA receptor gene IFIH1 (also called MDA5) cause a spectrum of neuroimmunological features consistently associated with an enhanced interferon state. Cellular and biochemical assays indicate that these mutations confer gain of function such that mutant IFIH1 binds RNA more avidly, leading to increased baseline and ligand-induced interferon signaling. Our results demonstrate that aberrant sensing of nucleic acids can cause immune upregulation.
470 citations
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TL;DR: The detailed variation with rigidity of the helium flux spectral index is presented for the first time and the spectral index progressively hardens at rigidities larger than 100 GV.
Abstract: Knowledge of the precise rigidity dependence of the helium flux is important in understanding the
origin, acceleration, and propagation of cosmic rays. A precise measurement of the helium flux in primary
cosmic rays with rigidity (momentum/charge) from 1.9 GV to 3 TV based on 50 million events is presented
and compared to the proton flux. The detailed variation with rigidity of the helium flux spectral index is
presented for the first time. The spectral index progressively hardens at rigidities larger than 100 GV. The
rigidity dependence of the helium flux spectral index is similar to that of the proton spectral index though
the magnitudes are different. Remarkably, the spectral index of the proton to helium flux ratio increases
with rigidity up to 45 GV and then becomes constant; the flux ratio above 45 GV is well described by a
single power law.
470 citations
Authors
Showing all 138091 results
Name | H-index | Papers | Citations |
---|---|---|---|
George M. Whitesides | 240 | 1739 | 269833 |
Peter Libby | 211 | 932 | 182724 |
Robert C. Nichol | 187 | 851 | 162994 |
Paul M. Thompson | 183 | 2271 | 146736 |
Terrie E. Moffitt | 182 | 594 | 150609 |
Douglas R. Green | 182 | 661 | 145944 |
Richard B. Lipton | 176 | 2110 | 140776 |
Robin M. Murray | 171 | 1539 | 116362 |
George P. Chrousos | 169 | 1612 | 120752 |
David A. Bennett | 167 | 1142 | 109844 |
Barry M. Popkin | 157 | 751 | 90453 |
David H. Adams | 155 | 1613 | 117783 |
Joao Seixas | 153 | 1538 | 115070 |
Matthias Egger | 152 | 901 | 184176 |
Ichiro Kawachi | 149 | 1216 | 90282 |