Institution
Sapienza University of Rome
Education•Rome, Lazio, Italy•
About: Sapienza University of Rome is a education organization based out in Rome, Lazio, Italy. It is known for research contribution in the topics: Population & Large Hadron Collider. The organization has 62002 authors who have published 155468 publications receiving 4397244 citations. The organization is also known as: La Sapienza & Università La Sapienza di Roma.
Papers published on a yearly basis
Papers
More filters
••
TL;DR: The current status of the Standard Model calculation of the anomalous magnetic moment of the muon is reviewed in this paper, where the authors present a detailed account of recent efforts to improve the calculation of these two contributions with either a data-driven, dispersive approach, or a first-principle, lattice approach.
801 citations
••
TL;DR: The results provide atomic-scale verification of a general mechanism originally proposed by Mars and van Krevelen in 1954 and are likely to be of general relevance for the mechanism of catalytic reactions at oxide surfaces.
Abstract: The structure of RuO(2)(110) and the mechanism for catalytic carbon monoxide oxidation on this surface were studied by low-energy electron diffraction, scanning tunneling microscopy, and density-functional calculations. The RuO(2)(110) surface exposes bridging oxygen atoms and ruthenium atoms not capped by oxygen. The latter act as coordinatively unsaturated sites-a hypothesis introduced long ago to account for the catalytic activity of oxide surfaces-onto which carbon monoxide can chemisorb and from where it can react with neighboring lattice-oxygen to carbon dioxide. Under steady-state conditions, the consumed lattice-oxygen is continuously restored by oxygen uptake from the gas phase. The results provide atomic-scale verification of a general mechanism originally proposed by Mars and van Krevelen in 1954 and are likely to be of general relevance for the mechanism of catalytic reactions at oxide surfaces.
801 citations
••
Medical Research Council1, University of Oxford2, National Institute for Health Research3, Structural Genomics Consortium4, University of Bristol5, University of Bath6, University of Queensland7, National Institutes of Health8, Cedars-Sinai Medical Center9, University of Toronto10, University of Alberta11, Memorial University of Newfoundland12, University of Leeds13, Norfolk and Norwich University Hospital14, Repatriation General Hospital15, University of Porto16, Sapienza University of Rome17, QIMR Berghofer Medical Research Institute18, Second Military Medical University19, Telethon Institute for Child Health Research20, Wellcome Trust Sanger Institute21, University of London22, Trinity College, Dublin23, Cardiff University24, Wellcome Trust25, Wellcome Trust Centre for Human Genetics26, St George's, University of London27, King's College London28, Churchill Hospital29, University of Leicester30, University of Cambridge31, Moorfields Eye Hospital32, University College London33, University of Texas Health Science Center at Houston34, Princess Alexandra Hospital35
TL;DR: In this paper, the identification of three variants in the RUNX3, LTBR-TNFRSF1A and IL12B regions convincingly associated with ankylosing spondylitis (P < 5 x 10(-8) in the combined discovery and replication datasets) and a further four loci at PTGER4, TBKBP1, ANTXR2 and CARD9 that show strong association across all their datasets (p < 5x 10(-6) overall, with support in each of the three datasets studied).
Abstract: Ankylosing spondylitis is a common form of inflammatory arthritis predominantly affecting the spine and pelvis that occurs in approximately 5 out of 1,000 adults of European descent. Here we report the identification of three variants in the RUNX3, LTBR-TNFRSF1A and IL12B regions convincingly associated with ankylosing spondylitis (P < 5 x 10(-8) in the combined discovery and replication datasets) and a further four loci at PTGER4, TBKBP1, ANTXR2 and CARD9 that show strong association across all our datasets (P < 5 x 10(-6) overall, with support in each of the three datasets studied). We also show that polymorphisms of ERAP1, which encodes an endoplasmic reticulum aminopeptidase involved in peptide trimming before HLA class I presentation, only affect ankylosing spondylitis risk in HLA-B27-positive individuals. These findings provide strong evidence that HLA-B27 operates in ankylosing spondylitis through a mechanism involving aberrant processing of antigenic peptides.
798 citations
••
TL;DR: In this article, the authors described linkage and association of type 1 diabetes to the CTLA-4 gene (cytotoxic T lymphocyte associated-4) on chromosome 2q33 (designated IDDM12), which is a strong candidate gene for T cell mediated autoimmune disease because it encodes a T cell receptor that mediates T cell apoptosis and is a vital negative regulator of T cell activation.
Abstract: Susceptibility to autoimmune insulin-dependent (type 1) diabetes mellitus is determined by a combination of environmental and genetic factors, which include variation in MHC genes on chromosome 6p21 (IDDM1) and the insulin gene on chromosome 11p15 (IDDM2). However, linkage to IDDM1 and IDDM2 cannot explain the clustering of type 1 diabetes in families, and a role for other genes is inferred. In the present report we describe linkage and association of type 1 diabetes to the CTLA-4 gene (cytotoxic T lymphocyte associated-4) on chromosome 2q33 (designated IDDM12). CTLA-4 is a strong candidate gene for T cell-mediated autoimmune disease because it encodes a T cell receptor that mediates T cell apoptosis and is a vital negative regulator of T cell activation. In addition, we provide supporting evidence that CTLA-4 is associated with susceptibility to Graves' disease, another organ-specific autoimmune disease.
798 citations
••
University of Birmingham1, Scripps Research Institute2, Public Health England3, University of São Paulo4, Scripps Health5, Harvard University6, Oswaldo Cruz Foundation7, Sapienza University of Rome8, University of Oxford9, Fred Hutchinson Cancer Research Center10, University of Washington11, University of Southampton12, Paul Ehrlich Institute13, University of Nottingham14
TL;DR: A protocol for generating coding-sequence-complete genomes, comprising an online primer design tool, a novel multiplex PCR enrichment protocol, optimized library preparation methods for the portable MinION sequencer and the Illumina range of instruments, and a bioinformatics pipeline for generating consensus sequences.
Abstract: Genome sequencing has become a powerful tool for studying emerging infectious diseases; however, genome sequencing directly from clinical samples (ie, without isolation and culture) remains challenging for viruses such as Zika, for which metagenomic sequencing methods may generate insufficient numbers of viral reads Here we present a protocol for generating coding-sequence-complete genomes, comprising an online primer design tool, a novel multiplex PCR enrichment protocol, optimized library preparation methods for the portable MinION sequencer (Oxford Nanopore Technologies) and the Illumina range of instruments, and a bioinformatics pipeline for generating consensus sequences The MinION protocol does not require an Internet connection for analysis, making it suitable for field applications with limited connectivity Our method relies on multiplex PCR for targeted enrichment of viral genomes from samples containing as few as 50 genome copies per reaction Viral consensus sequences can be achieved in 1-2 d by starting with clinical samples and following a simple laboratory workflow This method has been successfully used by several groups studying Zika virus evolution and is facilitating an understanding of the spread of the virus in the Americas The protocol can be used to sequence other viral genomes using the online Primal Scheme primer designer software It is suitable for sequencing either RNA or DNA viruses in the field during outbreaks or as an inexpensive, convenient method for use in the lab
797 citations
Authors
Showing all 62745 results
Name | H-index | Papers | Citations |
---|---|---|---|
Charles A. Dinarello | 190 | 1058 | 139668 |
Gregory Y.H. Lip | 169 | 3159 | 171742 |
Peter A. R. Ade | 162 | 1387 | 138051 |
H. Eugene Stanley | 154 | 1190 | 122321 |
Suvadeep Bose | 154 | 960 | 129071 |
P. de Bernardis | 152 | 680 | 117804 |
Bart Staels | 152 | 824 | 86638 |
Alessandro Melchiorri | 151 | 674 | 116384 |
Andrew H. Jaffe | 149 | 518 | 110033 |
F. Piacentini | 149 | 531 | 108493 |
Subir Sarkar | 149 | 1542 | 144614 |
Albert Bandura | 148 | 255 | 276143 |
Carlo Rovelli | 146 | 1502 | 103550 |
Robert C. Gallo | 145 | 825 | 68212 |
R. Kowalewski | 143 | 1815 | 135517 |