Institution
University of Paris
Education•Paris, France•
About: University of Paris is a education organization based out in Paris, France. It is known for research contribution in the topics: Population & Medicine. The organization has 102426 authors who have published 174180 publications receiving 5041753 citations. The organization is also known as: Sorbonne.
Topics: Population, Medicine, Context (language use), Transplantation, Gene
Papers published on a yearly basis
Papers
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University of North Carolina at Chapel Hill1, University of Pennsylvania2, University of Colorado Denver3, Tel Aviv University4, Baylor University Medical Center5, Durham University6, University of California, San Diego7, Mayo Clinic8, Northwestern University9, Nestlé10, Tufts University11, Boston Children's Hospital12, Icahn School of Medicine at Mount Sinai13, University of Texas Southwestern Medical Center14, Cincinnati Children's Hospital Medical Center15, Baylor College of Medicine16, Nationwide Children's Hospital17, University of Paris18, University of Health Sciences Antigua19, University of Illinois at Urbana–Champaign20, Shimane University21, University Hospitals Coventry and Warwickshire NHS Trust22, Harvard University23, Juntendo University24, University of Ljubljana25, National and Kapodistrian University of Athens26, University of Utah27, University of Adelaide28, University of South Florida29, University of Lausanne30, University College London31, Kaiser Permanente32, University of Newcastle33, Vanderbilt University34, Vrije Universiteit Brussel35, Federal University of Paraná36, Children's Memorial Hospital37, University of Amsterdam38
TL;DR: An updated diagnostic algorithm for EoE was developed, with removal of the PPI trial requirement, and the evidence suggests that PPIs are better classified as a treatment for esophageal eosinophilia that may be due to EOE than as a diagnostic criterion.
621 citations
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TL;DR: In this article, the longitudinal changes in insulin sensitivity during pregnancy were correlated with changes in placental hormones, cortisol, leptin, and tumor necrosis factor (TNF)-alpha.
Abstract: Historically, insulin resistance during pregnancy has been ascribed to increased production of placental hormones and cortisol. The purpose of this study was to test this hypothesis by correlating the longitudinal changes in insulin sensitivity during pregnancy with changes in placental hormones, cortisol, leptin, and tumor necrosis factor (TNF)-alpha. Insulin resistance was assessed in 15 women (5 with gestational diabetes mellitus [GDM] and 10 with normal glucose tolerance) using the euglycemic-hyperinsulinemic clamp procedure, before pregnancy (pregravid) and during early (12-14 weeks) and late (34-36 weeks) gestation. Body composition, plasma TNF-alpha, leptin, cortisol, and reproductive hormones (human chorionic gonadotropin, estradiol, progesterone, human placental lactogen, and prolactin) were measured in conjunction with the clamps. Placental TNF-alpha was measured in vitro using dually perfused human placental cotyledon from five additional subjects. Compared with pregravid, insulin resistance was evident during late pregnancy in all women (12.4 +/- 1.2 vs. 8.1 +/- 0.8 10(-2) mg. kg(-1) fat-free mass. min(-1). microU(-1). ml(-1)). TNF-alpha, leptin, cortisol, all reproductive hormones, and fat mass were increased in late pregnancy (P < 0.001). In vitro, most of the placental TNF-alpha (94%) was released into the maternal circulation; 6% was released to the fetal side. During late pregnancy, TNF-alpha was inversely correlated with insulin sensitivity (r = -0.69, P < 0.006). Furthermore, among all of the hormonal changes measured in this study, the change in TNF-alpha from pregravid to late pregnancy was the only significant predictor of the change in insulin sensitivity (r = -0.60, P < 0.02). The placental reproductive hormones and cortisol did not correlate with insulin sensitivity in late pregnancy. Multivariate stepwise regression analysis revealed that TNF-alpha was the most significant independent predictor of insulin sensitivity (r = -0.67, P < 0.0001), even after adjustment for fat mass by covariance (r = 0.46, P < 0.01). These observations challenge the view that the classical reproductive hormones are the primary mediators of change in insulin sensitivity during gestation and provide the basis for including TNF-alpha in a new paradigm to explain insulin resistance in pregnancy.
621 citations
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University of Queensland1, Nuffield Orthopaedic Centre2, Hanyang University3, Cedars-Sinai Medical Center4, National Institutes of Health5, University of Paris6, University of Oslo7, King Abdulaziz University8, Danube University Krems9, National Institute for Health and Welfare10, Second Military Medical University11, Ghent University12, National Autonomous University of Mexico13, University of Otago14, University of Toronto15, Royal Brisbane and Women's Hospital16, Autonomous University of Madrid17, Central University, India18, Wellcome Trust Sanger Institute19, University of Oxford20, Norfolk and Norwich University Hospital21, University of Cambridge22, University Health Network23, Memorial University of Newfoundland24, University of Alberta25, Nova Southeastern University26, Norwegian University of Science and Technology27, Universidad de La Sabana28, Spanish National Research Council29, Université Paris-Saclay30, Medical Research Council31
TL;DR: In this paper, the authors used the Illumina Immunochip microarray to perform a case-control association study involving 10,619 individuals with ankylosing spondylitis (cases) and 15,145 controls.
Abstract: Ankylosing spondylitis is a common, highly heritable inflammatory arthritis affecting primarily the spine and pelvis. In addition to HLA-B*27 alleles, 12 loci have previously been identified that are associated with ankylosing spondylitis in populations of European ancestry, and 2 associated loci have been identified in Asians. In this study, we used the Illumina Immunochip microarray to perform a case-control association study involving 10,619 individuals with ankylosing spondylitis (cases) and 15,145 controls. We identified 13 new risk loci and 12 additional ankylosing spondylitis-associated haplotypes at 11 loci. Two ankylosing spondylitis-associated regions have now been identified encoding four aminopeptidases that are involved in peptide processing before major histocompatibility complex (MHC) class I presentation. Protective variants at two of these loci are associated both with reduced aminopeptidase function and with MHC class I cell surface expression.
620 citations
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TL;DR: It is proved the existence of an optimal MAPE model and the universal consistency of Empirical Risk Minimization based on the MAPE is shown, and it is shown that finding the best model under theMAPE is equivalent to doing weighted Mean Absolute Error regression, and this weighting strategy is applied to kernel regression.
619 citations
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TL;DR: Compared with historical control subjects, patients who undergo thrombolysis within 6 hours of infarction onset may have a reduced risk of later VSD, and patients with VSDs selected for surgical repair had better outcomes than patients treated medically.
Abstract: Background —Ventricular septal defect (VSD) complicating acute myocardial infarction has been studied primarily in small, prethrombolytic-era trials. Our goal was to determine clinical predictors and angiographic and clinical outcomes of this complication in the thrombolytic era. Methods and Results —We compared enrollment characteristics, angiographic patterns, and outcomes (30-day and 1-year mortality) of patients enrolled in the Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries (GUSTO-I) trial with and without a confirmed diagnosis of VSD. Univariable and multivariable analyses were used to assess relations between enrollment factors and the development of VSD. In all, 84 of the 41 021 patients (0.2%) developed VSD, a smaller percentage than reported in the prethrombolytic era. The median time from symptom onset to VSD diagnosis was 1 day. Enrollment factors most associated with this complication were advanced age, anterior infarction, female sex, and no previous smoking. The infarct artery was more often the left anterior descending and more likely to be totally occluded in patients who developed VSD. Mortality at 30 days was higher in patients with VSDs than in those without this complication (73.8% versus 6.8%, P Conclusions —Compared with historical control subjects, patients who undergo thrombolysis within 6 hours of infarction onset may have a reduced risk of later VSD. If patients develop this mechanical complication, however, it typically occurs sooner than described in the prethrombolytic era. Despite improvements in medical therapy and percutaneous and surgical techniques, mortality with this complication remains extremely high.
619 citations
Authors
Showing all 102613 results
Name | H-index | Papers | Citations |
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Guido Kroemer | 236 | 1404 | 246571 |
David H. Weinberg | 183 | 700 | 171424 |
Paul M. Thompson | 183 | 2271 | 146736 |
Chris Sander | 178 | 713 | 233287 |
Sophie Henrot-Versille | 171 | 957 | 157040 |
Richard H. Friend | 169 | 1182 | 140032 |
George P. Chrousos | 169 | 1612 | 120752 |
Mika Kivimäki | 166 | 1515 | 141468 |
Martin Karplus | 163 | 831 | 138492 |
William J. Sandborn | 162 | 1317 | 108564 |
Darien Wood | 160 | 2174 | 136596 |
Monique M.B. Breteler | 159 | 546 | 93762 |
Paul Emery | 158 | 1314 | 121293 |
Wolfgang Wagner | 156 | 2342 | 123391 |
Joao Seixas | 153 | 1538 | 115070 |