Institution
Lund University
Education•Lund, Sweden•
About: Lund University is a education organization based out in Lund, Sweden. It is known for research contribution in the topics: Population & Cancer. The organization has 42345 authors who have published 124676 publications receiving 5016438 citations. The organization is also known as: Lunds Universitet & University of Lund.
Topics: Population, Cancer, Breast cancer, Insulin, Transplantation
Papers published on a yearly basis
Papers
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Wellcome Trust Sanger Institute1, University of Michigan2, University of Oxford3, University of Geneva4, University of Exeter5, Greifswald University Hospital6, National Research Council7, University of Bristol8, University of Colorado Boulder9, Fred Hutchinson Cancer Research Center10, University of Washington11, SUNY Downstate Medical Center12, Erasmus University Rotterdam13, University of Trieste14, VU University Amsterdam15, King's College London16, South London and Maudsley NHS Foundation Trust17, University of Edinburgh18, Harvard University19, National Institutes of Health20, Harokopio University21, Innsbruck Medical University22, Broad Institute23, Lund University24, University of Helsinki25, Norwegian University of Science and Technology26, University of Cambridge27, University of Minnesota28, Technische Universität München29, University of North Carolina at Chapel Hill30, University of Toronto31, McGill University32, Leiden University33, University of Pennsylvania34, University of Groningen35, Utrecht University36, Churchill Hospital37
TL;DR: A reference panel of 64,976 human haplotypes at 39,235,157 SNPs constructed using whole-genome sequence data from 20 studies of predominantly European ancestry leads to accurate genotype imputation at minor allele frequencies as low as 0.1% and a large increase in the number of SNPs tested in association studies.
Abstract: We describe a reference panel of 64,976 human haplotypes at 39,235,157 SNPs constructed using whole-genome sequence data from 20 studies of predominantly European ancestry. Using this resource leads to accurate genotype imputation at minor allele frequencies as low as 0.1% and a large increase in the number of SNPs tested in association studies, and it can help to discover and refine causal loci. We describe remote server resources that allow researchers to carry out imputation and phasing consistently and efficiently.
2,149 citations
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TL;DR: The evolutionary collision of the authors' ancient genome with the nutritional qualities of recently introduced foods may underlie many of the chronic diseases of Western civilization.
2,120 citations
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King's College London1, Memorial Sloan Kettering Cancer Center2, Harvard University3, University of Pennsylvania4, Cedars-Sinai Medical Center5, City of Hope National Medical Center6, University of Texas MD Anderson Cancer Center7, Lund University8, University of Cologne9, Peter MacCallum Cancer Centre10, National Institute for Health Research11, AstraZeneca12
TL;DR: Findings from this phase 2 study provide positive proof of concept of the efficacy and tolerability of genetically targeted treatment with olaparib in BRCA-mutated advanced ovarian cancer.
2,119 citations
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TL;DR: It is shown that the vasodilator response to anandamide in isolated arteries is capsaicin-sensitive and accompanied by release of calcitonin-gene-related peptide (CGRP), which indicates that the vanilloid receptor may be another molecular target for endogenousAnandamide, besides cannabinoid receptors, in the nervous and cardiovascular systems.
Abstract: The endogenous cannabinoid receptor agonist anandamide is a powerful vasodilator of isolated vascular preparations, but its mechanism of action is unclear. Here we show that the vasodilator response to anandamide in isolated arteries is capsaicin-sensitive and accompanied by release of calcitonin-gene-related peptide (CGRP). The selective CGRP-receptor antagonist 8-37 CGRP, but not the cannabinoid CB1 receptor blocker SR141716A, inhibited the vasodilator effect of anandamide. Other endogenous (2-arachidonylglycerol, palmitylethanolamide) and synthetic (HU 210, WIN 55,212-2, CP 55,940) CB1 and CB2 receptor agonists could not mimic the action of anandamide. The selective 'vanilloid receptor' antagonist capsazepine inhibited anandamide-induced vasodilation and release of CGRP. In patch-clamp experiments on cells expressing the cloned vanilloid receptor (VR1), anandamide induced a capsazepine-sensitive current in whole cells and isolated membrane patches. Our results indicate that anandamide induces vasodilation by activating vanilloid receptors on perivascular sensory nerves and causing release of CGRP. The vanilloid receptor may thus be another molecular target for endogenous anandamide, besides cannabinoid receptors, in the nervous and cardiovascular systems.
2,113 citations
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SUNY Downstate Medical Center1, McMaster University2, McGill University3, Harvard University4, Toronto General Hospital5, University of Birmingham6, University of Pisa7, Dalhousie University8, University of Manchester9, University College London10, University of California, Los Angeles11, United Hospitals12, Lund University13, Johns Hopkins University14, St. Vincent's Health System15
TL;DR: This damage index for SLE records damage occurring in patients with SLE regardless of its cause and was demonstrated to have content, face, criterion, and discriminant validity.
Abstract: Objective. To develop and perform an initial validation of a damage index for systemic lupus erythematosus (SLE).
Methods. A list of items considered to reflect damage in SLE was generated through a nominal group process. A consensus as to which items to be included in an index was reached, together with rules for ascertainment. Each center submitted 2 assessments, 5 years apart, on 2 patients with active and 2 with inactive disease, of whom 1 had increased damage and the other had stable disease. Analysis of variance was used to test the factors physician, time, amount of damage, and activity status.
Results. Nineteen physicians completed the damage index on 42 case scenarios. The analysis revealed that the damage index could identify changes in damage seen in patients with both active and inactive disease. Patients who had active disease at both time points had a higher increase in damage. There was good agreement among the physicians on the assessment of damage in these patients.
Conclusion. This damage index for SLE records damage occurring in patients with SLE regardless of its cause. The index was demonstrated to have content, face, criterion, and discriminant validity.
2,095 citations
Authors
Showing all 42777 results
Name | H-index | Papers | Citations |
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Yi Chen | 217 | 4342 | 293080 |
Fred H. Gage | 216 | 967 | 185732 |
Kari Stefansson | 206 | 794 | 174819 |
Mark I. McCarthy | 200 | 1028 | 187898 |
Ruedi Aebersold | 182 | 879 | 141881 |
Jie Zhang | 178 | 4857 | 221720 |
Feng Zhang | 172 | 1278 | 181865 |
Martin G. Larson | 171 | 620 | 117708 |
Michael Snyder | 169 | 840 | 130225 |
Unnur Thorsteinsdottir | 167 | 444 | 121009 |
Anders Björklund | 165 | 769 | 84268 |
Carl W. Cotman | 165 | 809 | 105323 |
Dennis R. Burton | 164 | 683 | 90959 |
Jaakko Kaprio | 163 | 1532 | 126320 |
Panos Deloukas | 162 | 410 | 154018 |