Institution
Erasmus University Rotterdam
Education•Rotterdam, Zuid-Holland, Netherlands•
About: Erasmus University Rotterdam is a education organization based out in Rotterdam, Zuid-Holland, Netherlands. It is known for research contribution in the topics: Population & Health care. The organization has 35466 authors who have published 91288 publications receiving 4510972 citations. The organization is also known as: EUR.
Papers published on a yearly basis
Papers
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TL;DR: This guideline was produced by a multidisciplinary group of experts in the field using the methodology of the Manual for ESHRE Guideline Development, including a thorough systematic search of the literature, quality assessment of the included papers up to September 2014 and consensus within the guideline group on all recommendations.
Abstract: study question: What is the optimal management of women with premature ovarian insufficiency (POI) based on the best available
evidence in the literature?
summary answer: The guideline development group (GDG) formulated 99 recommendations answering 31 key questions on the
diagnosis and treatment of women with POI.
what is known already: NA.
study design, size, duration: This guideline was produced by a multidisciplinary group of experts in the field using the methodology
of the Manual for ESHRE Guideline Development, including a thorough systematic search of the literature, quality assessment of the included
papers up to September 2014 and consensus within the guideline group on all recommendations. The GDG included a patient representative
to ensure input from women with POI. After finalization of the draft, the European Society for Human Reproduction and Embryology
(ESHRE) members and professional organizations were asked to review the guideline.
participants/materials, setting, methods: NA.
main results and the role of chance: The guideline provides 17 recommendations on diagnosis and assessment of POI and 46
recommendations on the different sequelae of POI and their consequences for monitoring and treatment. Furthermore, 24 recommendations
were formulated on hormone replacement therapy in women with POI, and two on alternative and complementary treatment. A chapter on
puberty induction resulted in five recommendations.
limitations, reasons for caution: The main limitation of the guideline is that, due to the lack of data, many of the recommendations
are based on expert opinion or indirect evidence from studies on post-menopausal women or women with Turner Syndrome.
wider implications of the findings: Despite the limitations, the guideline group is confident that this document will be able to
guide health care professionals in providing the best practice for managing women with POI given current evidence. Furthermore, the guideline
grouphas formulated research recommendations on the gaps in knowledge identified in the literature searches, in an attempt to stimulate research
on the key issues in POI.
801 citations
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TL;DR: This paper considers logistics network design in a reverse logistics context with a generic facility location model and uses this model to analyze the impact of product return flows on logistics networks.
Abstract: Efficient implementation of closed-loop supply chains requires setting up appropriate logistics structures for the arising flows of used and recovered products. In this paper we consider logistics network design in a reverse logistics context. We present a generic facility location model and discuss differences with traditional logistics settings. Moreover, we use our model to analyze the impact of product return flows on logistics networks. We show that the influence of product recovery is very much context dependent. While product recovery may efficiently be integrated in existing logistics structures in many cases, other examples require a more comprehensive approach redesigning a company's logistics network in an integral way
800 citations
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TL;DR: A genome-wide study to improve prognostic classification of ALL in children revealed a new ALL subtype, the underlying genetic abnormalities of which were characterised by comparative genomic hybridisation-arrays and molecular cytogenetics.
Abstract: Summary Background Genetic subtypes of acute lymphoblastic leukaemia (ALL) are used to determine risk and treatment in children. 25% of precursor B-ALL cases are genetically unclassified and have intermediate prognosis. We aimed to use a genome-wide study to improve prognostic classification of ALL in children. Methods We constructed a classifier based on gene expression in 190 children with newly diagnosed ALL (German Cooperative ALL [COALL] discovery cohort) by use of double-loop cross-validation and validated this in an independent cohort of 107 newly diagnosed patients (Dutch Childhood Oncology Group [DCOG] independent validation cohort). Hierarchical cluster analysis with classifying gene-probe sets revealed a new ALL subtype, the underlying genetic abnormalities of which were characterised by comparative genomic hybridisation-arrays and molecular cytogenetics. Findings Our classifier predicted ALL subtype with a median accuracy of 90·0% (IQR 88·3–91·7) in the discovery cohort and correctly identified 94 of 107 patients (accuracy 87·9%) in the independent validation cohort. Without our classifier, 44 children in the COALL cohort and 33 children in the DCOG cohort would have been classified as B-other. However, hierarchical clustering showed that many of these genetically unclassified cases clustered with BCR–ABL1 -positive cases: 30 (19%) of 154 children with precursor B-ALL in the COALL cohort and 14 (15%) of 92 children with precursor B-ALL in the DCOG cohort had this BCR–ABL1 -like disease. In the COALL cohort, these patients had unfavourable outcome (5-year disease-free survival 59·5%, 95% CI 37·1–81·9) compared with patients with other precursor B-ALL (84·4%, 76·8–92·1%; p=0·012), a prognosis similar to that of patients with BCR–ABL1 -positive ALL (51·9%, 23·1–80·6%). In the DCOG cohort, the prognosis of BCR–ABL1 -like disease (57·1%, 31·2–83·1%) was worse than that of other precursor B-ALL (79·2%, 70·2–88·3%; p=0.026), and similar to that of BCR–ABL1 -positive ALL (32·5%, 2·3–62·7%). 36 (82%) of the patients with BCR–ABL1 -like disease had deletions in genes involved in B-cell development, including IKZF1, TCF3, EBF1, PAX5, and VPREB1 ; only nine (36%) of 25 patients with B-other ALL had deletions in these genes (p=0·0002). Compared with other precursor B-ALL cells, BCR–ABL1 -like cells were 73 times more resistant to L-asparaginase (p=0·001) and 1·6 times more resistant to daunorubicin (p=0·017), but toxicity of prednisolone and vincristine did not differ. Interpretation New treatment strategies are needed to improve outcome for this newly identified high-risk subtype of ALL. Funding Dutch Cancer Society, Sophia Foundation for Medical Research, Paediatric Oncology Foundation Rotterdam, Centre of Medical Systems Biology of the Netherlands Genomics Initiative/Netherlands Organisation for Scientific Research, American National Institute of Health, American National Cancer Institute, and American Lebanese Syrian Associated Charities.
800 citations
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VU University Amsterdam1, Erasmus University Rotterdam2, Karolinska Institutet3, Charité4, Virginia Commonwealth University5, South London and Maudsley NHS Foundation Trust6, QIMR Berghofer Medical Research Institute7, King's College London8, University of Southern Denmark9, University of California, Riverside10, University of Southern California11, University of Minnesota12, University of Queensland13, University College London14, Johns Hopkins University15, University of California, Los Angeles16, University of Crete17, Harvard University18, Veterans Health Administration19, Icahn School of Medicine at Mount Sinai20, Yale University21, Haukeland University Hospital22, Trinity College, Dublin23, University of Edinburgh24, North Shore-LIJ Health System25, Hofstra University26, National Institutes of Health27, University of Bergen28, Oslo University Hospital29, National University of Ireland, Galway30, University of Helsinki31, University of Oslo32, Martin Luther University of Halle-Wittenberg33, Duke University34, Mental Health Research Institute35, National and Kapodistrian University of Athens36, University of Colorado Boulder37, Imperial College London38, University of Manchester39, Wellcome Trust40, Manchester Academic Health Science Centre41, Stanford University42, University of Oregon43, University of Toronto44, University of Michigan45, Erasmus University Medical Center46, Broad Institute47, University of North Carolina at Chapel Hill48
TL;DR: A large-scale genetic association study of intelligence identifies 190 new loci and implicates 939 new genes related to neurogenesis, neuron differentiation and synaptic structure, a major step forward in understanding the neurobiology of cognitive function as well as genetically related neurological and psychiatric disorders.
Abstract: Intelligence is highly heritable1 and a major determinant of human health and well-being2. Recent genome-wide meta-analyses have identified 24 genomic loci linked to variation in intelligence3-7, but much about its genetic underpinnings remains to be discovered. Here, we present a large-scale genetic association study of intelligence (n = 269,867), identifying 205 associated genomic loci (190 new) and 1,016 genes (939 new) via positional mapping, expression quantitative trait locus (eQTL) mapping, chromatin interaction mapping, and gene-based association analysis. We find enrichment of genetic effects in conserved and coding regions and associations with 146 nonsynonymous exonic variants. Associated genes are strongly expressed in the brain, specifically in striatal medium spiny neurons and hippocampal pyramidal neurons. Gene set analyses implicate pathways related to nervous system development and synaptic structure. We confirm previous strong genetic correlations with multiple health-related outcomes, and Mendelian randomization analysis results suggest protective effects of intelligence for Alzheimer's disease and ADHD and bidirectional causation with pleiotropic effects for schizophrenia. These results are a major step forward in understanding the neurobiology of cognitive function as well as genetically related neurological and psychiatric disorders.
800 citations
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TL;DR: In this paper, the authors address the relationship between business ownership and economic development and find that low barriers to entry and exit of businesses are necessary conditions for the equilibrium seeking mechanisms that are vital for a sound economic development.
Abstract: In the present paper we address the relationship between business ownership and economic development. We will focus upon three issues. First, how is the equilibrium rate of business ownership related to the stage of economic development? Second, what is the speed of convergence towards the equilibrium rate when the rate of business ownership is out-of-equilibrium? Third, to what extent does deviating from the equilibrium rate of business ownership hamper economic growth? Hypotheses concerning all three issues are formulated in the framework of a new two-equation model. We find confirmation for the hypothesized economic growth penalty on deviations from the equilibrium rate of business ownership using a data panel of 23 OECD countries. An important policy implication of our exercises is that low barriers to entry and exit of businesses are necessary conditions for the equilibrium seeking mechanisms that are vital for a sound economic development.
798 citations
Authors
Showing all 35695 results
Name | H-index | Papers | Citations |
---|---|---|---|
Walter C. Willett | 334 | 2399 | 413322 |
Meir J. Stampfer | 277 | 1414 | 283776 |
Albert Hofman | 267 | 2530 | 321405 |
Graham A. Colditz | 261 | 1542 | 256034 |
Paul M. Ridker | 233 | 1242 | 245097 |
Ralph B. D'Agostino | 226 | 1287 | 229636 |
John Q. Trojanowski | 226 | 1467 | 213948 |
David J. Hunter | 213 | 1836 | 207050 |
André G. Uitterlinden | 199 | 1229 | 156747 |
Robert M. Califf | 196 | 1561 | 167961 |
Eric J. Topol | 193 | 1373 | 151025 |
Frank E. Speizer | 193 | 636 | 135891 |
Bernard Rosner | 190 | 1162 | 147661 |
William B. Kannel | 188 | 533 | 175659 |
Patrick W. Serruys | 186 | 2427 | 173210 |