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Erasmus University Rotterdam

EducationRotterdam, 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.


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Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
Jeanne E. Savage1, Philip R. Jansen2, Philip R. Jansen1, Sven Stringer1, Kyoko Watanabe1, Julien Bryois3, Christiaan de Leeuw1, Mats Nagel, Swapnil Awasthi4, Peter B. Barr5, Jonathan R. I. Coleman6, Katrina L. Grasby7, Anke R. Hammerschlag1, Jakob Kaminski4, Robert Karlsson3, Eva Krapohl8, Max Lam, Marianne Nygaard9, Chandra A. Reynolds10, Joey W. Trampush11, Hannah Young12, Delilah Zabaneh8, Sara Hägg3, Narelle K. Hansell13, Ida K. Karlsson3, Sten Linnarsson3, Grant W. Montgomery7, Grant W. Montgomery13, Ana B. Muñoz-Manchado3, Erin Burke Quinlan8, Gunter Schumann8, Nathan G. Skene3, Nathan G. Skene14, Bradley T. Webb5, Tonya White2, Dan E. Arking15, Dimitrios Avramopoulos15, Robert M. Bilder16, Panos Bitsios17, Katherine E. Burdick18, Katherine E. Burdick19, Katherine E. Burdick20, Tyrone D. Cannon21, Ornit Chiba-Falek, Andrea Christoforou22, Elizabeth T. Cirulli, Eliza Congdon16, Aiden Corvin23, Gail Davies24, Ian J. Deary24, Pamela DeRosse25, Pamela DeRosse26, Dwight Dickinson27, Srdjan Djurovic28, Srdjan Djurovic29, Gary Donohoe30, Emily Drabant Conley, Johan G. Eriksson31, Thomas Espeseth32, Nelson A. Freimer16, Stella G. Giakoumaki17, Ina Giegling33, Michael Gill23, David C. Glahn21, Ahmad R. Hariri34, Alex Hatzimanolis35, Alex Hatzimanolis36, Matthew C. Keller37, Emma Knowles21, Deborah C. Koltai34, Bettina Konte33, Jari Lahti31, Stephanie Le Hellard28, Todd Lencz26, Todd Lencz25, David C. Liewald24, Edythe D. London16, Astri J. Lundervold28, Anil K. Malhotra26, Anil K. Malhotra25, Ingrid Melle28, Ingrid Melle32, Derek W. Morris30, Anna C. Need38, William Ollier39, Aarno Palotie40, Aarno Palotie18, Aarno Palotie31, Antony Payton39, Neil Pendleton41, Russell A. Poldrack42, Katri Räikkönen31, Ivar Reinvang32, Panos Roussos20, Panos Roussos19, Dan Rujescu33, Fred W. Sabb43, Matthew A. Scult34, Olav B. Smeland32, Nikolaos Smyrnis36, Nikolaos Smyrnis35, John M. Starr24, Vidar M. Steen28, Nikos C. Stefanis35, Nikos C. Stefanis36, Richard E. Straub15, Kjetil Sundet32, Henning Tiemeier2, Aristotle N. Voineskos44, Daniel R. Weinberger15, Elisabeth Widen31, Jin Yu, Gonçalo R. Abecasis45, Ole A. Andreassen32, Gerome Breen6, Lene Christiansen9, Birgit Debrabant9, Danielle M. Dick5, Andreas Heinz4, Jens Hjerling-Leffler3, M. Arfan Ikram46, Kenneth S. Kendler5, Nicholas G. Martin7, Sarah E. Medland7, Nancy L. Pedersen3, Robert Plomin8, Tinca J. C. Polderman1, Stephan Ripke47, Stephan Ripke4, Stephan Ripke18, Sophie van der Sluis, Patrick Sullivan3, Patrick Sullivan48, Scott I. Vrieze12, Margaret J. Wright13, Danielle Posthuma1 
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

Journal ArticleDOI
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

NameH-indexPapersCitations
Walter C. Willett3342399413322
Meir J. Stampfer2771414283776
Albert Hofman2672530321405
Graham A. Colditz2611542256034
Paul M. Ridker2331242245097
Ralph B. D'Agostino2261287229636
John Q. Trojanowski2261467213948
David J. Hunter2131836207050
André G. Uitterlinden1991229156747
Robert M. Califf1961561167961
Eric J. Topol1931373151025
Frank E. Speizer193636135891
Bernard Rosner1901162147661
William B. Kannel188533175659
Patrick W. Serruys1862427173210
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202397
2022317
20216,115
20205,342
20194,754
20184,357