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
More filters
••
TL;DR: It is shown that FMRP acts as a translational repressor of specific mRNAs at synapses, which could result in synaptic dysfunction phenotype of Fragile X patients when FMRp is not present.
692 citations
••
Erasmus University Rotterdam1, San Francisco VA Medical Center2, University of California, San Francisco3, University College Dublin4, Utrecht University5, Yale University6, University of North Carolina at Chapel Hill7, Queen's University8, Vrije Universiteit Brussel9, Maastricht University Medical Centre10, Lancaster University11, University of Sheffield12, University Hospital of Lausanne13, Ludwig Maximilian University of Munich14
TL;DR: A formal Delphi consensus process was used to help develop a definition of ACP and provide recommendations for its application, and it is believed that these recommendations can provide guidance for clinical practice, ACP policy, and research.
Abstract: Advance care planning (ACP) is increasingly implemented in oncology and beyond, but a definition of ACP and recommendations concerning its use are lacking. We used a formal Delphi consensus process to help develop a definition of ACP and provide recommendations for its application. Of the 109 experts (82 from Europe, 16 from North America, and 11 from Australia) who rated the ACP definitions and its 41 recommendations, agreement for each definition or recommendation was between 68-100%. ACP was defined as the ability to enable individuals to define goals and preferences for future medical treatment and care, to discuss these goals and preferences with family and health-care providers, and to record and review these preferences if appropriate. Recommendations included the adaptation of ACP based on the readiness of the individual; targeting ACP content as the individual's health condition worsens; and, using trained non-physician facilitators to support the ACP process. We present a list of outcome measures to enable the pooling and comparison of results of ACP studies. We believe that our recommendations can provide guidance for clinical practice, ACP policy, and research.
692 citations
••
TL;DR: It was found that not only victims and bully/victims but bullies as well were disliked and that parenting was unrelated to bullying and victimization once other factors were controlled.
Abstract: Research on bullying and victimization largely rests on univariate analyses and on reports from a single informant. Researchers may thus know too little about the simultaneous effects of various independent and dependent variables, and their research may be biased by shared method variance. The database for this Dutch study was large (N = 1,065) and rich enough to allow multivariate analysis and multisource information. In addition, the effect of familial vulnerability for internalizing and externalizing disorders was studied. Gender, aggressiveness, isolation, and dislikability were most strongly related to bullying and victimization. Among the many findings that deviated from or enhanced the univariate knowledge base were that not only victims and bully/victims but bullies as well were disliked and that parenting was unrelated to bullying and victimization once other factors were controlled.
692 citations
••
TL;DR: In this article, the translocation of the human cellular homologue (c-ab1) of the transforming sequence of Abelson murine leukaemia virus (A-MuLV) from chromosome 9 to the Philadelphia chromosome (Ph1) in chronic myelocytic leukemiaemia (CML) was investigated.
Abstract: The localization of cellular oncogenes near the break points of tumour-specific chromosomal aberrations suggests an involvement of these genes in the generation of neoplasms. Recently, we demonstrated the translocation of the human cellular homologue (c-ab1) of the transforming sequence of Abelson murine leukaemia virus (A-MuLV) from chromosome 9 to the Philadelphia chromosome (Ph1) in chronic myelocytic leukaemia (CML). In an attempt to investigate the significance of this translocation in the pathogenesis of CML, we have now studied two CML patients with complex translocations, t(9; 11; 22) and t(1; 9; 22), and two CML Ph1-negative patients with apparently normal karyotypes. In addition to using blot hybridization with human c-ab1 probes and DNA from rodent: CML cell hybrids as before, we have used in situ hybridization of these probes directly to metaphase chromosomes of CML patients. These studies show that the c-ab1 gene is translocated in Ph1-positive but not in Ph1-negative CML patients. CML without the Ph1 chromosome seems to be a distinct entity with a different origin, and this view is supported by clinical observations including correlations which reveal a poorer prognosis.
691 citations
••
TL;DR: The many SNPs associated with BMD map to genes in signaling pathways with relevance to bone metabolism and highlight the complex genetic architecture that underlies osteoporosis and variation in BMD.
Abstract: Bone mineral density (BMD) is a heritable complex trait used in the clinical diagnosis of osteoporosis and the assessment of fracture risk. We performed meta-analysis of five genome-wide association studies of femoral neck and lumbar spine BMD in 19,195 subjects of Northern European descent. We identified 20 BMD loci that reached genome-wide significance (GWS; P < 5 x 10(-8)), of which 13 map to regions not previously associated with this trait: 1p31.3 (GPR177), 2p21 (SPTBN1), 3p22 (CTNNB1), 4q21.1 (MEPE), 5q14 (MEF2C), 7p14 (STARD3NL), 7q21.3 (FLJ42280), 11p11.2 (LRP4, ARHGAP1, F2), 11p14.1 (DCDC5), 11p15 (SOX6), 16q24 (FOXL1), 17q21 (HDAC5) and 17q12 (CRHR1). The meta-analysis also confirmed at GWS level seven known BMD loci on 1p36 (ZBTB40), 6q25 (ESR1), 8q24 (TNFRSF11B), 11q13.4 (LRP5), 12q13 (SP7), 13q14 (TNFSF11) and 18q21 (TNFRSF11A). The many SNPs associated with BMD map to genes in signaling pathways with relevance to bone metabolism and highlight the complex genetic architecture that underlies osteoporosis and variation in BMD.
691 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 |