Institution
University of Amsterdam
Education•Amsterdam, Noord-Holland, Netherlands•
About: University of Amsterdam is a education organization based out in Amsterdam, Noord-Holland, Netherlands. It is known for research contribution in the topics: Population & Randomized controlled trial. The organization has 59309 authors who have published 140894 publications receiving 5984137 citations. The organization is also known as: UvA & Universiteit van Amsterdam.
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TL;DR: Using this resource, it is found—and confirm by independent approaches—that the proposed quiescent/‘+4’ stem cell markers Bmi1, Tert, Hopx and Lrig1 are robustly expressed in CBC cells.
Abstract: Two types of stem cells are currently defined in small intestinal crypts: cycling crypt base columnar (CBC) cells and quiescent ‘+4’ cells. Here, we combine transcriptomics with proteomics to define a definitive molecular signature for Lgr5 + CBC cells. Transcriptional profiling of FACS‐sorted Lgr5 + stem cells and their daughters using two microarray platforms revealed an mRNA stem cell signature of 384 unique genes. Quantitative mass spectrometry on the same cell populations identified 278 proteins enriched in intestinal stem cells. The mRNA and protein data sets showed a high level of correlation and a combined signature of 510 stem cell‐enriched genes was defined. Spatial expression patterns were further characterized by mRNA in‐situ hybridization, revealing that approximately half of the genes were expressed in a gradient with highest levels at the crypt bottom, while the other half was expressed uniquely in Lgr5 + stem cells. Lineage tracing using a newly established knock‐in mouse for one of the signature genes, Smoc2 , confirmed its stem cell specificity. Using this resource, we find—and confirm by independent approaches—that the proposed quiescent/‘+4’ stem cell markers Bmi1 , Tert , Hopx and Lrig1 are robustly expressed in CBC cells.
692 citations
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TL;DR: Results indicate that idiopathic olfactory dysfunction is associated with an increased risk of developing PD of at least 10%.
Abstract: Olfactory dysfunction is an early and common symptom in Parkinson's disease (PD). In an effort to determine whether otherwise unexplained (idiopathic) olfactory dysfunction is associated with an increased risk of developing PD, we designed a prospective study in a cohort of 361 asymptomatic relatives (parents, siblings, or children) of PD patients. A combination of olfactory detection, identification, and discrimination tasks was used to select groups of hyposmic (n = 40) and normosmic (n = 38) individuals for a 2-year clinical follow-up evaluation and sequential single-photon emission computed tomography (SPECT), using [123I]beta-CIT as a dopamine transporter ligand, to assess nigrostriatal dopaminergic function at baseline and 2 years from baseline. A validated questionnaire, sensitive to the presence of parkinsonism, was used in the follow-up of the remaining 283 relatives. Two years from baseline, 10% of the individuals with idiopathic hyposmia, who also had strongly reduced [123I]beta-CIT binding at baseline, had developed clinical PD as opposed to none of the other relatives in the cohort. In the remaining nonparkinsonian hyposmic relatives, the average rate of decline in dopamine transporter binding was significantly higher than in the normosmic relatives. These results indicate that idiopathic olfactory dysfunction is associated with an increased risk of developing PD of at least 10%.
691 citations
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TL;DR: The evaluation highlighted particular difficulties in scoring the items on uninterpretable results and withdrawals, and it is essential that reviewers tailor guidelines for scoring items to their review, and ensure that all reviewers are clear on how to score studies.
Abstract: A quality assessment tool for diagnostic accuracy studies, named QUADAS, has recently been developed. Although QUADAS has been used in several systematic reviews, it has not been formally validated. The objective was to evaluate the validity and usefulness of QUADAS. Three reviewers independently rated the quality of 30 studies using QUADAS. We assessed the proportion of agreements between each reviewer and the final consensus rating. This was done for all QUADAS items combined and for each individual item. Twenty reviewers who had used QUADAS in their reviews completed a short structured questionnaire on their experience of QUADAS. Over all items, the agreements between each reviewer and the final consensus rating were 91%, 90% and 85%. The results for individual QUADAS items varied between 50% and 100% with a median value of 90%. Items related to uninterpretable test results and withdrawals led to the most disagreements. The feedback on the content of the tool was generally positive with only small numbers of reviewers reporting problems with coverage, ease of use, clarity of instructions and validity. Major modifications to the content of QUADAS itself are not necessary. The evaluation highlighted particular difficulties in scoring the items on uninterpretable results and withdrawals. Revised guidelines for scoring these items are proposed. It is essential that reviewers tailor guidelines for scoring items to their review, and ensure that all reviewers are clear on how to score studies. Reviewers should consider whether all QUADAS items are relevant to their review, and whether additional quality items should be assessed as part of their review.
691 citations
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University of Washington1, University of Geneva2, Ghent University3, Salisbury University4, University Hospital Southampton NHS Foundation Trust5, Katholieke Universiteit Leuven6, Radboud University Nijmegen7, University of Amsterdam8, University College London9, University of Manchester10, University of Bern11, University of Naples Federico II12, University of Glasgow13, Pompeu Fabra University14, Utrecht University15, University of Oxford16, Wellcome Trust Sanger Institute17, University of Chicago18, Vanderbilt University19, Cold Spring Harbor Laboratory20, Howard Hughes Medical Institute21
TL;DR: Recurrent molecular lesions that elude syndromic classification and whose disease manifestations must be considered in a broader context of development as opposed to being assigned to a specific disease are identified.
Abstract: BACKGROUND: Duplications and deletions in the human genome can cause disease or predispose persons to disease. Advances in technologies to detect these changes allow for the routine identification of submicroscopic imbalances in large numbers of patients. METHODS: We tested for the presence of microdeletions and microduplications at a specific region of chromosome 1q21.1 in two groups of patients with unexplained mental retardation, autism, or congenital anomalies and in unaffected persons. RESULTS: We identified 25 persons with a recurrent 1.35-Mb deletion within 1q21.1 from screening 5218 patients. The microdeletions had arisen de novo in eight patients, were inherited from a mildly affected parent in three patients, were inherited from an apparently unaffected parent in six patients, and were of unknown inheritance in eight patients. The deletion was absent in a series of 4737 control persons (P=1.1x10(-7)). We found considerable variability in the level of phenotypic expression of the microdeletion; phenotypes included mild-to-moderate mental retardation, microcephaly, cardiac abnormalities, and cataracts. The reciprocal duplication was enriched in nine children with mental retardation or autism spectrum disorder and other variable features (P=0.02). We identified three deletions and three duplications of the 1q21.1 region in an independent sample of 788 patients with mental retardation and congenital anomalies. CONCLUSIONS: We have identified recurrent molecular lesions that elude syndromic classification and whose disease manifestations must be considered in a broader context of development as opposed to being assigned to a specific disease. Clinical diagnosis in patients with these lesions may be most readily achieved on the basis of genotype rather than phenotype.
690 citations
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University of Leicester1, Pennsylvania State University2, University of Warwick3, Harvard University4, University of Copenhagen5, Max Planck Society6, Goddard Space Flight Center7, University of California, Berkeley8, University of Amsterdam9, University of Iceland10, University of Exeter11, University of Bristol12, Spanish National Research Council13, European Southern Observatory14, Australian National University15, Special Astrophysical Observatory16, Space Telescope Science Institute17, Universities Space Research Association18, California Institute of Technology19, Liverpool John Moores University20, Pomona College21, University of Oxford22, McGill University23, University College London24, Stockholm University25, George Washington University26
TL;DR: In this paper, the authors reported that GRB 090423 lies at a redshift of z approximate to 8.2, implying that massive stars were being produced and dying as GRBs similar to 630 Myr after the Big Bang.
Abstract: Long-duration gamma-ray bursts (GRBs) are thought to result from the explosions of certain massive stars(1), and some are bright enough that they should be observable out to redshifts of z > 20 using current technology(2-4). Hitherto, the highest redshift measured for any object was z = 6.96, for a Lyman-alpha emitting galaxy(5). Here we report that GRB 090423 lies at a redshift of z approximate to 8.2, implying that massive stars were being produced and dying as GRBs similar to 630 Myr after the Big Bang. The burst also pinpoints the location of its host galaxy.
689 citations
Authors
Showing all 59759 results
Name | H-index | Papers | Citations |
---|---|---|---|
Richard A. Flavell | 231 | 1328 | 205119 |
Scott M. Grundy | 187 | 841 | 231821 |
Stuart H. Orkin | 186 | 715 | 112182 |
Kenneth C. Anderson | 178 | 1138 | 126072 |
David A. Weitz | 178 | 1038 | 114182 |
Dorret I. Boomsma | 176 | 1507 | 136353 |
Brenda W.J.H. Penninx | 170 | 1139 | 119082 |
Michael Kramer | 167 | 1713 | 127224 |
Nicholas J. White | 161 | 1352 | 104539 |
Lex M. Bouter | 158 | 767 | 103034 |
Wolfgang Wagner | 156 | 2342 | 123391 |
Jerome I. Rotter | 156 | 1071 | 116296 |
David Cella | 156 | 1258 | 106402 |
David Eisenberg | 156 | 697 | 112460 |
Naveed Sattar | 155 | 1326 | 116368 |