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: In this article, an integrative and comprehensive review of the 285 articles on servant leadership spanning 20 years (1998-2018) is presented. But, a lack of coherence and clarity around the construct has impeded its theory development.
Abstract: Notwithstanding the proliferation of servant leadership studies with over 100 articles published in the last four years alone, a lack of coherence and clarity around the construct has impeded its theory development. We provide an integrative and comprehensive review of the 285 articles on servant leadership spanning 20 years (1998–2018), and in so doing extend the field in four different ways. First, we provide a conceptual clarity of servant leadership vis-a-vis other value-based leadership approaches and offer a new definition of servant leadership. Second, we evaluate 16 existing measures of servant leadership in light of their respective rigor of scale construction and validation. Third, we map the theoretical and nomological network of servant leadership in relation to its antecedents, outcomes, moderators, mediators. We finally conclude by presenting a detailed future research agenda to bring the field forward encompassing both theoretical and empirical advancement. All in all, our review paints a holistic picture of where the literature has been and where it should go into the future.
689 citations
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TL;DR: This work has adapted the real-time TaqMan PCR technology to the analysis of 3C assays, resulting in a method that more accurately determines crosslinking frequencies than current semiquantitative 3C strategies that rely on measuring the intensity of ethidium bromide-stained PCR products separated by gel electrophoresis.
Abstract: Chromosome conformation capture (3C) technology is a pioneering methodology that allows in vivo genomic organization to be explored at a scale encompassing a few tens to a few hundred kilobase-pairs. Understanding the folding of the genome at this scale is particularly important in mammals where dispersed regulatory elements, like enhancers or insulators, are involved in gene regulation. 3C technology involves formaldehyde fixation of cells, followed by a polymerase chain reaction (PCR)-based analysis of the frequency with which pairs of selected DNA fragments are crosslinked in the population of cells. Accurate measurements of crosslinking frequencies require the best quantification techniques. We recently adapted the real-time TaqMan PCR technology to the analysis of 3C assays, resulting in a method that more accurately determines crosslinking frequencies than current semiquantitative 3C strategies that rely on measuring the intensity of ethidium bromide-stained PCR products separated by gel electrophoresis. Here, we provide a detailed protocol for this method, which we have named 3C-qPCR. Once preliminary controls and optimizations have been performed, the whole procedure (3C assays and quantitative analyses) can be completed in 7-9 days.
689 citations
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TL;DR: There was continuous circulation in east and Southeast Asia via a region-wide network of temporally overlapping epidemics and that epidemics in the temperate regions were seeded from this network each year, suggesting that once A (H3N2) viruses leave E-SE Asia, they are unlikely to contribute to long-term viral evolution.
Abstract: Antigenic and genetic analysis of the hemagglutinin of approximately 13,000 human influenza A (H3N2) viruses from six continents during 2002-2007 revealed that there was continuous circulation in east and Southeast Asia (E-SE Asia) via a region-wide network of temporally overlapping epidemics and that epidemics in the temperate regions were seeded from this network each year. Seed strains generally first reached Oceania, North America, and Europe, and later South America. This evidence suggests that once A (H3N2) viruses leave E-SE Asia, they are unlikely to contribute to long-term viral evolution. If the trends observed during this period are an accurate representation of overall patterns of spread, then the antigenic characteristics of A (H3N2) viruses outside E-SE Asia may be forecast each year based on surveillance within E-SE Asia, with consequent improvements to vaccine strain selection.
689 citations
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TL;DR: The data support the hypothesis that strictly lobar microbleeds are related to cerebral amyloid angiopathy, whereas microbleed in a deep or infratentorial location result from hypertensive or atherosclerotic microangiopathy.
Abstract: Background: Cerebral microbleeds are focal deposits of hemosiderin that can be visualized with MRI. Little is known on their prevalence in the general population and on their etiology. It has been suggested that, in analogy to spontaneous intracranial hemorrhage, the etiology of microbleeds differs according to their location in the brain, with lobar microbleeds being caused by cerebral amyloid angiopathy and deep or infratentorial microbleeds resulting from hypertension and atherosclerosis. We investigated the prevalence of and risk factors for microbleeds in the general population aged 60 years and older. Methods: This study is based on 1,062 persons (mean age 69.6 years) from the population-based Rotterdam Scan Study. MRI was performed at 1.5 T and included a sequence optimized to increase the conspicuity of microbleeds. We assessed the relation of APOE genotype, cardiovascular risk factors, and markers of small vessel disease to the presence and location of microbleeds with multiple logistic regression. Results: Overall prevalence of cerebral microbleeds was high and increased with age from 17.8% in persons aged 60-69 years to 38.3% in those over 80 years. APOE e4 carriers had significantly more often strictly lobar microbleeds than noncarriers. In contrast, cardiovascular risk factors and presence of lacunar infarcts and white matter lesions were associated with microbleeds in a deep or infratentorial location but not in a lobar location. Conclusion: The prevalence of cerebral microbleeds is high. Our data support the hypothesis that strictly lobar microbleeds are related to cerebral amyloid angiopathy, whereas microbleeds in a deep or infratentorial location result from hypertensive or atherosclerotic microangiopathy.
688 citations
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TL;DR: The relation of CBF velocity as measured with transcranial Doppler with dementia and markers of incipient dementia in 1,730 participants of the Rotterdam Study suggests cerebral hypoperfusion precedes and possibly contributes to onset of clinical dementia.
Abstract: Cerebral blood flow (CBF) velocity is decreased in patients with Alzheimer's disease. It is being debated whether this reflects diminished demand because of advanced neurodegeneration or that cerebral hypoperfusion contributes to dementia. We examined the relation of CBF velocity as measured with transcranial Doppler with dementia and markers of incipient dementia (ie, cognitive decline and hippocampal and amygdalar atrophy on magnetic resonance imaging) in 1,730 participants of the Rotterdam Study aged 55 years and older. Cognitive decline in the 6.5 years preceding CBF velocity measurement was assessed with repeated Mini-Mental State Examinations in nondemented subjects (n = 1,716). Hippocampal and amygdalar volumes were assessed in a subset of 170 nondemented subjects. Subjects with greater CBF velocity were less likely to have dementia. Furthermore, in nondemented subjects, greater CBF velocity was related to significantly less cognitive decline over the preceding period (odds ratio per standard deviation increase in mean CBF 0.74 [95% confidence interval, 0.58-0.98]) and larger hippocampal and amygdalar volumes. A low CBF is associated with dementia, but also with markers of incipient dementia. Although we cannot exclude that this is caused by preclinical neurodegeneration leading to hypoperfusion, it does suggest that cerebral hypoperfusion precedes and possibly contributes to onset of clinical dementia.
687 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 |