Institution
Radboud University Nijmegen
Education•Nijmegen, Gelderland, Netherlands•
About: Radboud University Nijmegen is a education organization based out in Nijmegen, Gelderland, Netherlands. It is known for research contribution in the topics: Population & Randomized controlled trial. The organization has 35417 authors who have published 83035 publications receiving 3285064 citations. The organization is also known as: Catholic University of Nijmegen & Radboud University.
Papers published on a yearly basis
Papers
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TL;DR: A life-span perspective on one component of the evolutionary theory of loneliness—a component the authors refer to as the reaffiliation motive (RAM) that represents the motivation to reconnect with others that is triggered by perceived social isolation.
Abstract: Most people have experienced loneliness and have been able to overcome it to reconnect with other people. In the current review, we provide a life-span perspective on one component of the evolutionary theory of loneliness—a component we refer to as the reaffiliation motive (RAM). The RAM represents the motivation to reconnect with others that is triggered by perceived social isolation. Loneliness is often a transient experience because the RAM leads to reconnection, but sometimes this motivation can fail, leading to prolonged loneliness. We review evidence of how aspects of the RAM change across development and how these aspects can fail for different reasons across the life span. We conclude with a discussion of age-appropriate interventions that may help to alleviate prolonged loneliness.
503 citations
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TL;DR: Polymeric building blocks containing terminal azide and alkyne functionalities are prepared via atom transfer radical polymerization (ATRP) and used to modularly synthesize block copolymers via 1,3-dipolar cycloaddition reactions, which are quantitative according to SEC measurements.
503 citations
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TL;DR: Mortality risk, particularly by heart failure, is increased by virtually all complications, particularly in the young, and is equally hazardous in younger as in older patients.
Abstract: Aims Mortality in adults with congenital heart disease is known to be increased, yet its extent and the major mortality risks are unclear.
Methods and results The Dutch CONCOR national registry for adult congenital heart disease was linked to the national mortality registry. Cox's regression was used to assess mortality predictors. Of 6933 patients, 197 (2.8%) died during a follow-up of 24 865 patient-years. Compared with the general national population, there was excess mortality, particularly in the young. Median age at death was 48.8 years. Of all deaths, 77% had a cardiovascular origin; 45% were due to chronic heart failure (26%, age 51.0 years) or sudden death (19%, age 39.1 years). Age predicted mortality, as did gender, severity of defect, number of interventions, and number of complications [hazard ratio (HR) range 1.1–5.9, P < 0.05]. Several complications predicted all-cause mortality beyond the effects of age, gender, and congenital heart disease severity, i.e. endocarditis, supraventricular arrhythmias, ventricular arrhythmias, conduction disturbances, myocardial infarction, and pulmonary hypertension (HR range 1.4–3.1, P < 0.05). These risks were similar in patients above and below 40 years of age. Almost all complications predicted death due to heart failure (HR range 2.0–5.1, P < 0.05); conduction disturbances and pulmonary hypertension predicted sudden death (HR range 2.0–4.7, P < 0.05).
Conclusion Mortality is increased in adults with congenital heart disease, particularly in the young. The vast majority die from cardiovascular causes. Mortality risk, particularly by heart failure, is increased by virtually all complications. Complications are equally hazardous in younger as in older patients.
503 citations
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TL;DR: Time series prediction is performed by support vector machines, Elman recurrent neural networks, and autoregressive moving average (ARMA) models and it appears that the AR MA model performs best for the ARMA data set while the SVM and the Elman networks perform similarly.
501 citations
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Georgia Institute of Technology1, Leipzig University2, Johns Hopkins University3, University of Cambridge4, University of Tartu5, Ontario Institute for Cancer Research6, University of Washington7, VU University Amsterdam8, University of Chicago9, Greifswald University Hospital10, University of Bristol11, Erasmus University Rotterdam12, University of Exeter13, University of Lausanne14, University of Geneva15, Swiss Institute of Bioinformatics16, University of Helsinki17, Weizmann Institute of Science18, Agency for Science, Technology and Research19, University of Queensland20, Leiden University Medical Center21, University of Liège22, University of Oxford23, University of Tampere24, Stanford University25, Turku University Hospital26, Maastricht University Medical Centre27, Karolinska Institutet28, Radboud University Nijmegen29, Utrecht University30, European Bioinformatics Institute31
TL;DR: It is observed that cis-eQTLs can be detected for 88% of the studied genes, but that they have a different genetic architecture compared to disease-associated variants, limiting the ability to use cis- eZTLs to pinpoint causal genes within susceptibility loci.
Abstract: While many disease-associated variants have been identified through genome-wide association studies, their downstream molecular consequences remain unclear. To identify these effects, we performed cis- and trans-expression quantitative trait locus (eQTL) analysis in blood from 31,684 individuals through the eQTLGen Consortium. We observed that cis-eQTLs can be detected for 88% of the studied genes, but that they have a different genetic architecture compared to disease-associated variants, limiting our ability to use cis-eQTLs to pinpoint causal genes within susceptibility loci. In contrast, trans-eQTLs (detected for 37% of 10,317 studied trait-associated variants) were more informative. Multiple unlinked variants, associated to the same complex trait, often converged on trans-genes that are known to play central roles in disease etiology. We observed the same when ascertaining the effect of polygenic scores calculated for 1,263 genome-wide association study (GWAS) traits. Expression levels of 13% of the studied genes correlated with polygenic scores, and many resulting genes are known to drive these traits.
500 citations
Authors
Showing all 35749 results
Name | H-index | Papers | Citations |
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Charles A. Dinarello | 190 | 1058 | 139668 |
Richard H. Friend | 169 | 1182 | 140032 |
Yang Gao | 168 | 2047 | 146301 |
Ian J. Deary | 166 | 1795 | 114161 |
David T. Felson | 153 | 861 | 133514 |
Margaret A. Pericak-Vance | 149 | 826 | 118672 |
Fernando Rivadeneira | 146 | 628 | 86582 |
Shah Ebrahim | 146 | 733 | 96807 |
Mihai G. Netea | 142 | 1170 | 86908 |
Mingshui Chen | 141 | 1543 | 125369 |
George Alverson | 140 | 1653 | 105074 |
Barry Blumenfeld | 140 | 1909 | 105694 |
Harvey B Newman | 139 | 1594 | 88308 |
Tariq Aziz | 138 | 1646 | 96586 |
Stylianos E. Antonarakis | 138 | 746 | 93605 |