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Institution

Radboud University Nijmegen

EducationNijmegen, 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
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Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
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

Posted ContentDOI
Urmo Võsa, Annique Claringbould, Harm-Jan Westra, Marc Jan Bonder, Patrick Deelen, Biao Zeng1, Holger Kirsten2, Ashis Saha3, Roman Kreuzhuber4, Silva Kasela5, Natalia Pervjakova5, Alvaes I6, Marie-Julie Favé6, Mawusse Agbessi6, Mark W. Christiansen7, Rick Jansen8, Ilkka Seppälä, Lin Tong9, Alexander Teumer10, Katharina Schramm, Gibran Hemani11, Joost Verlouw12, Hanieh Yaghootkar13, Reyhan Sonmez14, Andrew A. Brown15, Andrew A. Brown16, Kukushkina5, Anette Kalnapenkis5, Sina Rüeger14, Eleonora Porcu14, Jaanika Kronberg-Guzman5, Jarno Kettunen17, Joseph E. Powell18, Bernett Lee19, Futao Zhang20, Wibowo Arindrarto21, Frank Beutner2, Harm Brugge, Dmitreva J22, Mahmoud Elansary22, Benjamin P. Fairfax23, Michel Georges22, Bastiaan T. Heijmans21, Mika Kähönen24, Yungil Kim3, Julian C. Knight23, Peter Kovacs2, Knut Krohn2, Shuang Li, Markus Loeffler2, Urko M. Marigorta1, Hailiang Mei21, Yukihide Momozawa22, Martina Müller-Nurasyid, Matthias Nauck10, Michel G. Nivard8, Brenda W.J.H. Penninx8, Jonathan K. Pritchard25, Olli T. Raitakari26, Rotzchke O19, Eline Slagboom21, Coen D.A. Stehouwer27, Michael Stumvoll2, Patrick F. Sullivan28, Peter A C 't Hoen29, Joachim Thiery2, Anke Tönjes2, van Dongen J2, van Iterson M2, Jan H. Veldink30, Uwe Völker10, C Wijmenga, Morris A. Swertz, Anand Kumar Andiappan19, Grant W. Montgomery20, Samuli Ripatti17, Markus Perola17, Z. Kutalik14, Emmanouil T. Dermitzakis15, Sven Bergmann14, Timothy M. Frayling13, van Meurs J14, Holger Prokisch, Habibul Ahsan9, Brandon L. Pierce9, Terho Lehtimäki24, D.I. Boomsma8, Bruce M. Psaty7, Sina A. Gharib7, Philip Awadalla6, Lili Milani5, Willem H. Ouwehand4, Kate Downes4, Oliver Stegle31, Alexis Battle3, Jian Yang20, Peter M. Visscher20, Markus Scholz2, Greg Gibson1, Tõnu Esko5, Lude Franke 
19 Oct 2018-bioRxiv
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

NameH-indexPapersCitations
Charles A. Dinarello1901058139668
Richard H. Friend1691182140032
Yang Gao1682047146301
Ian J. Deary1661795114161
David T. Felson153861133514
Margaret A. Pericak-Vance149826118672
Fernando Rivadeneira14662886582
Shah Ebrahim14673396807
Mihai G. Netea142117086908
Mingshui Chen1411543125369
George Alverson1401653105074
Barry Blumenfeld1401909105694
Harvey B Newman139159488308
Tariq Aziz138164696586
Stylianos E. Antonarakis13874693605
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023123
2022492
20216,380
20206,080
20195,747
20185,114