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Institution

University of Duisburg-Essen

EducationEssen, Nordrhein-Westfalen, Germany
About: University of Duisburg-Essen is a education organization based out in Essen, Nordrhein-Westfalen, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 16072 authors who have published 39972 publications receiving 1109199 citations.


Papers
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Journal ArticleDOI
TL;DR: The smartphone technology is introduced as a challenge for diagnostics in the study of Internet use disorders and the term “smartphone addiction” is reflected on and it is believed that it is necessary to divide research on Internet use disorder (IUD) into a mobile and non-mobile IUD branch.
Abstract: AimsThe present theoretical paper introduces the smartphone technology as a challenge for diagnostics in the study of Internet use disorders and reflects on the term “smartphone addiction.”MethodsS...

197 citations

Journal ArticleDOI
TL;DR: Intravital two-photon microscopy is used to document neutrophils and brain-resident microglia in mice after induction of experimental stroke and indicates that neutrophil invasion of the ischemic brain is rapid, massive, and a key mediator of functional impairment, while peripheral T-cells promote brain damage.
Abstract: Neuronal injury from ischemic stroke is aggravated by invading peripheral immune cells. Early infiltrates of neutrophil granulocytes and T-cells influence the outcome of stroke. So far, however, neither the timing nor the cellular dynamics of neutrophil entry, its consequences for the invaded brain area, or the relative importance of T-cells has been extensively studied in an intravital setting. Here, we have used intravital two-photon microscopy to document neutrophils and brain-resident microglia in mice after induction of experimental stroke. We demonstrated that neutrophils immediately rolled, firmly adhered, and transmigrated at sites of endothelial activation in stroke-affected brain areas. The ensuing neutrophil invasion was associated with local blood–brain barrier breakdown and infarct formation. Brain-resident microglia recognized both endothelial damage and neutrophil invasion. In a cooperative manner, they formed cytoplasmic processes to physically shield activated endothelia and trap infiltrating neutrophils. Interestingly, the systemic blockade of very-late-antigen-4 immediately and very effectively inhibited the endothelial interaction and brain entry of neutrophils. This treatment thereby strongly reduced the ischemic tissue injury and effectively protected the mice from stroke-associated behavioral impairment. Behavioral preservation was also equally well achieved with the antibody-mediated depletion of myeloid cells or specifically neutrophils. In contrast, T-cell depletion more effectively reduced the infarct volume without improving the behavioral performance. Thus, neutrophil invasion of the ischemic brain is rapid, massive, and a key mediator of functional impairment, while peripheral T-cells promote brain damage. Acutely depleting T-cells and inhibiting brain infiltration of neutrophils might, therefore, be a powerful early stroke treatment.

196 citations

Journal ArticleDOI
TL;DR: A large-scale survey of current DL evaluation activities has resulted in a description of the state of the art in the field, and a new framework for the evaluation of DLs, as well as for recording, describing and analyzing the related research field is proposed.
Abstract: Digital libraries (DLs) are new and innovative information systems, under constant development and change, and therefore evaluation is of critical importance to ensure not only their correct evolution but also their acceptance by the user and application communities. The Evaluation activity of the DELOS Network of Excellence has performed a large-scale survey of current DL evaluation activities. This study has resulted in a description of the state of the art in the field, which is presented in this paper. The paper also proposes a new framework for the evaluation of DLs, as well as for recording, describing and analyzing the related research field. The framework includes a methodology for the classification of current evaluation procedures. The objective is to provide a set of flexible and adaptable guidelines for DL evaluation.

196 citations

Journal ArticleDOI
TL;DR: The molecular analysis of composite Hodgkin's and non‐Hodgkin's lymphomas indicated that many cases develop from a common GC B‐cell precursor in a multistep transformation process with both shared and distinct oncogenic events.
Abstract: Hodgkin's and Reed/Sternberg (HRS) cells, the tumour cells in classical Hodgkin's lymphoma (HL), represent transformed B cells in nearly all cases. The detection of destructive somatic mutations in the rearranged immunoglobulin (Ig) genes of HRS cells in classical HL indicated that they originate from preapoptotic germinal centre (GC) B cells that lost the capacity to express a high-affinity B-cell receptor (BCR). Several aberrantly activated signalling pathways and transcription factors have been identified that contribute to the rescue of HRS cells from apoptosis. Among the deregulated signalling pathways, activation of multiple receptor tyrosine kinases in HRS cells appears to be a specific feature of HL. In about 40% of cases of classical HL the HRS cells are infected by Epstein-Barr virus (EBV), indicating an important role of EBV in HL pathogenesis. Interestingly, nearly all cases of HL with destructive Ig gene mutations eliminating BCR expression (e.g. nonsense mutations) are EBV-positive, suggesting that EBV-encoded genes have a particular function to prevent apoptosis of HRS-cell precursors that acquired such crippling mutations. This idea is further supported by the recent demonstration that isolated human GC B cells harbouring crippled Ig genes can be rescued by EBV from cell death, giving rise to lymphoblastoid cell lines. The molecular analysis of composite Hodgkin's and non-Hodgkin's lymphomas indicated that many cases develop from a common GC B-cell precursor in a multistep transformation process with both shared and distinct oncogenic events.

196 citations

Journal ArticleDOI
Tim Ripperger1, Stefan S. Bielack, Arndt Borkhardt2, Ines B. Brecht3, Ines B. Brecht4, Birgit Burkhardt4, Gabriele Calaminus4, Klaus-Michael Debatin5, Hedwig E. Deubzer6, Uta Dirksen4, Cornelia Eckert6, Angelika Eggert6, Miriam Erlacher7, Gudrun Fleischhack8, Michael C. Frühwald4, Astrid Gnekow4, Gudrun Goehring1, Norbert Graf9, Helmut Hanenberg2, Julia Hauer2, Barbara Hero10, Simone Hettmer7, Katja von Hoff11, Martin A. Horstmann11, Juliane Hoyer3, Thomas Illig1, Peter Kaatsch12, Roland Kappler13, Kornelius Kerl4, Thomas Klingebiel14, Udo Kontny, Uwe Kordes11, Dieter Körholz15, Ewa Koscielniak, Christof M. Kramm16, Michaela Kuhlen2, Andreas E. Kulozik17, Britta Lamottke1, Ivo Leuschner18, Dietmar R. Lohmann, Andrea Meinhardt15, Markus Metzler3, Lüder Hinrich Meyer5, Olga Moser, Michaela Nathrath19, Charlotte M. Niemeyer7, Rainer Nustede1, Kristian W. Pajtler17, Kristian W. Pajtler20, Claudia Paret, Mareike Rasche8, Dirk Reinhardt8, Olaf Rieß21, Alexandra Russo, Stefan Rutkowski11, Brigitte Schlegelberger1, Dominik T. Schneider, Reinhard Schneppenheim11, Martin Schrappe18, Christopher Schroeder21, Dietrich von Schweinitz13, Thorsten Simon10, Monika Sparber-Sauer, Claudia Spix12, Martin Stanulla1, Doris Steinemann1, Brigitte Strahm7, Petra Temming8, Kathrin Thomay1, André O. von Bueren16, Peter Vorwerk22, Olaf Witt17, Marcin W. Wlodarski7, Willy Wössmann15, Martin Zenker22, Stefanie Zimmermann14, Stefan M. Pfister17, Stefan M. Pfister20, Christian P. Kratz1 
TL;DR: This review summarizes the current knowledge of cancer predisposition syndromes in pediatric oncology and provides essential information on clinical situations in which a childhood cancer genetic predisposition syndrome should be suspected.
Abstract: Heritable predisposition is an important cause of cancer in children and adolescents. Although a large number of cancer predisposition genes and their associated syndromes and malignancies have already been described, it appears likely that there are more pediatric cancer patients in whom heritable cancer predisposition syndromes have yet to be recognized. In a consensus meeting in the beginning of 2016, we convened experts in Human Genetics and Pediatric Hematology/Oncology to review the available data, to categorize the large amount of information, and to develop recommendations regarding when a cancer predisposition syndrome should be suspected in a young oncology patient. This review summarizes the current knowledge of cancer predisposition syndromes in pediatric oncology and provides essential information on clinical situations in which a childhood cancer predisposition syndrome should be suspected.

196 citations


Authors

Showing all 16364 results

NameH-indexPapersCitations
Rui Zhang1512625107917
Olli T. Raitakari1421232103487
Anders Hamsten13961188144
Robert Huber13967173557
Christopher T. Walsh13981974314
Patrick D. McGorry137109772092
Stanley Nattel13277865700
Luis M. Liz-Marzán13261661684
Dirk Schadendorf1271017105777
William Wijns12775295517
Raimund Erbel125136474179
Khalil Amine11865250111
Hans-Christoph Diener118102591710
Bruce A.J. Ponder11640354796
Andre Franke11568255481
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023117
2022496
20213,694
20203,449
20193,155
20182,761