Institution
University of Duisburg-Essen
Education•Essen, 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 published on a yearly basis
Papers
More filters
••
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
••
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
••
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
••
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
••
Hannover Medical School1, University of Düsseldorf2, University of Erlangen-Nuremberg3, Boston Children's Hospital4, University of Ulm5, Charité6, University of Freiburg7, University of Duisburg-Essen8, Saarland University9, University of Cologne10, University of Hamburg11, University of Mainz12, Ludwig Maximilian University of Munich13, Goethe University Frankfurt14, University of Giessen15, University of Göttingen16, University Hospital Heidelberg17, University of Kiel18, Technische Universität München19, German Cancer Research Center20, University of Tübingen21, Otto-von-Guericke University Magdeburg22
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
Name | H-index | Papers | Citations |
---|---|---|---|
Rui Zhang | 151 | 2625 | 107917 |
Olli T. Raitakari | 142 | 1232 | 103487 |
Anders Hamsten | 139 | 611 | 88144 |
Robert Huber | 139 | 671 | 73557 |
Christopher T. Walsh | 139 | 819 | 74314 |
Patrick D. McGorry | 137 | 1097 | 72092 |
Stanley Nattel | 132 | 778 | 65700 |
Luis M. Liz-Marzán | 132 | 616 | 61684 |
Dirk Schadendorf | 127 | 1017 | 105777 |
William Wijns | 127 | 752 | 95517 |
Raimund Erbel | 125 | 1364 | 74179 |
Khalil Amine | 118 | 652 | 50111 |
Hans-Christoph Diener | 118 | 1025 | 91710 |
Bruce A.J. Ponder | 116 | 403 | 54796 |
Andre Franke | 115 | 682 | 55481 |