Institution
University of Kiel
Education•Kiel, Germany•
About: University of Kiel is a education organization based out in Kiel, Germany. It is known for research contribution in the topics: Population & Crystal structure. The organization has 27816 authors who have published 57114 publications receiving 2061802 citations. The organization is also known as: Christian Albrechts University & Christian-Albrechts-Universität zu Kiel.
Topics: Population, Crystal structure, Transplantation, Gene, Receptor
Papers published on a yearly basis
Papers
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TL;DR: The missing induction of both inducible &bgr;-defensins in CD as compared with UC may cause a defect in barrier function that predisposes to bacterial invasion.
Abstract: Antimicrobial peptides such as defensins provide nonspecific mucosal defense against a multitude of microorganisms. Recently, it has been shown that luminal bacteria may invade the mucosa in inflammatory bowel diseases, suggesting a defect in innate mucosal immunity. The aim of this study was to investigate the expression of human beta-defensins (HBD) in controls, Crohn's disease (CD), ulcerative colitis (UC), and unspecific inflammation. Up to 4 biopsies were taken from 103 patients (33 controls, 24 with Crohn's disease, 36 with ulcerative colitis, 10 with unspecific colitis). Mucosal mRNA was measured using real-time fluorescence temperature cycler reverse-transcription polymerase chain reaction with primers for HBD-1, HBD-2, HBD-3, tumor necrosis factor alpha, and interleukin 8. Mucosal HBD-1 expression was marginally decreased in both CD and UC. HBD-2 was increased exclusively in UC but not in CD. The expression of the novel defensin HBD-3 was strongly correlated with HBD-2 and also raised predominantly in UC. The expression of both inducible beta-defensins was enhanced in the state of inflammation. Expression of HBD-2 showed a weak correlation with interleukin 8 only in inflamed CD biopsies but not with tumor necrosis factor alpha. The missing induction of both inducible beta-defensins in CD as compared with UC may cause a defect in barrier function that predisposes to bacterial invasion.
300 citations
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22 Apr 2012TL;DR: Kieker as mentioned in this paper is an extensible framework for monitoring and analyzing the runtime behavior of concurrent or distributed software systems, which provides measurement probes for application performance monitoring and control-flow tracing.
Abstract: Kieker is an extensible framework for monitoring and analyzing the runtime behavior of concurrent or distributed software systems. It provides measurement probes for application performance monitoring and control-flow tracing. Analysis plugins extract and visualize architectural models, augmented by quantitative observations. Configurable readers and writers allow Kieker to be used for online and offline analysis. This paper reviews the Kieker framework focusing on its features, its provided extension points for custom components, as well the imposed monitoring overhead.
300 citations
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TL;DR: In this paper, the authors investigated the relationship between government support for R&D and expenditure financed privately by firms using a comprehensive plant level data set for the manufacturing sector in the Republic of Ireland.
Abstract: This paper investigates the relationship between government support for R&D and R&D expenditure financed privately by firms using a comprehensive plant level data set for the manufacturing sector in the Republic of Ireland. We find that for domestic plants small grants serve to increase private R&D spending, while too large a grant may crowd out private financing of R&D. In contrast, evidence for foreign establishments suggests that grant provision causes neither additionality nor crowding out effects of private R&D financing, regardless of the size of the subsidy.
300 citations
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TL;DR: The economics profession appears to have been unaware of the long build-up to the current worldwide financial crisis, and to have significantly underestimated its dimensions once it started to unfold as mentioned in this paper.
Abstract: The economics profession appears to have been unaware of the long build-up to the current worldwide financial crisis and to have significantly underestimated its dimensions once it started to unfold. In our view, this lack of understanding is due to a misallocation of research efforts in economics. We trace the deeper roots of this failure to the profession's focus on models that, by design, disregard key elements driving outcomes in real-world markets. The economics profession has failed in communicating the limitations, weaknesses, and even dangers of its preferred models to the public. This state of affairs makes clear the need for a major reorientation of focus in the research economists undertake, as well as for the establishment of an ethical code that would ask economists to understand and communicate the limitations and potential misuses of their models.
300 citations
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TL;DR: The usefulness of joint analyses of clinically distinct immune-mediated diseases and the map of shared genetic risk loci revealed in silico expression quantitative trait locus analyses revealed that the associations at ZMIZ1 and near SOCS1 have a potential functional effect on gene expression.
Abstract: Psoriasis (PS) and Crohn disease (CD) have been shown to be epidemiologically, pathologically, and therapeutically connected, but little is known about their shared genetic causes. We performed meta-analyses of five published genome-wide association studies on PS (2,529 cases and 4,955 controls) and CD (2,142 cases and 5,505 controls), followed up 20 loci that showed strongest evidence for shared disease association and, furthermore, tested cross-disease associations for previously reported PS and CD risk alleles in additional 6,115 PS cases, 4,073 CD cases, and 10,100 controls. We identified seven susceptibility loci outside the human leukocyte antigen region (9p24 near JAK2, 10q22 at ZMIZ1 , 11q13 near PRDX5 , 16p13 near SOCS1 , 17q21 at STAT3 , 19p13 near FUT2 , and 22q11 at YDJC ) shared between PS and CD with genome-wide significance (p −8 ) and confirmed four already established PS and CD risk loci ( IL23R , IL12B , REL , and TYK2 ). Three of the shared loci are also genome-wide significantly associated with PS alone (10q22 at ZMIZ1 , p rs1250544 = 3.53 × 10 −8 , 11q13 near PRDX5 , p rs694739 = 3.71 × 10 −09 , 22q11 at YDJC , p rs181359 = 8.02 × 10 −10 ). In addition, we identified one susceptibility locus for CD (16p13 near SOCS1 , p rs4780355 = 4.99 × 10 −8 ). Refinement of association signals identified shared genome-wide significant associations for exonic SNPs at 10q22 ( ZMIZ1 ) and in silico expression quantitative trait locus analyses revealed that the associations at ZMIZ1 and near SOCS1 have a potential functional effect on gene expression. Our results show the usefulness of joint analyses of clinically distinct immune-mediated diseases and enlarge the map of shared genetic risk loci.
300 citations
Authors
Showing all 28103 results
Name | H-index | Papers | Citations |
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Stefan Schreiber | 178 | 1233 | 138528 |
Jun Wang | 166 | 1093 | 141621 |
William J. Sandborn | 162 | 1317 | 108564 |
Jens Nielsen | 149 | 1752 | 104005 |
Tak W. Mak | 148 | 807 | 94871 |
Annette Peters | 138 | 1114 | 101640 |
Severine Vermeire | 134 | 1086 | 76352 |
Peter M. Rothwell | 134 | 779 | 67382 |
Dusan Bruncko | 132 | 1042 | 84709 |
Gideon Bella | 129 | 1301 | 87905 |
Dirk Schadendorf | 127 | 1017 | 105777 |
Neal L. Benowitz | 126 | 792 | 60658 |
Thomas Schwarz | 123 | 701 | 54560 |
Meletios A. Dimopoulos | 122 | 1371 | 71871 |
Christian Weber | 122 | 776 | 53842 |