Institution
University of Konstanz
Education•Konstanz, Baden-Württemberg, Germany•
About: University of Konstanz is a education organization based out in Konstanz, Baden-Württemberg, Germany. It is known for research contribution in the topics: Population & Visualization. The organization has 12115 authors who have published 27401 publications receiving 951162 citations. The organization is also known as: University of Constance & Universität Konstanz.
Topics: Population, Visualization, Membrane, Visual analytics, Silicon
Papers published on a yearly basis
Papers
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TL;DR: The authors discusses recent research on party politics and the welfare state that differs from traditional "partisan politics theory" that states that left-wing and right-wing parties hold contrasting positions on welfare issues, depending on the interests of their respective electorates.
Abstract: This article discusses recent research on party politics and the welfare state that differs from traditional ‘partisan politics theory’. The traditional approach states that left-wing and right-wing parties hold contrasting positions on welfare issues, depending on the interests of their respective electorates. This view has recently been challenged by three strands of research, which emphasize (1) the effects of electoral change on parties’ policy positions, (2) the role of context, notably electoral institutions, party competition and the configuration of party systems, and (3) the impact of different linkages between parties and electorates (particularistic versus programmatic). The implications of these arguments for the applicability of partisan theory are presented, and theoretical and empirical issues are identified for further research.
192 citations
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TL;DR: This work presents a model for the control of growth in the wing imaginal disc of Drosophila, which can account for the uniform occurrence and termination of growth, and shows that the model indeed yields uniform growth.
192 citations
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TL;DR: Functional integrity and efficient recruitment of left frontal language areas seems to be critical for successful word retrieval in old age.
Abstract: As we age, our ability to select and to produce words changes, yet we know little about the underlying neural substrate of word-finding difficulties in old adults. This study was designed to elucidate changes in specific frontally mediated retrieval processes involved in word-finding difficulties associated with advanced age. We implemented two overt verbal (semantic and phonemic) fluency tasks during fMRI and compared brain activity patterns of old and young adults. Performance during the phonemic task was comparable for both age groups and mirrored by strongly left-lateralized (frontal) activity patterns. On the other hand, a significant drop of performance during the semantic task in the older group was accompanied by additional right (inferior and middle) frontal activity, which was negatively correlated with performance. Moreover, the younger group recruited different subportions of the left inferior frontal gyrus for both fluency tasks, whereas the older participants failed to show this distinction. Thus, functional integrity and efficient recruitment of left frontal language areas seems to be critical for successful word retrieval in old age.
192 citations
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Yale University1, University of Toronto2, University of Wisconsin-Madison3, Rush University Medical Center4, Flinders University5, University of Göttingen6, University of Washington7, University of Bonn8, University of Konstanz9, University of Cambridge10, Brandeis University11, Max Planck Society12, University of Texas Medical Branch13, University of Oxford14, University of York15, University of California, San Diego16, Cornell University17, University of Sydney18, Imperial College London19
192 citations
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TL;DR: It is shown that TNF-α induction by Borrelia lysate was impaired in heterozygous TLR-2 knockout mice, while reactivity to lipoteichoic acid, another TLR -2 ligand signaling via TLr-2/TLR-6 heterodimers, was unaffected, suggesting that Arg753Gln may protect from the development of late stage LD due to a reduced signaling viaTLR/TLr-1.
Abstract: Lyme disease (LD) is caused by Borrelia burgdorferi and displays different stages, including localized, early disseminated, and persistent infection, all of which are associated with profound inflammatory reactions in the host. Induction of proinflammatory cytokines by B. burgdorferi is mainly mediated by outer surface proteins interacting with TLR-2/TLR-1 heterodimers. In this study, we show that TNF-alpha induction by Borrelia lysate was impaired in heterozygous TLR-2 knockout mice, while reactivity to lipoteichoic acid, another TLR-2 ligand signaling via TLR-2/TLR-6 heterodimers, was unaffected. Blood from individuals heterozygous for the TLR-2 polymorphism Arg753Gln was tested for cytokine release upon stimulation with Borrelia lysate, and induction of TNF-alpha and IFN-gamma was significantly lower as compared with individuals not exhibiting this variation. Overexpression of TLR-2 carrying the Arg753Gln polymorphism in HEK 293 cells led to a significantly stronger impairment of activation by TLR-2/TLR-1 ligands as compared with TLR-2/TLR-6 ligands. To study whether heterozygosity for the Arg753Gln variant of TLR-2 influenced susceptibility for LD, we analyzed 155 patients for this polymorphism. The Arg753Gln variant occurs at a significantly lower frequency in LD patients as compared with matched controls (5.8 vs 13.5%, odds ratio 0.393, 95% confidence interval 0.17-0.89, p = 0.033), with an even more pronounced difference when late stage disease was observed (2.3 vs 12.5%, odds ratio 0.163, 95% confidence interval 0.04-0.76, p = 0.018). These data suggest that Arg753Gln may protect from the development of late stage LD due to a reduced signaling via TLR-2/TLR-1.
191 citations
Authors
Showing all 12272 results
Name | H-index | Papers | Citations |
---|---|---|---|
Robert E. W. Hancock | 152 | 775 | 88481 |
Lloyd J. Old | 152 | 775 | 101377 |
Andrew White | 149 | 1494 | 113874 |
Stefanie Dimmeler | 147 | 574 | 81658 |
Rudolf Amann | 143 | 459 | 85525 |
Niels Birbaumer | 142 | 835 | 77853 |
Thomas P. Russell | 141 | 1012 | 80055 |
Emmanuelle Perez | 138 | 1550 | 99016 |
Shlomo Havlin | 131 | 1013 | 83347 |
Bruno S. Frey | 119 | 900 | 65368 |
Roald Hoffmann | 116 | 870 | 59470 |
Michael G. Fehlings | 116 | 1189 | 57003 |
Yves Van de Peer | 115 | 494 | 61479 |
Axel Meyer | 112 | 511 | 51195 |
Manuela Campanelli | 111 | 675 | 48563 |