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Institution

University of Konstanz

EducationKonstanz, 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.


Papers
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Journal ArticleDOI
TL;DR: Novel developments in the post-synthetic labelling approach as new insights into DNA polymerase substrate specificity allowed generation and amplification of labelled DNA strands are summarized herein.

199 citations

Journal ArticleDOI
TL;DR: In this article, the authors propose two new concepts, that of the synthetic situation and that of time transactions, which are situations that include electronically transmitted on-screen projections that add informational depth and new response requirements to the "ecological huddle" (Goffman 1964:135) of the natural situation.
Abstract: It proposes two new concepts, that of the synthetic situation and that of time transactions. Synthetic situations are situations that include electronically transmitted on-screen projections that add informational depth and new response requirements to the “ecological huddle” (Goffman 1964:135) of the natural situation. Global situations invariably include such components; we also find that temporal forms of integration may substitute for joint territoriality of copresence in the natural situation. Based on research on global currency trading and other empirical examples, I identify four types of synthetic situations and describe the synthetic situation’s informational character, its ontological fluidity, and the phenomenon that syn thetic situations may become role-others for participants. I outline the response system of synthetic situations, sketching out the concepts of response presence and its implications in this context as well as the importance of embodiment. I also discuss time transactions and the idea of fatefulness as a symbolic charge linked to the synthetic components of the situation.

199 citations

Journal ArticleDOI
TL;DR: It is shown that good pivots are outliers, but that selecting outliers does not ensure that good pivotots are selected, and an efficiency measure to compare two pivot sets is proposed.

199 citations

Journal ArticleDOI
TL;DR: Three studies explored the role of hedonic contingency theory as an explanation for the link between positive mood and cognitive flexibility and indicated that the hedonics may be an important contributing mechanism behind the positive mood-cognitive flexibility link.
Abstract: Three studies explored the role of hedonic contingency theory as an explanation for the link between positive mood and cognitive flexibility. Study 1 examined the determinants of activity choice for participants in happy, sad, or neutral moods. Consistent with hedonic contingency theory, happy participants weighted potential for creativity as well as the pleasantness of the task more heavily in their preference ratings. In Study 2, participants were given either a neutral or mood-threatening item generation task to perform. Results illustrated that happy participants exhibited greater cognitive flexibility in all cases; when confronted with a potentially mood-threatening task, happy participants were able to creatively transform the task so as to maintain positive mood and interest. Finally, Study 3 manipulated participants’ beliefs that moods could or could not be altered. Results replicated the standard positive mood-increased cognitive flexibility effect in the nonmood-freezing condition, but no effects of mood on creativity were found in the mood-freezing condition. These studies indicate that the hedonic contingency theory may be an important contributing mechanism behind the positive mood–cognitive flexibility link.

198 citations

Journal ArticleDOI
TL;DR: The correlation between mtROS formation and acetylcholine-dependent relaxation revealed that mitochondrial radical formation significantly contributes to age-dependent endothelial dysfunction.
Abstract: Aims Imbalance between pro- and antioxidant species (e.g. during aging) plays a crucial role for vascular function and is associated with oxidative gene regulation and modification. Vascular aging is associated with progressive deterioration of vascular homeostasis leading to reduced relaxation, hypertrophy, and a higher risk of thrombotic events. These effects can be explained by a reduction in free bioavailable nitric oxide that is inactivated by an age-dependent increase in superoxide formation. In the present study, mitochondria as a source of reactive oxygen species (ROS) and the contribution of manganese superoxide dismutase (MnSOD, SOD-2) and aldehyde dehydrogenase (ALDH-2) were investigated. Methods and results Age-dependent effects on vascular function were determined in aortas of C57/Bl6 wild-type (WT), ALDH-2−/−, MnSOD+/+, and MnSOD+/− mice by isometric tension measurements in organ chambers. Mitochondrial ROS formation was measured by luminol (L-012)-enhanced chemiluminescence and 2-hydroxyethidium formation with an HPLC-based assay in isolated heart mitochondria. ROS-mediated mitochondrial DNA (mtDNA) damage was detected by a novel and modified version of the fluorescent-detection alkaline DNA unwinding (FADU) assay. Endothelial dysfunction was observed in aged C57/Bl6 WT mice in parallel to increased mitochondrial ROS formation and oxidative mtDNA damage. In contrast, middle-aged ALDH-2−/− mice showed a marked vascular dysfunction that was similar in old ALDH-2−/− mice suggesting that ALDH-2 exerts age-dependent vasoprotective effects. Aged MnSOD+/− mice showed the most pronounced phenotype such as severely impaired vasorelaxation, highest levels of mitochondrial ROS formation and mtDNA damage. Conclusion The correlation between mtROS formation and acetylcholine-dependent relaxation revealed that mitochondrial radical formation significantly contributes to age-dependent endothelial dysfunction.

198 citations


Authors

Showing all 12272 results

NameH-indexPapersCitations
Robert E. W. Hancock15277588481
Lloyd J. Old152775101377
Andrew White1491494113874
Stefanie Dimmeler14757481658
Rudolf Amann14345985525
Niels Birbaumer14283577853
Thomas P. Russell141101280055
Emmanuelle Perez138155099016
Shlomo Havlin131101383347
Bruno S. Frey11990065368
Roald Hoffmann11687059470
Michael G. Fehlings116118957003
Yves Van de Peer11549461479
Axel Meyer11251151195
Manuela Campanelli11167548563
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202360
2022202
20211,361
20201,299
20191,166
20181,082