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: Sensory discrimination was normal and mislocalization (referral of stimulation-induced sensation to a phantom limb) was absent in the congenital amputees and the role of peripheral and central factors in the understanding of phantom limb pain and phantom limb phenomena is discussed.
Abstract: The relationship between phantom limb phenomena and cortical reorganization was examined in five subjects with congenital absence of an upper limb and nine traumatic amputees. Neuromagnetic source imaging revealed minimal reorganization of primary somatosensory cortex in the congenital amputees (M=0.69 cm, SD 0.24) and the traumatic amputees without phantom limb pain (M=0.27 cm, SD 0.25); the amputees with phantom limb pain showed massive cortical reorganization (M=2.22 cm, SD 0.78). Phantom limb pain and nonpainful phantom limb phenomena were absent in the congenital amputees. Whereas phantom limb pain was positively related to cortical reorganization (r=0.87), nonpainful phantom phenomena were not significantly correlated with cortical reorganization (r=0.34). Sensory discrimination was normal and mislocalization (referral of stimulation-induced sensation to a phantom limb) was absent in the congenital amputees. The role of peripheral and central factors in the understanding of phantom limb pain and phantom limb phenomena is discussed in view of these findings.
293 citations
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TL;DR: Factor structure was generally invariant across random selected groups, gender, and BMI, which indicates a high stability for the Eating Motivation Survey, and implications of the fifteen distinct motivations to choose foods in everyday life are discussed.
293 citations
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TL;DR: It is demonstrated that pretreatment with highly purified lipoteichoic acid (LTA) results in suppression of cytokine release on restimulation with LTA in both C3H/HeN and C3h/HeJ mice, but not in macrophages from Toll-like receptor (TLR)-2-deficient mice.
Abstract: Exposure of macrophages to LPS induces a state of hyporesponsiveness to subsequent stimulation with LPS termed LPS desensitization or tolerance. To date, it is not known whether similar mechanisms of macrophage refractoriness are induced on contact with components of Gram-positive bacteria. In the present study, we demonstrate that pretreatment with highly purified lipoteichoic acid (LTA) results in suppression of cytokine release on restimulation with LTA in vitro and in vivo in both C3H/HeN and C3H/HeJ mice, but not in macrophages from Toll-like receptor (TLR)-2-deficient mice. Furthermore, desensitization in response to LPS or LTA exposure also inhibits responses to the other stimulus (“cross-tolerance”), suggesting that signaling pathways shared by TLR2 and TLR4 are impaired during tolerance. Finally, we show that LPS- or LTA-induced cross-tolerance is not transferred to hyporesponsive cells cocultured with LPS/LTA-responsive macrophages, showing that soluble mediators do not suffice for tolerance induction in neighboring cells.
293 citations
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TL;DR: A new type of sulfate-reducing bacteria with ellipsoidal to lemon-shaped cells was regularly enriched from anaerobic freshwater and marine mud samples when mineral media with propionate and sulfate were used.
Abstract: A new type of sulfate-reducing bacteria with ellipsoidal to lemon-shaped cells was regularly enriched from anaerobic freshwater and marine mud samples when mineral media with propionate and sulfate were used. Three strains (1pr3, 2pr4, 3pr10) were isolated in pure culture. Propionate, lactate and alcohols were used as electron donors and carbon sources. Growth on H2 required acetate as a carbon source in the presence of CO2. Stoichiometric measurements revealed that oxidation of propionate was incomplete and led to acetate as an endproduct. Instead of sulfate, strain 1pr3 was shown to reduce sulfite and thiosulfate to H2S; nitrate also served as electron acceptor and was reduced to ammonia. With lactate or pyruvate, all three strains were able to grow without external electron acceptor and formed propionate and acetate as fermentation products. None of the strains contained desulfoviridin. In strain 1pr3 cytochromes of the b- and c-type were identified. Strain 1pr3 is described as type strain of the new species and genus, Desulfobulbus propionicus.
292 citations
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TL;DR: Nitrate tolerance is mediated, at least in significant part, by inhibition of vascular ALDH-2 and that mitochondrial ROS contribute to this inhibition, and GTN tolerance may be viewed as a metabolic syndrome characterized by mitochondrial dysfunction.
Abstract: Recent studies suggest that mitochondrial aldehyde dehydrogenase (ALDH-2) plays a central role in the process of nitroglycerin (glyceryl trinitrate, GTN) biotransformation in vivo and that its inhibition accounts for mechanism-based tolerance in vitro. The extent to which ALDH-2 contributes to GTN tolerance (impaired relaxation to GTN) and cross-tolerance (impaired endothelium-dependent relaxation) in vivo remain to be elucidated. Rats were treated for three days with GTN. Infusions were accompanied by decreases in vascular ALDH-2 activity, GTN biotransformation, and cGMP-dependent kinase (cGK-I) activity. Further, whereas in control vessels, multiple inhibitors and substrates of ALDH-2 reduced both GTN-stimulation of cGKI and GTN-induced vasodilation, these agents had little effect on tolerant vessels. A state of functional tolerance (in the GTN/cGMP pathway) was recapitulated in cultured endothelial cells by knocking down mitochondrial DNA (rho(0) cells). In addition, GTN increased the production of reactive oxygen species (ROS) by mitochondria, and these increases were associated with impaired relaxation to acetylcholine. Finally, antioxidants/reductants decreased mitochondrial ROS production and restored ALDH-2 activity. These observations suggest that nitrate tolerance is mediated, at least in significant part, by inhibition of vascular ALDH-2 and that mitochondrial ROS contribute to this inhibition. Thus, GTN tolerance may be viewed as a metabolic syndrome characterized by mitochondrial dysfunction.
292 citations
Authors
Showing all 12272 results
Name | H-index | Papers | Citations |
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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 |