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Institution

University of Fribourg

EducationFribourg, Freiburg, Switzerland
About: University of Fribourg is a education organization based out in Fribourg, Freiburg, Switzerland. It is known for research contribution in the topics: Population & Context (language use). The organization has 6040 authors who have published 14975 publications receiving 542500 citations. The organization is also known as: UNIFR & Universität Freiburg.


Papers
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Journal ArticleDOI
TL;DR: In this paper, a Minority Game based model of a financial market where adaptive agents (the speculators) interact with deterministic agents (called producers) is presented, and transitions between equilibrium and out of equilibrium behavior are observed when the relative number of speculators to the complexity of information or to the number of producers are changed.
Abstract: We present and study a Minority Game based model of a financial market where adaptive agents—the speculators—interact with deterministic agents—called producers. Speculators trade only if they detect predictable patterns which grant them a positive gain. Indeed the average number of active speculators grows with the amount of information that producers inject into the market. Transitions between equilibrium and out of equilibrium behavior are observed when the relative number of speculators to the complexity of information or to the number of producers are changed. When the system is out of equilibrium, stylized facts arise, such as fat tailed distribution of returns and volatility clustering. Without speculators, the price follows a random walk; this implies that stylized facts arise because of the presence of speculators. Furthermore, if speculators abandon price taking behavior, stylized facts disappear.

132 citations

Journal ArticleDOI
22 Apr 2011-PLOS ONE
TL;DR: The data demonstrate a causal role of the hyperactive S6K1 in eNOS uncoupling leading to endothelial dysfunction and vascular aging, and resveratrol improves endothelial function in aging, at least in part, through inhibition of S 6K1.
Abstract: Mammalian target of rapamycin (mTOR)/S6K1 signalling emerges as a critical regulator of aging. Yet, a role of mTOR/S6K1 in aging-associated vascular endothelial dysfunction remains unknown. In this study, we investigated the role of S6K1 in aging-associated endothelial dysfunction and effects of the polyphenol resveratrol on S6K1 in aging endothelial cells. We show here that senescent endothelial cells displayed higher S6K1 activity, increased superoxide production and decreased bioactive nitric oxide (NO) levels than young endothelial cells, which is contributed by eNOS uncoupling. Silencing S6K1 in senescent cells reduced superoxide generation and enhanced NO production. Conversely, over-expression of a constitutively active S6K1 mutant in young endothelial cells mimicked endothelial dysfunction of the senescent cells through eNOS uncoupling and induced premature cellular senescence. Like the mTOR/S6K1 inhibitor rapamycin, resveratrol inhibited S6K1 signalling, resulting in decreased superoxide generation and enhanced NO levels in the senescent cells. Consistent with the data from cultured cells, an enhanced S6K1 activity, increased superoxide generation, and decreased bioactive NO levels associated with eNOS uncoupling were also detected in aortas of old WKY rats (aged 20–24 months) as compared to the young animals (1–3 months). Treatment of aortas of old rats with resveratrol or rapamycin inhibited S6K1 activity, oxidative stress, and improved endothelial NO production. Our data demonstrate a causal role of the hyperactive S6K1 in eNOS uncoupling leading to endothelial dysfunction and vascular aging. Resveratrol improves endothelial function in aging, at least in part, through inhibition of S6K1. Targeting S6K1 may thus represent a novel therapeutic approach for aging-associated vascular disease.

131 citations

Journal ArticleDOI
TL;DR: With an experimental setup reflecting physiological exposure conditions in the human lung more realistic, the present study indicates that Ag-NPs do not cause adverse effects and cells were only sensitive to high Ag-ion concentrations.
Abstract: Due to its antibacterial properties, silver (Ag) has been used in more consumer products than any other nanomaterial so far. Despite the promising advantages posed by using Ag-nanoparticles (NPs), their interaction with mammalian systems is currently not fully understood. An exposure route via inhalation is of primary concern for humans in an occupational setting. Aim of this study was therefore to investigate the potential adverse effects of aerosolised Ag-NPs using a human epithelial airway barrier model composed of A549, monocyte derived macrophage and dendritic cells cultured in vitro at the air-liquid interface. Cell cultures were exposed to 20 nm citrate-coated Ag-NPs with a deposition of 30 and 278 ng/cm2 respectively and incubated for 4 h and 24 h. To elucidate whether any effects of Ag-NPs are due to ionic effects, Ag-Nitrate (AgNO3) solutions were aerosolised at the same molecular mass concentrations. Agglomerates of Ag-NPs were detected at 24 h post exposure in vesicular structures inside cells but the cellular integrity was not impaired upon Ag-NP exposures. Minimal cytotoxicity, by measuring the release of lactate dehydrogenase, could only be detected following a higher concentrated AgNO3-solution. A release of pro-inflammatory markers TNF-α and IL-8 was neither observed upon Ag-NP and AgNO3 exposures as well as was not affected when cells were pre-stimulated with lipopolysaccharide (LPS). Also, an induction of mRNA expression of TNF-α and IL-8, could only be observed for the highest AgNO3 concentration alone or even significantly increased when pre-stimulated with LPS after 4 h. However, this effect disappeared after 24 h. Furthermore, oxidative stress markers (HMOX-1, SOD-1) were expressed after 4 h in a concentration dependent manner following AgNO3 exposures only. With an experimental setup reflecting physiological exposure conditions in the human lung more realistic, the present study indicates that Ag-NPs do not cause adverse effects and cells were only sensitive to high Ag-ion concentrations. Chronic exposure scenarios however, are needed to reveal further insight into the fate of Ag-NPs after deposition and cell interactions.

131 citations

Journal ArticleDOI
Georges Aad1, Brad Abbott2, Jalal Abdallah3, S. Abdel Khalek4  +2817 moreInstitutions (207)
TL;DR: In this paper, the nuclear modification factors R-AA and R-CP are presented in detail as a function of centrality, p(T) and eta, which is determined by the response of the forward calorimeters located on both sides of the interaction point.
Abstract: Charged-particle spectra obtained in Pb+Pb interactions at root s(NN) = 2.76TeV and pp interactions at root s(NN) = 2.76TeV with the ATLAS detector at the LHC are presented, using data with integrated luminosities of 0.15 nb(-1) and 4.2 pb(-1), respectively, in a wide transverse momentum (0.5 < p(T) < 150 GeV) and pseudorapidity (vertical bar eta vertical bar < 2) range. For Pb+Pb collisions, the spectra are presented as a function of collision centrality, which is determined by the response of the forward calorimeters located on both sides of the interaction point. The nuclear modification factors R-AA and R-CP are presented in detail as a function of centrality, p(T) and eta. They show a distinct p(T)-dependence with a pronounced minimum at about 7 GeV. Above 60 GeV, R-AA is consistent with a plateau at a centrality-dependent value, within the uncertainties. The value is 0.55 +/- 0.01(stat.) +/- 0.04(syst.) in the most central collisions. The R-AA distribution is consistent with flat vertical bar eta vertical bar dependence over the whole transverse momentum range in all centrality classes.

131 citations

Journal ArticleDOI
TL;DR: Lipase double-mutant cells in which the third lipase is expressed from the inducible GAL1 promoter have greatly reduced steady-state levels of steryl esters, indicating that overexpression of any of the three lipases is sufficient for steryl Ester mobilization in vivo.
Abstract: Sterol homeostasis in eukaryotic cells relies on the reciprocal interconversion of free sterols and steryl esters. The formation of steryl esters is well characterized, but the mechanisms that control steryl ester mobilization upon cellular demand are less well understood. We have identified a family of three lipases of Saccharomyces cerevisiae that are required for efficient steryl ester mobilization. These lipases, encoded by YLL012/ YEH1, YLR020/YEH2, and TGL1, are paralogues of the mammalian acid lipase family, which is composed of the lysosomal acid lipase, the gastric lipase, and four novel as yet uncharacterized human open reading frames. Lipase triple-mutant yeast cells are completely blocked in steryl ester hydrolysis but do not affect the mobilization of triacylglycerols, indicating that the three lipases are required for steryl ester mobilization in vivo. Lipase single mutants mobilize steryl esters to various degrees, indicating partial functional redundancy of the three gene products. Lipase double-mutant cells in which the third lipase is expressed from the inducible GAL1 promoter have greatly reduced steady-state levels of steryl esters, indicating that overexpression of any of the three lipases is sufficient for steryl ester mobilization in vivo. The three yeast enzymes constitute a novel class of membrane-anchored lipases that differ in topology and subcellular localization.

131 citations


Authors

Showing all 6204 results

NameH-indexPapersCitations
Jens Nielsen1491752104005
Sw. Banerjee1461906124364
Hans Peter Beck143113491858
Patrice Nordmann12779067031
Abraham Z. Snyder12532991997
Csaba Szabó12395861791
Robert Edwards12177574552
Laurent Poirel11762153680
Thomas Münzel116105557716
David G. Amaral11230249094
F. Blanc107151458418
Markus Stoffel10262050796
Vincenzo Balzani10147645722
Enrico Bertini9986538167
Sandeep Kumar94156338652
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202367
2022348
20211,110
20201,112
2019966
2018924