Institution
University of Basel
Education•Basel, Basel-Stadt, Switzerland•
About: University of Basel is a education organization based out in Basel, Basel-Stadt, Switzerland. It is known for research contribution in the topics: Population & Gene. The organization has 25084 authors who have published 52975 publications receiving 2388002 citations. The organization is also known as: Universität Basel & Basel University.
Topics: Population, Gene, Medicine, Context (language use), Transplantation
Papers published on a yearly basis
Papers
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TL;DR: The priority heuristic is generalized from the framework of fast and frugal heuristics from inferences to preferences and predicts the Allais paradox, and how accurately the heuristic predicts people's choices is tested.
Abstract: Bernoulli's framework of expected utility serves as a model for various psychological processes, including motivation, moral sense, attitudes, and decision making. To account for evidence at variance with expected utility, the authors generalize the framework of fast and frugal heuristics from inferences to preferences. The priority heuristic predicts (a) the Allais paradox, (b) risk aversion for gains if probabilities are high, (c) risk seeking for gains if probabilities are low (e.g., lottery tickets), (d) risk aversion for losses if probabilities are low (e.g., buying insurance), (e) risk seeking for losses if probabilities are high, (f) the certainty effect, (g) the possibility effect, and (h) intransitivities. The authors test how accurately the heuristic predicts people's choices, compared with previously proposed heuristics and 3 modifications of expected utility theory: security-potential/aspiration theory, transfer-of-attention-exchange model, and cumulative prospect theory.
667 citations
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TL;DR: These observations demonstrate that the relaxation channels of a single quantum emitter can be controlled by coupling to an efficiently radiating metallic nanoantenna.
Abstract: The interaction of a single quantum dot with a bowtie antenna is demonstrated for visible light. The antenna is generated at the apex of a ${\mathrm{Si}}_{3}{\mathrm{N}}_{4}$ atomic force microscopy tip by focused ion beam milling. When scanned over the quantum dot, its photoluminescence is enhanced while its excited-state lifetime is decreased. Our observations demonstrate that the relaxation channels of a single quantum emitter can be controlled by coupling to an efficiently radiating metallic nanoantenna.
667 citations
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TL;DR: Metabolic labeling with 5-bromouridine 5′-triphosphate in the presence of actinomycin D revealed that the membranous web is the site of viral RNA synthesis and therefore represents the replication complex of HCV.
Abstract: Formation of a membrane-associated replication complex, composed of viral proteins, replicating RNA, and altered cellular membranes, is a characteristic feature of plus-strand RNA viruses. Here, we demonstrate the presence of a specific membrane alteration, designated the membranous web, that contains hepatitis C virus (HCV) nonstructural proteins, as well as viral plus-strand RNA, in Huh-7 cells harboring autonomously replicating subgenomic HCV RNAs. Metabolic labeling with 5-bromouridine 5'-triphosphate in the presence of actinomycin D revealed that the membranous web is the site of viral RNA synthesis and therefore represents the replication complex of HCV.
666 citations
Broad Institute1, University of Oxford2, University of Bern3, Swiss Federal Institute of Aquatic Science and Technology4, Wellcome Trust/Cancer Research UK Gurdon Institute5, Wellcome Trust Sanger Institute6, University of Konstanz7, Agency for Science, Technology and Research8, Reed College9, Stanford University10, California Institute of Technology11, Benaroya Research Institute12, University of Rennes13, Georgia Institute of Technology14, University of Maryland, College Park15, University of Basel16, University of Texas at Austin17, Tokyo Institute of Technology18, National Museum of Natural History19, University of Stirling20, Carnegie Institution for Science21, National Cheng Kung University22, Science for Life Laboratory23, Norwich University24
TL;DR: It is concluded that a number of molecular mechanisms shaped East African cichlid genomes, and that amassing of standing variation during periods of relaxed purifying selection may have been important in facilitating subsequent evolutionary diversification.
Abstract: Cichlid fishes are famous for large, diverse and replicated adaptive radiations in the Great Lakes of East Africa. To understand the molecular mechanisms underlying cichlid phenotypic diversity, we sequenced the genomes and transcriptomes of five lineages of African cichlids: the Nile tilapia (Oreochromis niloticus), an ancestral lineage with low diversity; and four members of the East African lineage: Neolamprologus brichardi/pulcher (older radiation, Lake Tanganyika), Metriaclima zebra (recent radiation, Lake Malawi), Pundamilia nyererei (very recent radiation, Lake Victoria), and Astatotilapia burtoni (riverine species around Lake Tanganyika). We found an excess of gene duplications in the East African lineage compared to tilapia and other teleosts, an abundance of non-coding element divergence, accelerated coding sequence evolution, expression divergence associated with transposable element insertions, and regulation by novel microRNAs. In addition, we analysed sequence data from sixty individuals representing six closely related species from Lake Victoria, and show genome-wide diversifying selection on coding and regulatory variants, some of which were recruited from ancient polymorphisms. We conclude that a number of molecular mechanisms shaped East African cichlid genomes, and that amassing of standing variation during periods of relaxed purifying selection may have been important in facilitating subsequent evolutionary diversification.
666 citations
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TL;DR: The concept that activation of the endogenous IFN system in CHC not only is ineffective in clearing the infection but also may impede the response to therapy, most likely by inducing a refractory state of the IFN signaling pathway, is supported.
Abstract: Hepatitis C virus (HCV) infection is a major cause of chronic liver disease worldwide. The current standard therapy for chronic hepatitis C (CHC) consists of a combination of pegylated IFN alpha (pegIFNalpha) and ribavirin. It achieves a sustained viral clearance in only 50-60% of patients. To learn more about molecular mechanisms underlying treatment failure, we investigated IFN-induced signaling in paired liver biopsies collected from CHC patients before and after administration of pegIFNalpha. In patients with a rapid virological response to treatment, pegIFNalpha induced a strong up-regulation of IFN-stimulated genes (ISGs). As shown previously, nonresponders had high expression levels of ISGs before therapy. Analysis of posttreatment biopsies of these patients revealed that pegIFNalpha did not induce expression of ISGs above the pretreatment levels. In accordance with ISG expression data, phosphorylation, DNA binding, and nuclear localization of STAT1 indicated that the IFN signaling pathway in nonresponsive patients is preactivated and refractory to further stimulation. Some features characteristic of nonresponders were more accentuated in patients infected with HCV genotypes 1 and 4 compared with genotypes 2 and 3, providing a possible explanation for the poor response of the former group to therapy. Taken together with previous findings, our data support the concept that activation of the endogenous IFN system in CHC not only is ineffective in clearing the infection but also may impede the response to therapy, most likely by inducing a refractory state of the IFN signaling pathway.
665 citations
Authors
Showing all 25374 results
Name | H-index | Papers | Citations |
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Yang Yang | 171 | 2644 | 153049 |
Martin Karplus | 163 | 831 | 138492 |
Frank J. Gonzalez | 160 | 1144 | 96971 |
Paul Emery | 158 | 1314 | 121293 |
Matthias Egger | 152 | 901 | 184176 |
Don W. Cleveland | 152 | 444 | 84737 |
Ashok Kumar | 151 | 5654 | 164086 |
Kurt Wüthrich | 143 | 739 | 103253 |
Thomas J. Smith | 140 | 1775 | 113919 |
Robert Huber | 139 | 671 | 73557 |
Peter Robmann | 135 | 1438 | 97569 |
Ernst Detlef Schulze | 133 | 670 | 69504 |
Michael Levine | 129 | 586 | 55963 |
Claudio Santoni | 129 | 1027 | 80598 |
Pablo Garcia-Abia | 126 | 989 | 78690 |