Institution
University of Vienna
Education•Vienna, Austria•
About: University of Vienna is a education organization based out in Vienna, Austria. It is known for research contribution in the topics: Population & Context (language use). The organization has 44686 authors who have published 95840 publications receiving 2907492 citations.
Topics: Population, Context (language use), Stars, Computer science, Galaxy
Papers published on a yearly basis
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TL;DR: In this paper, the performance of recent density functionals for the exchange-correlation energy of a nonmolecular solid, by applying accurate calculations with the GAUSSIAN, BAND, and VASP codes to a test set of 24 solid metals and nonmetals.
Abstract: We assess the performance of recent density functionals for the exchange-correlation energy of a nonmolecular solid, by applying accurate calculations with the GAUSSIAN, BAND, and VASP codes to a test set of 24 solid metals and nonmetals. The functionals tested are the modified Perdew-Burke-Ernzerhof generalized gradient approximation PBEsol GGA, the second-order GGA SOGGA, and the Armiento-Mattsson 2005 AM05 GGA. For completeness, we also test more standard functionals: the local density approximation, the original PBE GGA, and the Tao-Perdew-Staroverov-Scuseria meta-GGA. We find that the recent density functionals for solids reach a high accuracy for bulk properties lattice constant and bulk modulus. For the cohesive energy, PBE is better than PBEsol overall, as expected, but PBEsol is actually better for the alkali metals and alkali halides. For fair comparison of calculated and experimental results, we consider the zeropoint phonon and finite-temperature effects ignored by many workers. We show how GAUSSIAN basis sets and inaccurate experimental reference data may affect the rating of the quality of the functionals. The results show that PBEsol and AM05 perform somewhat differently from each other for alkali metal, alkaline-earth metal, and alkali halide crystals where the maximum value of the reduced density gradient is about 2, but perform very similarly for most of the other solids where it is often about 1. Our explanation for this is consistent with the importance of exchange-correlation nonlocality in regions of core-valence overlap.
683 citations
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TL;DR: TGF-beta 1 is involved in the initiation of apoptosis in the liver and that the mature form of TGF- beta 1 is the active principle, according to previous studies.
Abstract: In previous studies hepatocytes undergoing cell death by apoptosis but not normal hepatocytes in rat liver showed immunostaining for transforming growth factor beta 1 (TGF-beta 1). Staining was much stronger with antibodies recognizing the pro-region of TGF-beta 1 than the mature peptide itself. Therefore we investigated the ability of both forms of TGF-beta 1 to induce apoptosis in primary cultures of rat hepatocytes. Mature TGF-beta 1 induced rounding up of the cells and fragmentation into multiple vesicles. As revealed by the DNA-specific stain H33258, the chromatin of these cells condensed and segregated into masses at the nuclear membrane; this was obviously followed by fragmentation of the nucleus. Ultrastructurally the cytoplasm was well preserved, as demonstrated by the presence of intact cell organelles. These features strongly suggest the occurrence of apoptosis. Quantification of nuclei with condensed chromatin revealed that mature TGF-beta 1 was 30-fold more effective than the TGF-beta 1 latency-associated protein complex. Finally, we administered TGF-beta 1 in vivo using an experimental model in which regression of rat liver was initiated by a short preceding treatment with the hepatomitogen cyproterone acetate. Two doses of TGF-beta 1, each 1 nM/kg, augmented the incidence of apoptotic hepatocytes 5-fold. Equimolar doses of TGF-beta 1 latency-associated protein complex were ineffective. These studies suggest that TGF-beta 1 is involved in the initiation of apoptosis in the liver and that the mature form of TGF-beta 1 is the active principle.
681 citations
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TL;DR: It is concluded that xiap represents one of the NF-κB–regulated genes that counteracts the apoptotic signals caused by TNF-α and thereby prevents ECs from undergoing apoptosis during inflammation.
Abstract: By differential screening of tumor necrosis factor alpha (TNF-alpha) and lipopolysaccharide (LPS)- activated endothelial cells (ECs), we have identified a cDNA clone that turned out to be a member of the inhibitor of apoptosis (iap) gene family. iap genes function to protect cells from undergoing apoptotic death in response to a variety of stimuli. These iap genes, hiap1, hiap2, and xiap were found to be strongly upregulated upon treatment of ECs with the inflammatory cytokines TNF-alpha, interleukin 1beta, and LPS, reagents that lead to activation of the nuclear transcription factor kappaB (NF-kappaB). Indeed, overexpression of IkappaBalpha, an inhibitor of NF-kappaB, suppresses the induced expression of iap genes and sensitizes ECs to TNF-alpha-induced apoptosis. Ectopic expression of one member of the human iap genes, human X-chromosome-linked iap (xiap), using recombinant adenovirus overrules the IkappaBalpha effect and protects ECs from TNF-alpha- induced apoptosis. We conclude that xiap represents one of the NF-kappaB-regulated genes that counteracts the apoptotic signals caused by TNF-alpha and thereby prevents ECs from undergoing apoptosis during inflammation.
681 citations
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TL;DR: Some myths about model selection are debunked, in particular the myth that consistent model selection has no effect on subsequent inference asymptotically and an “impossibility” result regarding the estimation of the finite-sample distribution of post-model-selection estimators.
Abstract: Model selection has an important impact on subsequent inference. Ignoring the model selection step leads to invalid inference. We discuss some intricate aspects of data-driven model selection that do not seem to have been widely appreciated in the literature. We debunk some myths about model selection, in particular the myth that consistent model selection has no effect on subsequent inference asymptotically. We also discuss an “impossibility” result regarding the estimation of the finite-sample distribution of post-model-selection estimators.
680 citations
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TL;DR: The 20210A prothrombin variant is a common abnormality, with a prevalence of carriership between one and four percent, and is more common in southern than in northern Europe.
Abstract: A variant in prothrombin (clotting factor II), a G to A transition at nucleotide position 20210, has recently been shown to be associated with the prothrombin plasma levels and the risk of both venous and arterial thrombosis. The purpose of this study was to investigate the prevalence of carriership of this mutation in various populations. We combined data from 11 centres in nine countries, where tests for this mutation had been performed in groups representing the general population. We calculated an overall prevalence estimate, by a precision-weighted method, and, since the distribution of the prevalences did not appear homogeneous, by an unweighted average of the prevalences. We examined differences in the prevalences by geographical location and ethnic background as a possible explanation for the heterogeneity. Among a total of 5527 individuals who had been tested, 111 heterozygous carriers of the 20210A mutation were found. The prevalence estimates varied from 0.7 to 4.0 between the centres. The overall prevalence estimate was 2.0 percent (CI95 1.4-2.6%). The variation around the summary estimate appeared more than was expected by chance alone, and this heterogeneity could be explained by geographic differences. In southern Europe, the prevalence was 3.0 percent (CI95 2.3 to 3.7%), nearly twice as high as the prevalence in northern Europe (1.7%, CI95 1.3 to 2.2%). The prothrombin variant appeared very rare in individuals from Asian and African descent. The 20210A prothrombin variant is a common abnormality, with a prevalence of carriership between one and four percent. It is more common in southern than in northern Europe. Since this distribution within Europe is very different to that of another prothrombotic mutation (factor V Leiden or factor V R506Q), founder effects are the most likely explanation for the geographical distribution of both mutations.
678 citations
Authors
Showing all 45262 results
Name | H-index | Papers | Citations |
---|---|---|---|
Tomas Hökfelt | 158 | 1033 | 95979 |
Wolfgang Wagner | 156 | 2342 | 123391 |
Hans Lassmann | 155 | 724 | 79933 |
Stanley J. Korsmeyer | 151 | 316 | 113691 |
Charles B. Nemeroff | 149 | 979 | 90426 |
Martin A. Nowak | 148 | 591 | 94394 |
Barton F. Haynes | 144 | 911 | 79014 |
Yi Yang | 143 | 2456 | 92268 |
Peter Palese | 132 | 526 | 57882 |
Gérald Simonneau | 130 | 587 | 90006 |
Peter M. Elias | 127 | 581 | 49825 |
Erwin F. Wagner | 125 | 375 | 59688 |
Anton Zeilinger | 125 | 631 | 71013 |
Wolfgang Waltenberger | 125 | 854 | 75841 |
Michael Wagner | 124 | 351 | 54251 |