Institution
Pompeu Fabra University
Education•Barcelona, Spain•
About: Pompeu Fabra University is a education organization based out in Barcelona, Spain. It is known for research contribution in the topics: Population & Gene. The organization has 8093 authors who have published 23570 publications receiving 858431 citations. The organization is also known as: Universitat Pompeu Fabra & UPF.
Topics: Population, Gene, European union, Genome, Context (language use)
Papers published on a yearly basis
Papers
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TL;DR: In this paper, the authors introduce bounded rationality into a standard consumption-based asset pricing model with a representative agent and time separable preferences, and show that it improves empirical performance.
Abstract: Introducing bounded rationality into a standard consumption based asset pricing model with a representative agent and time separable preferences strongly improves empirical performance. Learning causes momentum and mean reversion of returns and thereby excess volatility, persistence of price-dividend ratios, long-horizon return predictability and a risk premium, as in the habit model of Campbell and Cochrane (1999), but for lower risk aversion. This is obtained, even though we restrict consideration to learning schemes that imply only small deviations from full rationality. The findings are robust to the particular learning rule used and the value chosen for the single free parameter introduced by learning, provided agents forecast future stock prices using past information on prices.
225 citations
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TL;DR: It is shown that Hog1 regulates cell cycle progression at the G1 phase by a dual mechanism that involves downregulation of cyclin expression and direct targeting of the CDK-inhibitor protein Sic1.
Abstract: Activation of stress-activated protein kinases (SAPKs) is essential for proper cell adaptation to extracellular stimuli. The exposure of yeast cells to high osmolarity, or mutations that lead to activation of the Hog1 SAPK, result in cell-cycle arrest1,2,3,4. The mechanisms by which Hog1 and SAPKs in general regulate cell-cycle progression are not completely understood5,6,7,8. Here we show that Hog1 regulates cell cycle progression at the G1 phase by a dual mechanism that involves downregulation of cyclin expression and direct targeting of the CDK-inhibitor protein Sic1. Hog1 interacts physically with Sic1 in vivo and in vitro, and phosphorylates a single residue at the carboxyl terminus of Sic1, which, in combination with the downregulation of cyclin expression, results in Sic1 stabilization and inhibition of cell-cycle progression. Cells lacking Sic1 or containing a Sic1 allele mutated in the Hog1 phosphorylation site are unable to arrest at G1 phase after Hog1 activation, and become sensitive to osmostress. Together, our data indicate that the Sic1 CDK-inhibitor is the molecular target for the SAPK Hog1 that is required to modulate cell-cycle progression in response to stress.
225 citations
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TL;DR: In this article, the effect of social pressure on voting behavior in small and close-knit communities in Switzerland was investigated. And the main hypothesis is that social pressure creates incentives to vote for the purpose of being seen at the voting act.
Abstract: This paper uses a natural experiment to document the impact of social pressure on voting behavior. The main hypothesis is that social pressure creates incentives to vote for the purpose of being seen at the voting act. This incentive is particularly high in small and close-knit communities. Empirically, I analyze the effect of postal voting on voter participation in Switzerland. Optional postal voting decreased the voting costs, but simultaneously removed the social pressure to vote. In spite of the large reduction in voting costs, the effect on aggregate turnout was small. However, voter participation was more negatively affected in the smaller communities. This lends support to the view that social incentives played a role for certain people's voting decisions. (JEL: H0, Z13)
225 citations
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Charité1, Boston University2, Otto-von-Guericke University Magdeburg3, Radboud University Nijmegen4, Max Delbrück Center for Molecular Medicine5, Ankara University6, University of Zurich7, Sanjay Gandhi Post Graduate Institute of Medical Sciences8, University of Parma9, Charles University in Prague10, Sapienza University of Rome11, University of Copenhagen12, Pompeu Fabra University13, Innsbruck Medical University14, University of Barcelona15, University of Verona16, University of Rome Tor Vergata17, Carol Davila University of Medicine and Pharmacy18, University of Ulm19, Heidelberg University20, University of Münster21, University of Greifswald22, Leipzig University23
TL;DR: The G191R variant of PRSS2 mitigates intrapancreatic trypsin activity and thereby protects against chronic pancreatitis.
Abstract: Chronic pancreatitis is a common inflammatory disease of the pancreas. Mutations in the genes encoding cationic trypsinogen (PRSS1) and the pancreatic secretory trypsin inhibitor (SPINK1) are associated with chronic pancreatitis. Because increased proteolytic activity owing to mutated PRSS1 enhances the risk for chronic pancreatitis, mutations in the gene encoding anionic trypsinogen (PRSS2) may also predispose to disease. Here we analyzed PRSS2 in individuals with chronic pancreatitis and controls and found, to our surprise, that a variant of codon 191 (G191R) is overrepresented in control subjects: G191R was present in 220/6,459 (3.4%) controls but in only 32/2,466 (1.3%) affected individuals (odds ratio 0.37; P = 1.1 x 10(-8)). Upon activation by enterokinase or trypsin, purified recombinant G191R protein showed a complete loss of trypsin activity owing to the introduction of a new tryptic cleavage site that renders the enzyme hypersensitive to autocatalytic proteolysis. In conclusion, the G191R variant of PRSS2 mitigates intrapancreatic trypsin activity and thereby protects against chronic pancreatitis.
225 citations
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TL;DR: In this article, the authors review the expected future WLAN scenarios and use cases that justify the push for a new PHY/MAC IEEE 802.11 amendment, and discuss some of the network-level functionalities that are required to fully improve the user experience in next-generation WLANs.
Abstract: IEEE 802.11ax-2019 will replace both IEEE 802.11n-2009 and IEEE 802.11ac-2013 as the next high-throughput WLAN amendment. In this article, we review the expected future WLAN scenarios and use cases that justify the push for a new PHY/MAC IEEE 802.11 amendment. After that, we overview a set of new technical features that may be included in the IEEE 802.11ax-2019 amendment, and describe both their advantages and drawbacks. Finally, we discuss some of the network-level functionalities that are required to fully improve the user experience in next-generation WLANs and note their relation with other ongoing IEEE 802.11 amendments.
224 citations
Authors
Showing all 8248 results
Name | H-index | Papers | Citations |
---|---|---|---|
Andrei Shleifer | 171 | 514 | 271880 |
Paul Elliott | 153 | 773 | 103839 |
Bert Brunekreef | 124 | 806 | 81938 |
Philippe Aghion | 122 | 507 | 73438 |
Anjana Rao | 118 | 337 | 61395 |
Jordi Sunyer | 115 | 798 | 57211 |
Kenneth J. Arrow | 113 | 411 | 111221 |
Xavier Estivill | 110 | 673 | 59568 |
Roderic Guigó | 108 | 304 | 106914 |
Mark J. Nieuwenhuijsen | 107 | 647 | 49080 |
Jordi Alonso | 107 | 523 | 64058 |
Alfonso Valencia | 106 | 542 | 55192 |
Luis Serrano | 105 | 452 | 42515 |
Vadim N. Gladyshev | 102 | 490 | 34148 |
Josep M. Antó | 100 | 493 | 38663 |