@article{ErdmengerFernandezFloryetal.2017, author = {Erdmenger, Johanna and Fern{\´a}ndez, Daniel and Flory, Mario and Meg{\´i}as, Eugenio and Straub, Ann-Kathrin and Witkowski, Piotr}, title = {Time evolution of entanglement for holographic steady state formation}, series = {Journal of High Energy Physics}, volume = {2017}, journal = {Journal of High Energy Physics}, number = {10}, doi = {10.1007/JHEP10(2017)034}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-173798}, year = {2017}, abstract = {Within gauge/gravity duality, we consider the local quench-like time evolution obtained by joining two 1+1-dimensional heat baths at different temperatures at time \(t\) = 0. A steady state forms and expands in space. For the 2+1-dimensional gravity dual, we find that the "shockwaves" expanding the steady-state region are of spacelike nature in the bulk despite being null at the boundary. However, they do not transport information. Moreover, by adapting the time-dependent Hubeny-Rangamani-Takayanagi prescription, we holographically calculate the entanglement entropy and also the mutual information for different entangling regions. For general temperatures, we find that the entanglement entropy increase rate satisfies the same bound as in the 'entanglement tsunami' setups. For small temperatures of the two baths, we derive an analytical formula for the time dependence of the entanglement entropy. This replaces the entanglement tsunami-like behaviour seen for high temperatures. Finally, we check that strong subadditivity holds in this time-dependent system, as well as further more general entanglement inequalities for five or more regions recently derived for the static case.}, language = {en} } @article{DavisYuKeenanetal.2013, author = {Davis, Lea K. and Yu, Dongmei and Keenan, Clare L. and Gamazon, Eric R. and Konkashbaev, Anuar I. and Derks, Eske M. and Neale, Benjamin M. and Yang, Jian and Lee, S. Hong and Evans, Patrick and Barr, Cathy L. and Bellodi, Laura and Benarroch, Fortu and Berrio, Gabriel Bedoya and Bienvenu, Oscar J. and Bloch, Michael H. and Blom, Rianne M. and Bruun, Ruth D. and Budman, Cathy L. and Camarena, Beatriz and Campbell, Desmond and Cappi, Carolina and Cardona Silgado, Julio C. and Cath, Danielle C. and Cavallini, Maria C. and Chavira, Denise A. and Chouinard, Sylvian and Conti, David V. and Cook, Edwin H. and Coric, Vladimir and Cullen, Bernadette A. and Deforce, Dieter and Delorme, Richard and Dion, Yves and Edlund, Christopher K. and Egberts, Karin and Falkai, Peter and Fernandez, Thomas V. and Gallagher, Patience J. and Garrido, Helena and Geller, Daniel and Girard, Simon L. and Grabe, Hans J. and Grados, Marco A. and Greenberg, Benjamin D. and Gross-Tsur, Varda and Haddad, Stephen and Heiman, Gary A. and Hemmings, Sian M. J. and Hounie, Ana G. and Illmann, Cornelia and Jankovic, Joseph and Jenike, Micheal A. and Kennedy, James L. and King, Robert A. and Kremeyer, Barbara and Kurlan, Roger and Lanzagorta, Nuria and Leboyer, Marion and Leckman, James F. and Lennertz, Leonhard and Liu, Chunyu and Lochner, Christine and Lowe, Thomas L. and Macciardi, Fabio and McCracken, James T. and McGrath, Lauren M. and Restrepo, Sandra C. Mesa and Moessner, Rainald and Morgan, Jubel and Muller, Heike and Murphy, Dennis L. and Naarden, Allan L. and Ochoa, William Cornejo and Ophoff, Roel A. and Osiecki, Lisa and Pakstis, Andrew J. and Pato, Michele T. and Pato, Carlos N. and Piacentini, John and Pittenger, Christopher and Pollak, Yehunda and Rauch, Scott L. and Renner, Tobias J. and Reus, Victor I. and Richter, Margaret A. and Riddle, Mark A. and Robertson, Mary M. and Romero, Roxana and Ros{\`a}rio, Maria C. and Rosenberg, David and Rouleau, Guy A. and Ruhrmann, Stephan and Ruiz-Linares, Andreas and Sampaio, Aline S. and Samuels, Jack and Sandor, Paul and Sheppard, Broke and Singer, Harvey S. and Smit, Jan H. and Stein, Dan J. and Strengman, E. and Tischfield, Jay A. and Valencia Duarte, Ana V. and Vallada, Homero and Van Nieuwerburgh, Flip and Veenstra-VanderWeele, Jeremy and Walitza, Susanne and Wang, Ying and Wendland, Jens R. and Westenberg, Herman G. M. and Shugart, Yin Yao and Miguel, Euripedes C. and McMahon, William and Wagner, Michael and Nicolini, Humberto and Posthuma, Danielle and Hanna, Gregory L. and Heutink, Peter and Denys, Damiaan and Arnold, Paul D. and Oostra, Ben A. and Nestadt, Gerald and Freimer, Nelson B. and Pauls, David L. and Wray, Naomi R. and Stewart, S. Evelyn and Mathews, Carol A. and Knowles, James A. and Cox, Nancy J. and Scharf, Jeremiah M.}, title = {Partitioning the Heritability of Tourette Syndrome and Obsessive Compulsive Disorder Reveals Differences in Genetic Architecture}, series = {PLoS Genetics}, volume = {9}, journal = {PLoS Genetics}, number = {10}, issn = {1553-7390}, doi = {10.1371/journal.pgen.1003864}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127377}, pages = {e1003864}, year = {2013}, abstract = {The direct estimation of heritability from genome-wide common variant data as implemented in the program Genome-wide Complex Trait Analysis (GCTA) has provided a means to quantify heritability attributable to all interrogated variants. We have quantified the variance in liability to disease explained by all SNPs for two phenotypically-related neurobehavioral disorders, obsessive-compulsive disorder (OCD) and Tourette Syndrome (TS), using GCTA. Our analysis yielded a heritability point estimate of 0.58 (se = 0.09, p = 5.64e-12) for TS, and 0.37 (se = 0.07, p = 1.5e-07) for OCD. In addition, we conducted multiple genomic partitioning analyses to identify genomic elements that concentrate this heritability. We examined genomic architectures of TS and OCD by chromosome, MAF bin, and functional annotations. In addition, we assessed heritability for early onset and adult onset OCD. Among other notable results, we found that SNPs with a minor allele frequency of less than 5\% accounted for 21\% of the TS heritability and 0\% of the OCD heritability. Additionally, we identified a significant contribution to TS and OCD heritability by variants significantly associated with gene expression in two regions of the brain (parietal cortex and cerebellum) for which we had available expression quantitative trait loci (eQTLs). Finally we analyzed the genetic correlation between TS and OCD, revealing a genetic correlation of 0.41 (se = 0.15, p = 0.002). These results are very close to previous heritability estimates for TS and OCD based on twin and family studies, suggesting that very little, if any, heritability is truly missing (i.e., unassayed) from TS and OCD GWAS studies of common variation. The results also indicate that there is some genetic overlap between these two phenotypically-related neuropsychiatric disorders, but suggest that the two disorders have distinct genetic architectures.}, language = {en} } @article{JiangOronClarketal.2016, author = {Jiang, Yuxiang and Oron, Tal Ronnen and Clark, Wyatt T. and Bankapur, Asma R. and D'Andrea, Daniel and Lepore, Rosalba and Funk, Christopher S. and Kahanda, Indika and Verspoor, Karin M. and Ben-Hur, Asa and Koo, Da Chen Emily and Penfold-Brown, Duncan and Shasha, Dennis and Youngs, Noah and Bonneau, Richard and Lin, Alexandra and Sahraeian, Sayed M. E. and Martelli, Pier Luigi and Profiti, Giuseppe and Casadio, Rita and Cao, Renzhi and Zhong, Zhaolong and Cheng, Jianlin and Altenhoff, Adrian and Skunca, Nives and Dessimoz, Christophe and Dogan, Tunca and Hakala, Kai and Kaewphan, Suwisa and Mehryary, Farrokh and Salakoski, Tapio and Ginter, Filip and Fang, Hai and Smithers, Ben and Oates, Matt and Gough, Julian and T{\"o}r{\"o}nen, Petri and Koskinen, Patrik and Holm, Liisa and Chen, Ching-Tai and Hsu, Wen-Lian and Bryson, Kevin and Cozzetto, Domenico and Minneci, Federico and Jones, David T. and Chapman, Samuel and BKC, Dukka and Khan, Ishita K. and Kihara, Daisuke and Ofer, Dan and Rappoport, Nadav and Stern, Amos and Cibrian-Uhalte, Elena and Denny, Paul and Foulger, Rebecca E. and Hieta, Reija and Legge, Duncan and Lovering, Ruth C. and Magrane, Michele and Melidoni, Anna N. and Mutowo-Meullenet, Prudence and Pichler, Klemens and Shypitsyna, Aleksandra and Li, Biao and Zakeri, Pooya and ElShal, Sarah and Tranchevent, L{\´e}on-Charles and Das, Sayoni and Dawson, Natalie L. and Lee, David and Lees, Jonathan G. and Sillitoe, Ian and Bhat, Prajwal and Nepusz, Tam{\´a}s and Romero, Alfonso E. and Sasidharan, Rajkumar and Yang, Haixuan and Paccanaro, Alberto and Gillis, Jesse and Sede{\~n}o-Cort{\´e}s, Adriana E. and Pavlidis, Paul and Feng, Shou and Cejuela, Juan M. and Goldberg, Tatyana and Hamp, Tobias and Richter, Lothar and Salamov, Asaf and Gabaldon, Toni and Marcet-Houben, Marina and Supek, Fran and Gong, Qingtian and Ning, Wei and Zhou, Yuanpeng and Tian, Weidong and Falda, Marco and Fontana, Paolo and Lavezzo, Enrico and Toppo, Stefano and Ferrari, Carlo and Giollo, Manuel and Piovesan, Damiano and Tosatto, Silvio C. E. and del Pozo, Angela and Fern{\´a}ndez, Jos{\´e} M. and Maietta, Paolo and Valencia, Alfonso and Tress, Michael L. and Benso, Alfredo and Di Carlo, Stefano and Politano, Gianfranco and Savino, Alessandro and Rehman, Hafeez Ur and Re, Matteo and Mesiti, Marco and Valentini, Giorgio and Bargsten, Joachim W. and van Dijk, Aalt D. J. and Gemovic, Branislava and Glisic, Sanja and Perovic, Vladmir and Veljkovic, Veljko and Almeida-e-Silva, Danillo C. and Vencio, Ricardo Z. N. and Sharan, Malvika and Vogel, J{\"o}rg and Kansakar, Lakesh and Zhang, Shanshan and Vucetic, Slobodan and Wang, Zheng and Sternberg, Michael J. E. and Wass, Mark N. and Huntley, Rachael P. and Martin, Maria J. and O'Donovan, Claire and Robinson, Peter N. and Moreau, Yves and Tramontano, Anna and Babbitt, Patricia C. and Brenner, Steven E. and Linial, Michal and Orengo, Christine A. and Rost, Burkhard and Greene, Casey S. and Mooney, Sean D. and Friedberg, Iddo and Radivojac, Predrag and Veljkovic, Nevena}, title = {An expanded evaluation of protein function prediction methods shows an improvement in accuracy}, series = {Genome Biology}, volume = {17}, journal = {Genome Biology}, number = {184}, doi = {10.1186/s13059-016-1037-6}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-166293}, year = {2016}, abstract = {Background A major bottleneck in our understanding of the molecular underpinnings of life is the assignment of function to proteins. While molecular experiments provide the most reliable annotation of proteins, their relatively low throughput and restricted purview have led to an increasing role for computational function prediction. However, assessing methods for protein function prediction and tracking progress in the field remain challenging. Results We conducted the second critical assessment of functional annotation (CAFA), a timed challenge to assess computational methods that automatically assign protein function. We evaluated 126 methods from 56 research groups for their ability to predict biological functions using Gene Ontology and gene-disease associations using Human Phenotype Ontology on a set of 3681 proteins from 18 species. CAFA2 featured expanded analysis compared with CAFA1, with regards to data set size, variety, and assessment metrics. To review progress in the field, the analysis compared the best methods from CAFA1 to those of CAFA2. Conclusions The top-performing methods in CAFA2 outperformed those from CAFA1. This increased accuracy can be attributed to a combination of the growing number of experimental annotations and improved methods for function prediction. The assessment also revealed that the definition of top-performing algorithms is ontology specific, that different performance metrics can be used to probe the nature of accurate predictions, and the relative diversity of predictions in the biological process and human phenotype ontologies. While there was methodological improvement between CAFA1 and CAFA2, the interpretation of results and usefulness of individual methods remain context-dependent.}, language = {en} } @article{TrafimowAmrheinAreshenkoffetal.2018, author = {Trafimow, David and Amrhein, Valentin and Areshenkoff, Corson N. and Barrera-Causil, Carlos J. and Beh, Eric J. and Bilgi{\c{c}}, Yusuf K. and Bono, Roser and Bradley, Michael T. and Briggs, William M. and Cepeda-Freyre, H{\´e}ctor A. and Chaigneau, Sergio E. and Ciocca, Daniel R. and Correa, Juan C. and Cousineau, Denis and de Boer, Michiel R. and Dhar, Subhra S. and Dolgov, Igor and G{\´o}mez-Benito, Juana and Grendar, Marian and Grice, James W. and Guerrero-Gimenez, Martin E. and Guti{\´e}rrez, Andr{\´e}s and Huedo-Medina, Tania B. and Jaffe, Klaus and Janyan, Armina and Karimnezhad, Ali and Korner-Nievergelt, Fr{\"a}nzi and Kosugi, Koji and Lachmair, Martin and Ledesma, Rub{\´e}n D. and Limongi, Roberto and Liuzza, Marco T. and Lombardo, Rosaria and Marks, Michael J. and Meinlschmidt, Gunther and Nalborczyk, Ladislas and Nguyen, Hung T. and Ospina, Raydonal and Perezgonzalez, Jose D. and Pfister, Roland and Rahona, Juan J. and Rodr{\´i}guez-Medina, David A. and Rom{\~a}o, Xavier and Ruiz-Fern{\´a}ndez, Susana and Suarez, Isabel and Tegethoff, Marion and Tejo, Mauricio and van de Schoot, Rens and Vankov, Ivan I. and Velasco-Forero, Santiago and Wang, Tonghui and Yamada, Yuki and Zoppino, Felipe C. M. and Marmolejo-Ramos, Fernando}, title = {Manipulating the Alpha Level Cannot Cure Significance Testing}, series = {Frontiers in Psychology}, volume = {9}, journal = {Frontiers in Psychology}, number = {699}, issn = {1664-1078}, doi = {10.3389/fpsyg.2018.00699}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-189973}, year = {2018}, abstract = {We argue that making accept/reject decisions on scientific hypotheses, including a recent call for changing the canonical alpha level from p = 0.05 to p = 0.005, is deleterious for the finding of new discoveries and the progress of science. Given that blanket and variable alpha levels both are problematic, it is sensible to dispense with significance testing altogether. There are alternatives that address study design and sample size much more directly than significance testing does; but none of the statistical tools should be taken as the new magic method giving clear-cut mechanical answers. Inference should not be based on single studies at all, but on cumulative evidence from multiple independent studies. When evaluating the strength of the evidence, we should consider, for example, auxiliary assumptions, the strength of the experimental design, and implications for applications. To boil all this down to a binary decision based on a p-value threshold of 0.05, 0.01, 0.005, or anything else, is not acceptable.}, language = {en} }