@article{GomezHFelipeMedinaSanchezMartinetal.2016, author = {Gom{\´e}z-H, Laura and Felipe-Medina, Natalia and S{\´a}nchez-Mart{\´i}n, Manuel and Davies, Owen R. and Ramos, Isabel and Garc{\´i}a-Tu{\~n}{\´o}n, Ignacio and de Rooij, Dirk G. and Dereli, Ihsan and T{\´o}th, Attila and Barbero, Jos{\´e} Luis and Benavente, Ricardo and Llano, Elena and Pendas, Alberto M.}, title = {C14ORF39/SIX6OS1 is a constituent of the synaptonemal complex and is essential for mouse fertility}, series = {Nature Communications}, volume = {7}, journal = {Nature Communications}, doi = {10.1038/ncomms13298}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-165907}, pages = {13298}, year = {2016}, abstract = {Meiotic recombination generates crossovers between homologous chromosomes that are essential for genome haploidization. The synaptonemal complex is a 'zipper'-like protein assembly that synapses homologue pairs together and provides the structural framework for processing recombination sites into crossovers. Humans show individual differences in the number of crossovers generated across the genome. Recently, an anonymous gene variant in C14ORF39/SIX6OS1 was identified that influences the recombination rate in humans. Here we show that C14ORF39/SIX6OS1 encodes a component of the central element of the synaptonemal complex. Yeast two-hybrid analysis reveals that SIX6OS1 interacts with the well-established protein synaptonemal complex central element 1 (SYCE1). Mice lacking SIX6OS1 are defective in chromosome synapsis at meiotic prophase I, which provokes an arrest at the pachytene-like stage and results in infertility. In accordance with its role as a modifier of the human recombination rate, SIX6OS1 is essential for the appropriate processing of intermediate recombination nodules before crossover formation.}, 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} } @article{RuizHerediaSanchezVegaOnechaetal.2018, author = {Ruiz-Heredia, Yanira and S{\´a}nchez-Vega, Beatriz and Onecha, Esther and Barrio, Santiago and Alonso, Rafael and Carlos Mart{\´i}nez-Avila, Jose and Cuenca, Isabel and Agirre, Xabier and Braggio, Esteban and Hern{\´a}ndez, Miguel-T. and Mart{\´i}nez, Rafael and Rosi{\~n}ol, Laura and Gutierrez, Norma and Martin-Ramos, Marisa and Ocio, Enrique M. and Echeveste, Mar{\´i}a-Asunci{\´o}n and P{\´e}rez de Oteyza, Jaime and Oriol, Albert and Bargay, Joan and Gironella, Mercedes and Ayala, Rosa and Blad{\´e}, Joan and Mateos, Mar{\´i}a-Victoria and Kortum, Klaus M. and Stewart, Keith and Garc{\´i}a-Sanz, Ram{\´o}n and San Miguel, Jes{\´u}s and Jos{\´e} Lahuerta, Juan and Martinez-Lopez, Joaqu{\´i}n}, title = {Mutational screening of newly diagnosed multiple myeloma patients by deep targeted sequencing}, series = {Haematologica}, volume = {103}, journal = {Haematologica}, number = {11}, doi = {10.3324/haematol.2018.188839}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-227151}, pages = {e544-e548}, year = {2018}, abstract = {no abstract available}, language = {en} }