@article{PostemaHoogmanAmbrosinoetal.2021,
  author    = {Postema, Merel C. and Hoogman, Martine and Ambrosino, Sara and Asherson, Philip and Banaschewski, Tobias and Bandeira, Cibele E. and Baranov, Alexandr and Bau, Claiton H.D. and Baumeister, Sarah and Baur-Streubel, Ramona and Bellgrove, Mark A. and Biederman, Joseph and Bralten, Janita and Brandeis, Daniel and Brem, Silvia and Buitelaar, Jan K. and Busatto, Geraldo F. and Castellanos, Francisco X. and Cercignani, Mara and Chaim-Avancini, Tiffany M. and Chantiluke, Kaylita C. and Christakou, Anastasia and Coghill, David and Conzelmann, Annette and Cubillo, Ana I. and Cupertino, Renata B. and de Zeeuw, Patrick and Doyle, Alysa E. and Durston, Sarah and Earl, Eric A. and Epstein, Jeffery N. and Ethofer, Thomas and Fair, Damien A. and Fallgatter, Andreas J. and Faraone, Stephen V. and Frodl, Thomas and Gabel, Matt C. and Gogberashvili, Tinatin and Grevet, Eugenio H. and Haavik, Jan and Harrison, Neil A. and Hartman, Catharina A. and Heslenfeld, Dirk J. and Hoekstra, Pieter J. and Hohmann, Sarah and H{\o}vik, Marie F. and Jernigan, Terry L. and Kardatzki, Bernd and Karkashadze, Georgii and Kelly, Clare and Kohls, Gregor and Konrad, Kerstin and Kuntsi, Jonna and Lazaro, Luisa and Lera-Miguel, Sara and Lesch, Klaus-Peter and Louza, Mario R. and Lundervold, Astri J. and Malpas, Charles B and Mattos, Paulo and McCarthy, Hazel and Namazova-Baranova, Leyla and Nicolau, Rosa and Nigg, Joel T. and Novotny, Stephanie E. and Oberwelland Weiss, Eileen and O'Gorman Tuura, Ruth L. and Oosterlaan, Jaap and Oranje, Bob and Paloyelis, Yannis and Pauli, Paul and Picon, Felipe A. and Plessen, Kerstin J. and Ramos-Quiroga, J. Antoni and Reif, Andreas and Reneman, Liesbeth and Rosa, Pedro G.P. and Rubia, Katya and Schrantee, Anouk and Schweren, Lizanne J.S. and Seitz, Jochen and Shaw, Philip and Silk, Tim J. and Skokauskas, Norbert and Soliva Vila, Juan C. and Stevens, Michael C. and Sudre, Gustavo and Tamm, Leanne and Tovar-Moll, Fernanda and van Erp, Theo G.M. and Vance, Alasdair and Vilarroya, Oscar and Vives-Gilabert, Yolanda and von Polier, Georg G. and Walitza, Susanne and Yoncheva, Yuliya N. and Zanetti, Marcus V. and Ziegler, Georg C. and Glahn, David C. and Jahanshad, Neda and Medland, Sarah E. and Thompson, Paul M. and Fisher, Simon E. and Franke, Barbara and Francks, Clyde},
  title     = {Analysis of structural brain asymmetries in attention-deficit/hyperactivity disorder in 39 datasets},
  series = {Journal of Child Psychology and Psychiatry},
  volume    = {62},
  journal   = {Journal of Child Psychology and Psychiatry},
  number    = {10},
  doi       = {10.1111/jcpp.13396},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-239968},
  pages     = {1202 -- 1219},
  year      = {2021},
  abstract  = {Objective Some studies have suggested alterations of structural brain asymmetry in attention-deficit/hyperactivity disorder (ADHD), but findings have been contradictory and based on small samples. Here, we performed the largest ever analysis of brain left-right asymmetry in ADHD, using 39 datasets of the ENIGMA consortium. Methods We analyzed asymmetry of subcortical and cerebral cortical structures in up to 1,933 people with ADHD and 1,829 unaffected controls. Asymmetry Indexes (AIs) were calculated per participant for each bilaterally paired measure, and linear mixed effects modeling was applied separately in children, adolescents, adults, and the total sample, to test exhaustively for potential associations of ADHD with structural brain asymmetries. Results There was no evidence for altered caudate nucleus asymmetry in ADHD, in contrast to prior literature. In children, there was less rightward asymmetry of the total hemispheric surface area compared to controls (t = 2.1, p = .04). Lower rightward asymmetry of medial orbitofrontal cortex surface area in ADHD (t = 2.7, p = .01) was similar to a recent finding for autism spectrum disorder. There were also some differences in cortical thickness asymmetry across age groups. In adults with ADHD, globus pallidus asymmetry was altered compared to those without ADHD. However, all effects were small (Cohen's d from -0.18 to 0.18) and would not survive study-wide correction for multiple testing. Conclusion Prior studies of altered structural brain asymmetry in ADHD were likely underpowered to detect the small effects reported here. Altered structural asymmetry is unlikely to provide a useful biomarker for ADHD, but may provide neurobiological insights into the trait.},
  language  = {en}
}
@article{WeberLassalleHaukeRamseretal.2018,
  author    = {Weber-Lassalle, Nana and Hauke, Jan and Ramser, Juliane and Richters, Lisa and Groß, Eva and Bl{\"u}mcke, Britta and Gehrig, Andrea and Kahlert, Anne-Karin and M{\"u}ller, Clemens R. and Hackmann, Karl and Honisch, Ellen and Weber-Lassalle, Konstantin and Niederacher, Dieter and Borde, Julika and Thiele, Holger and Ernst, Corinna and Altm{\"u}ller, Janine and Neidhardt, Guido and N{\"u}rnberg, Peter and Klaschik, Kristina and Schroeder, Christopher and Platzer, Konrad and Volk, Alexander E. and Wang-Gohrke, Shan and Just, Walter and Auber, Bernd and Kubisch, Christian and Schmidt, Gunnar and Horvath, Judit and Wappenschmidt, Barbara and Engel, Christoph and Arnold, Norbert and Dworniczak, Bernd and Rhiem, Kerstin and Meindl, Alfons and Schmutzler, Rita K. and Hahnen, Eric},
  title     = {BRIP1 loss-of-function mutations confer high risk for familial ovarian cancer, but not familial breast cancer},
  series = {Breast Cancer Research},
  volume    = {20},
  journal   = {Breast Cancer Research},
  doi       = {10.1186/s13058-018-0935-9},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-233433},
  year      = {2018},
  abstract  = {Background Germline mutations in the BRIP1 gene have been described as conferring a moderate risk for ovarian cancer (OC), while the role of BRIP1 in breast cancer (BC) pathogenesis remains controversial. Methods To assess the role of deleterious BRIP1 germline mutations in BC/OC predisposition, 6341 well-characterized index patients with BC, 706 index patients with OC, and 2189 geographically matched female controls were screened for loss-of-function (LoF) mutations and potentially damaging missense variants. All index patients met the inclusion criteria of the German Consortium for Hereditary Breast and Ovarian Cancer for germline testing and tested negative for pathogenic BRCA1/2 variants. Results BRIP1 LoF mutations confer a high OC risk in familial index patients (odds ratio (OR) = 20.97, 95\% confidence interval (CI) = 12.02-36.57, P < 0.0001) and in the subgroup of index patients with late-onset OC (OR = 29.91, 95\% CI = 14.99-59.66, P < 0.0001). No significant association of BRIP1 LoF mutations with familial BC was observed (OR = 1.81 95\% CI = 1.00-3.30, P = 0.0623). In the subgroup of familial BC index patients without a family history of OC there was also no apparent association (OR = 1.42, 95\% CI = 0.70-2.90, P = 0.3030). In 1027 familial BC index patients with a family history of OC, the BRIP1 mutation prevalence was significantly higher than that observed in controls (OR = 3.59, 95\% CI = 1.43-9.01; P = 0.0168). Based on the negative association between BRIP1 LoF mutations and familial BC in the absence of an OC family history, we conclude that the elevated mutation prevalence in the latter cohort was driven by the occurrence of OC in these families. Compared with controls, predicted damaging rare missense variants were significantly more prevalent in OC (P = 0.0014) but not in BC (P = 0.0693) patients. Conclusions To avoid ambiguous results, studies aimed at assessing the impact of candidate predisposition gene mutations on BC risk might differentiate between BC index patients with an OC family history and those without. In familial cases, we suggest that BRIP1 is a high-risk gene for late-onset OC but not a BC predisposition gene, though minor effects cannot be excluded.},
  language  = {en}
}
@article{GrossheinrichFirkSchulteRuetheretal.2018,
  author    = {Grossheinrich, Nicola and Firk, Christine and Schulte-R{\"u}ther, Martin and von Leupoldt, Andreas and Konrad, Kerstin and Huestegge, Lynn},
  title     = {Looking while unhappy: a mood-congruent attention bias toward sad adult faces in children},
  series = {Frontiers in Psychology},
  volume    = {9},
  journal   = {Frontiers in Psychology},
  number    = {2577},
  doi       = {10.3389/fpsyg.2018.02577},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-177688},
  year      = {2018},
  abstract  = {A negative mood-congruent attention bias has been consistently observed, for example, in clinical studies on major depression. This bias is assumed to be dysfunctional in that it supports maintaining a sad mood, whereas a potentially adaptive role has largely been neglected. Previous experiments involving sad mood induction techniques found a negative mood-congruent attention bias specifically for young individuals, explained by an adaptive need for information transfer in the service of mood regulation. In the present study we investigated the attentional bias in typically developing children (aged 6-12 years) when happy and sad moods were induced. Crucially, we manipulated the age (adult vs. child) of the displayed pairs of facial expressions depicting sadness, anger, fear and happiness. The results indicate that sad children indeed exhibited a mood specific attention bias toward sad facial expressions. Additionally, this bias was more pronounced for adult faces. Results are discussed in the context of an information gain which should be stronger when looking at adult faces due to their more expansive life experience. These findings bear implications for both research methods and future interventions.},
  language  = {en}
}
@article{FoerstnerReuscherHaberzettletal.2018,
  author    = {F{\"o}rstner, Konrad U and Reuscher, Carina M and Haberzettl, Kerstin and Weber, Lennart and Klug, Gabriele},
  title     = {RNase E cleavage shapes the transcriptome of Rhodobacter sphaeroides and strongly impacts phototrophic growth},
  series = {Life Science Alliance},
  volume    = {1},
  journal   = {Life Science Alliance},
  number    = {4},
  doi       = {10.26508/lsa.201800080},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-177139},
  pages     = {e201800080},
  year      = {2018},
  abstract  = {Bacteria adapt to changing environmental conditions by rapid changes in their transcriptome. This is achieved not only by adjusting rates of transcription but also by processing and degradation of RNAs. We applied TIER-Seq (transiently inactivating an endoribonuclease followed by RNA-Seq) for the transcriptome-wide identification of RNase E cleavage sites and of 5′ RNA ends, which are enriched when RNase E activity is reduced in Rhodobacter sphaeroides. These results reveal the importance of RNase E for the maturation and turnover of mRNAs, rRNAs, and sRNAs in this guanine-cytosine-rich α-proteobacterium, some of the latter have well-described functions in the oxidative stress response. In agreement with this, a role of RNase E in the oxidative stress response is demonstrated. A remarkably strong phenotype of a mutant with reduced RNase E activity was observed regarding the formation of photosynthetic complexes and phototrophic growth, whereas there was no effect on chemotrophic growth.},
  language  = {en}
}