TY  - JOUR
A1  - Biedermann, B.
A1  - Billoni, M.
A1  - Denner, A.
A1  - Dittmaier, S.
A1  - Hofer, L.
A1  - Jäger, B.
A1  - Salfelder, L.
T1  - Next-to-leading-order electroweak corrections to pp -> W\(^{+}\)W\(^{-}\) -> 4 leptons at the LHC
JF  - JOURNAL OF HIGH ENERGY PHYSICS
N2  - We present results of the first calculation of next-to-leading-order electroweak corrections to W-boson pair production at the LHC that fully takes into account leptonic W-boson decays and off-shell effects. Employing realistic event selections, we discuss the corrections in situations that are typical for the study of W-boson pairs as a signal process or of Higgs-boson decays H → WW∗, to which W-boson pair production represents an irreducible background. In particular, we compare the full off-shell results, obtained treating the W-boson resonances in the complex-mass scheme, to previous results in the so-called double-pole approximation, which is based on an expansion of the loop amplitudes about the W resonance poles. At small and intermediate scales, i.e. in particular in angular and rapidity distributions, the two approaches show the expected agreement at the level of fractions of a percent, but larger differences appear in the TeV range. For transverse-momentum distributions, the differences can even exceed the 10% level in the TeV range where “background diagrams” with one instead of two resonant W bosons gain in importance because of recoil effects.
KW  - NLO Computations
KW  - W-boson
KW  - LHC
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-167790
VL  - 06
IS  - 065
ER  - 
TY  - JOUR
A1  - Mitjans, M.
A1  - Begemann, M.
A1  - Ju, A.
A1  - Dere, E.
A1  - Wüstefeld, L.
A1  - Hofer, S.
A1  - Hassouna, I.
A1  - Balkenhol, J.
A1  - Oliveira, B.
A1  - Van der Auwera, S.
A1  - Tammer, R.
A1  - Hammerschmidt, K.
A1  - Völzke, H.
A1  - Homuth, G.
A1  - Cecconi, F.
A1  - Chowdhury, K.
A1  - Grabe, H.
A1  - Frahm, J.
A1  - Boretius, S.
A1  - Dandekar, T.
A1  - Ehrenreich, H.
T1  - Sexual dimorphism of \(AMBRA1\)-related autistic features in human and mouse
JF  - Translational Psychiatry
N2  - \(Ambra1\) is linked to autophagy and neurodevelopment. Heterozygous \(Ambra1\) deficiency induces autism-like behavior in a sexually dimorphic manner. Extraordinarily, autistic features are seen in female mice only, combined with stronger Ambra1 protein reduction in brain compared to males. However, significance of \(AMBRA1\) for autistic phenotypes in humans and, apart from behavior, for other autism-typical features, namely early brain enlargement or increased seizure propensity, has remained unexplored. Here we show in two independent human samples that a single normal \(AMBRA1\) genotype, the intronic SNP rs3802890-AA, is associated with autistic features in women, who also display lower \(AMBRA1\) mRNA expression in peripheral blood mononuclear cells relative to female GG carriers. Located within a non-coding RNA, likely relevant for mRNA and protein interaction, rs3802890 (A versus G allele) may affect its stability through modification of folding, as predicted by \(in\) \(silico\) analysis. Searching for further autism-relevant characteristics in \(Ambra1^{+/−}\) mice, we observe reduced interest of female but not male mutants regarding pheromone signals of the respective other gender in the social intellicage set-up. Moreover, altered pentylentetrazol-induced seizure propensity, an \(in\) \(vivo\) readout of neuronal excitation–inhibition dysbalance, becomes obvious exclusively in female mutants. Magnetic resonance imaging reveals mild prepubertal brain enlargement in both genders, uncoupling enhanced brain dimensions from the primarily female expression of all other autistic phenotypes investigated here. These data support a role of \(AMBRA1/Ambra1\) partial loss-of-function genotypes for female autistic traits. Moreover, they suggest \(Ambra1\) heterozygous mice as a novel multifaceted and construct-valid genetic mouse model for female autism.
KW  - biology
KW  - clinical genetics
KW  - molecular neuroscience
Y1  - 2017
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-173782
VL  - 2017
IS  - 7
ER  - 
TY  - JOUR
A1  - Hibar, Derrek P.
A1  - Adams, Hieab H.H.
A1  - Jahanshad, Neda
A1  - Chauhan, Ganesh
A1  - Stein, Jason L
A1  - Hofer, Edith
A1  - Renteria, Miguel E.
A1  - Bis, Joshua C.
A1  - Arias-Vasquez, Alejandro
A1  - Ikram, M. Kamran
A1  - Desrivières, Sylvane
A1  - Vernooij, Meike W.
A1  - Abramovic, Lucija
A1  - Alhusaini, Saud
A1  - Amin, Najaf
A1  - Andersson, Micael
A1  - Arfanakis, Konstantinos
A1  - Aribisala, Benjamin S.
A1  - Armstrong, Nicola J.
A1  - Athanasiu, Lavinia
A1  - Axelsson, Tomas
A1  - Beecham, Ashley H.
A1  - Beiser, Alexa
A1  - Bernard, Manon
A1  - Blanton, Susan H.
A1  - Bohlken, Marc M.
A1  - Boks, Marco P.
A1  - Bralten, Janita
A1  - Brickman, Adam M.
A1  - Carmichael, Owen
T1  - Novel genetic loci associated with hippocampal volume
JF  - Nature Communications
N2  - The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer’s disease (r\(_g\)=−0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness.
KW  - brain
KW  - hippocampal formation
KW  - neuropsychiatric disorders
KW  - Alzheimer’s disease
KW  - genetic loci
KW  - hippocampal volume
Y1  - 2017
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-182115
VL  - 8
ER  -