@article{ZahnertLoewenheimBeutneretal.2016,
  author    = {Zahnert, Thomas and L{\"o}wenheim, Hubert and Beutner, Dirk and Hagen, Rudolf and Ernst, Arneborg and Pau, Hans-Wilhelm and Zehlicke, Thorsten and K{\"u}hne, Hilke and Friese, Natascha and Tropitzsch, Anke and L{\"u}ers, Jan-Christoffer and Mlynski, Robert and Todt, Ingo and H{\"u}ttenbrink, Karl-Bernd},
  title     = {Multicenter Clinical Trial of Vibroplasty Couplers to Treat Mixed/Conductive Hearing Loss: First Results},
  series = {Audiology and Neurotology},
  volume    = {21},
  journal   = {Audiology and Neurotology},
  number    = {4},
  issn      = {1420-3030},
  doi       = {10.1159/000444616},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-199129},
  pages     = {212-222},
  year      = {2016},
  abstract  = {Objective: To evaluate the safety and effectiveness of round window (RW), oval window (OW), CliP and Bell couplers for use with an active middle ear implant. Methods: This is a multicenter, long-term, prospective trial with consecutive enrollment, involving 6 university hospitals in Germany. Bone conduction, air conduction, implant-aided warble-tone thresholds and Freiburger monosyllable word recognition scores were compared with unaided preimplantation results in 28 moderate-to-profound hearing-impaired patients after 12 months of follow-up. All patients had previously undergone failed reconstruction surgeries (up to 5 or more). In a subset of patients, additional speech tests at 12 months postoperatively were used to compare the aided with the unaided condition after implantation with the processor switched off. An established quality-of-life questionnaire for hearing aids was used to determine patient satisfaction. Results: Postoperative bone conduction remained stable. Mean functional gain for all couplers was 37 dB HL (RW = 42 dB, OW = 35 dB, Bell = 38 dB, CliP = 27 dB). The mean postoperative Freiburger monosyllable score was 71\% at 65 dB SPL. The postimplantation mean SRT<sub>50</sub> (speech reception in quiet for 50\% understanding of words in sentences) improved on average by 23 dB over unaided testing and signal-to-noise ratios also improved in all patients. The International Outcome Inventory for Hearing Aids (IOI-HA)quality-of-life questionnaire was scored very positively by all patients. Conclusion: A significant improvement was seen with all couplers, and patients were satisfied with the device at 12 months postoperatively. These results demonstrate that an active implant is an advantage in achieving good hearing benefit in patients with prior failed reconstruction surgery.},
  language  = {en}
}
@article{DenglerMaldanerGlaeskeretal.2016,
  author    = {Dengler, Julius and Maldaner, Nicolai and Gl{\"a}sker, Sven and Endres, Matthias and Wagner, Martin and Malzahn, Uwe and Heuschmann, Peter U. and Vajkoczy, Peter},
  title     = {Outcome of Surgical or Endovascular Treatment of Giant Intracranial Aneurysms, with Emphasis on Age, Aneurysm Location, and Unruptured Aneuryms - A Systematic Review and Meta-Analysis},
  series = {Cerebrovascular Diseases},
  volume    = {41},
  journal   = {Cerebrovascular Diseases},
  number    = {3-4},
  organization    = {Giant Intracranial Aneurysm Study Group},
  issn      = {1015-9770},
  doi       = {10.1159/000443485},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-196792},
  pages     = {187-198},
  year      = {2016},
  abstract  = {Background: Designing treatment strategies for unruptured giant intracranial aneurysms (GIA) is difficult as evidence of large clinical trials is lacking. We examined the outcome following surgical or endovascular GIA treatment focusing on patient age, GIA location and unruptured GIA. Methods: Medline and Embase were searched for studies reporting on GIA treatment outcome published after January 2000. We calculated the proportion of good outcome (PGO) for all included GIA and for unruptured GIA by meta-analysis using a random effects model. Results: We included 54 studies containing 64 study populations with 1,269 GIA at a median follow-up time (FU-T) of 26.4 months (95\% CI 10.8-42.0). PGO was 80.9\% (77.4-84.4) in the analysis of all GIA compared to 81.2\% (75.3-86.1) in the separate analysis of unruptured GIA. For each year added to patient age, PGO decreased by 0.8\%, both for all GIA and unruptured GIA. For all GIA, surgical treatment resulted in a PGO of 80.3\% (95\% CI 76.0-84.6) compared to 84.2\% (78.5-89.8, p = 0.27) after endovascular treatment. In unruptured GIA, PGO was 79.7\% (95\% CI 71.5-87.8) after surgical treatment and 84.9\% (79.1-90.7, p = 0.54) after endovascular treatment. PGO was lower in high quality studies and in studies presenting aggregate instead of individual patient data. In unruptured GIA, the OR for good treatment outcome was 5.2 (95\% CI 2.0-13.0) at the internal carotid artery compared to 0.1 (0.1-0.3, p < 0.1) in the posterior circulation. Patient sex, FU-T and prevalence of ruptured GIA were not associated with PGO. Conclusions: We found that the chances of good outcome after surgical or endovascular GIA treatment mainly depend on patient age and aneurysm location rather than on the type of treatment conducted. Our analysis may inform future research on GIA.},
  language  = {en}
}
@techreport{MetzgerRafetsederSchroederetal.2016,
  type      = {Working Paper},
  author    = {Metzger, Florian and Rafetseder, Albert and Schr{\"o}der, Svenja and Zwickl, Patrick},
  title     = {The Prospects of Cloud Gaming: Do the Benefits Outweigh the Costs?},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-242452},
  pages     = {10},
  year      = {2016},
  abstract  = {In recent years, cloud gaming has become a popular research topic and has claimed many benefits in the commercial domain over conventional gaming. While, cloud gaming platforms have frequently failed in the past, they have received a new impetus over the last years that brought it to the edge of commercial breakthrough. The fragility of the cloud gaming market may be caused by the high investment costs, offered pricing models or competition from existing "{\`a} la carte" platforms. This paper aims at investigating the costs and benefits of both platform types through a twofold approach. We first take on the perspective of the customers, and investigate several cloud gaming platforms and their pricing models in comparison to the costs of other gaming platforms. Then, we explore engagement metrics in order to assess the enjoyment of playing the offered games. Lastly, coming from the perspective of the service providers, we aim to identify challenges in cost-effectively operating a large-scale cloud gaming service while maintaining high QoE values. Our analysis provides initial, yet still comprehensive reasons and models for the prospects of cloud gaming in a highly competitive market.},
  subject      = {Cloud Computing},
  language  = {en}
}
@article{VanHauteDietmannKremeretal.2016,
  author    = {Van Haute, Lindsey and Dietmann, Sabine and Kremer, Laura and Hussain, Shobbir and Pearce, Sarah F. and Powell, Christopher A. and Rorbach, Joanna and Lantaff, Rebecca and Blanco, Sandra and Sauer, Sascha and Kotzaeridou, Urania and Hoffmann, Georg F. and Memari, Yasin and Kolb-Kokocinski, Anja and Durbin, Richard and Mayr, Johannes A. and Frye, Michaela and Prokisch, Holger and Minczuk, Michal},
  title     = {Deficient methylation and formylation of mt-tRNA(Met) wobble cytosine in a patient carrying mutations in NSUN3},
  series = {Nature Communications},
  volume    = {7},
  journal   = {Nature Communications},
  doi       = {10.1038/ncomms12039},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-165998},
  pages     = {12039},
  year      = {2016},
  abstract  = {Epitranscriptome modifications are required for structure and function of RNA and defects in these pathways have been associated with human disease. Here we identify the RNA target for the previously uncharacterized 5-methylcytosine (m5C) methyltransferase NSun3 and link m5C RNA modifications with energy metabolism. Using whole-exome sequencing, we identified loss-of-function mutations in NSUN3 in a patient presenting with combined mitochondrial respiratory chain complex deficiency. Patient-derived fibroblasts exhibit severe defects in mitochondrial translation that can be rescued by exogenous expression of NSun3. We show that NSun3 is required for deposition of m5C at the anticodon loop in the mitochondrially encoded transfer RNA methionine (mt-tRNAMet). Further, we demonstrate that m5C deficiency in mt-tRNAMet results in the lack of 5-formylcytosine (f5C) at the same tRNA position. Our findings demonstrate that NSUN3 is necessary for efficient mitochondrial translation and reveal that f5C in human mitochondrial RNA is generated by oxidative processing of m5C.},
  language  = {en}
}
@article{MitchellLiWeinholdetal.2016,
  author    = {Mitchell, Jonathan S. and Li, Ni and Weinhold, Niels and F{\"o}rsti, Asta and Ali, Mina and van Duin, Mark and Thorleifsson, Gudmar and Johnson, David C. and Chen, Bowang and Halvarsson, Britt-Marie and Gudbjartsson, Daniel F. and Kuiper, Rowan and Stephens, Owen W. and Bertsch, Uta and Broderick, Peter and Campo, Chiara and Einsele, Hermann and Gregory, Walter A. and Gullberg, Urban and Henrion, Marc and Hillengass, Jens and Hoffmann, Per and Jackson, Graham H. and Johnsson, Ellinor and J{\"o}ud, Magnus and Kristinsson, Sigurdur Y. and Lenhoff, Stig and Lenive, Oleg and Mellqvist, Ulf-Henrik and Migliorini, Gabriele and Nahi, Hareth and Nelander, Sven and Nickel, Jolanta and N{\"o}then, Markus M. and Rafnar, Thorunn and Ross, Fiona M. and da Silva Filho, Miguel Inacio and Swaminathan, Bhairavi and Thomsen, Hauke and Turesson, Ingemar and Vangsted, Annette and Vogel, Ulla and Waage, Anders and Walker, Brian A. and Wihlborg, Anna-Karin and Broyl, Annemiek and Davies, Faith E. and Thorsteinsdottir, Unnur and Langer, Christian and Hansson, Markus and Kaiser, Martin and Sonneveld, Pieter and Stefansson, Kari and Morgan, Gareth J. and Goldschmidt, Hartmut and Hemminki, Kari and Nilsson, Bj{\"o}rn and Houlston, Richard S.},
  title     = {Genome-wide association study identifies multiple susceptibility loci for multiple myeloma},
  series = {Nature Communications},
  volume    = {7},
  journal   = {Nature Communications},
  doi       = {10.1038/ncomms12050},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-165983},
  pages     = {12050},
  year      = {2016},
  abstract  = {Multiple myeloma (MM) is a plasma cell malignancy with a significant heritable basis. Genome-wide association studies have transformed our understanding of MM predisposition, but individual studies have had limited power to discover risk loci. Here we perform a meta-analysis of these GWAS, add a new GWAS and perform replication analyses resulting in 9,866 cases and 239,188 controls. We confirm all nine known risk loci and discover eight new loci at 6p22.3 (rs34229995, P=1.31 × 10-8), 6q21 (rs9372120, P=9.09 × 10-15), 7q36.1 (rs7781265, P=9.71 × 10-9), 8q24.21 (rs1948915, P=4.20 × 10-11), 9p21.3 (rs2811710, P=1.72 × 10-13), 10p12.1 (rs2790457, P=1.77 × 10-8), 16q23.1 (rs7193541, P=5.00 × 10-12) and 20q13.13 (rs6066835, P=1.36 × 10-13), which localize in or near to JARID2, ATG5, SMARCD3, CCAT1, CDKN2A, WAC, RFWD3 and PREX1. These findings provide additional support for a polygenic model of MM and insight into the biological basis of tumour development.},
  language  = {en}
}
@article{HanzelmannJooFranzWachteletal.2016,
  author    = {Hanzelmann, Dennis and Joo, Hwang-Soo and Franz-Wachtel, Mirita and Hertlein, Tobias and Stevanovic, Stefan and Macek, Boris and Wolz, Christiane and G{\"o}tz, Friedrich and Otto, Michael and Kretschmer, Dorothee and Peschel, Andreas},
  title     = {Toll-like receptor 2 activation depends on lipopeptide shedding by bacterial surfactants},
  series = {Nature Communications},
  volume    = {7},
  journal   = {Nature Communications},
  doi       = {10.1038/ncomms12304},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-165975},
  pages     = {12304},
  year      = {2016},
  abstract  = {Sepsis caused by Gram-positive bacterial pathogens is a major fatal disease but its molecular basis remains elusive. Toll-like receptor 2 (TLR2) has been implicated in the orchestration of inflammation and sepsis but its role appears to vary for different pathogen species and clones. Accordingly, Staphylococcus aureus clinical isolates differ substantially in their capacity to activate TLR2. Here we show that strong TLR2 stimulation depends on high-level production of phenol-soluble modulin (PSM) peptides in response to the global virulence activator Agr. PSMs are required for mobilizing lipoproteins, the TLR2 agonists, from the staphylococcal cytoplasmic membrane. Notably, the course of sepsis caused by PSM-deficient S. aureus is similar in wild-type and TLR2-deficient mice, but TLR2 is required for protection of mice against PSM-producing S. aureus. Thus, a crucial role of TLR2 depends on agonist release by bacterial surfactants. Modulation of this process may lead to new therapeutic strategies against Gram-positive infections.},
  language  = {en}
}
@article{BaptistaKeszeiOliveiraetal.2016,
  author    = {Baptista, Marisa A.P. and Keszei, Marton and Oliveira, Mariana and Sunahara, Karen K.S. and Andersson, John and Dahlberg, Carin I.M. and Worth, Austen J. and Lied{\´e}n, Agne and Kuo, I-Chun and Wallin, Robert P.A. and Snapper, Scott B. and Eidsmo, Liv and Scheynius, Annika and Karlsson, Mikael C.I. and Bouma, Gerben and Burns, Siobhan O. and Forsell, Mattias N.E. and Thrasher, Adrian J. and Nyl{\´e}n, Susanne and Westerberg, Lisa S.},
  title     = {Deletion of Wiskott-Aldrich syndrome protein triggers Rac2 activity and increased cross-presentation by dendritic cells},
  series = {Nature Communications},
  volume    = {7},
  journal   = {Nature Communications},
  doi       = {10.1038/ncomms12175},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-165966},
  pages     = {12175},
  year      = {2016},
  abstract  = {Wiskott-Aldrich syndrome (WAS) is caused by loss-of-function mutations in theWASp gene. Decreased cellular responses in WASp-deficient cells have been interpreted to mean that WASp directly regulates these responses in WASp-sufficient cells. Here, we identify an exception to this concept and show that WASp-deficient dendritic cells have increased activation of Rac2 that support cross-presentation to CD8þ T cells. Using two different skin pathology models, WASp-deficient mice show an accumulation of dendritic cells in the skin and increased expansion of IFNg-producing CD8þ T cells in the draining lymph node and spleen. Specific deletion of WASp in dendritic cells leads to marked expansion of CD8þ T cells at the expense of CD4þ T cells. WASp-deficient dendritic cells induce increased cross-presentation to CD8þ T cells by activating Rac2 that maintains a near neutral pH of phagosomes. Our data reveals an intricate balance between activation of WASp and Rac2 signalling pathways in dendritic cells.},
  language  = {en}
}
@article{KnorrSokkarSchottetal.2016,
  author    = {Knorr, Johannes and Sokkar, Pandian and Schott, Sebastian and Costa, Paolo and Thiel, Walter and Sander, Wolfram and Sanchez-Garcia, Elsa and Nuernberger, Patrick},
  title     = {Competitive solvent-molecule interactions govern primary processes of diphenylcarbene in solvent mixtures},
  series = {Nature Communications},
  volume    = {7},
  journal   = {Nature Communications},
  doi       = {10.1038/ncomms12968},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-165954},
  pages     = {12968},
  year      = {2016},
  abstract  = {Photochemical reactions in solution often proceed via competing reaction pathways comprising intermediates that capture a solvent molecule. A disclosure of the underlying reaction mechanisms is challenging due to the rapid nature of these processes and the intricate identification of how many solvent molecules are involved. Here combining broadband femtosecond transient absorption and quantum mechanics/molecular mechanics simulations, we show for one of the most reactive species, diphenylcarbene, that the decision-maker is not the nearest solvent molecule but its neighbour. The hydrogen bonding dynamics determine which reaction channels are accessible in binary solvent mixtures at room temperature. In-depth analysis of the amount of nascent intermediates corroborates the importance of a hydrogen-bonded complex with a protic solvent molecule, in striking analogy to complexes found at cryogenic temperatures. Our results show that adjacent solvent molecules take the role of key abettors rather than bystanders for the fate of the reactive intermediate.},
  language  = {en}
}
@article{WawraFeselWidmeretal.2016,
  author    = {Wawra, Stephan and Fesel, Philipp and Widmer, Heidi and Timm, Malte and Seibel, J{\"u}rgen and Leson, Lisa and Kesseler, Leona and Nostadt, Robin and Hilbert, Magdalena and Langen, Gregor and Zuccaro, Alga},
  title     = {The fungal-specific beta-glucan-binding lectin FGB1 alters cell-wall composition and suppresses glucan-triggered immunity in plants},
  series = {Nature Communications},
  volume    = {7},
  journal   = {Nature Communications},
  doi       = {10.1038/ncomms13188},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-165945},
  pages     = {13188},
  year      = {2016},
  abstract  = {β-glucans are well-known modulators of the immune system in mammals but little is known about β-glucan triggered immunity in planta. Here we show by isothermal titration calorimetry, circular dichroism spectroscopy and nuclear magnetic resonance spectroscopy that the FGB1 gene from the root endophyte Piriformospora indica encodes for a secreted fungal-specific β-glucan-binding lectin with dual function. This lectin has the potential to both alter fungal cell wall composition and properties, and to efficiently suppress β-glucan-triggered immunity in different plant hosts, such as Arabidopsis, barley and Nicotiana benthamiana. Our results hint at the existence of fungal effectors that deregulate innate sensing of β-glucan in plants.},
  language  = {en}
}
@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}
}