@article{BoltzeKleinschnitzReymannetal.2012,
  author    = {Boltze, Johannes and Kleinschnitz, Christoph and Reymann, Klaus G. and Reiser, Georg and Wagner, Daniel-Christoph and Kranz, Alexander and Michalski, Dominik},
  title     = {Neurovascular pathophysiology in cerebral ischemia, dementia and the ageing brain - current trends in basic, translational and clinical research},
  series = {Experimental \& Translational Stroke Medicine},
  volume    = {4},
  journal   = {Experimental \& Translational Stroke Medicine},
  number    = {14},
  doi       = {doi:10.1186/2040-7378-4-14},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-126679},
  year      = {2012},
  abstract  = {The 7th International Symposium on Neuroprotection and Neurorepair was held from May 2nd to May 5th, 2012 in Potsdam, Germany. The symposium, which directly continues the successful Magdeburg meeting series, attracted over 330 colleagues from 29 countries to discuss recent findings and advances in the field. The focus of the 2012 symposium was widened from stroke and traumatic brain injury to neurodegenerative diseases, notably dementia, and more generally the ageing brain. Thereby, emphasis was given on neurovascular aspects of neurodegeneration and stroke including the blood-brain barrier, recent findings regarding the pathomechanism of Alzheimer's disease, and brain imaging approaches. In addition, neurobiochemical aspects of neuroprotection, the role of astrogliosis, the clinical progress of cell-based approaches as well as translational hurdles and opportunities were discussed in-depth. This review summarizes some of the most stimulating discussions and reports from the meeting.},
  language  = {en}
}
@article{MinnerupSutherlandBuchanetal.2012,
  author    = {Minnerup, Jens and Sutherland, Brad A. and Buchan, Alastair M. and Kleinschnitz, Christoph},
  title     = {Neuroprotection for Stroke: Current Status and Future Perspectives},
  series = {International Journal of Molecular Science},
  volume    = {13},
  journal   = {International Journal of Molecular Science},
  number    = {9},
  doi       = {10.3390/ijms130911753},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134730},
  pages     = {11753-11772},
  year      = {2012},
  abstract  = {Neuroprotection aims to prevent salvageable neurons from dying. Despite showing efficacy in experimental stroke studies, the concept of neuroprotection has failed in clinical trials. Reasons for the translational difficulties include a lack of methodological agreement between preclinical and clinical studies and the heterogeneity of stroke in humans compared to homogeneous strokes in animal models. Even when the international recommendations for preclinical stroke research, the Stroke Academic Industry Roundtable (STAIR) criteria, were followed, we have still seen limited success in the clinic, examples being NXY-059 and haematopoietic growth factors which fulfilled nearly all the STAIR criteria. However, there are a number of neuroprotective treatments under investigation in clinical trials such as hypothermia and ebselen. Moreover, promising neuroprotective treatments based on a deeper understanding of the complex pathophysiology of ischemic stroke such as inhibitors of NADPH oxidases and PSD-95 are currently evaluated in preclinical studies. Further concepts to improve translation include the investigation of neuroprotectants in multicenter preclinical Phase III-type studies, improved animal models, and close alignment between clinical trial and preclinical methodologies. Future successful translation will require both new concepts for preclinical testing and innovative approaches based on mechanistic insights into the ischemic cascade.},
  language  = {en}
}
@article{IpKronerGrohetal.2012,
  author    = {Ip, Chi Wang and Kroner, Antje and Groh, Janos and Huber, Marianne and Klein, Dennis and Spahn, Irene and Diem, Ricarda and Williams, Sarah K. and Nave, Klaus-Armin and Edgar, Julia M. and Martini, Rudolf},
  title     = {Neuroinflammation by Cytotoxic T-Lymphocytes Impairs Retrograde Axonal Transport in an Oligodendrocyte Mutant Mouse},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {8},
  doi       = {10.1371/journal.pone.0042554},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134982},
  pages     = {e42554},
  year      = {2012},
  abstract  = {Mice overexpressing proteolipid protein (PLP) develop a leukodystrophy-like disease involving cytotoxic, CD8+ T-lymphocytes. Here we show that these cytotoxic T-lymphocytes perturb retrograde axonal transport. Using fluorogold stereotactically injected into the colliculus superior, we found that PLP overexpression in oligodendrocytes led to significantly reduced retrograde axonal transport in retina ganglion cell axons. We also observed an accumulation of mitochondria in the juxtaparanodal axonal swellings, indicative for a disturbed axonal transport. PLP overexpression in the absence of T-lymphocytes rescued retrograde axonal transport defects and abolished axonal swellings. Bone marrow transfer from wildtype mice, but not from perforin- or granzyme B-deficient mutants, into lymphocyte-deficient PLP mutant mice led again to impaired axonal transport and the formation of axonal swellings, which are predominantly located at the juxtaparanodal region. This demonstrates that the adaptive immune system, including cytotoxic T-lymphocytes which release perforin and granzyme B, are necessary to perturb axonal integrity in the PLP-transgenic disease model. Based on our observations, so far not attended molecular and cellular players belonging to the immune system should be considered to understand pathogenesis in inherited myelin disorders with progressive axonal damage.},
  language  = {en}
}
@article{StippekohlWinklerWalteretal.2012,
  author    = {Stippekohl, Bastian and Winkler, Markus H. and Walter, Bertram and Kagerer, Sabine and Mucha, Ronald F. and Pauli, Paul and Vaitl, Dieter and Stark, Rudolf},
  title     = {Neural Responses to Smoking Stimuli Are Influenced by Smokers' Attitudes towards Their Own Smoking Behaviour},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {11},
  doi       = {10.1371/journal.pone.0046782},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-124393},
  year      = {2012},
  abstract  = {An important feature of addiction is the high drug craving that may promote the continuation of consumption. Environmental stimuli classically conditioned to drug-intake have a strong motivational power for addicts and can elicit craving. However, addicts differ in the attitudes towards their own consumption behavior: some are content with drug taking (consonant users) whereas others are discontent (dissonant users). Such differences may be important for clinical practice because the experience of dissonance might enhance the likelihood to consider treatment. This fMRI study investigated in smokers whether these different attitudes influence subjective and neural responses to smoking stimuli. Based on self-characterization, smokers were divided into consonant and dissonant smokers. These two groups were presented smoking stimuli and neutral stimuli. Former studies have suggested differences in the impact of smoking stimuli depending on the temporal stage of the smoking ritual they are associated with. Therefore, we used stimuli associated with the beginning (BEGIN-smoking-stimuli) and stimuli associated with the terminal stage (END-smoking-stimuli) of the smoking ritual as distinct stimulus categories. Stimulus ratings did not differ between both groups. Brain data showed that BEGIN-smoking-stimuli led to enhanced mesolimbic responses (amygdala, hippocampus, insula) in dissonant compared to consonant smokers. In response to END-smoking-stimuli, dissonant smokers showed reduced mesocortical responses (orbitofrontal cortex, subcallosal cortex) compared to consonant smokers. These results suggest that smoking stimuli with a high incentive value (BEGIN-smoking-stimuli) are more appetitive for dissonant than consonant smokers at least on the neural level. To the contrary, smoking stimuli with low incentive value (END-smoking-stimuli) seem to be less appetitive for dissonant smokers than consonant smokers. These differences might be one reason why dissonant smokers experience difficulties in translating their attitudes into an actual behavior change.},
  language  = {en}
}
@article{KlingelhoefferKaemmererKoospaletal.2012,
  author    = {Klingelhoeffer, Chr{\´i}stoph and K{\"a}mmerer, Ulrike and Koospal, Monika and M{\"u}hling, Bettina and Schneider, Manuela and Kapp, Michaela and K{\"u}bler, Alexander, and Germer, Christoph-Thomas and Otto, Christoph},
  title     = {Natural resistance to ascorbic acid induced oxidative stress is mainly mediated by catalase activity in human cancer cells and catalase-silencing sensitizes to oxidative stress},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75142},
  year      = {2012},
  abstract  = {Background: Ascorbic acid demonstrates a cytotoxic effect by generating hydrogen peroxide, a reactive oxygen species (ROS) involved in oxidative cell stress. A panel of eleven human cancer cell lines, glioblastoma and carcinoma, were exposed to serial dilutions of ascorbic acid (5-100 mmol/L). The purpose of this study was to analyse the impact of catalase, an important hydrogen peroxide-detoxifying enzyme, on the resistance of cancer cells to ascorbic acid mediated oxidative stress. Methods: Effective concentration (EC50) values, which indicate the concentration of ascorbic acid that reduced the number of viable cells by 50\%, were detected with the crystal violet assay. The level of intracellular catalase protein and enzyme activity was determined. Expression of catalase was silenced by catalase-specific short hairpin RNA (sh-RNA) in BT-20 breast carcinoma cells. Oxidative cell stress induced apoptosis was measured by a caspase luminescent assay. Results: The tested human cancer cell lines demonstrated obvious differences in their resistance to ascorbic acid mediated oxidative cell stress. Forty-five percent of the cell lines had an EC50>20 mmol/L and fifty-five percent had an EC50<20 mmol/L. With an EC50 of 2.6-5.5 mmol/L, glioblastoma cells were the most susceptible cancer cell lines analysed in this study. A correlation between catalase activity and the susceptibility to ascorbic acid was observed. To study the possible protective role of catalase on the resistance of cancer cells to oxidative cell stress, the expression of catalase in the breast carcinoma cell line BT-20, which cells were highly resistant to the exposure to ascorbic acid (EC50: 94,9 mmol/L), was silenced with specific sh-RNA. The effect was that catalase-silenced BT-20 cells (BT-20 KD-CAT) became more susceptible to high concentrations of ascorbic acid (50 and 100 mmol/L). Conclusions: Fifty-five percent of the human cancer cell lines tested were unable to protect themselves against oxidative stress mediated by ascorbic acid induced hydrogen peroxide production. The antioxidative enzyme catalase is important to protect cancer cells against cytotoxic hydrogen peroxide. Silenced catalase expression increased the susceptibility of the formerly resistant cancer cell line BT-20 to oxidative stress.},
  subject      = {Medizin},
  language  = {en}
}
@article{Gallo2012,
  author    = {Gallo, Lorenzo},
  title     = {Natural hybrids in Sedum series Rupestria Berger (Crassulaceae): a review of taxonomy and nomenclature},
  doi       = {10.3264/FG.2012.0710},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-71945},
  year      = {2012},
  abstract  = {The nothotaxa of the genus Sedum series Rupestria Berger (Crassulaceae) are reviewed, three new hybrids (S. ×affomarcoi, S. ×henkii and S. ×pascalianum) are described and Sedum brevierei Chass. is typified. The identity of the western (French) populations of S. rupestre L. subsp. erectum 't Hart is also clarified, and a table with all known combinations is given.},
  subject      = {Botanik},
  language  = {en}
}
@article{BenkertDietzHartmannetal.2012,
  author    = {Benkert, Thomas F. and Dietz, Lena and Hartmann, Elena M. and Leich, Ellen and Rosenwald, Andreas and Serfling, Edgar and Buttmann, Mathias and Berberich-Siebelt, Friederike},
  title     = {Natalizumab Exerts Direct Signaling Capacity and Supports a Pro-Inflammatory Phenotype in Some Patients with Multiple Sclerosis},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-77905},
  year      = {2012},
  abstract  = {Natalizumab is a recombinant monoclonal antibody raised against integrin alpha-4 (CD49d). It is approved for the treatment of patients with multiple sclerosis (MS), a chronic inflammatory autoimmune disease of the CNS. While having shown high therapeutic efficacy, treatment by natalizumab has been linked to progressive multifocal leukoencephalopathy (PML) as a serious adverse effect. Furthermore, drug cessation sometimes induces rebound disease activity of unknown etiology. Here we investigated whether binding of this adhesion-blocking antibody to T lymphocytes could modulate their phenotype by direct induction of intracellular signaling events. Primary CD4+ T lymphocytes either from healthy donors and treated with natalizumab in vitro or from MS patients receiving their very first dose of natalizumab were analyzed. Natalizumab induced a mild upregulation of IL-2, IFN-c and IL-17 expression in activated primary human CD4+ T cells propagated ex vivo from healthy donors, consistent with a pro-inflammatory costimulatory effect on lymphokine expression. Along with this, natalizumab binding triggered rapid MAPK/ERK phosphorylation. Furthermore, it decreased CD49d surface expression on effector cells within a few hours. Sustained CD49d downregulation could be attributed to integrin internalization and degradation. Importantly, also CD4+ T cells from some MS patients receiving their very first dose of natalizumab produced more IL-2, IFN-c and IL-17 already 24 h after infusion. Together these data indicate that in addition to its adhesion-blocking mode of action natalizumab possesses mild direct signaling capacities, which can support a pro-inflammatory phenotype of peripheral blood T lymphocytes. This might explain why a rebound of disease activity or IRIS is observed in some MS patients after natalizumab cessation.},
  subject      = {Medizin},
  language  = {en}
}
@article{HornBaumannPereiraetal.2012,
  author    = {Horn, Michael and Baumann, Reto and Pereira, Jorge A. and Sidiropoulos, P{\´a}ris N. M. and Somandin, Christian and Welzl, Hans and Stendel, Claudia and L{\"u}hmann, Tessa and Wessig, Carsten and Toyka, Klaus V. and Relvas, Jo{\~a}o B. and Senderek, Jan and Suter, Ueli},
  title     = {Myelin is dependent on the Charcot-Marie-Tooth Type 4H disease culprit protein FRABIN/FGD4 in Schwann cells},
  series = {Brain},
  volume    = {135},
  journal   = {Brain},
  doi       = {10.1093/brain/aws275},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-125390},
  pages     = {3567-3583},
  year      = {2012},
  abstract  = {Studying the function and malfunction of genes and proteins associated with inherited forms of peripheral neuropathies has provided multiple clues to our understanding of myelinated nerves in health and disease. Here, we have generated a mouse model for the peripheral neuropathy Charcot-Marie-Tooth disease type 4H by constitutively disrupting the mouse orthologue of the suspected culprit gene FGD4 that encodes the small RhoGTPase Cdc42-guanine nucleotide exchange factor Frabin. Lack of Frabin/Fgd4 causes dysmyelination in mice in early peripheral nerve development, followed by profound myelin abnormalities and demyelination at later stages. At the age of 60 weeks, this was accompanied by electrophysiological deficits. By crossing mice carrying alleles of Frabin/Fgd4 flanked by loxP sequences with animals expressing Cre recombinase in a cell type-specific manner, we show that Schwann cell-autonomous Frabin/Fgd4 function is essential for proper myelination without detectable primary contributions from neurons. Deletion of Frabin/Fgd4 in Schwann cells of fully myelinated nerve fibres revealed that this protein is not only required for correct nerve development but also for accurate myelin maintenance. Moreover, we established that correct activation of Cdc42 is dependent on Frabin/Fgd4 function in healthy peripheral nerves. Genetic disruption of Cdc42 in Schwann cells of adult myelinated nerves resulted in myelin alterations similar to those observed in Frabin/Fgd4-deficient mice, indicating that Cdc42 and the Frabin/Fgd4-Cdc42 axis are critical for myelin homeostasis. In line with known regulatory roles of Cdc42, we found that Frabin/Fgd4 regulates Schwann cell endocytosis, a process that is increasingly recognized as a relevant mechanism in peripheral nerve pathophysiology. Taken together, our results indicate that regulation of Cdc42 by Frabin/Fgd4 in Schwann cells is critical for the structure and function of the peripheral nervous system. In particular, this regulatory link is continuously required in adult fully myelinated nerve fibres. Thus, mechanisms regulated by Frabin/Fgd4-Cdc42 are promising targets that can help to identify additional regulators of myelin development and homeostasis, which may crucially contribute also to malfunctions in different types of peripheral neuropathies.},
  language  = {en}
}
@article{JiangChenBelimovetal.2012,
  author    = {Jiang, Fan and Chen, Lin and Belimov, Andrey A. and Shaposhnikov, Alexander I. and Gong, Fan and Meng, Xu and Hartung, Wolfram and Jeschke, Dieter W. and Davies, William J. and Dodd, Ian C.},
  title     = {Multiple impacts of the plant growth-promoting rhizobacterium Variovorax paradoxus 5C-2 on nutrient and ABA relations of Pisum sativum},
  series = {Journal of Experimental Botany},
  volume    = {63},
  journal   = {Journal of Experimental Botany},
  number    = {18},
  doi       = {10.1093/jxb/ers301},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127011},
  pages     = {6421-6430},
  year      = {2012},
  abstract  = {Resolving the physiological mechanisms by which rhizobacteria enhance plant growth is difficult, since many such bacteria contain multiple plant growth-promoting properties. To understand further how the 1-aminocyclopropane-1-carboxylate (ACC) deaminase (ACCd)-containing rhizobacterium Variovorax paradoxus 5C-2 affects plant growth, the flows and partitioning of mineral nutrients and abscisic acid (ABA) and ABA metabolism were studied in pea (Pisum sativum) plants following rhizosphere bacterial inoculation. Although root architecture was not affected, inoculation increased root and shoot biomass, and stomatal conductance, by 20, 15, and 24\%, respectively, and increased N, P, K, Ca, and Mg uptake by 16, 81, 50, 46, and 58\%, respectively. P deposition in inoculated plant roots was 4.9 times higher than that in uninoculated controls. Rhizobacterial inoculation increased root to shoot xylem flows and shoot to root phloem flows of K by 1.8- and 2.1-fold, respectively. In control plants, major sinks for K deposition were the roots and upper shoot (43\% and 49\% of total uptake, respectively), while rhizobacterial inoculation increased K distribution to the lower shoot at the expense of other compartments (xylem, phloem, and upper shoot). Despite being unable to metabolize ABA in vitro, V. paradoxus 5C-2 decreased root ABA concentrations and accumulation by 40-60\%. Although inoculation decreased xylem ABA flows, phloem ABA flows increased. Whether bacterial ACCd attenuates root to shoot ABA signalling requires further investigation, since ABA is critical to maintain growth of droughted plants, and ACCd-containing organisms have been advocated as a means of minimizing growth inhibition of plants in drying soil.},
  language  = {en}
}
@article{GrafePreiningerSztatecsnyetal.2012,
  author    = {Grafe, T. Ulmar and Preininger, Doris and Sztatecsny, Marc and Kasah, Rosli and Dehling, J. Maximilian and Proksch, Sebastian and H{\"o}dl, Walter},
  title     = {Multimodal Communication in a Noisy Environment: A Case Study of the Bornean Rock Frog Staurois parvus},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {5},
  doi       = {10.1371/journal.pone.0037965},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-133718},
  year      = {2012},
  abstract  = {High background noise is an impediment to signal detection and perception. We report the use of multiple solutions to improve signal perception in the acoustic and visual modality by the Bornean rock frog, Staurois parvus. We discovered that vocal communication was not impaired by continuous abiotic background noise characterised by fast-flowing water. Males modified amplitude, pitch, repetition rate and duration of notes within their advertisement call. The difference in sound pressure between advertisement calls and background noise at the call dominant frequency of 5578 Hz was 8 dB, a difference sufficient for receiver detection. In addition, males used several visual signals to communicate with conspecifics with foot flagging and foot flashing being the most common and conspicuous visual displays, followed by arm waving, upright posture, crouching, and an open-mouth display. We used acoustic playback experiments to test the efficacy-based alerting signal hypothesis of multimodal communication. In support of the alerting hypothesis, we found that acoustic signals and foot flagging are functionally linked with advertisement calling preceding foot flagging. We conclude that S. parvus has solved the problem of continuous broadband low-frequency noise by both modifying its advertisement call in multiple ways and by using numerous visual signals. This is the first example of a frog using multiple acoustic and visual solutions to communicate in an environment characterised by continuous noise.},
  language  = {en}
}
@article{ReiterRitterNordbecketal.2012,
  author    = {Reiter, Theresa and Ritter, Oliver and Nordbeck, Peter and Beer, Meinrad and Bauer, Wolfgang Rudolf},
  title     = {MRI-guided ablation of wide complex tachycardia in a univentricular heart},
  series = {World Journal of Cardiology},
  volume    = {4},
  journal   = {World Journal of Cardiology},
  number    = {8},
  doi       = {10.4330/wjc.v4.i8.260},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-123165},
  pages     = {260-263},
  year      = {2012},
  abstract  = {Magnetic resonance imaging can be used for preprocedural assessment of complex anatomy for radiofrequency (RF) ablations, e.g., in a univentricular heart. This case report features the treatment of a young patient with a functionally univentricular heart who suffered from persistent sudden onset tachycardia with wide complexes that required RF ablation as treatment.},
  language  = {en}
}
@article{BiedererMirsadraeeBeeretal.2012,
  author    = {Biederer, J{\"u}rgen and Mirsadraee, S. and Beer, M. and Molinari, F. and Hintze, C. and Bauman, G. and Both, M. and Van Beek, E. J. R. and Wild, J. and Puderbach, M.},
  title     = {MRI of the lung (3/3)—current applications and future perspectives},
  series = {Insights into Imaging},
  volume    = {3},
  journal   = {Insights into Imaging},
  number    = {4},
  doi       = {10.1007/s13244-011-0142-z},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-124348},
  pages     = {373-386},
  year      = {2012},
  abstract  = {Background MRI of the lung is recommended in a number of clinical indications. Having a non-radiation alternative is particularly attractive in children and young subjects, or pregnant women. Methods Provided there is sufficient expertise, magnetic resonance imaging (MRI) may be considered as the preferential modality in specific clinical conditions such as cystic fibrosis and acute pulmonary embolism, since additional functional information on respiratory mechanics and regional lung perfusion is provided. In other cases, such as tumours and pneumonia in children, lung MRI may be considered an alternative or adjunct to other modalities with at least similar diagnostic value. Results In interstitial lung disease, the clinical utility of MRI remains to be proven, but it could provide additional information that will be beneficial in research, or at some stage in clinical practice. Customised protocols for chest imaging combine fast breath-hold acquisitions from a "buffet" of sequences. Having introduced details of imaging protocols in previous articles, the aim of this manuscript is to discuss the advantages and limitations of lung MRI in current clinical practice. Conclusion New developments and future perspectives such as motion-compensated imaging with self-navigated sequences or fast Fourier decomposition MRI for non-contrast enhanced ventilation- and perfusion-weighted imaging of the lung are discussed. Main Messages • MRI evolves as a third lung imaging modality, combining morphological and functional information. • It may be considered first choice in cystic fibrosis and pulmonary embolism of young and pregnant patients. • In other cases (tumours, pneumonia in children), it is an alternative or adjunct to X-ray and CT. • In interstitial lung disease, it serves for research, but the clinical value remains to be proven. • New users are advised to make themselves familiar with the particular advantages and limitations.},
  language  = {en}
}
@article{BiedererBeerHirschetal.2012,
  author    = {Biederer, J. and Beer, M. and Hirsch, W. and Wild, J. and Fabel, M. and Puderbach, M. and Van Beek, E. J. R.},
  title     = {MRI of the lung (2/3). Why … when … how?},
  series = {Insights into Imaging},
  volume    = {3},
  journal   = {Insights into Imaging},
  number    = {4},
  doi       = {10.1007/s13244-011-0146-8},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-124268},
  pages     = {355-371},
  year      = {2012},
  abstract  = {Background Among the modalities for lung imaging, proton magnetic resonance imaging (MRI) has been the latest to be introduced into clinical practice. Its value to replace X-ray and computed tomography (CT) when radiation exposure or iodinated contrast material is contra-indicated is well acknowledged: i.e. for paediatric patients and pregnant women or for scientific use. One of the reasons why MRI of the lung is still rarely used, except in a few centres, is the lack of consistent protocols customised to clinical needs. Methods This article makes non-vendor-specific protocol suggestions for general use with state-of-the-art MRI scanners, based on the available literature and a consensus discussion within a panel of experts experienced in lung MRI. Results Various sequences have been successfully tested within scientific or clinical environments. MRI of the lung with appropriate combinations of these sequences comprises morphological and functional imaging aspects in a single examination. It serves in difficult clinical problems encountered in daily routine, such as assessment of the mediastinum and chest wall, and even might challenge molecular imaging techniques in the near future. Conclusion This article helps new users to implement appropriate protocols on their own MRI platforms. Main Messages • MRI of the lung can be readily performed on state-of-the-art 1.5-T MRI scanners. • Protocol suggestions based on the available literature facilitate its use for routine • MRI offers solutions for complicated thoracic masses with atelectasis and chest wall invasion. • MRI is an option for paediatrics and science when CT is contra-indicated},
  language  = {en}
}
@article{WildMarshallBocketal.2012,
  author    = {Wild, J. M. and Marshall, H. and Bock, M. and Schad, L. R. and Jakob, P. M. and Puderbach, M. and Molinari, F. and Van Beek, E. J. R. and Biederer, J.},
  title     = {MRI of the lung (1/3): methods},
  series = {Insights into Imaging},
  volume    = {3},
  journal   = {Insights into Imaging},
  number    = {4},
  doi       = {10.1007/s13244-012-0176-x},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-124238},
  pages     = {345-353},
  year      = {2012},
  abstract  = {Proton magnetic resonance imaging (MRI) has recently emerged as a clinical tool to image the lungs. This paper outlines the current technical aspects of MRI pulse sequences, radiofrequency (RF) coils and MRI system requirements needed for imaging the pulmonary parenchyma and vasculature. Lung MRI techniques are presented as a "technical toolkit", from which MR protocols will be composed in the subsequent papers for comprehensive imaging of lung disease and function (parts 2 and 3). This paper is pitched at MR scientists, technicians and radiologists who are interested in understanding and establishing lung MRI methods. Images from a 1.5 T scanner are used for illustration of the sequences and methods that are highlighted. Main Messages • Outline of the hardware and pulse sequence requirements for proton lung MRI • Overview of pulse sequences for lung parenchyma, vascular and functional imaging with protons • Demonstration of the pulse-sequence building blocks for clinical lung MRI protocols},
  language  = {en}
}
@article{GaletzkaHansmannElHajjetal.2012,
  author    = {Galetzka, Danuta and Hansmann, Tamara and El Hajj, Nady and Weis, Eva and Irmscher, Benjamin and Ludwig, Marco and Schneider-R{\"a}tzke, Brigitte and Kohlschmidt, Nicolai and Beyer, Vera and Bartsch, Oliver and Zechner, Ulrich and Spix, Claudia and Haaf, Thomas},
  title     = {Monozygotic twins discordant for constitutive BRCA1 promoter methylation, childhood cancer and secondary cancer},
  series = {Epigenetics},
  volume    = {7},
  journal   = {Epigenetics},
  number    = {1},
  doi       = {10.4161/epi.7.1.18814},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-125386},
  pages     = {47-54},
  year      = {2012},
  abstract  = {We describe monozygotic twins discordant for childhood leukemia and secondary thyroid carcinoma. We used bisulfite pyrosequencing to compare the constitutive promoter methylation of BRCA1 and several other tumor suppressor genes in primary fibroblasts. The affected twin displayed an increased BRCA1 methylation (12\%), compared with her sister (3\%). Subsequent bisulfite plasmid sequencing demonstrated that 13\% (6 of 47) BRCA1 alleles were fully methylated in the affected twin, whereas her sister displayed only single CpG errors without functional implications. This between-twin methylation difference was also found in irradiated fibroblasts and untreated saliva cells. The BRCA1 epimutation may have originated by an early somatic event in the affected twin: approximately 25\% of her body cells derived from different embryonic cell lineages carry one epigenetically inactivated BRCA1 allele. This epimutation was associated with reduced basal protein levels and a higher induction of BRCA1 after DNA damage. In addition, we performed a genome-wide microarray analysis of both sisters and found several copy number variations, i.e., heterozygous deletion and reduced expression of the RSPO3 gene in the affected twin. This monozygotic twin pair represents an impressive example of epigenetic somatic mosaicism, suggesting a role for constitutive epimutations, maybe along with de novo genetic alterations in recurrent tumor development.},
  language  = {en}
}
@article{DreyerGomezPorrasRianoPachonetal.2012,
  author    = {Dreyer, Ingo and Gomez-Porras, Judith Lucia and Ria{\~n}o-Pach{\´o}n, Diego Mauricio and Hedrich, Rainer and Geiger, Dietmar},
  title     = {Molecular Evolution of Slow and Quick Anion Channels (SLACs and QUACs/ALMTs)},
  series = {Frontiers in Plant Science},
  volume    = {3},
  journal   = {Frontiers in Plant Science},
  issn      = {1664-462X},
  doi       = {10.3389/fpls.2012.00263},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-189345},
  pages     = {263},
  year      = {2012},
  abstract  = {Electrophysiological analyses conducted about 25 years ago detected two types of anion channels in the plasma membrane of guard cells. One type of channel responds slowly to changes in membrane voltage while the other responds quickly. Consequently, they were named SLAC, for SLow Anion Channel, and QUAC, for QUick Anion Channel. Recently, genes SLAC1 and QUAC1/ALMT12, underlying the two different anion current components, could be identified in the model plant Arabidopsis thaliana. Expression of the gene products in Xenopus oocytes confirmed the quick and slow current kinetics. In this study we provide an overview on our current knowledge on slow and quick anion channels in plants and analyze the molecular evolution of ALMT/QUAC-like and SLAC-like channels. We discovered fingerprints that allow screening databases for these channel types and were able to identify 192 (177 non-redundant) SLAC-like and 422 (402 non-redundant) ALMT/QUAC-like proteins in the fully sequenced genomes of 32 plant species. Phylogenetic analyses provided new insights into the molecular evolution of these channel types. We also combined sequence alignment and clustering with predictions of protein features, leading to the identification of known conserved phosphorylation sites in SLAC1-like channels along with potential sites that have not been yet experimentally confirmed. Using a similar strategy to analyze the hydropathicity of ALMT/QUAC-like channels, we propose a modified topology with additional transmembrane regions that integrates structure and function of these membrane proteins. Our results suggest that cross-referencing phylogenetic analyses with position-specific protein properties and functional data could be a very powerful tool for genome research approaches in general.},
  language  = {en}
}
@article{RatzkaFoersterLiangetal.2012,
  author    = {Ratzka, Carolin and F{\"o}rster, Frank and Liang, Chunguang and Kupper, Maria and Dandekar, Thomas and Feldhaar, Heike and Gross, Roy},
  title     = {Molecular characterization of antimicrobial peptide genes of the carpenter ant Camponotus floridanus},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75985},
  year      = {2012},
  abstract  = {The production of antimicrobial peptides (AMPs) is a major defense mechanism against pathogen infestation and of particular importance for insects relying exclusively on an innate immune system. Here, we report on the characterization of three AMPs from the carpenter ant Camponotus floridanus. Due to sequence similarities and amino acid composition these peptides can be classified into the cysteine-rich (e.g. defensin) and glycine-rich (e.g. hymenoptaecin) AMP groups, respectively. The gene and cDNA sequences of these AMPs were established and their expression was shown to be induced by microbial challenge. We characterized two different defensin genes. The defensin-2 gene has a single intron, whereas the defensin-1 gene has two introns. The deduced amino acid sequence of the C. floridanus defensins is very similar to other known ant defensins with the exception of a short C-terminal extension of defensin-1. The hymenoptaecin gene has a single intron and a very peculiar domain structure. The corresponding precursor protein consists of a signal- and a pro-sequence followed by a hymenoptaecin-like domain and six directly repeated hymenoptaecin domains. Each of the hymenoptaecin domains is flanked by an EAEP-spacer sequence and a RR-site known to be a proteolytic processing site. Thus, proteolytic processing of the multipeptide precursor may generate several mature AMPs leading to an amplification of the immune response. Bioinformatical analyses revealed the presence of hymenoptaecin genes with similar multipeptide precursor structure in genomes of other ant species suggesting an evolutionary conserved important role of this gene in ant immunity.},
  subject      = {Biologie},
  language  = {en}
}
@article{GrassmannFritscheKeilhaueretal.2012,
  author    = {Grassmann, Felix and Fritsche, Lars G. and Keilhauer, Claudia N. and Heid, Iris M. and Weber, Bernhard H. F.},
  title     = {Modelling the Genetic Risk in Age-Related Macular Degeneration},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {5},
  doi       = {10.1371/journal.pone.0037979},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-131315},
  pages     = {e37979},
  year      = {2012},
  abstract  = {Late-stage age-related macular degeneration (AMD) is a common sight-threatening disease of the central retina affecting approximately 1 in 30 Caucasians. Besides age and smoking, genetic variants from several gene loci have reproducibly been associated with this condition and likely explain a large proportion of disease. Here, we developed a genetic risk score (GRS) for AMD based on 13 risk variants from eight gene loci. The model exhibited good discriminative accuracy, area-under-curve (AUC) of the receiver-operating characteristic of 0.820, which was confirmed in a cross-validation approach. Noteworthy, younger AMD patients aged below 75 had a significantly higher mean GRS (1.87, 95\% CI: 1.69-2.05) than patients aged 75 and above (1.45, 95\% CI: 1.36-1.54). Based on five equally sized GRS intervals, we present a risk classification with a relative AMD risk of 64.0 (95\% CI: 14.11-1131.96) for individuals in the highest category (GRS 3.44-5.18, 0.5\% of the general population) compared to subjects with the most common genetic background (GRS -0.05-1.70, 40.2\% of general population). The highest GRS category identifies AMD patients with a sensitivity of 7.9\% and a specificity of 99.9\% when compared to the four lower categories. Modeling a general population around 85 years of age, 87.4\% of individuals in the highest GRS category would be expected to develop AMD by that age. In contrast, only 2.2\% of individuals in the two lowest GRS categories which represent almost 50\% of the general population are expected to manifest AMD. Our findings underscore the large proportion of AMD cases explained by genetics particularly for younger AMD patients. The five-category risk classification could be useful for therapeutic stratification or for diagnostic testing purposes once preventive treatment is available.},
  language  = {en}
}
@article{RuczyńskiBartoń2012,
  author    = {Ruczyński, Ireneusz and Bartoń, Kamil A.},
  title     = {Modelling Sensory Limitation: The Role of Tree Selection, Memory and Information Transfer in Bats' Roost Searching Strategies},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {9},
  doi       = {10.1371/journal.pone.0044897},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-133963},
  pages     = {e44897},
  year      = {2012},
  abstract  = {Sensory limitation plays an important role in the evolution of animal behaviour. Animals have to find objects of interest (e.g. food, shelters, predators). When sensory abilities are strongly limited, animals adjust their behaviour to maximize chances for success. Bats are nocturnal, live in complex environments, are capable of flight and must confront numerous perceptual challenges (e.g. limited sensory range, interfering clutter echoes). This makes them an excellent model for studying the role of compensating behaviours to decrease costs of finding resources. Cavity roosting bats are especially interesting because the availability of tree cavities is often limited, and their quality is vital for bats during the breeding season. From a bat's sensory point of view, cavities are difficult to detect and finding them requires time and energy. However, tree cavities are also long lasting, allowing information transfer among conspecifics. Here, we use a simple simulation model to explore the benefits of tree selection, memory and eavesdropping (compensation behaviours) to searches for tree cavities by bats with short and long perception range. Our model suggests that memory and correct discrimination of tree suitability are the basic strategies decreasing the cost of roost finding, whereas perceptual range plays a minor role in this process. Additionally, eavesdropping constitutes a buffer that reduces the costs of finding new resources (such as roosts), especially when they occur in low density. We conclude that natural selection may promote different strategies of roost finding in relation to habitat conditions and cognitive skills of animals.},
  language  = {en}
}
@article{HoennemannSanzMorenoWolfetal.2012,
  author    = {H{\"o}nnemann, Jan and Sanz-Moreno, Adrian and Wolf, Elmar and Eilers, Martin and Els{\"a}sser, Hans-Peter},
  title     = {Miz1 Is a Critical Repressor of cdkn1a during Skin Tumorigenesis},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {4},
  doi       = {10.1371/journal.pone.0034885},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-133285},
  pages     = {e34885},
  year      = {2012},
  abstract  = {The transcription factor Miz1 forms repressive DNA-binding complexes with the Myc, Gfi-1 and Bcl-6 oncoproteins. Known target genes of these complexes encode the cyclin-dependent kinase inhibitors (CKIs) cdkn2b (p15\(^{Ink4}\)), cdkn1a (p21\(^{Cip1}\)), and cdkn1c (p57\(^{Kip2}\)). Whether Miz1-mediated repression is important for control of cell proliferation in vivo and for tumor formation is unknown. Here we show that deletion of the Miz1 POZ domain, which is critical for Miz1 function, restrains the development of skin tumors in a model of chemically-induced, Ras-dependent tumorigenesis. While the stem cell compartment appears unaffected, interfollicular keratinocytes lacking functional Miz1 exhibit a reduced proliferation and an accelerated differentiation of the epidermis in response to the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). Tumorigenesis, proliferation and normal differentiation are restored in animals lacking cdkn1a, but not in those lacking cdkn2b. Our data demonstrate that Miz1-mediated attenuation of cell cycle arrest pathways via repression of cdkn1a has a critical role during tumorigenesis in the skin.},
  language  = {en}
}
@article{ReiterRitterPrinceetal.2012,
  author    = {Reiter, Theresa and Ritter, Oliver and Prince, Martin R. and Nordbeck, Peter and Wanner, Christoph and Nagel, Eike and Bauer, Wolfgang R.},
  title     = {Minimizing Risk of Nephrogenic systemic fibrosis in Cardiovascular Magnetic Resonance},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75068},
  year      = {2012},
  abstract  = {Nephrogenic Systemic Fibrosis is a rare condition appearing only in patients with severe renal impairment or failure and presents with dermal lesions and involvement of internal organs. Although many cases are mild, an estimated 5 \% have a progressive debilitating course. To date, there is no known effective treatment thus stressing the necessity of ample prevention measures. An association with the use of Gadolinium based contrast agents (GBCA) makes Nephrogenic Systemic Fibrosis a potential side effect of contrast enhanced magnetic resonance imaging and offers the opportunity for prevention by limiting use of gadolinium based contrast agents in renal failure patients. In itself toxic, Gadolinium is embedded into chelates that allow its safe use as a contrast agent. One NSF theory is that Gadolinium chelates distribute into the extracellular fluid compartment and set Gadolinium ions free, depending on multiple factors among which the duration of chelates exposure is directly related to the renal function. Major medical societies both in Europe and in North America have developed guidelines for the usage of GBCA. Since the establishment of these guidelines and the increased general awareness of this condition, the occurrence of NSF has been nearly eliminated. Giving an overview over the current knowledge of NSF pathobiochemistry, pathogenesis and treatment options this review focuses on the guidelines of the European Medicines Agency, the European Society of Urogenital Radiology, the FDA and the American College of Radiology from 2008 up to 2011 and the transfer of this knowledge into every day practice.},
  subject      = {CMR},
  language  = {en}
}
@article{HaeringKiesel2012,
  author    = {Haering, Carola and Kiesel, Andrea},
  title     = {Mine is earlier than yours: Causal beliefs influence the perceived time of action effects},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-76229},
  year      = {2012},
  abstract  = {When a key press causes a stimulus, the key press is perceived later and the stimulus earlier than key presses and stimuli presented independently. This bias in time perception has been linked to the intention to produce the effect and thus been called intentional binding (IB). In recent studies it has been shown that the IB effect is stronger when participants believed that they caused the effect stimulus compared to when they believed that another person caused the effect (Desantis et al., 2011). In this experiment we ask whether causal beliefs influence the perceived time of an effect when the putative effect occurs temporally close to another stimulus that is also an effect. In our study two participants performed the same task on connected computers with separate screens. Each trial started synchro- nously on both computers. When a participant pressed a key, a red and a yellow stimulus appeared as action effects simultaneously or with a slight delay of up to 50 ms. The partic- ipants' task was to judge the temporal order of these two effect stimuli. Participants were either told that one participant caused one of the two stimuli while the other participant seated at the other computer caused the other stimulus, or each participant was told that he/she caused both stimuli. The different causal beliefs changed the perceived time of the effects' appearance relative to each other. When participants believed they each caused one effect, their "own" effect was perceived earlier than the other participant's effect. When the participants believed each caused both effects, no difference in the perceived temporal order of the red and yellow effect was found. These results confirm that higher order causal beliefs change the perceived time of an action effect even in a setting in which the occurrence of the putative effect can be directly compared to a reference stimulus.},
  subject      = {Psychologie},
  language  = {en}
}
@article{JazbutyteFiedlerKneitzetal.2012,
  author    = {Jazbutyte, Virginija and Fiedler, Jan and Kneitz, Susanne and Galuppo, Paolo and Just, Annette and Holzmann, Angelika and Bauersachs, Johann and Thum, Thomas},
  title     = {MicroRNA-22 increases senescence and activates cardiac fibroblasts in the aging heart},
  series = {AGE},
  volume    = {35},
  journal   = {AGE},
  number    = {3},
  doi       = {10.1007/s11357-012-9407-9},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-126745},
  pages     = {747-762},
  year      = {2012},
  abstract  = {MicroRNAs (miRs) are small non- coding RNA molecules controlling a plethora of biological processes such as development, cellular survival and senescence. We here determined miRs differentially regulated during cardiac postnatal development and aging. Cardiac function, morphology and miR expression profiles were determined in neonatal, 4 weeks, 6 months and 19 months old normotensive male healthy C57/Bl6N mice. MiR-22 was most prominently upregulated during cardiac aging. Cardiac expression of its bioinformatically predicted target mimecan (osteoglycin, OGN) was gradually decreased with advanced age. Luciferase reporter assays validated mimecan as a bona fide miR-22 target. Both, miR-22 and its target mimecan were co- expressed in cardiac fibroblasts and smooth muscle cells. Functionally, miR-22 overexpression induced cellular senescence and promoted migratory activity of cardiac fibroblasts. Small interference RNA-mediated silencing of mimecan in cardiac fibroblasts mimicked the miR-22-mediated effects. Rescue experiments revealed that the effects of miR-22 on cardiac fibroblasts were only partially mediated by mimecan. In conclusion, miR-22 upregulation in the aging heart contributed at least partly to accelerated cardiac fibroblast senescence and increased migratory activity. Our results suggest an involvement of miR-22 in age-associated cardiac changes, such as cardiac fibrosis.},
  language  = {en}
}
@article{BlachutzikDemirKreuzeretal.2012,
  author    = {Blachutzik, J{\"o}rg O. and Demir, Faith and Kreuzer, Ines and Hedrich, Rainer and Harms, Gregory S.},
  title     = {Methods of staining and visualization of sphingolipid enriched and non-enriched plasma membrane regions of Arabidopsis thaliana with fluorescent dyes and lipid analogues},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75433},
  year      = {2012},
  abstract  = {Background: Sterols and Sphingolipids form lipid clusters in the plasma membranes of cell types throughout the animal and plant kingdoms. These lipid domains provide a medium for protein signaling complexes at the plasma membrane and are also observed to be principal regions of membrane contact at the inception of infection. We visualized different specific fluorescent lipophilic stains of the both sphingolipid enriched and non-sphingolipid enriched regions in the plasma membranes of live protoplasts of Arabidopsis thaliana. Results: Lipid staining protocols for several fluorescent lipid analogues in plants are presented. The most emphasis was placed on successful protocols for the single and dual staining of sphingolipid enriched regions and exclusion of sphingolipid enriched regions on the plasma membrane of Arabidopsis thaliana protoplasts. A secondary focus was placed to ensure that these staining protocols presented still maintain cell viability. Furthermore, the protocols were successfully tested with the spectrally sensitive dye Laurdan. Conclusion: Almost all existing staining procedures of the plasma membrane with fluorescent lipid analogues are specified for animal cells and tissues. In order to develop lipid staining protocols for plants, procedures were established with critical steps for the plasma membrane staining of Arabidopsis leaf tissue and protoplasts. The success of the plasma membrane staining protocols was additionally verified by measurements of lipid dynamics by the fluorescence recovery after photobleaching technique and by the observation of new phenomena such as time dependent lipid polarization events in living protoplasts, for which a putative physiological relevance is suggested.},
  subject      = {Arabidopsis thaliana},
  language  = {de}
}
@article{OPUS4-12799,
  title     = {Measurements of the pseudorapidity dependence of the total transverse energy in proton-proton collisions at √s=7 TeV with ATLAS},
  series = {Journal of High Energy Physics},
  volume    = {11},
  journal   = {Journal of High Energy Physics},
  number    = {033},
  organization    = {ATLAS Collaboration},
  doi       = {10.1007/JHEP11(2012)033},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127998},
  year      = {2012},
  abstract  = {This paper describes measurements of the sum of the transverse energy of particles as a function of particle pseudorapidity, η, in proton-proton collisions at a centre-of-mass energy, √s=7 TeV using the ATLAS detector at the Large Hadron Collider. The measurements are performed in the region |η| < 4.8 for two event classes: those requiring the presence of particles with a low transverse momentum and those requiring particles with a significant transverse momentum. In the second dataset measurements are made in the region transverse to the hard scatter. The distributions are compared to the predictions of various Monte Carlo event generators, which generally tend to underestimate the amount of transverse energy at high |η|.},
  language  = {en}
}
@article{OPUS4-12780,
  title     = {Measurement of τ polarization in W→τν decays with the ATLAS detector in pp collisions at s√=7 TeV},
  series = {The European Physical Journal C},
  volume    = {72},
  journal   = {The European Physical Journal C},
  number    = {2062},
  organization    = {ATLAS Collaboration},
  doi       = {10.1140/epjc/s10052-012-2062-6},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127807},
  year      = {2012},
  abstract  = {In this paper, a measurement of τ polarization in W→τν decays is presented. It is measured from the energies of the decay products in hadronic τ decays with a single final state charged particle. The data, corresponding to an integrated luminosity of 24 pb\(^{-1}\), were collected by the ATLAS experiment at the Large Hadron Collider in 2010. The measured value of the τ polarization is P\(_τ\)=-1.06±0.04 (stat)\(^{+0.05}_{-0.07}\) (syst), in agreement with the Standard Model prediction, and is consistent with a physically allowed 95 \% CL interval [-1,-0.91]. Measurements of τ polarization have not previously been made at hadron colliders.},
  language  = {en}
}
@article{OPUS4-12796,
  title     = {Measurement of W\(^{±}\)Z production in proton-proton collisions at √s=7 TeV with the ATLAS detector},
  series = {European Physical Journal C},
  volume    = {72},
  journal   = {European Physical Journal C},
  number    = {2173},
  organization    = {ATLAS Collaboration},
  doi       = {10.1140/epjc/s10052-012-2173-0},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127963},
  year      = {2012},
  abstract  = {A study of W\(^{±}\)Z production in proton-proton collisions at √s=7 TeV is presented using data corresponding to an integrated luminosity of 4.6 fb\(^{-1}\) collected with the ATLAS detector at the Large Hadron Collider in 2011. In total, 317 candidates, with a background expectation of 68±10 events, are observed in double-leptonic decay final states with electrons, muons and missing transverse momentum. The total cross-section is determined to be σ\(^{tot}_{WZ}\)=19.0\(^{+1.4}_{-1.3}\)(stat.)±0.9(syst.)±0.4(lumi.) pb, consistent with the Standard Model expectation of 17.6\(^{+1.1}_{-1.0}\) pb. Limits on anomalous triple gauge boson couplings are derived using the transverse momentum spectrum of Z bosons in the selected events. The cross-section is also presented as a function of Z boson transverse momentum and diboson invariant mass.},
  language  = {en}
}
@article{OPUS4-12741,
  title     = {Measurement of the W boson polarization in top quark decays with the ATLAS detector},
  series = {Journal of High Energy Physics},
  volume    = {06},
  journal   = {Journal of High Energy Physics},
  number    = {88},
  organization    = {ATLAS Collaboration},
  doi       = {10.1007/JHEP06(2012)088},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127417},
  year      = {2012},
  abstract  = {This paper presents measurements of the polarization of W bosons in top quark decays, derived from \(t\overline{t}\) events with missing transverse momentum, one charged lepton and at least four jets, or two charged leptons and at least two jets. Data from pp collisions at a centre-of-mass energy of 7 TeV were collected with the ATLAS experiment at the LHC and correspond to an integrated luminosity of 1.04 fb\(^{-1}\). The measured fractions of longitudinally, left- and right-handed polarization are F\(_0\) = 0.67 ± 0.07, F\(_L\) = 0.32 ± 0.04 and F\(_R\) = 0.01 ± 0.05, in agreement with the Standard Model predictions. As the polarization of the W bosons in top quark decays is sensitive to the Wtb vertex Lorentz structure and couplings, the measurements were used to set limits on anomalous contributions to the Wtb couplings.},
  language  = {en}
}
@article{OPUS4-12891,
  title     = {Measurement of the top quark mass with the template method in the \(t\overline t\)→lepton+jets channel using ATLAS data},
  series = {The European Physical Journal C},
  volume    = {72},
  journal   = {The European Physical Journal C},
  number    = {2046},
  organization    = {ATLAS Collaboration},
  doi       = {10.1140/epjc/s10052-012-2046-6},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-128912},
  year      = {2012},
  abstract  = {The top quark mass has been measured using the template method in the \(t\overline t\)→lepton+jets channel based on data recorded in 2011 with the ATLAS detector at the LHC. The data were taken at a proton-proton centre-of-mass energy of √s=7 TeV and correspond to an integrated luminosity of 1.04 fb\(^{-1}\). The analyses in the e+jets and μ+jets decay channels yield consistent results. The top quark mass is measured to be m\(_{top}\)=174.5±0.6\(_{stat}\)±2.3\(_{syst}\) GeV.},
  language  = {en}
}
@article{OPUS4-12761,
  title     = {Measurement of the polarisation of W bosons produced with large transverse momentum in pp collisions at √s=7 TeV with the ATLAS experiment},
  series = {The European Physical Journal C},
  volume    = {72},
  journal   = {The European Physical Journal C},
  number    = {2001},
  organization    = {ATLAS Collaboration},
  doi       = {10.1140/epjc/s10052-012-2001-6},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127615},
  year      = {2012},
  abstract  = {This paper describes an analysis of the angular distribution of W→eν and W→μν decays, using data from pp collisions at s√=7 TeV recorded with the ATLAS detector at the LHC in 2010, corresponding to an integrated luminosity of about 35 pb\(^{-1}\). Using the decay lepton transverse momentum and the missing transverse momentum, the W decay angular distribution projected onto the transverse plane is obtained and analysed in terms of helicity fractions f\(_0\), f\(_L\) and f\(_R\) over two ranges of W transverse momentum (p\(^W_T\)):35<p\(^W_T\)<50 GeV and p\(^W_T\)>50 GeV. Good agreement is found with theoretical predictions. For p\(^W_T\)>50 GeV, the values of f\(_0\) and f\(_L\)-f\(_R\), averaged over charge and lepton flavour, are measured to be: f\(_0\)=0.127±0.030±0.108 and f\(_L\)-f\(_R\)=0.252±0.017±0.030, where the first uncertainties are statistical, and the second include all systematic effects.},
  language  = {en}
}
@article{OPUS4-12892,
  title     = {Measurement of the cross section for top-quark pair production in pp collisions at √s=7TeV with the ATLAS detector using final states with two high-p\(_T\) leptons},
  series = {Journal of High Energy Physics},
  volume    = {5},
  journal   = {Journal of High Energy Physics},
  number    = {59},
  organization    = {ATLAS Collaboration},
  doi       = {10.1007/JHEP05(2012)059},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-128924},
  year      = {2012},
  abstract  = {A measurement is reported of the production cross section of top-quark pairs (\(t\overline t\)) in proton-proton collisions at a center-of-mass energy of 7 TeV recorded with the ATLAS detector at the LHC. Candidate events have a signature consistent with containing two isolated leptons, large missing transverse momentum, and at least two jets. Using a data sample corresponding to an integrated luminosity of 0.70 fb\(^{-1}\), a \(t\overline t\) production cross section σ\(_{t\overline t}\)=176±5(stat.)\(^{+14}_{-11}\)(syst.)±8(lum.) pb is measured for an assumed top-quark mass of m\(_t\)  = 172.5 GeV. This measurement is in good agreement with Standard Model predictions.},
  language  = {en}
}
@article{OPUS4-12890,
  title     = {Measurement of the charge asymmetry in top quark pair production in pp collisions at √s=7 TeV using the ATLAS detector},
  series = {The European Physical Journal C},
  volume    = {72},
  journal   = {The European Physical Journal C},
  number    = {2039},
  organization    = {ATLAS Collaboration},
  doi       = {10.1140/epjc/s10052-012-2039-5},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-128904},
  year      = {2012},
  abstract  = {A measurement of the top-antitop production charge asymmetry A C is presented using data corresponding to an integrated luminosity of 1.04 fb\(^{-1}\) of pp collisions at √s=7 TeV collected by the ATLAS detector at the LHC. Events are selected with a single lepton (electron or muon), missing transverse momentum and at least four jets of which at least one jet is identified as coming from a b-quark. A kinematic fit is used to reconstruct the t\(\overline t\) event topology. After background subtraction, a Bayesian unfolding procedure is performed to correct for acceptance and detector effects. The measured value of A\(_C\) is AC=-0.019±0.028 (stat.)±0.024 (syst.), consistent with the prediction from the MC@NLO Monte Carlo generator of A\(_C\) =0.006±0.002. Measurements of A\(_C\) in two ranges of invariant mass of the top-antitop pair are also shown.},
  language  = {en}
}
@article{OPUS4-12735,
  title     = {Measurement of inclusive two-particle angular correlations in pp collisions with the ATLAS detector at the LHC},
  series = {Journal of High Energy Physics},
  volume    = {05},
  journal   = {Journal of High Energy Physics},
  number    = {157},
  organization    = {ATLAS Collaboration},
  doi       = {10.1007/JHEP05(2012)157},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127350},
  year      = {2012},
  abstract  = {We present a measurement of two-particle angular correlations in proton- proton collisions at √s=900 GeV and 7 TeV. The collision events were collected during 2009 and 2010 with the ATLAS detector at the Large Hadron Collider using a single-arm minimum bias trigger. Correlations are measured for charged particles produced in the kinematic range of transverse momentum p\(_T\)  > 100 MeV and pseudorapidity |η| < 2.5. A complex structure in pseudorapidity and azimuth is observed at both collision energies. Results are compared to PYTHIA 8 and HERWIG++ as well as to the AMBT2B, DW and Perugia 2011 tunes of PYTHIA 6. The data are not satisfactorily described by any of these models.},
  language  = {en}
}
@article{OPUS4-12781,
  title     = {Measurement of event shapes at large momentum transfer with the ATLAS detector in pp collisions at √s=7 TeV},
  series = {The European Physical Journal C},
  volume    = {72},
  journal   = {The European Physical Journal C},
  number    = {2211},
  organization    = {ATLAS Collaboration},
  doi       = {10.1140/epjc/s10052-012-2211-y},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127813},
  year      = {2012},
  abstract  = {A measurement of event shape variables is presented for large momentum transfer proton-proton collisions using the ATLAS detector at the Large Hadron Collider. Six event shape variables calculated using hadronic jets are studied in inclusive multi-jet events in 35 pb\(^{-1}\) of integrated luminosity at a center-of-mass energy of √s=7 TeV. These measurements are compared to predictions by three Monte Carlo event generators containing leading-logarithmic parton showers matched to leading order matrix elements for 2→2 and 2→n (n=2,…,6) scattering. Measurements of the third-jet resolution parameter, aplanarity, thrust, sphericity, and transverse sphericity are generally well described. The mean value of each event shape variable is evaluated as a function of the average momentum of the two leading jets p\(_{T,1}\) and p\(_{T,2}\), with a mean p\(_T\) approaching 1 TeV.},
  language  = {en}
}
@article{OPUS4-12893,
  title     = {Measurement of \(t\overline t\) production with a veto on additional central jet activity in pp collisions at √s=7 TeV using the ATLAS detector},
  series = {European Physical Journal C},
  volume    = {72},
  journal   = {European Physical Journal C},
  number    = {2043},
  organization    = {ATLAS Collaboration},
  doi       = {10.1140/epjc/s10052-012-2043-9},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-128931},
  year      = {2012},
  abstract  = {A measurement of the jet activity in \(t\overline t\) events produced in proton-proton collisions at a centre-of-mass energy of 7 TeV is presented, using 2.05 fb\(^{-1}\) of integrated luminosity collected by the ATLAS detector at the Large Hadron Collider. The \(t\overline t\) events are selected in the dilepton decay channel with two identified b-jets from the top quark decays. Events are vetoed if they contain an additional jet with transverse momentum above a threshold in a central rapidity interval. The fraction of events surviving the jet veto is presented as a function of this threshold for four different central rapidity interval definitions. An alternate measurement is also performed, in which events are vetoed if the scalar transverse momentum sum of the additional jets in each rapidity interval is above a threshold. In both measurements, the data are corrected for detector effects and compared to the theoretical models implemented in MC@NLO, Powheg, Alpgen and Sherpa. The experimental uncertainties are often smaller than the spread of theoretical predictions, allowing deviations between data and theory to be observed in some regions of phase space.},
  language  = {en}
}
@article{KneisslAbelRasbachetal.2012,
  author    = {Kneissl, Sabrina and Abel, Tobias and Rasbach, Anke and Brynza, Julia and Schneider-Schaulies, J{\"u}rgen and Buchholz, Christian J.},
  title     = {Measles Virus Glycoprotein-Based Lentiviral Targeting Vectors That Avoid Neutralizing Antibodies},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {10},
  doi       = {10.1371/journal.pone.0046667},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134993},
  pages     = {e46667},
  year      = {2012},
  abstract  = {Lentiviral vectors (LVs) are potent gene transfer vehicles frequently applied in research and recently also in clinical trials. Retargeting LV entry to cell types of interest is a key issue to improve gene transfer safety and efficacy. Recently, we have developed a targeting method for LVs by incorporating engineered measles virus (MV) glycoproteins, the hemagglutinin (H), responsible for receptor recognition, and the fusion protein into their envelope. The H protein displays a single-chain antibody (scFv) specific for the target receptor and is ablated for recognition of the MV receptors CD46 and SLAM by point mutations in its ectodomain. A potential hindrance to systemic administration in humans is pre-existing MV-specific immunity due to vaccination or natural infection. We compared transduction of targeting vectors and non-targeting vectors pseudotyped with MV glycoproteins unmodified in their ectodomains (MV-LV) in presence of \(\alpha\)-MV antibody-positive human plasma. At plasma dilution 1: 160 MV-LV was almost completely neutralized, whereas targeting vectors showed relative transduction efficiencies from 60\% to 90\%. Furthermore, at plasma dilution 1: 80 an at least 4-times higher multiplicity of infection (MOI) of MV-LV had to be applied to obtain similar transduction efficiencies as with targeting vectors. Also when the vectors were normalized to their p24 values, targeting vectors showed partial protection against \(\alpha\)-MV antibodies in human plasma. Furthermore, the monoclonal neutralizing antibody K71 with a putative epitope close to the receptor binding sites of H, did not neutralize the targeting vectors, but did neutralize MV-LV. The observed escape from neutralization may be due to the point mutations in the H ectodomain that might have destroyed antibody binding sites. Furthermore, scFv mediated cell entry via the target receptor may proceed in presence of a-MV antibodies interfering with entry via the natural MV receptors. These results are promising for in vivo applications of targeting vectors in humans.},
  language  = {en}
}
@article{WeiseStoll2012,
  author    = {Weise, Gesa and Stoll, Guido},
  title     = {Magnetic resonance imaging of blood brain/nerve barrier dysfunction and leukocyte infiltration: closely related or discordant?},
  series = {Frontiers in Neurology},
  volume    = {3},
  journal   = {Frontiers in Neurology},
  number    = {178},
  doi       = {10.3389/fneur.2012.00178},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-123359},
  year      = {2012},
  abstract  = {Unlike other organs the nervous system is secluded from the rest of the organism by the blood brain barrier (BBB) or blood nerve barrier (BNB) preventing passive influx of fluids from the circulation. Similarly, leukocyte entry to the nervous system is tightly controlled. Breakdown of these barriers and cellular inflammation are hallmarks of inflammatory as well as ischemic neurological diseases and thus represent potential therapeutic targets. The spatiotemporal relationship between BBB/BNB disruption and leukocyte infiltration has been a matter of debate. We here review contrast-enhanced magnetic resonance imaging (MRI) as a non-invasive tool to depict barrier dysfunction and its relation to macrophage infiltration in the central and peripheral nervous system under pathological conditions. Novel experimental contrast agents like Gadofluorine M (Gf) allow more sensitive assessment of BBB dysfunction than conventional Gadolinium (Gd)-DTPA enhanced MRI. In addition, Gf facilitates visualization of functional and transient alterations of the BBB remote from lesions. Cellular contrast agents such as superparamagnetic iron oxide particles (SPIO) and perfluorocarbons enable assessment of leukocyte (mainly macrophage) infiltration by MR technology. Combined use of these MR contrast agents disclosed that leukocytes can enter the nervous system independent from a disturbance of the BBB, and vice versa, a dysfunctional BBB/BNB by itself is not sufficient to attract inflammatory cells from the circulation. We will illustrate these basic imaging findings in animal models of multiple sclerosis, cerebral ischemia, and traumatic nerve injury and review corresponding findings in patients.},
  language  = {en}
}
@article{NeuhausSamwerKunzmannetal.2012,
  author    = {Neuhaus, Winfried and Samwer, Fabian and Kunzmann, Steffen and Muellenbach, Ralph and Wirth, Michael and Speer, Christian P. and Roewer, Norbert and F{\"o}rster, Carola},
  title     = {Lung endothelial cells strengthen, but brain endothelial cells weaken barrier properties of a human alveolar epithelium cell culture model},
  series = {Differentiation},
  volume    = {84},
  journal   = {Differentiation},
  number    = {4},
  doi       = {10.1016/j.diff.2012.08.006},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-90284},
  pages     = {294-304},
  year      = {2012},
  abstract  = {The blood-air barrier in the lung consists of the alveolar epithelium, the underlying capillary endothelium, their basement membranes and the interstitial space between the cell layers. Little is known about the interactions between the alveolar and the blood compartment. The aim of the present study was to gain first insights into the possible interplay between these two neighboured cell layers. We established an in vitro Transwell model of the alveolar epithelium based on human cell line H441 and investigated the influence of conditioned medium obtained from human lung endothelial cell line HPMEC-ST1.6R on the barrier properties of the H441 layers. As control for tissue specificity H441 layers were exposed to conditioned medium from human brain endothelial cell line hCMEC/D3. Addition of dexamethasone was necessary to obtain stable H441 cell layers. Moreover, dexamethasone increased expression of cell type I markers (caveolin-1, RAGE) and cell type II marker SP-B, whereas decreased the transepithelial electrical resistance (TEER) in a concentration dependent manner. Soluble factors obtained from the lung endothelial cell line increased the barrier significantly proven by TEER values and fluorescein permeability on the functional level and by the differential expression of tight junctional proteins on the molecular level. In contrast to this, soluble factors derived from brain endothelial cells weakened the barrier significantly. In conclusion, soluble factors from lung endothelial cells can strengthen the alveolar epithelium barrier in vitro, which suggests communication between endothelial and epithelial cells regulating the integrity of the blood-air barrier.},
  language  = {en}
}
@article{OttoRubenwolfBurgeretal.2012,
  author    = {Otto, Wolfgang and Rubenwolf, Peter C. and Burger, Maximilian and Fritsche, Hans-Martin and R{\"o}ßler, Wolfgang and May, Matthias and Hartmann, Arndt and Hofst{\"a}dter, Ferdinand and Wieland, Wolf F. and Denzinger, Stefan},
  title     = {Loss of aquaporin 3 protein expression constitutes an independent prognostic factor for progression-free survival: an immunohistochemical study on stage pT1 urothelial bladder cancer},
  series = {BMC Cancer},
  volume    = {12},
  journal   = {BMC Cancer},
  number    = {459},
  doi       = {10.1186/1471-2407-12-459},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-135679},
  year      = {2012},
  abstract  = {Background: Treatment of patients with stage pT1 urothelial bladder cancer (UBC) continues to be a challenge due to its unpredictable clinical course. Reliable molecular markers that help to determine appropriate individual treatment are still lacking. Loss of aquaporin (AQP) 3 protein expression has previously been shown in muscle-invasive UBC. The aim of the present study was to investigate the prognostic value of AQP3 protein expression with regard to the prognosis of stage pT1 UBC. Method: AQP 3 protein expression was investigated by immunohistochemistry in specimens of 87 stage T1 UBC patients, who were diagnosed by transurethral resection of the bladder (TURB) and subsequent second resection at a high-volume urological centre between 2002 and 2009. Patients underwent adjuvant instillation therapy with Bacillus Calmette-Guerin (BCG). Loss of AQP3 protein expression was defined as complete absence of the protein within the whole tumour. Expression status was correlated retrospectively with clinicopathological and follow-up data (median: 31 months). Multivariate Cox regression analysis was used to assess the value of AQP3 tumour expression with regard to recurrence-free (RFS), progression-free (PFS) and cancer-specific survival (CSS). RFS, PFS and CSS were calculated by Kaplan-Meier analysis and Log rank test. Results: 59\% of patients were shown to exhibit AQP3-positive tumours, whereas 41\% of tumours did not express the marker. Loss of AQP3 protein expression was associated with a statistically significantly worse PFS (20\% vs. 72\%, p=0.020). This finding was confirmed by multivariate Cox regression analysis (HR 7.58, CI 1.29 - 44.68; p=0.025). Conclusions: Loss of AQP3 protein expression in pT1 UBC appears to play a key role in disease progression and is associated with worse PFS. Considering its potential prognostic value, assessment of AQP3 protein expression could be used to help stratify the behavior of patients with pT1 UBC.},
  language  = {en}
}
@article{ThangarajSelvarajFrankBenderetal.2012,
  author    = {Thangaraj Selvaraj, Bhuvaneish and Frank, Nicolas and Bender, Florian L. P. and Asan, Esther and Sendtner, Michael},
  title     = {Local axonal function of STAT3 rescues axon degeneration in the pmn model of motoneuron disease},
  series = {The Journal of Cell Biology},
  volume    = {199},
  journal   = {The Journal of Cell Biology},
  number    = {3},
  doi       = {10.1083/jcb.201203109},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-154675},
  pages     = {437 -- 451},
  year      = {2012},
  abstract  = {Axonal maintenance, plasticity, and regeneration are influenced by signals from neighboring cells, in particular Schwann cells of the peripheral nervous system. Schwann cells produce neurotrophic factors, but the mechanisms by which ciliary neurotrophic factor (CNTF) and other neurotrophic molecules modify the axonal cytoskeleton are not well understood. In this paper, we show that activated signal transducer and activator of transcription-3 (STAT3), an intracellular mediator of the effects of CNTF and other neurotrophic cytokines, acts locally in axons of motoneurons to modify the tubulin cytoskeleton. Specifically, we show that activated STAT3 interacted with stathmin and inhibited its microtubule-destabilizing activity. Thus, ectopic CNTF-mediated activation of STAT3 restored axon elongation and maintenance in motoneurons from progressive motor neuronopathy mutant mice, a mouse model of motoneuron disease. This mechanism could also be relevant for other neurodegenerative diseases and provide a target for new therapies for axonal degeneration.},
  language  = {en}
}
@article{MenescalSchmidtLiedtkeetal.2012,
  author    = {Menescal, Luciana and Schmidt, Cornelia and Liedtke, Daniel and Schartl, Manfred},
  title     = {Liver hyperplasia after tamoxifen induction of Myc in a transgenic medaka model},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75316},
  year      = {2012},
  abstract  = {Myc is a global transcriptional regulator and one of the most frequently overexpressed oncoproteins in human tumors. It is well established that activation of Myc leads to enhanced cell proliferation but can also lead to increased apoptosis. The use of animal models expressing deregulated levels of Myc has helped to both elucidate its function in normal cells and give insight into how Myc initiates and maintains tumorigenesis. Analyses of the medaka (Oryzias latipes) genome uncovered the unexpected presence of two Myc gene copies in this teleost species. Comparison of these Myc versions to other vertebrate species revealed that one gene, myc17, differs by the loss of some conserved regulatory protein motifs present in all other known Myc genes. To investigate how such differences might affect the basic biological functions of Myc, we generated a tamoxifeninducible in vivo model utilizing a natural, fish-specific Myc gene. Using this model we show that, when activated, Myc17 leads to increased proliferation and to apoptosis in a dose-dependent manner, similar to human Myc. We have also shown that long-term Myc17 activation triggers liver hyperplasia in adult fish, allowing this newly established transgenic medaka model to be used to study the transition from hyperplasia to liver cancer and to identify Myc-induced tumorigenesis modifiers.},
  subject      = {Biologie},
  language  = {en}
}
@article{GresleAlexandrouWuetal.2012,
  author    = {Gresle, Melissa M. and Alexandrou, Estella and Wu, Qizhu and Egan, Gary and Jokubaitis, Vilija and Ayers, Margaret and Jonas, Anna and Doherty, William and Friedhuber, Anna and Shaw, Gerry and Sendtner, Michael and Emery, Ben and Kilpatrick, Trevor and Butzkueven, Helmut},
  title     = {Leukemia Inhibitory Factor Protects Axons in Experimental Autoimmune Encephalomyelitis via an Oligodendrocyte-Independent Mechanism},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {10},
  doi       = {10.1371/journal.pone.0047379},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134617},
  pages     = {e47379},
  year      = {2012},
  abstract  = {Leukemia inhibitory factor (LIF) and Ciliary Neurotrophic factor (CNTF) are members of the interleukin-6 family of cytokines, defined by use of the gp130 molecule as an obligate receptor. In the murine experimental autoimmune encephalomyelitis (EAE) model, antagonism of LIF and genetic deletion of CNTF worsen disease. The potential mechanism of action of these cytokines in EAE is complex, as gp130 is expressed by all neural cells, and could involve immuno-modulation, reduction of oligodendrocyte injury, neuronal protection, or a combination of these actions. In this study we aim to investigate whether the beneficial effects of CNTF/LIF signalling in EAE are associated with axonal protection; and whether this requires signalling through oligodendrocytes. We induced MOG\(_{35-55}\) EAE in CNTF, LIF and double knockout mice. On a CNTF null background, LIF knockout was associated with increased EAE severity (EAE grade 2.1\(\pm\)0.14 vs 2.6\(\pm\)0.19; P<0.05). These mice also showed increased axonal damage relative to LIF heterozygous mice, as indicated by decreased optic nerve parallel diffusivity on MRI (1540\(\pm\)207 \(\mu\)m\(^2\)-/s vs 1310\(\pm\)175 \(\mu\)m\(^2\)-/s; P<0.05), and optic nerve (-12.5\%) and spinal cord (-16\%) axon densities; and increased serum neurofilament-H levels (2.5 fold increase). No differences in inflammatory cell numbers or peripheral auto-immune T-cell priming were evident. Oligodendrocyte-targeted gp130 knockout mice showed that disruption of CNTF/LIF signalling in these cells has no effect on acute EAE severity. These studies demonstrate that endogenous CNTF and LIF act centrally to protect axons from acute inflammatory destruction via an oligodendrocyte-independent mechanism.},
  language  = {en}
}
@article{NeuschKuhlmannKressetal.2012,
  author    = {Neusch, Clemens and Kuhlmann, Tanja and Kress, Wolfram and Schneider-Gold, Christiane},
  title     = {Late-onset myopathy of the posterior calf muscles mimicking Miyoshi myopathy unrelated to dysferlin mutation: a case report},
  series = {Journal of Medical Case Reports},
  volume    = {6},
  journal   = {Journal of Medical Case Reports},
  number    = {345},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-124365},
  year      = {2012},
  abstract  = {Introduction Miyoshi myopathy, a type of distal myopathy with predominant involvement of the posterior calf muscles, has been assigned to mutations in the dysferlin gene. However, many of the late-onset limb-girdle and distal myopathies that resemble dysferlinopathy or Miyoshi myopathy remain unclassified, even after extensive immunohistological and genetic analysis. Case presentation We report the case of a 59-year-old Caucasian man with distal myopathy and exercise-induced myalgia, preferentially of the leg muscles, closely resembling the Miyoshi phenotype. Magnetic resonance imaging of his calf muscles showed typical fatty replacement of the medial heads of the gastrocnemius muscles and soleus muscles, with progression to the adductor longus muscles over a time course of two years. However, genetic analysis revealed that the phenotype of our patient was not related to a mutation in the dysferlin gene but to a novel homozygous splice mutation in the anoctamin 5 gene. Mutations in the anoctamin 5 gene have so far been identified only in some cases of limb-girdle and distal myopathy. Mutations in the anoctamin 5 gene have been assigned to limb-girdle muscular dystrophy type 2L, while distal Miyoshi-like phenotypes have been classified as Miyoshi myopathy type 3. Conclusion The case presented in this report further strengthens the underlying genetic heterogeneity in Miyoshi myopathy-like phenotypes and adds another family to non-dysferlin, Miyoshi myopathy type 3 of late-onset. Furthermore, our case supports the recent observation that anoctamin 5 mutations are a primary cause of distal non-dysferlin myopathies. Therefore, given the increasing number of anoctamin 5 mutations in Miyoshi-like phenotypes, genetic analysis should include an anoctamin 5 screen in late-onset limb-girdle and distal myopathies.},
  language  = {en}
}
@article{StoeltingWiesnervanVlietetal.2012,
  author    = {St{\"o}lting, Miriam and Wiesner, Christiane and van Vliet, Vanessa and Butt, Elke and Pavenst{\"a}dt, Hermann and Linder, Stefan and Kremerskothen, Joachim},
  title     = {Lasp-1 Regulates Podosome Function},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {4},
  doi       = {10.1371/journal.pone.0035340},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134315},
  pages     = {e35340},
  year      = {2012},
  abstract  = {Eukaryotic cells form a variety of adhesive structures to connect with their environment and to regulate cell motility. In contrast to classical focal adhesions, podosomes, highly dynamic structures of different cell types, are actively engaged in matrix remodelling and degradation. Podosomes are composed of an actin-rich core region surrounded by a ring-like structure containing signalling molecules, motor proteins as well as cytoskeleton-associated proteins. Lasp-1 is a ubiquitously expressed, actin-binding protein that is known to regulate cytoskeleton architecture and cell migration. This multidomain protein is predominantely present at focal adhesions, however, a second pool of Lasp-1 molecules is also found at lamellipodia and vesicle-like microdomains in the cytosol. In this report, we show that Lasp-1 is a novel component and regulator of podosomes. Immunofluorescence studies reveal a localization of Lasp-1 in the podosome ring structure, where it colocalizes with zyxin and vinculin. Life cell imaging experiments demonstrate that Lasp-1 is recruited in early steps of podosome assembly. A siRNA-mediated Lasp-1 knockdown in human macrophages affects podosome dynamics as well as their matrix degradation capacity. In summary, our data indicate that Lasp-1 is a novel component of podosomes and is involved in the regulation of podosomal function.},
  language  = {en}
}
@article{OPUS4-12897,
  title     = {Jet mass and substructure of inclusive jets in √s=7 TeV pp collisions with the ATLAS experiment},
  series = {Journal of High Energy Physics},
  volume    = {05},
  journal   = {Journal of High Energy Physics},
  number    = {128},
  organization    = {ATLAS Collaboration},
  doi       = {10.1007/JHEP05(2012)128},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-128970},
  year      = {2012},
  abstract  = {Recent studies have highlighted the potential of jet substructure techniques to identify the hadronic decays of boosted heavy particles. These studies all rely upon the assumption that the internal substructure of jets generated by QCD radiation is well understood. In this article, this assumption is tested on an inclusive sample of jets recorded with the ATLAS detector in 2010, which corresponds to 35 pb\(^{-1}\) of pp collisions delivered by the LHC at √s=7TeV. In a subsample of events with single pp collisions, measurements corrected for detector efficiency and resolution are presented with full systematic uncertainties. Jet invariant mass, k\(_t\) splitting scales and N-subjettiness variables are presented for anti-k\(_t\) R = 1.0 jets and Cambridge-Aachen R = 1.2 jets. Jet invariant-mass spectra for Cambridge-Aachen R = 1.2 jets after a splitting and filtering procedure are also presented. Leading-order parton-shower Monte Carlo predictions for these variables are found to be broadly in agreement with data. The dependence of mean jet mass on additional pp interactions is also explored.},
  language  = {en}
}
@article{BrechtWeissbrichBraunetal.2012,
  author    = {Brecht, Isabel and Weissbrich, Benedikt and Braun, Julia and Toyka, Klaus Viktor and Weishaupt, Andreas and Buttmann, Mathias},
  title     = {Intrathecal, Polyspecific Antiviral Immune Response in Oligoclonal Band Negative Multiple Sclerosis},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {7},
  doi       = {10.1371/journal.pone.0040431},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134426},
  pages     = {e40431},
  year      = {2012},
  abstract  = {Background: Oligoclonal bands (OCB) are detected in the cerebrospinal fluid (CSF) in more than 95\% of patients with multiple sclerosis (MS) in the Western hemisphere. Here we evaluated the intrathecal, polyspecific antiviral immune response as a potential diagnostic CSF marker for OCB-negative MS patients. Methodology/Principal Findings: We tested 46 OCB-negative German patients with paraclinically well defined, definite MS. Sixteen OCB-negative patients with a clear diagnosis of other autoimmune CNS disorders and 37 neurological patients without evidence for autoimmune CNS inflammation served as control groups. Antibodies against measles, rubella, varicella zoster and herpes simplex virus in paired serum and CSF samples were determined by ELISA, and virus-specific immunoglobulin G antibody indices were calculated. An intrathecal antibody synthesis against at least one neurotropic virus was detected in 8 of 26 (31\%) patients with relapsing-remitting MS, 8 of 12 (67\%) with secondary progressive MS and 5 of 8 (63\%) with primary progressive MS, in 3 of 16 (19\%) CNS autoimmune and 3 of 37 (8\%) non-autoimmune control patients. Antibody synthesis against two or more viruses was found in 11 of 46 (24\%) MS patients but in neither of the two control groups. On average, MS patients with a positive antiviral immune response were older and had a longer disease duration than those without. Conclusion: Determination of the intrathecal, polyspecific antiviral immune response may allow to establish a CSF-supported diagnosis of MS in OCB-negative patients when two or more of the four virus antibody indices are elevated.},
  language  = {en}
}
@article{RoierLeitnerIwashkiwetal.2012,
  author    = {Roier, Sandro and Leitner, Deborah R. and Iwashkiw, Jeremy and Schild-Pr{\"u}fert, Kristina and Feldman, Mario F. and Krohne, Georg and Reidl, Joachim and Schild, Stefan},
  title     = {Intranasal Immunization with Nontypeable Haemophilus influenzae Outer Membrane Vesicles Induces Cross-Protective Immunity in Mice},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {8},
  doi       = {10.1371/journal.pone.0042664},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-135201},
  pages     = {e42664},
  year      = {2012},
  abstract  = {Haemophilus influenzae is a Gram-negative human-restricted bacterium that can act as a commensal and a pathogen of the respiratory tract. Especially nontypeable H. influenzae (NTHi) is a major threat to public health and is responsible for several infectious diseases in humans, such as pneumonia, sinusitis, and otitis media. Additionally, NTHi strains are highly associated with exacerbations in patients suffering from chronic obstructive pulmonary disease. Currently, there is no licensed vaccine against NTHi commercially available. Thus, this study investigated the utilization of outer membrane vesicles (OMVs) as a potential vaccine candidate against NTHi infections. We analyzed the immunogenic and protective properties of OMVs derived from various NTHi strains by means of nasopharyngeal immunization and colonization studies with BALB/c mice. The results presented herein demonstrate that an intranasal immunization with NTHi OMVs results in a robust and complex humoral and mucosal immune response. Immunoprecipitation revealed the most important immunogenic proteins, such as the heme utilization protein, protective surface antigen D15, heme binding protein A, and the outer membrane proteins P1, P2, P5 and P6. The induced immune response conferred not only protection against colonization with a homologous NTHi strain, which served as an OMV donor for the immunization mixtures, but also against a heterologous NTHi strain, whose OMVs were not part of the immunization mixtures. These findings indicate that OMVs derived from NTHi strains have a high potential to act as a vaccine against NTHi infections.},
  language  = {en}
}
@article{FraunholzSinha2012,
  author    = {Fraunholz, Martin and Sinha, Bhanu},
  title     = {Intracellular staphylococcus aureus: Live-in and let die},
  series = {Frontiers in Cellular and Infection Microbiology},
  volume    = {2},
  journal   = {Frontiers in Cellular and Infection Microbiology},
  number    = {43},
  doi       = {10.3389/fcimb.2012.00043},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-123374},
  year      = {2012},
  abstract  = {Staphylococcus aureus uses a plethora of virulence factors to accommodate a diversity of niches in its human host. Aside from the classical manifestations of S. aureus-induced diseases, the pathogen also invades and survives within mammalian host cells. The survival strategies of the pathogen are as diverse as strains or host cell types used. S. aureus is able to replicate in the phagosome or freely in the cytoplasm of its host cells. It escapes the phagosome of professional and non-professional phagocytes, subverts autophagy, induces cell death mechanisms such as apoptosis and pyronecrosis, and even can induce anti-apoptotic programs in phagocytes. The focus of this review is to present a guide to recent research outlining the variety of intracellular fates of S. aureus.},
  language  = {en}
}
@article{HerbertMuthPollatosetal.2012,
  author    = {Herbert, Beate M. and Muth, Eric R. and Pollatos, Olga and Herbert, Cornelia},
  title     = {Interoception across Modalities: On the Relationship between Cardiac Awareness and the Sensitivity for Gastric Functions},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {5},
  doi       = {10.1371/journal.pone.0036646},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-130733},
  pages     = {e36646},
  year      = {2012},
  abstract  = {The individual sensitivity for ones internal bodily signals ("interoceptive awareness") has been shown to be of relevance for a broad range of cognitive and affective functions. Interoceptive awareness has been primarily assessed via measuring the sensitivity for ones cardiac signals ("cardiac awareness") which can be non-invasively measured by heartbeat perception tasks. It is an open question whether cardiac awareness is related to the sensitivity for other bodily, visceral functions. This study investigated the relationship between cardiac awareness and the sensitivity for gastric functions in healthy female persons by using non-invasive methods. Heartbeat perception as a measure for cardiac awareness was assessed by a heartbeat tracking task and gastric sensitivity was assessed by a water load test. Gastric myoelectrical activity was measured by electrogastrography (EGG) and subjective feelings of fullness, valence, arousal and nausea were assessed. The results show that cardiac awareness was inversely correlated with ingested water volume and with normogastric activity after water load. However, persons with good and poor cardiac awareness did not differ in their subjective ratings of fullness, nausea and affective feelings after drinking. This suggests that good heartbeat perceivers ingested less water because they subjectively felt more intense signals of fullness during this lower amount of water intake compared to poor heartbeat perceivers who ingested more water until feeling the same signs of fullness. These findings demonstrate that cardiac awareness is related to greater sensitivity for gastric functions, suggesting that there is a general sensitivity for interoceptive processes across the gastric and cardiac modality.},
  language  = {en}
}
@article{BauneKonradGrotegerdetal.2012,
  author    = {Baune, Bernhard T. and Konrad, Carsten and Grotegerd, Dominik and Suslow, Thomas and Birosova, Eva and Ohrmann, Patricia and Bauer, Jochen and Arolt, Volker and Heindel, Walter and Domschke, Katharina and Sch{\"o}ning, Sonja and Rauch, Astrid V. and Uhlmann, Christina and Kugel, Harald and Dannlowski, Udo},
  title     = {Interleukin-6 gene (IL-6): a possible role in brain morphology in the healthy adult brain},
  series = {Journal of Neuroinflammation},
  volume    = {9},
  journal   = {Journal of Neuroinflammation},
  number    = {125},
  doi       = {10.1186/1742-2094-9-125},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-130804},
  year      = {2012},
  abstract  = {Background: Cytokines such as interleukin 6 (IL-6) have been implicated in dual functions in neuropsychiatric disorders. Little is known about the genetic predisposition to neurodegenerative and neuroproliferative properties of cytokine genes. In this study the potential dual role of several IL-6 polymorphisms in brain morphology is investigated. Methodology: In a large sample of healthy individuals (N = 303), associations between genetic variants of IL-6 (rs1800795; rs1800796, rs2069833, rs2069840) and brain volume (gray matter volume) were analyzed using voxel-based morphometry (VBM). Selection of single nucleotide polymorphisms (SNPs) followed a tagging SNP approach (e. g., Stampa algorigthm), yielding a capture 97.08\% of the variation in the IL-6 gene using four tagging SNPs. Principal findings/results In a whole-brain analysis, the polymorphism rs1800795 (-174 C/G) showed a strong main effect of genotype (43 CC vs. 150 CG vs. 100 GG; x = 24, y = -10, z = -15; F(2,286) = 8.54, p(uncorrected) = 0.0002; p(AlphaSim-corrected) = 0.002; cluster size k = 577) within the right hippocampus head. Homozygous carriers of the G-allele had significantly larger hippocampus gray matter volumes compared to heterozygous subjects. None of the other investigated SNPs showed a significant association with grey matter volume in whole-brain analyses. Conclusions/significance: These findings suggest a possible neuroprotective role of the G-allele of the SNP rs1800795 on hippocampal volumes. Studies on the role of this SNP in psychiatric populations and especially in those with an affected hippocampus (e.g., by maltreatment, stress) are warranted.},
  language  = {en}
}
@article{BeisserGrohmeKopkaetal.2012,
  author    = {Beisser, Daniela and Grohme, Markus A. and Kopka, Joachim and Frohme, Marcus and Schill, Ralph O. and Hengherr, Steffen and Dandekar, Thomas and Klau, Gunnar W. and Dittrich, Marcus and M{\"u}ller, Tobias},
  title     = {Integrated pathway modules using time-course metabolic profiles and EST data from Milnesium tardigradum},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75241},
  year      = {2012},
  abstract  = {Background: Tardigrades are multicellular organisms, resistant to extreme environmental changes such as heat, drought, radiation and freezing. They outlast these conditions in an inactive form (tun) to escape damage to cellular structures and cell death. Tardigrades are apparently able to prevent or repair such damage and are therefore a crucial model organism for stress tolerance. Cultures of the tardigrade Milnesium tardigradum were dehydrated by removing the surrounding water to induce tun formation. During this process and the subsequent rehydration, metabolites were measured in a time series by GC-MS. Additionally expressed sequence tags are available, especially libraries generated from the active and inactive state. The aim of this integrated analysis is to trace changes in tardigrade metabolism and identify pathways responsible for their extreme resistance against physical stress. Results: In this study we propose a novel integrative approach for the analysis of metabolic networks to identify modules of joint shifts on the transcriptomic and metabolic levels. We derive a tardigrade-specific metabolic network represented as an undirected graph with 3,658 nodes (metabolites) and 4,378 edges (reactions). Time course metabolite profiles are used to score the network nodes showing a significant change over time. The edges are scored according to information on enzymes from the EST data. Using this combined information, we identify a key subnetwork (functional module) of concerted changes in metabolic pathways, specific for de- and rehydration. The module is enriched in reactions showing significant changes in metabolite levels and enzyme abundance during the transition. It resembles the cessation of a measurablemetabolism (e.g. glycolysis and amino acid anabolism) during the tun formation, the production of storage metabolites and bioprotectants, such as DNA stabilizers, and the generation of amino acids and cellular components from monosaccharides as carbon and energy source during rehydration. Conclusions: The functional module identifies relationships among changed metabolites (e.g. spermidine) and reactions and provides first insights into important altered metabolic pathways. With sparse and diverse data available, the presented integrated metabolite network approach is suitable to integrate all existing data and analyse it in a combined manner.},
  subject      = {Milnesium tardigradum},
  language  = {en}
}
@article{VarykhalovMarchenkoSanchezBarrigaetal.2012,
  author    = {Varykhalov, A. and Marchenko, D. and S{\´a}nchez-Barriga, J. and Scholz, M. R. and Verberck, B. and Trauzettel, B. and Wehling, T. O. and Carbone, C. and Rader, O.},
  title     = {Intact Dirac Cones at Broken Sublattice Symmetry: Photoemission Study of Graphene on Ni and Co},
  series = {Physical Review X},
  volume    = {2},
  journal   = {Physical Review X},
  number    = {041017},
  doi       = {10.1103/PhysRevX.2.041017},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-135732},
  year      = {2012},
  abstract  = {The appearance of massless Dirac fermions in graphene requires two equivalent carbon sublattices of trigonal shape. While the generation of an effective mass and a band gap at the Dirac point remains an unresolved problem for freestanding extended graphene, it is well established by breaking translational symmetry by confinement and by breaking sublattice symmetry by interaction with a substrate. One of the strongest sublattice-symmetry-breaking interactions with predicted and measured band gaps ranging from 400 meV to more than 3 eV has been attributed to the interfaces of graphene with Ni and Co, which are also promising spin-filter interfaces. Here, we apply angle-resolved photoemission to epitaxial graphene on Ni (111) and Co(0001) to show the presence of intact Dirac cones 2.8 eV below the Fermi level. Our results challenge the common belief that the breaking of sublattice symmetry by a substrate and the opening of the band gap at the Dirac energy are in a straightforward relation. A simple effective model of a biased bilayer structure composed of graphene and a sublattice-symmetry-broken layer, corroborated by density-functional-theory calculations, demonstrates the general validity of our conclusions.},
  language  = {en}
}
@article{JanczykHeinemannPfister2012,
  author    = {Janczyk, Markus and Heinemann, Alexander and Pfister, Roland},
  title     = {Instant attraction: Immediate action-effect bindings occur for both, stimulus- and goal-driven actions},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-76203},
  year      = {2012},
  abstract  = {Flexible behavior is only possible if contingencies between own actions and following environmental effects are acquired as quickly as possible; and recent findings indeed point toward an immediate formation of action-effect bindings already after a single coupling of an action and its effect. The present study explored whether these short-term bindings occur for both, stimulus- and goal-driven actions ("forced-choice actions" vs. "free-choice actions"). Two experiments confirmed that immediate action-effect bindings are formed for both types of actions and affect upcoming behavior. These findings support the view that action-effect binding is a ubiquitous phenomenon which occurs for any type of action.},
  subject      = {Psychologie},
  language  = {en}
}
@article{SaidPolatSteinetal.2012,
  author    = {Said, Harun M. and Polat, Buelent and Stein, Susanne and Guckenberger, Mathias and Hagemann, Carsten and Staab, Adrian and Katzer, Astrid and Anacker, Jelena and Flentje, Michael and Vordermark, Dirk},
  title     = {Inhibition of N-Myc down regulated gene 1 in in vitro cultured human glioblastoma cells},
  series = {World Journal of Clinical Oncology},
  volume    = {3},
  journal   = {World Journal of Clinical Oncology},
  number    = {7},
  doi       = {10.5306/wjco.v3.i7.104},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-123385},
  pages     = {104-110},
  year      = {2012},
  abstract  = {AIM: To study short dsRNA oligonucleotides (siRNA) as a potent tool for artificially modulating gene expression of N-Myc down regulated gene 1 (NDRG1) gene induced under different physiological conditions (Normoxia and hypoxia) modulating NDRG1 transcription, mRNA stability and translation. METHODS: A cell line established from a patient with glioblastoma multiforme. Plasmid DNA for transfections was prepared with the Endofree Plasmid Maxi kit. From plates containing 5 x 10(7) cells, nuclear extracts were prepared according to previous protocols. The pSUPER-NDRG1 vectors were designed, two sequences were selected from the human NDRG1 cDNA (5'-GCATTATTGGCATGGGAAC-3' and 5'-ATGCAGAGTAACGTGGAAG-3'. reverse transcription polymerase chain reaction was performed using primers designed using published information on -actin and hypoxia-inducible factor (HIF)-1 mRNA sequences in GenBank. NDRG1 mRNA and protein level expression results under different conditions of hypoxia or reoxygenation were compared to aerobic control conditions using the Mann-Whitney U test. Reoxygenation values were also compared to the NDRG1 levels after 24 h of hypoxia (P < 0.05 was considered significant). RESULTS: siRNA- and iodoacetate (IAA)-mediated downregulation of NDRG1 mRNA and protein expression in vitro in human glioblastoma cell lines showed a nearly complete inhibition of NDRG1 expression when compared to the results obtained due to the inhibitory role of glycolysis inhibitor IAA. Hypoxia responsive elements bound by nuclear HIF-1 in human glioblastoma cells in vitro under different oxygenation conditions and the clearly enhanced binding of nuclear extracts from glioblastoma cell samples exposed to extreme hypoxic conditions confirmed the HIF-1 Western blotting results. CONCLUSION: NDRG1 represents an additional diagnostic marker for brain tumor detection, due to the role of hypoxia in regulating this gene, and it can represent a potential target for tumor treatment in human glioblastoma. The siRNA method can represent an elegant alternative to modulate the expression of the hypoxia induced NDRG1 gene and can help to monitor the development of the cancer disease treatment outcome through monitoring the expression of this gene in the patients undergoing the different therapeutic treatment alternatives available nowadays.},
  language  = {en}
}
@article{BenderReschKleinetal.2012,
  author    = {Bender, Stephan and Resch, Franz and Klein, Christoph and Renner, Tobias and Fallgatter, Andreas J. and Weisbrod, Matthias and Romanos, Marcel},
  title     = {Influence of Stimulant Medication and Response Speed on Lateralization of Movement-Related Potentials in Attention-Deficit/Hyperactivity Disorder},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {6},
  doi       = {10.1371/journal.pone.0039012},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-135262},
  pages     = {e39012},
  year      = {2012},
  abstract  = {Background: Hyperactivity is one of the core symptoms in attention deficit hyperactivity disorder (ADHD). However, it remains unclear in which way the motor system itself and its development are affected by the disorder. Movement-related potentials (MRP) can separate different stages of movement execution, from the programming of a movement to motor post-processing and memory traces. Pre-movement MRP are absent or positive during early childhood and display a developmental increase of negativity. Methods: We examined the influences of response-speed, an indicator of the level of attention, and stimulant medication on lateralized MRP in 16 children with combined type ADHD compared to 20 matched healthy controls. Results: We detected a significantly diminished lateralisation of MRP over the pre-motor and primary motor cortex during movement execution (initial motor potential peak, iMP) in patients with ADHD. Fast reactions (indicating increased visuo-motor attention) led to increased lateralized negativity during movement execution only in healthy controls, while in children with ADHD faster reaction times were associated with more positive amplitudes. Even though stimulant medication had some effect on attenuating group differences in lateralized MRP, this effect was insufficient to normalize lateralized iMP amplitudes. Conclusions: A reduced focal (lateralized) motor cortex activation during the command to muscle contraction points towards an immature motor system and a maturation delay of the (pre-) motor cortex in children with ADHD. A delayed maturation of the neuronal circuitry, which involves primary motor cortex, may contribute to ADHD pathophysiology.},
  language  = {en}
}
@article{KirschHerbortButzetal.2012,
  author    = {Kirsch, Wladimir and Herbort, Oliver and Butz, Martin V. and Kunde, Wilfried},
  title     = {Influence of Motor Planning on Distance Perception within the Peripersonal Space},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75332},
  year      = {2012},
  abstract  = {We examined whether movement costs as defined by movement magnitude have an impact on distance perception in near space. In Experiment 1, participants were given a numerical cue regarding the amplitude of a hand movement to be carried out. Before the movement execution, the length of a visual distance had to be judged. These visual distances were judged to be larger, the larger the amplitude of the concurrently prepared hand movement was. In Experiment 2, in which numerical cues were merely memorized without concurrent movement planning, this general increase of distance with cue size was not observed. The results of these experiments indicate that visual perception of near space is specifically affected by the costs of planned hand movements.},
  subject      = {Psychologie},
  language  = {en}
}
@article{DurrenbergerGruenblattFernandoetal.2012,
  author    = {Durrenberger, Pascal F. and Gr{\"u}nblatt, Edna and Fernando, Francesca S. and Monoranu, Camelia Maria and Evans, Jordan and Riederer, Peter and Reynolds, Richard and Dexter, David T.},
  title     = {Inflammatory Pathways in Parkinson's Disease; A BNE Microarray Study},
  series = {Parkinson's Disease},
  volume    = {2012},
  journal   = {Parkinson's Disease},
  number    = {214714},
  doi       = {10.1155/2012/214714},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-124380},
  year      = {2012},
  abstract  = {The aetiology of Parkinson's disease (PD) is yet to be fully understood but it is becoming more and more evident that neuronal cell death may be multifactorial in essence. The main focus of PD research is to better understand substantia nigra homeostasis disruption, particularly in relation to the wide-spread deposition of the aberrant protein α-synuclein. Microarray technology contributed towards PD research with several studies to date and one gene, ALDH1A1 (Aldehyde dehydrogenase 1 family, member A1), consistently reappeared across studies including the present study, highlighting dopamine (DA) metabolism dysfunction resulting in oxidative stress and most probably leading to neuronal cell death. Neuronal cell death leads to increased inflammation through the activation of astrocytes and microglia. Using our dataset, we aimed to isolate some of these pathways so to offer potential novel neuroprotective therapeutic avenues. To that effect our study has focused on the upregulation of P2X7 (purinergic receptor P2X, ligand-gated ion channel, 7) receptor pathway (microglial activation) and on the NOS3 (nitric oxide synthase 3) pathway (angiogenesis). In summary, although the exact initiator of striatal DA neuronal cell death remains to be determined, based on our analysis, this event does not remain without consequence. Extracellular ATP and reactive astrocytes appear to be responsible for the activation of microglia which in turn release proinflammatory cytokines contributing further to the parkinsonian condition. In addition to tackling oxidative stress pathways we also suggest to reduce microglial and endothelial activation to support neuronal outgrowth.},
  language  = {en}
}
@article{AzzamiRitterTautzetal.2012,
  author    = {Azzami, Klara and Ritter, Wolfgang and Tautz, J{\"u}rgen and Beier, Hildburg},
  title     = {Infection of honey bees with acute bee paralysis virus does not trigger humoral or cellular immune responses},
  series = {Archives of Virology},
  volume    = {157},
  journal   = {Archives of Virology},
  number    = {4},
  doi       = {10.1007/s00705-012-1223-0},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-126863},
  pages     = {689-702},
  year      = {2012},
  abstract  = {We have studied the responses of honey bees at different life stages (Apis mellifera) to controlled infection with acute bee paralysis virus and have identified the haemolymph of infected larvae and adult worker bees as the compartment where massive propagation of ABPV occurs. Insects respond with a broad spectrum of induced innate immune reactions to bacterial infections, whereas defence mechanisms based on RNA interference play a major role in antiviral immunity. In this study, we have determined that honey bee larvae and adult workers do not produce a humoral immune reaction upon artificial infection with ABPV, in contrast to control individuals challenged with Escherichia coli. ABPV-infected bees produced neither elevated levels of specific antimicrobial peptides (AMPs), such as hymenoptaecin and defensin, nor any general antimicrobial activity, as revealed by inhibition-zone assays. Additionally, adult bees did not generate melanised nodules upon ABPV infection, an important cellular immune function activated by bacteria and viruses in some insects. Challenge of bees with both ABPV and E. coli showed that innate humoral and cellular immune reactions are induced in mixed infections, albeit at a reduced level.},
  language  = {en}
}
@article{NolteZadehKhorasaniSafarovetal.2012,
  author    = {Nolte, Thomas and Zadeh-Khorasani, Maryam and Safarov, Orkhan and Rueff, Franziska and Varga, Rita and Herbach, Nadja and Wanke, R{\"u}diger and Wollenberg, Andreas and Mueller, Thomas and Gropp, Roswitha and Wolf, Eckhard and Siebeck, Matthias},
  title     = {Induction of oxazolone-mediated features of atopic dermatitis in NOD-scid \(IL2Rγ^{null}\) mice engrafted with human peripheral blood mononuclear cells},
  series = {Disease Models and Mechanisms},
  volume    = {6},
  journal   = {Disease Models and Mechanisms},
  doi       = {10.1242/dmm.009167},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-124150},
  pages     = {125-134},
  year      = {2012},
  abstract  = {Animal models mimicking human diseases have been used extensively to study the pathogenesis of autoimmune diseases and the efficacy of potential therapeutics. They are, however, limited with regard to their similarity to the human disease and cannot be used if the antagonist and its cognate receptor require high similarity in structure or binding. Here, we examine the induction of oxazolone-mediated features of atopic dermatitis (AD) in NOD-scid IL2Rγnull mice engrafted with human peripheral blood mononuclear cells (PBMC). The mice developed the same symptoms as immunocompetent BALB/c mice. Histological alterations induced by oxazolone were characterized by keratosis, epithelial hyperplasia and influx of inflammatory cells into the dermis and epidermis. The cellular infiltrate was identified as human leukocytes, with T cells being the major constituent. In addition, oxazolone increased human serum IgE levels. The response, however, required the engraftment of PBMC derived from patients suffering from AD, which suggests that this model reflects the immunological status of the donor. Taken together, the model described here has the potential to evaluate the efficacy of therapeutics targeting human lymphocytes in vivo and, in addition, might be developed further to elucidate molecular mechanisms inducing and sustaining flares of the disease.},
  language  = {en}
}
@article{SteinertWeissenbergerKunzetal.2012,
  author    = {Steinert, Andre F. and Weissenberger, Manuel and Kunz, Manuela and Gilbert, Fabian and Ghivizzani, Steven C. and Goebel, Sascha and Jakob, Franz and N{\"o}th, Ulrich and Rudert, Maximilian},
  title     = {Indian hedgehog gene transfer is a chondrogenic inducer of human mesenchymal stem cells},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75425},
  year      = {2012},
  abstract  = {Introduction: To date, no single most-appropriate factor or delivery method has been identified for the purpose of mesenchymal stem cell (MSC)-based treatment of cartilage injury. Therefore, in this study we tested whether gene delivery of the growth factor Indian hedgehog (IHH) was able to induce chondrogenesis in human primary MSCs, and whether it was possible by such an approach to modulate the appearance of chondrogenic hypertrophy in pellet cultures in vitro. Methods: First-generation adenoviral vectors encoding the cDNA of the human IHH gene were created by cre-lox recombination and used alone or in combination with adenoviral vectors, bone morphogenetic protein-2 (Ad.BMP- 2), or transforming growth factor beta-1 (Ad.TGF-b1) to transduce human bone-marrow derived MSCs at 5 × 102 infectious particles/cell. Thereafter, 3 × 105 cells were seeded into aggregates and cultured for 3 weeks in serumfree medium, with untransduced or marker gene transduced cultures as controls. Transgene expressions were determined by ELISA, and aggregates were analysed histologically, immunohistochemically, biochemically and by RT-PCR for chondrogenesis and hypertrophy. Results: IHH, TGF-b1 and BMP-2 genes were equipotent inducers of chondrogenesis in primary MSCs, as evidenced by strong staining for proteoglycans, collagen type II, increased levels of glycosaminoglycan synthesis, and expression of mRNAs associated with chondrogenesis. IHH-modified aggregates, alone or in combination, also showed a tendency to progress towards hypertrophy, as judged by the expression of alkaline phosphatase and stainings for collagen type X and Annexin 5. Conclusion: As this study provides evidence for chondrogenic induction of MSC aggregates in vitro via IHH gene delivery, this technology may be efficiently employed for generating cartilaginous repair tissues in vivo.},
  subject      = {Medizin},
  language  = {en}
}
@article{SchusterWessigSchimmeretal.2012,
  author    = {Schuster, Frank and Wessig, Carsten and Schimmer, Christoph and Johannsen, Stephan and Lazarus, Marc and Aleksic, Ivan and Leyh, Rainer and Roewer, Norbert},
  title     = {In vitro contracture test results and anaesthetic management of a patient with emery-dreifuss muscular dystrophy for cardiac transplantation},
  series = {Case Reports in Anesthesiology},
  volume    = {2012},
  journal   = {Case Reports in Anesthesiology},
  number    = {349046},
  doi       = {10.1155/2012/349046},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-123413},
  year      = {2012},
  abstract  = {Emery-Dreifuss muscular dystrophy (EDMD) is a hereditary neuromuscular disorder characterized by slowly progressive muscle weakness, early contractures, and dilated cardiomyopathy. We reported an uneventful general anaesthesia using total intravenous anaesthesia (TIVA) for cardiac transplantation in a 19-year-old woman suffering from EDMD. In vitro contracture test results of two pectoralis major muscle bundles of the patient suggest that exposition to triggering agents does not induce a pathological sarcoplasmic calcium release in the lamin A/C phenotype. However, due to the lack of evidence in the literature, we would recommend TIVA for patients with EDMD if general anaesthesia is required.},
  language  = {en}
}
@article{JakobEbertRudertetal.2012,
  author    = {Jakob, Franz and Ebert, Regina and Rudert, Maximilian and N{\"o}th, Ulrich and Walles, Heike and Docheva, Denitsa and Schieker, Matthias and Meinel, Lorenz and Groll, J{\"u}rgen},
  title     = {In situ guided tissue regeneration in musculoskeletal diseases and aging},
  series = {Cell and Tissue Research},
  volume    = {347},
  journal   = {Cell and Tissue Research},
  number    = {3},
  doi       = {10.1007/s00441-011-1237-z},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-124738},
  pages     = {725-735},
  year      = {2012},
  abstract  = {In situ guided tissue regeneration, also addressed as in situ tissue engineering or endogenous regeneration, has a great potential for population-wide "minimal invasive" applications. During the last two decades, tissue engineering has been developed with remarkable in vitro and preclinical success but still the number of applications in clinical routine is extremely small. Moreover, the vision of population-wide applications of ex vivo tissue engineered constructs based on cells, growth and differentiation factors and scaffolds, must probably be deemed unrealistic for economic and regulation-related issues. Hence, the progress made in this respect will be mostly applicable to a fraction of post-traumatic or post-surgery situations such as big tissue defects due to tumor manifestation. Minimally invasive procedures would probably qualify for a broader application and ideally would only require off the shelf standardized products without cells. Such products should mimic the microenvironment of regenerating tissues and make use of the endogenous tissue regeneration capacities. Functionally, the chemotaxis of regenerative cells, their amplification as a transient amplifying pool and their concerted differentiation and remodeling should be addressed. This is especially important because the main target populations for such applications are the elderly and diseased. The quality of regenerative cells is impaired in such organisms and high levels of inhibitors also interfere with regeneration and healing. In metabolic bone diseases like osteoporosis, it is already known that antagonists for inhibitors such as activin and sclerostin enhance bone formation. Implementing such strategies into applications for in situ guided tissue regeneration should greatly enhance the efficacy of tailored procedures in the future.},
  language  = {en}
}
@article{DossoYeoKonateetal.2012,
  author    = {Dosso, Kanvaly and Yeo, Kolo and Konate, Souleymane and Linsenmair, Karl Eduard},
  title     = {Importance of protected areas for biodiversity conservation in central Cote d'Ivoire: Comparison of termite assemblages between two neighboring areas under differing levels of disturbance},
  series = {Journal of Insect Science},
  volume    = {12},
  journal   = {Journal of Insect Science},
  number    = {131},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-133218},
  year      = {2012},
  abstract  = {To highlight human impact on biodiversity in the Lamto region, termites were studied with regard to their use as bio-indicators of habitat change in the tropics. Using a standardized method, termites were sampled in the three most common habitat types, i.e., in semi-deciduous forest, savanna woodland, and annually burned savanna, all inside Lamto Reserve and its surrounding rural domain. Termite species richness fell from 25 species in the Lamto forest to 13 species in the rural area, involving strong modification in the species composition (species turnover = 59 \%). In contrast, no significant change in diversity was found between the Lamto savannas and the rural ones. In addition, the relative abundance of termites showed a significantly greater decline in the rural domain, even in the species Ancistrotermes cavithorax (Sjostedt) (Isoptera: Termitidae), which is known to be ecologically especially versatile. Overall, the findings of this study suggest further investigation around Lamto Reserve on the impact of human activities on biodiversity, focusing on forest conversion to land uses (e.g. agricultural and silvicultural systems).},
  language  = {en}
}
@article{GutknechtAraragiMerkeretal.2012,
  author    = {Gutknecht, Lise and Araragi, Naozumi and Merker, S{\"o}ren and Waider, Jonas and Sommerlandt, Frank M. J. and Mlinar, Boris and Baccini, Gilda and Mayer, Ute and Proft, Florian and Hamon, Michel and Schmitt, Angelika G. and Corradetti, Renato and Lanfumey, Laurence and Lesch, Klaus-Peter},
  title     = {Impacts of Brain Serotonin Deficiency following Tph2 Inactivation on Development and Raphe Neuron Serotonergic Specification},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {8},
  doi       = {10.1371/journal.pone.0043157},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-133728},
  year      = {2012},
  abstract  = {Brain serotonin (5-HT) is implicated in a wide range of functions from basic physiological mechanisms to complex behaviors, including neuropsychiatric conditions, as well as in developmental processes. Increasing evidence links 5-HT signaling alterations during development to emotional dysregulation and psychopathology in adult age. To further analyze the importance of brain 5-HT in somatic and brain development and function, and more specifically differentiation and specification of the serotonergic system itself, we generated a mouse model with brain-specific 5-HT deficiency resulting from a genetically driven constitutive inactivation of neuronal tryptophan hydroxylase-2 (Tph2). Tph2 inactivation (Tph2-/-) resulted in brain 5-HT deficiency leading to growth retardation and persistent leanness, whereas a sex- and age-dependent increase in body weight was observed in Tph2+/- mice. The conserved expression pattern of the 5-HT neuron-specific markers (except Tph2 and 5-HT) demonstrates that brain 5-HT synthesis is not a prerequisite for the proliferation, differentiation and survival of raphe neurons subjected to the developmental program of serotonergic specification. Furthermore, although these neurons are unable to synthesize 5-HT from the precursor tryptophan, they still display electrophysiological properties characteristic of 5-HT neurons. Moreover, 5-HT deficiency induces an up-regulation of 5-HT\(_{1A}\) and 5-HT\(_{1B}\) receptors across brain regions as well as a reduction of norepinephrine concentrations accompanied by a reduced number of noradrenergic neurons. Together, our results characterize developmental, neurochemical, neurobiological and electrophysiological consequences of brain-specific 5-HT deficiency, reveal a dual dose-dependent role of 5-HT in body weight regulation and show that differentiation of serotonergic neuron phenotype is independent from endogenous 5-HT synthesis.},
  language  = {en}
}
@article{KleinertTonyKrauseetal.2012,
  author    = {Kleinert, Stefan and Tony, Hans-Peter and Krause, Andreas and Feuchtenberger, Martin and Wassenberg, Siegfried and Richter, Constanze and R{\"a}ther, Ekkehard and Spieler, Wolfgang and Gnann, Holger and Wittig, Bianca M.},
  title     = {Impact of patient and disease characteristics on therapeutic success during adalimumab treatment of patients with rheumatoid arthritis: data from a German noninterventional observational study},
  series = {Rheumatology International},
  volume    = {32},
  journal   = {Rheumatology International},
  number    = {9},
  doi       = {10.1007/s00296-011-2033-5},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-125118},
  pages     = {2759-2767},
  year      = {2012},
  abstract  = {The objective of this study was to use data from a noninterventional study to evaluate the effectiveness of adalimumab in rheumatoid arthritis (RA) patients during routine clinical practice and to explore the potential impact of patient and disease characteristics in response to adalimumab therapy. A total of 2,625 RA patients with specified data at baseline (prior to initiating adalimumab treatment) and 12 months entered this study between April 2003 and March 2009. We evaluated response to adalimumab therapy and conducted stepwise regression and subgroup analyses of factors influencing therapeutic response. During the 1-year adalimumab treatment period, disease activity decreased from a baseline mean disease activity score-28 joints (DAS28) of 5.9-3.9, while functional capacity improved from 59.0 to 68.4 Funktionsfragebogen Hannover (FFbH) percentage points. In multivariate regression models, high baseline DAS28 was the strongest positive predictor for decrease in disease activity, and high baseline functional capacity was associated with reduced gains in functional capacity. Male gender was a positive predictor of therapeutic response for both disease activity and functional capacity, while older age and multiple previous biologics were associated with a reduced therapeutic response. Subset analyses provided further support for the impact of baseline DAS28, FFbH, and prior biologic therapy on therapeutic response during treatment. We conclude that treatment with adalimumab leads to decreased disease activity and improved function during routine clinical practice. Patients with high disease activity and low functional capacity are particularly benefitted by adalimumab therapy.},
  language  = {en}
}
@article{KleinertTonyKrauseetal.2012,
  author    = {Kleinert, Stefan and Tony, Hans-Peter and Krause, Andreas and Feuchtenberger, Martin and Wassenberg, Siegfried and Richter, Constanze and R{\"o}ther, Ekkehard and Spieler, Wolfgang and Gnann, Holger and Wittig, Bianca M.},
  title     = {Impact of patient and disease characteristics on therapeutic success during adalimumab treatment of patients with rheumatoid arthritis: data from a German},
  series = {Rheumatology International},
  volume    = {32},
  journal   = {Rheumatology International},
  number    = {9},
  doi       = {10.1007/s00296-011-2033-5},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-126220},
  pages     = {2759-2767},
  year      = {2012},
  abstract  = {The objective of this study was to use data from a noninterventional study to evaluate the effectiveness of adalimumab in rheumatoid arthritis (RA) patients during routine clinical practice and to explore the potential impact of patient and disease characteristics in response to adalimumab therapy. A total of 2,625 RA patients with specified data at baseline (prior to initiating adalimumab treatment) and 12 months entered this study between April 2003 and March 2009. We evaluated response to adalimumab therapy and conducted stepwise regression and subgroup analyses of factors influencing therapeutic response. During the 1-year adalimumab treatment period, disease activity decreased from a baseline mean disease activity score-28 joints (DAS28) of 5.9-3.9, while functional capacity improved from 59.0 to 68.4 Funktionsfragebogen Hannover (FFbH) percentage points. In multivariate regression models, high baseline DAS28 was the strongest positive predictor for decrease in disease activity, and high baseline functional capacity was associated with reduced gains in functional capacity. Male gender was a positive predictor of therapeutic response for both disease activity and functional capacity, while older age and multiple previous biologics were associated with a reduced therapeutic response. Subset analyses provided further support for the impact of baseline DAS28, FFbH, and prior biologic therapy on therapeutic response during treatment. We conclude that treatment with adalimumab leads to decreased disease activity and improved function during routine clinical practice. Patients with high disease activity and low functional capacity are particularly benefitted by adalimumab therapy.},
  language  = {en}
}
@article{BiermannHeilmannDidieetal.2012,
  author    = {Biermann, Daniel and Heilmann, Andreas and Didi{\´e}, Michael and Schlossarek, Saskia and Wahab, Azadeh and Grimm, Michael and R{\"o}mer, Maria and Reichenspurner, Hermann and Sultan, Karim R. and Steenpass, Anna and Erg{\"u}n, S{\"u}leyman and Donzelli, Sonia and Carrier, Lucie and Ehmke, Heimo and Zimmermann, Wolfram H. and Hein, Lutz and B{\"o}ger, Rainer H. and Benndorf, Ralf A.},
  title     = {Impact of AT2 Receptor Deficiency on Postnatal Cardiovascular Development},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {10},
  doi       = {10.1371/journal.pone.0047916},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134902},
  pages     = {e47916},
  year      = {2012},
  abstract  = {Background: The angiotensin II receptor subtype 2 (AT2 receptor) is ubiquitously and highly expressed in early postnatal life. However, its role in postnatal cardiac development remained unclear. Methodology/Principal Findings: Hearts from 1, 7, 14 and 56 days old wild-type (WT) and AT2 receptor-deficient (KO) mice were extracted for histomorphometrical analysis as well as analysis of cardiac signaling and gene expression. Furthermore, heart and body weights of examined animals were recorded and echocardiographic analysis of cardiac function as well as telemetric blood pressure measurements were performed. Moreover, gene expression, sarcomere shortening and calcium transients were examined in ventricular cardiomyocytes isolated from both genotypes. KO mice exhibited an accelerated body weight gain and a reduced heart to body weight ratio as compared to WT mice in the postnatal period. However, in adult KO mice the heart to body weight ratio was significantly increased most likely due to elevated systemic blood pressure. At postnatal day 7 ventricular capillarization index and the density of \(\alpha\)-smooth muscle cell actin-positive blood vessels were higher in KO mice as compared to WT mice but normalized during adolescence. Echocardiographic assessment of cardiac systolic function at postnatal day 7 revealed decreased contractility of KO hearts in response to beta-adrenergic stimulation. Moreover, cardiomyocytes from KO mice showed a decreased sarcomere shortening and an increased peak Ca\(^{2+}\) transient in response to isoprenaline when stimulated concomitantly with angiotensin II. Conclusion: The AT2 receptor affects postnatal cardiac growth possibly via reducing body weight gain and systemic blood pressure. Moreover, it moderately attenuates postnatal vascularization of the heart and modulates the beta adrenergic response of the neonatal heart. These AT2 receptor-mediated effects may be implicated in the physiological maturation process of the heart.},
  language  = {en}
}
@article{PrustyBoehmeBergmannetal.2012,
  author    = {Prusty, Bhupesh K. and B{\"o}hme, Linda and Bergmann, Birgit and Siegl, Christine and Krause, Eva and Mehlitz, Adrian and Rudel, Thomas},
  title     = {Imbalanced oxidative stress causes chlamydial persistence during non-productive Human Herpes Virus co-infection},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-76215},
  year      = {2012},
  abstract  = {Both human herpes viruses and Chlamydia are highly prevalent in the human population and are detected together in different human disorders. Here, we demonstrate that co-infection with human herpes virus 6 (HHV6) interferes with the developmental cycle of C. trachomatis and induces persistence. Induction of chlamydial persistence by HHV6 is independent of productive virus infection, but requires the interaction and uptake of the virus by the host cell. On the other hand, viral uptake is strongly promoted under co-infection conditions. Host cell glutathione reductase activity was suppressed by HHV6 causing NADPH accumulation, decreased formation of reduced glutathione and increased oxidative stress. Prevention of oxidative stress restored infectivity of Chlamydia after HHV6-induced persistence. We show that co-infection with Herpes simplex virus 1 or human Cytomegalovirus also induces chlamydial persistence by a similar mechanism suggesting that Chlamydia -human herpes virus co-infections are evolutionary shaped interactions with a thus far unrecognized broad significance.},
  subject      = {Biologie},
  language  = {en}
}
@article{HaddadChenCarlinetal.2012,
  author    = {Haddad, Dana and Chen, Chun-Hao and Carlin, Sean and Silberhumer, Gerd and Chen, Nanhai G. and Zhang, Qian and Longo, Valerie and Carpenter, Susanne G. and Mittra, Arjun and Carson, Joshua and Au, Joyce and Gonen, Mithat and Zanzonico, Pat B. and Szalay, Aladar A. and Fong, Yuman},
  title     = {Imaging Characteristics, Tissue Distribution, and Spread of a Novel Oncolytic Vaccinia Virus Carrying the Human Sodium Iodide Symporter},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {8},
  doi       = {10.1371/journal.pone.0041647},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-130041},
  pages     = {e41647},
  year      = {2012},
  abstract  = {Introduction: Oncolytic viruses show promise for treating cancer. However, to assess therapy and potential toxicity, a noninvasive imaging modality is needed. This study aims to determine the in vivo biodistribution, and imaging and timing characteristics of a vaccinia virus, GLV-1h153, encoding the human sodium iodide symporter (hNIS. Methods: GLV-1h153 was modified from GLV-1h68 to encode the hNIS gene. Timing of cellular uptake of radioiodide \(^{131}\)I in human pancreatic carcinoma cells PANC-1 was assessed using radiouptake assays. Viral biodistribution was determined in nude mice bearing PANC-1 xenografts, and infection in tumors confirmed histologically and optically via Green Fluorescent Protein (GFP) and bioluminescence. Timing characteristics of enhanced radiouptake in xenografts were assessed via \(^{124}\)I-positron emission tomography (PET). Detection of systemic administration of virus was investigated with both \(^{124}\)I-PET and 99m-technecium gamma-scintigraphy. Results: GLV-1h153 successfully facilitated time-dependent intracellular uptake of \(^{131}\)I in PANC-1 cells with a maximum uptake at 24 hours postinfection (P < 0.05). In vivo, biodistribution profiles revealed persistence of virus in tumors 5 weeks postinjection at 10\(^9\) plaque-forming unit (PFU)/gm tissue, with the virus mainly cleared from all other major organs. Tumor infection by GLV-1h153 was confirmed via optical imaging and histology. GLV-1h153 facilitated imaging virus replication in tumors via PET even at 8 hours post radiotracer injection, with a mean \% ID/gm of 3.82 \(\pm\) 60.46 (P < 0.05) 2 days after intratumoral administration of virus, confirmed via tissue radiouptake assays. One week post systemic administration, GLV1h153-infected tumors were detected via \(^{124}\)I-PET and 99m-technecium-scintigraphy. Conclusion: GLV-1h153 is a promising oncolytic agent against pancreatic cancer with a promising biosafety profile. GLV-1h153 facilitated time-dependent hNIS-specific radiouptake in pancreatic cancer cells, facilitating detection by PET with both intratumoral and systemic administration. Therefore, GLV-1h153 is a promising candidate for the noninvasive imaging of virotherapy and warrants further study into longterm monitoring of virotherapy and potential radiocombination therapies with this treatment and imaging modality.},
  language  = {en}
}
@article{LaugFehrholzSchuetzeetal.2012,
  author    = {Laug, Roderich and Fehrholz, Markus and Sch{\"u}tze, Norbert and Kramer, Boris W. and Krump-Konvalinkova, Vera and Speer, Christian P. and Kunzmann, Steffen},
  title     = {IFN-gamma and TNF-alpha synergize to inhibit CTGF expression in human lung endothelial cells},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-76253},
  year      = {2012},
  abstract  = {Connective tissue growth factor (CTGF/CCN2) is an angiogenetic and profibrotic factor, acting downstream of TGF-b, involved in both airway- and vascular remodeling. While the T-helper 1 (Th1) cytokine interferon-gamma (IFN-c) is well characterized as immune-modulatory and anti-fibrotic cytokine, the role of IFN-c in lung endothelial cells (LEC) is less defined. Tumour necrosis factor alpha (TNF-a) is another mediator that drives vascular remodeling in inflammation by influencing CTGF expression. In the present study we investigated the influence of IFN-c and TNF-a on CTGF expression in human LEC (HPMEC-ST1.6R) and the effect of CTGF knock down on human LEC. IFN-c and TNF-a down-regulated CTGF in human LEC at the promoter-, transcriptional- and translational-level in a dose- and time-dependent manner. The inhibitory effect of IFN-c on CTGF-expression could be almost completely compensated by the Jak inhibitor AG-490, showing the involvement of the Jak-Stat signaling pathway. Besides the inhibitory effect of IFN-c and TNF-a alone on CTGF expression and LEC proliferation, these cytokines had an additive inhibitory effect on proliferation as well as on CTGF expression when administered together. To study the functional role of CTGF in LEC, endogenous CTGF expression was down-regulated by a lentiviral system. CTGF silencing in LEC by transduction of CTGF shRNA reduced cell proliferation, but did not influence the anti-proliferative effect of IFN-c and TNF-a. In conclusion, our data demonstrated that CTGF was negatively regulated by IFN-c in LEC in a Jak/Stat signaling pathway-dependent manner. In addition, an additive effect of IFN-c and TNF-a on inhibition of CTGF expression and cell proliferation could be found. The inverse correlation between IFN-c and CTGF expression in LEC could mean that screwing the Th2 response to a Th1 response with an additional IFN-c production might be beneficial to avoid airway remodeling in asthma.},
  subject      = {Medizin},
  language  = {en}
}
@article{BugaScholzKumaretal.2012,
  author    = {Buga, Ana-Maria and Scholz, Claus J{\"u}rgen and Kumar, Senthil and Herndon, James G. and Alexandru, Dragos and Cojocaru, Gabriel Radu and Dandekar, Thomas and Popa-Wagner, Aurel},
  title     = {Identification of New Therapeutic Targets by Genome-Wide Analysis of Gene Expression in the Ipsilateral Cortex of Aged Rats after Stroke},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {12},
  doi       = {10.1371/journal.pone.0050985},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-130657},
  pages     = {e50985},
  year      = {2012},
  abstract  = {Background: Because most human stroke victims are elderly, studies of experimental stroke in the aged rather than the young rat model may be optimal for identifying clinically relevant cellular responses, as well for pinpointing beneficial interventions. Methodology/Principal Findings: We employed the Affymetrix platform to analyze the whole-gene transcriptome following temporary ligation of the middle cerebral artery in aged and young rats. The correspondence, heat map, and dendrogram analyses independently suggest a differential, age-group-specific behaviour of major gene clusters after stroke. Overall, the pattern of gene expression strongly suggests that the response of the aged rat brain is qualitatively rather than quantitatively different from the young, i.e. the total number of regulated genes is comparable in the two age groups, but the aged rats had great difficulty in mounting a timely response to stroke. Our study indicates that four genes related to neuropathic syndrome, stress, anxiety disorders and depression (Acvr1c, Cort, Htr2b and Pnoc) may have impaired response to stroke in aged rats. New therapeutic options in aged rats may also include Calcrl, Cyp11b1, Prcp, Cebpa, Cfd, Gpnmb, Fcgr2b, Fcgr3a, Tnfrsf26, Adam 17 and Mmp14. An unexpected target is the enzyme 3-hydroxy-3-methylglutaryl-Coenzyme A synthase 1 in aged rats, a key enzyme in the cholesterol synthesis pathway. Post-stroke axonal growth was compromised in both age groups. Conclusion/Significance: We suggest that a multi-stage, multimodal treatment in aged animals may be more likely to produce positive results. Such a therapeutic approach should be focused on tissue restoration but should also address other aspects of patient post-stroke therapy such as neuropathic syndrome, stress, anxiety disorders, depression, neurotransmission and blood pressure.},
  language  = {en}
}
@article{OPUS4-12959,
  title     = {Hunt for new phenomena using large jet multiplicities and missing transverse momentum with ATLAS in 4.7 fb\(^{-1}\) of √s=7TeV proton-proton collisions},
  series = {The Journal of High Energy Physics},
  volume    = {07},
  journal   = {The Journal of High Energy Physics},
  number    = {167},
  organization    = {ATLAS Collaboration},
  doi       = {10.1007/JHEP07(2012)167},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-129591},
  year      = {2012},
  abstract  = {Results are presented of a search for new particles decaying to large numbers of jets in association with missing transverse momentum, using 4.7 fb\(^{-1}\) of pp collision data at √s=7TeV collected by the ATLAS experiment at the Large Hadron Collider in 2011. The event selection requires missing transverse momentum, no isolated electrons or muons, and from ≥6 to ≥9 jets. No evidence is found for physics beyond the Standard Model. The results are interpreted in the context of a MSUGRA/CMSSM supersymmetric model, where, for large universal scalar mass m 0, gluino masses smaller than 840 GeV are excluded at the 95\% confidence level, extending previously published limits. Within a simplified model containing only a gluino octet and a neutralino, gluino masses smaller than 870 GeV are similarly excluded for neutralino masses below 100 GeV.},
  language  = {en}
}
@article{HansenSeilerRumpfetal.2012,
  author    = {Hansen, Niels and Seiler, Carola and Rumpf, Julian and Kraft, Peter and Dlaske, Henry and Abele-Horn, Marianne and Muellges, Wolfgang},
  title     = {Human Tuberculous Meningitis Caused by \(Mycobacterium\) \(caprae\)},
  series = {Case Reports in Neurology},
  volume    = {4},
  journal   = {Case Reports in Neurology},
  number    = {1},
  doi       = {10.1159/000337299},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-123425},
  pages     = {54-60},
  year      = {2012},
  abstract  = {INTRODUCTION: Tuberculous meningitis (TM) causes substantial morbidity and mortality in humans. Human TM has been known to be induced by bacteria from the Mycobacterium tuberculosis complex (MTBC), such as M. tuberculosis and M. bovis. CASE PRESENTATION: We describe a case of meningitis treated with fosfomycin, which showed partial effectiveness in an 80-year-old patient. After a lethal myocardial infarction, M. caprae (MC) was identified in cerebrospinal fluid culture. This isolated acid-fast organism was first identified as MTBC by MTBC-specific PCR (16S rDNA-PCR). Furthermore, species-specific identification of the isolate was done by gyrB PCR-restriction fragment length polymorphism analysis of a part of gyrB DNA. Colony morphology of the isolated MC strain showed dysgonic growth on Lowenstein-Jensen medium. The strain was susceptible to pyrazinamide (PZA). CONCLUSION: This isolated strain was convincingly identified as MC according to the phenotypic and genotypic characteristics and PZA sensitivity. This is the first report of MC causing TM.},
  language  = {en}
}
@article{VieiraJonesDanonetal.2012,
  author    = {Vieira, Jacqueline and Jones, Alex R. and Danon, Antoine and Sakuma, Michiyo and Hoang, Nathalie and Robles, David and Tait, Shirley and Heyes, Derren J. and Picot, Marie and Yoshii, Taishi and Helfrich-F{\"o}rster, Charlotte and Soubigou, Guillaume and Coppee, Jean-Yves and Klarsfeld, Andr{\´e} and Rouyer, Francois and Scrutton, Nigel S. and Ahmad, Margaret},
  title     = {Human Cryptochrome-1 Confers Light Independent Biological Activity in Transgenic Drosophila Correlated with Flavin Radical Stability},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {3},
  doi       = {10.1371/journal.pone.0031867},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134513},
  pages     = {e31867},
  year      = {2012},
  abstract  = {Cryptochromes are conserved flavoprotein receptors found throughout the biological kingdom with diversified roles in plant development and entrainment of the circadian clock in animals. Light perception is proposed to occur through flavin radical formation that correlates with biological activity in vivo in both plants and Drosophila. By contrast, mammalian (Type II) cryptochromes regulate the circadian clock independently of light, raising the fundamental question of whether mammalian cryptochromes have evolved entirely distinct signaling mechanisms. Here we show by developmental and transcriptome analysis that Homo sapiens cryptochrome - 1 (HsCRY1) confers biological activity in transgenic expressing Drosophila in darkness, that can in some cases be further stimulated by light. In contrast to all other cryptochromes, purified recombinant HsCRY1 protein was stably isolated in the anionic radical flavin state, containing only a small proportion of oxidized flavin which could be reduced by illumination. We conclude that animal Type I and Type II cryptochromes may both have signaling mechanisms involving formation of a flavin radical signaling state, and that light independent activity of Type II cryptochromes is a consequence of dark accumulation of this redox form in vivo rather than of a fundamental difference in signaling mechanism.},
  language  = {en}
}
@article{RauBaurGeier2012,
  author    = {Rau, Monika and Baur, Katharina and Geier, Andreas},
  title     = {Host Genetic Variants in the Pathogenesis of Hepatitis C.},
  series = {Viruses},
  volume    = {4},
  journal   = {Viruses},
  number    = {12},
  doi       = {10.3390/v4123281},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-123611},
  pages     = {3281-302},
  year      = {2012},
  abstract  = {Direct-acting antiviral drugs (DAAs) are currently replacing antiviral therapy for Hepatitis C infection. Treatment related side effects are even worse and the emergence of resistant viruses must be avoided because of the direct-antiviral action. Altogether it remains a challenge to take treatment decisions in a clinical setting with cost restrictions. Genetic host factors are hereby essential to implement an individualized treatment concept. In recent years results on different genetic variants have been published with a strong association with therapy response, fibrosis and treatment-related side effects. Polymorphisms of the IL28B gene were identified as accurate predictors for therapy response and spontaneous clearance of HCV infection and are already used for diagnostic decisions. For RBV-induced side effects, such as hemolytic anemia, associations to genetic variants of inosine triphosphatase (ITPA) were described and different SLC28 transporters for RBV-uptake have been successfully analyzed. Fibrosis progression has been associated with variants of Vitamin D receptor (VDR) and ABCB11 (bile salt export pump). Cirrhotic patients especially have a high treatment risk and low therapy response, so that personalized antiviral treatment is mandatory. This review focuses on different host genetic variants in the pathogenesis of Hepatitis C at the beginning of a new area of treatment.},
  language  = {en}
}
@article{NaidooDuPreezStuartHilletal.2012,
  author    = {Naidoo, Robin and Du Preez, Pierre and Stuart-Hill, Greg and Jago, Mark and Wegmann, Martin},
  title     = {Home on the Range: Factors Explaining Partial Migration of African Buffalo in a Tropical Environment},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {5},
  doi       = {10.1371/journal.pone.0036527},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134935},
  pages     = {e36527},
  year      = {2012},
  abstract  = {Partial migration (when only some individuals in a population undertake seasonal migrations) is common in many species and geographical contexts. Despite the development of modern statistical methods for analyzing partial migration, there have been no studies on what influences partial migration in tropical environments. We present research on factors affecting partial migration in African buffalo (Syncerus caffer) in northeastern Namibia. Our dataset is derived from 32 satellite tracking collars, spans 4 years and contains over 35,000 locations. We used remotely sensed data to quantify various factors that buffalo experience in the dry season when making decisions on whether and how far to migrate, including potential man-made and natural barriers, as well as spatial and temporal heterogeneity in environmental conditions. Using an information-theoretic, non-linear regression approach, our analyses showed that buffalo in this area can be divided into 4 migratory classes: migrants, non-migrants, dispersers, and a new class that we call "expanders". Multimodel inference from least-squares regressions of wet season movements showed that environmental conditions (rainfall, fires, woodland cover, vegetation biomass), distance to the nearest barrier (river, fence, cultivated area) and social factors (age, size of herd at capture) were all important in explaining variation in migratory behaviour. The relative contributions of these variables to partial migration have not previously been assessed for ungulates in the tropics. Understanding the factors driving migratory decisions of wildlife will lead to better-informed conservation and land-use decisions in this area.},
  language  = {en}
}
@article{KasangUlmerDonhauseretal.2012,
  author    = {Kasang, Christa and Ulmer, Albrecht and Donhauser, Norbert and Schmidt, Barabara and Stich, August and Klinker, Hartwig and Kalluvya, Samuel and Koutsilieri, Eleni and Rethwilm, Axel and Scheller, Carsten},
  title     = {HIV patients treated with low-dose prednisolone exhibit lower immune activation than untreated patients},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75100},
  year      = {2012},
  abstract  = {Background: HIV-associated general immune activation is a strong predictor for HIV disease progression, suggesting that chronic immune activation may drive HIV pathogenesis. Consequently, immunomodulating agents may decelerate HIV disease progression. Methods: In an observational study, we determined immune activation in HIV patients receiving low-dose (5 mg/day) prednisolone with or without highly-active antiretroviral therapy (HAART) compared to patients without prednisolone treatment. Lymphocyte activation was determined by flow cytometry detecting expression of CD38 on CD8(+) T cells. The monocyte activation markers sCD14 and LPS binding protein (LBP) as well as inflammation markers soluble urokinase plasminogen activated receptor (suPAR) and sCD40L were determined from plasma by ELISA. Results: CD38-expression on CD8+ T lymphocytes was significantly lower in prednisolone-treated patients compared to untreated patients (median 55.40\% [percentile range 48.76-67.70] versus 73.34\% [65.21-78.92], p = 0.0011, Mann-Whitney test). Similarly, we detected lower levels of sCD14 (3.6 μg/ml [2.78-5.12] vs. 6.11 μg/ml [4.58-7.70]; p = 0.0048), LBP (2.18 ng/ml [1.59-2.87] vs. 3.45 ng/ml [1.84-5.03]; p = 0.0386), suPAR antigen (2.17 μg/ml [1.65-2.81] vs. 2.56 μg/ml [2.24-4.26]; p = 0.0351) and a trend towards lower levels of sCD40L (2.70 pg/ml [1.90-4.00] vs. 3.60 pg/ml [2.95-5.30]; p = 0.0782). Viral load in both groups was similar (0.8 × 105 ng/ml [0.2-42.4 × 105] vs. 1.1 × 105 [0.5-12.2 × 105]; p = 0.3806). No effects attributable to prednisolone were observed when patients receiving HAART in combination with prednisolone were compared to patients who received HAART alone. Conclusions: Patients treated with low-dose prednisolone display significantly lower general immune activation than untreated patients. Further longitudinal studies are required to assess whether treatment with low-dose prednisolone translates into differences in HIV disease progression.},
  subject      = {HIV},
  language  = {en}
}
@article{GrundmeierHammWeissbrichetal.2012,
  author    = {Grundmeier, Natalie and Hamm, Henning and Weissbrich, Benedikt and Lang, Sabrina Christine and Br{\"o}cker, Eva-Bettina and Kerstan, Andreas},
  title     = {High-risk human papillomavirus infection in Bowen's disease of the nail unit: report of three cases and review of the literature},
  series = {Dermatology},
  volume    = {223},
  journal   = {Dermatology},
  number    = {4},
  issn      = {1018-8665},
  doi       = {10.1159/000335371},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-196638},
  pages     = {293 -- 300},
  year      = {2012},
  abstract  = {Background: Bowen's disease (BD) of the nail unit is associated with human papillomavirus (HPV) infection. Objective: This study aimed to investigate the frequency of high-risk HPV infection, gender, age and digital distribution in this condition. Methods: Biopsy specimens of 3 consecutive cases with periungual BD were investigated for the presence of HPV DNA by in situ hybridization and by polymerase chain reaction (PCR). Furthermore, 74 cases of ungual BD conducted with HPV genotyping as reported in the literature were reviewed. Results: PCR of biopsy specimens revealed in 2 cases infection with HPV-16 and in 1 case with HPV-73. Additionally, in 1 HPV-16-positive case HPV-31/33 was detected by in situ hybridization. In line, review of the literature demonstrated a clear association of HPV-positive BD with high-risk HPV types. Interestingly, age at diagnosis was significantly lower in women. Whereas in both genders the second to fourth fingers on both hands were commonly diseased, only in men the thumbs were also prominently affected. Conclusions: Infection with high-risk HPV types is common in BD of the nail unit suggesting the aetiological cause. Therefore, patients and partners should be closely followed up for digital and genital HPV-associated lesions.},
  language  = {en}
}
@article{RoehrichNgwaWiesneretal.2012,
  author    = {R{\"o}hrich, Christian Rene and Ngwa, Che Julius and Wiesner, Jochen and Schmidtberg, Henrike and Degenkolb, Thomas and Kollewe, Christian and Fischer, Rainer and Pradel, Gabriele and Vilcinskas, Andreas},
  title     = {Harmonine, a defence compound from the harlequin ladybird, inhibits mycobacterial growth and demonstrates multi-stage antimalarial activity},
  series = {Biology Letters},
  volume    = {8},
  journal   = {Biology Letters},
  doi       = {10.1098/rsbl.2011.0760},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127079},
  pages     = {308-311},
  year      = {2012},
  abstract  = {The harlequin ladybird beetle Harmonia axyridis has been introduced in many countries as a biological control agent, but has become an invasive species threatening the biodiversity of native ladybirds. Its invasive success has been attributed to its vigorous resistance against diverse pathogens. This study demonstrates that harmonine ((17R,9Z)-1,17-diaminooctadec-9-ene), which is present in H. axyridis haemolymph, displays broad-spectrum antimicrobial activity that includes human pathogens. Antibacterial activity is most pronounced against fast-growing mycobacteria and Mycobacterium tuberculosis, and the growth of both chloroquine-sensitive and -resistant Plasmodium falciparum strains is inhibited. Harmonine displays gametocytocidal activity, and inhibits the exflagellation of microgametocytes and zygote formation. In an Anopheles stephensi mosquito feeding model, harmonine displays transmission-blocking activity.},
  language  = {en}
}
@article{StraussMoskalenkoTiurbeetal.2012,
  author    = {Strauss, Armin and Moskalenko, Vasily and Tiurbe, Christian and Chodnevskaja, Irina and Timm, Stephan and Wiegering, Verena A. and Germer, Chrioph Thomas and Ulrichs, Karin},
  title     = {Goettingen Minipigs (GMP): Comparison of Two Different Models for Inducing Diabetes},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75119},
  year      = {2012},
  abstract  = {Purpose: Preclinical experiments on large animals are indispensable for evaluating the effectiveness of diabetes therapies. Miniature swine are well suited for such studies due to their physiological and pathophysiological responses. Methods: We compare two methods for inducing diabetes in Goettingen minipigs (GMP), in five with the beta cell toxin streptozotocin (STZ) and in five other GMP by total pancreatectomy (PE). Glucose homeostasis was assessed with the intravenous glucose-tolerance test (IVGTT) and continual monitoring of interstitial glucose levels. At conclusion of the observation period, the pancreata were examined histologically. Three non-diabetic GMP served as control group. Results: The IVGTT revealed markedly diabetic profiles in both GMP groups. STZ-GMP were found to harbor residual C-peptides and scattered insulin-positive cells in the pancreas. PE-GMP survived the total pancreatectomy only with intensive postoperative care. Conclusions: Although both methods reliably induced diabetes in GMP, the PE-GMP clearly had more health problems and required a greater expenditure of time and resources. The PE-GMP model, however, was better at eliminating endogenous insulin and C-peptide than the STZ-GMP model.},
  subject      = {G{\"o}ttingen},
  language  = {en}
}
@article{SchaeferVogelVillmann2012,
  author    = {Schaefer, Natscha and Vogel, Nicolas and Villmann, Carmen},
  title     = {Glycine receptor mutants of the mouse: what are possible routes of inhibitory compensation?},
  series = {Frontiers in Molecular Neuroscience},
  volume    = {5},
  journal   = {Frontiers in Molecular Neuroscience},
  number    = {98},
  doi       = {10.3389/fnmol.2012.00098},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-123839},
  year      = {2012},
  abstract  = {Defects in glycinergic inhibition result in a complex neuromotor disorder in humans known as hyperekplexia (OMIM 149400) with similar phenotypes in rodents characterized by an exaggerated startle reflex and hypertonia. Analogous to genetic defects in humans single point mutations, microdeletions, or insertions in the Glra1 gene but also in the Glrb gene underlie the pathology in mice. The mutations either localized in the (spasmodic, oscillator, cincinnati, Nmf11) or the (spastic) subunit of the glycine receptor (GlyR) are much less tolerated in mice than in humans, leaving the question for the existence of different regulatory elements of the pathomechanisms in humans and rodents. In addition to the spontaneous mutations, new insights into understanding of the regulatory pathways in hyperekplexia or glycine encephalopathy arose from the constantly increasing number of knock-out as well as knock-in mutants of GlyRs. Over the last five years, various efforts using in vivo whole cell recordings provided a detailed analysis of the kinetic parameters underlying glycinergic dysfunction. Presynaptic compensation as well as postsynaptic compensatory mechanisms in these mice by other GlyR subunits or GABA(A) receptors, and the role of extra-synaptic GlyRs is still a matter of debate. A recent study on the mouse mutant oscillator displayed a novel aspect for compensation of functionality by complementation of receptor domains that fold independently. This review focuses on defects in glycinergic neurotransmission in mice discussed with the background of human hyperekplexia en route to strategies of compensation.},
  language  = {en}
}
@article{LioliouSharmaCaldelarietal.2012,
  author    = {Lioliou, Efthimia and Sharma, Cynthia M. and Caldelari, Isabelle and Helfer, Anne-Catherine and Fechter, Pierre and Vandenesch, Fran{\c{c}}ois and Vogel, J{\"o}rg and Romby, Pascale},
  title     = {Global Regulatory Functions of the Staphylococcus aureus Endoribonuclease III in Gene Expression},
  series = {PLoS Genetics},
  volume    = {8},
  journal   = {PLoS Genetics},
  number    = {6},
  doi       = {10.1371/journal.pgen.1002782},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127219},
  pages     = {e1002782},
  year      = {2012},
  abstract  = {RNA turnover plays an important role in both virulence and adaptation to stress in the Gram-positive human pathogen Staphylococcus aureus. However, the molecular players and mechanisms involved in these processes are poorly understood. Here, we explored the functions of S. aureus endoribonuclease III (RNase III), a member of the ubiquitous family of double-strand-specific endoribonucleases. To define genomic transcripts that are bound and processed by RNase III, we performed deep sequencing on cDNA libraries generated from RNAs that were co-immunoprecipitated with wild-type RNase III or two different cleavage-defective mutant variants in vivo. Several newly identified RNase III targets were validated by independent experimental methods. We identified various classes of structured RNAs as RNase III substrates and demonstrated that this enzyme is involved in the maturation of rRNAs and tRNAs, regulates the turnover of mRNAs and non-coding RNAs, and autoregulates its synthesis by cleaving within the coding region of its own mRNA. Moreover, we identified a positive effect of RNase III on protein synthesis based on novel mechanisms. RNase III-mediated cleavage in the 5′ untranslated region (5′UTR) enhanced the stability and translation of cspA mRNA, which encodes the major cold-shock protein. Furthermore, RNase III cleaved overlapping 5′UTRs of divergently transcribed genes to generate leaderless mRNAs, which constitutes a novel way to co-regulate neighboring genes. In agreement with recent findings, low abundance antisense RNAs covering 44\% of the annotated genes were captured by co-immunoprecipitation with RNase III mutant proteins. Thus, in addition to gene regulation, RNase III is associated with RNA quality control of pervasive transcription. Overall, this study illustrates the complexity of post-transcriptional regulation mediated by RNase III.},
  language  = {en}
}
@article{TretterMukherjeeMaricetal.2012,
  author    = {Tretter, Verena and Mukherjee, Jayanta and Maric, Hans-Michael and Schindelin, Hermann and Sieghart, Werner and Moss, Stephen J.},
  title     = {Gephyrin, the enigmatic organizer at GABAergic synapses},
  series = {Frontiers in Cellular Neuroscience},
  volume    = {6},
  journal   = {Frontiers in Cellular Neuroscience},
  number    = {23},
  doi       = {10.3389/fncel.2012.00023},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-133356},
  year      = {2012},
  abstract  = {GABA(A) receptors are clustered at synaptic sites to achieve a high density of postsynaptic receptors opposite the input axonal terminals. This allows for an efficient propagation of GABA mediated signals, which mostly result in neuronal inhibition. A key organizer for inhibitory synaptic receptors is the 93 kDa protein gephyrin that forms oligomeric superstructures beneath the synaptic area. Gephyrin has long been known to be directly associated with glycine receptor beta subunits that mediate synaptic inhibition in the spinal cord. Recently, synaptic GABA(A) receptors have also been shown to directly interact with gephyrin and interaction sites have been identified and mapped within the intracellular loops of the GABA(A) receptor alpha 1, alpha 2, and alpha 3 subunits. Gephyrin-binding to GABA(A) receptors seems to be at least one order of magnitude weaker than to glycine receptors (GlyRs) and most probably is regulated by phosphorylation. Gephyrin not only has a structural function at synaptic sites, but also plays a crucial role in synaptic dynamics and is a platform for multiple protein-protein interactions, bringing receptors, cytoskeletal proteins and downstream signaling proteins into close spatial proximity.},
  language  = {en}
}
@article{KirylukYifuSannaCherchietal.2012,
  author    = {Kiryluk, Krzysztof and Yifu, Li and Sanna-Cherchi, Simone and Rohanizadegan, Mersedeh and Suzuki, Hitoshi and Eitner, Frank and Snyder, Holly J. and Choi, Murim and Hou, Ping and Scolari, Francesco and Izzi, Claudia and Gigante, Maddalena and Gesualdo, Loreto and Savoldi, Silvana and Amoroso, Antonio and Cusi, Daniele and Zamboli, Pasquale and Julian, Bruce A. and Novak, Jan and Wyatt, Robert J. and Mucha, Krzysztof and Perola, Markus and Kristiansson, Kati and Viktorin, Alexander and Magnusson, Patrik K. and Thorleifsson, Gudmar and Thorsteinsdottir, Unnur and Stefansson, Kari and Boland, Anne and Metzger, Marie and Thibaudin, Lise and Wanner, Christoph and Jager, Kitty J. and Goto, Shin and Maixnerova, Dita and Karnib, Hussein H. and Nagy, Judit and Panzer, Ulf and Xie, Jingyuan and Chen, Nan and Tesar, Vladimir and Narita, Ichiei and Berthoux, Francois and Floege, J{\"u}rgen and Stengel, Benedicte and Zhang, Hong and Lifton, Richard P. and Gharavi, Ali G.},
  title     = {Geographic Differences in Genetic Susceptibility to IgA Nephropathy: GWAS Replication Study and Geospatial Risk Analysis},
  series = {PLoS Genetics},
  volume    = {8},
  journal   = {PLoS Genetics},
  number    = {6},
  doi       = {10.1371/journal.pgen.1002765},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-130195},
  pages     = {e1002765},
  year      = {2012},
  abstract  = {IgA nephropathy (IgAN), major cause of kidney failure worldwide, is common in Asians, moderately prevalent in Europeans, and rare in Africans. It is not known if these differences represent variation in genes, environment, or ascertainment. In a recent GWAS, we localized five IgAN susceptibility loci on Chr.6p21 (HLA-DQB1/DRB1, PSMB9/TAP1, and DPA1/DPB2 loci), Chr.1q32 (CFHR3/R1 locus), and Chr.22q12 (HORMAD2 locus). These IgAN loci are associated with risk of other immune-mediated disorders such as type I diabetes, multiple sclerosis, or inflammatory bowel disease. We tested association of these loci in eight new independent cohorts of Asian, European, and African-American ancestry (N = 4,789), followed by meta-analysis with risk-score modeling in 12 cohorts (N = 10,755) and geospatial analysis in 85 world populations. Four susceptibility loci robustly replicated and all five loci were genome-wide significant in the combined cohort (P = 5x10\(^{-32}\) 3x10\(^{-10}\), with heterogeneity detected only at the PSMB9/TAP1 locus (I\(^{-2}\) = 0.60). Conditional analyses identified two new independent risk alleles within the HLA-DQB1/DRB1 locus, defining multiple risk and protective haplotypes within this interval. We also detected a significant genetic interaction, whereby the odds ratio for the HORMAD2 protective allele was reversed in homozygotes for a CFHR3/R1 deletion (P = 2.5x10\(^{-4}\)). A seven-SNP genetic risk score, which explained 4.7\% of overall IgAN risk, increased sharply with Eastward and Northward distance from Africa (r = 0.30, P = 3x10\(^{-128}\)). This model paralleled the known East-West gradient in disease risk. Moreover, the prediction of a South-North axis was confirmed by registry data showing that the prevalence of IgAN-attributable kidney failure is increased in Northern Europe, similar to multiple sclerosis and type I diabetes. Variation at IgAN susceptibility loci correlates with differences in disease prevalence among world populations. These findings inform genetic, biological, and epidemiological investigations of IgAN and permit cross-comparison with other complex traits that share genetic risk loci and geographic patterns with IgAN.},
  language  = {en}
}
@article{KniesSchusterAmezianeetal.2012,
  author    = {Knies, Kerstin and Schuster, Beatrice and Ameziane, Najim and Rooimans, Martin and Bettecken, Thomas and de Winter, Johan and Schindler, Detlev},
  title     = {Genotyping of Fanconi Anemia Patients by Whole Exome Sequencing: Advantages and Challenges},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-77985},
  year      = {2012},
  abstract  = {Fanconi anemia (FA) is a rare genomic instability syndrome. Disease-causing are biallelic mutations in any one of at least 15 genes encoding members of the FA/BRCA pathway of DNA-interstrand crosslink repair. Patients are diagnosed based upon phenotypical manifestationsand the diagnosis of FA is confirmed by the hypersensitivity of cells to DNA interstrand crosslinking agents. Customary molecular diagnostics has become increasingly cumbersome, time-consuming and expensive the more FA genes have been identified. We performed Whole Exome Sequencing (WES) in four FA patients in order to investigate the potential of this method for FA genotyping. In search of an optimal WES methodology we explored different enrichment and sequencing techniques. In each case we were able to identify the pathogenic mutations so that WES provided both, complementation group assignment and mutation detection in a single approach. The mutations included homozygous and heterozygous single base pair substitutions and a two-base-pair duplication in FANCJ, -D1, or - D2. Different WES strategies had no critical influence on the individual outcome. However, database errors and in particular pseudogenes impose obstacles that may prevent correct data perception and interpretation, and thus cause pitfalls. With these difficulties in mind, our results show that WES is a valuable tool for the molecular diagnosis of FA and a sufficiently safe technique, capable of engaging increasingly in competition with classical genetic approaches.},
  subject      = {Medizin},
  language  = {en}
}
@article{AgostonLiHaslingeretal.2012,
  author    = {Agoston, Zsuzsa and Li, Naixin and Haslinger, Anja and Wizenmann, Andrea and Schulte, Dorothea},
  title     = {Genetic and physical interaction of Meis2, Pax3 and Pax7 during dorsal midbrain development},
  series = {BMC Developmental Biology},
  volume    = {12},
  journal   = {BMC Developmental Biology},
  number    = {10},
  doi       = {10.1186/1471-213X-12-10},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-132626},
  year      = {2012},
  abstract  = {Background: During early stages of brain development, secreted molecules, components of intracellular signaling pathways and transcriptional regulators act in positive and negative feed-back or feed-forward loops at the mid-hindbrain boundary. These genetic interactions are of central importance for the specification and subsequent development of the adjacent mid-and hindbrain. Much less, however, is known about the regulatory relationship and functional interaction of molecules that are expressed in the tectal anlage after tectal fate specification has taken place and tectal development has commenced. Results: Here, we provide experimental evidence for reciprocal regulation and subsequent cooperation of the paired-type transcription factors Pax3, Pax7 and the TALE-homeodomain protein Meis2 in the tectal anlage. Using in ovo electroporation of the mesencephalic vesicle of chick embryos we show that (i) Pax3 and Pax7 mutually regulate each other's expression in the mesencephalic vesicle, (ii) Meis2 acts downstream of Pax3/7 and requires balanced expression levels of both proteins, and (iii) Meis2 physically interacts with Pax3 and Pax7. These results extend our previous observation that Meis2 cooperates with Otx2 in tectal development to include Pax3 and Pax7 as Meis2 interacting proteins in the tectal anlage. Conclusion: The results described here suggest a model in which interdependent regulatory loops involving Pax3 and Pax7 in the dorsal mesencephalic vesicle modulate Meis2 expression. Physical interaction with Meis2 may then confer tectal specificity to a wide range of otherwise broadly expressed transcriptional regulators, including Otx2, Pax3 and Pax7.},
  language  = {en}
}
@article{BurekSalvadorFoerster2012,
  author    = {Burek, Malgorzata and Salvador, Ellaine and F{\"o}rster, Carola Y.},
  title     = {Generation of an Immortalized Murine Brain Microvascular Endothelial Cell Line as an In Vitro Blood Brain Barrier Model},
  series = {Journal of Visualized Experiments},
  volume    = {66},
  journal   = {Journal of Visualized Experiments},
  number    = {e4022},
  doi       = {10.3791/4022},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-126702},
  year      = {2012},
  abstract  = {Epithelial and endothelial cells (EC) are building paracellular barriers which protect the tissue from the external and internal environment. The blood-brain barrier (BBB) consisting of EC, astrocyte end-feet, pericytes and the basal membrane is responsible for the protection and homeostasis of the brain parenchyma. In vitro BBB models are common tools to study the structure and function of the BBB at the cellular level. A considerable number of different in vitro BBB models have been established for research in different laboratories to date. Usually, the cells are obtained from bovine, porcine, rat or mouse brain tissue (discussed in detail in the review by Wilhelm et al. 1). Human tissue samples are available only in a restricted number of laboratories or companies 2,3. While primary cell preparations are time consuming and the EC cultures can differ from batch to batch, the establishment of immortalized EC lines is the focus of scientific interest. Here, we present a method for establishing an immortalized brain microvascular EC line from neonatal mouse brain. We describe the procedure step-by-step listing the reagents and solutions used. The method established by our lab allows the isolation of a homogenous immortalized endothelial cell line within four to five weeks. The brain microvascular endothelial cell lines termed cEND 4 (from cerebral cortex) and cerebEND 5 (from cerebellar cortex), were isolated according to this procedure in the F{\"o}rster laboratory and have been effectively used for explanation of different physiological and pathological processes at the BBB. Using cEND and cerebEND we have demonstrated that these cells respond to glucocorticoid- 4,6-9 and estrogen-treatment 10 as well as to pro-infammatory mediators, such as TNFalpha 5,8. Moreover, we have studied the pathology of multiple sclerosis 11 and hypoxia 12,13 on the EC-level. The cEND and cerebEND lines can be considered as a good tool for studying the structure and function of the BBB, cellular responses of ECs to different stimuli or interaction of the EC with lymphocytes or cancer cells.},
  language  = {en}
}
@article{WeberScholzDomschkeetal.2012,
  author    = {Weber, Heike and Scholz, Claus J{\"u}rgen and Domschke, Katharina and Baumann, Christian and Klauke, Benedikt and Jacob, Christian P. and Maier, Wolfgang and Fritze, J{\"u}rgen and Bandelow, Borwin and Zwanzger, Peter Michael and Lang, Thomas and Fehm, Lydia and Str{\"o}hle, Andreas and Hamm, Alfons and Gerlach, Alexander L. and Alpers, Georg W. and Kircher, Tilo and Wittchen, Hans-Ulrich and Arolt, Volker and Pauli, Paul and Deckert, J{\"u}rgen and Reif, Andreas},
  title     = {Gender Differences in Associations of Glutamate Decarboxylase 1 Gene (GAD1) Variants with Panic Disorder},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75830},
  year      = {2012},
  abstract  = {Background: Panic disorder is common (5\% prevalence) and females are twice as likely to be affected as males. The heritable component of panic disorder is estimated at 48\%. Glutamic acid dehydrogenase GAD1, the key enzyme for the synthesis of the inhibitory and anxiolytic neurotransmitter GABA, is supposed to influence various mental disorders, including mood and anxiety disorders. In a recent association study in depression, which is highly comorbid with panic disorder, GAD1 risk allele associations were restricted to females. Methodology/Principal Findings: Nineteen single nucleotide polymorphisms (SNPs) tagging the common variation in GAD1 were genotyped in two independent gender and age matched case-control samples (discovery sample n = 478; replication sample n = 584). Thirteen SNPs passed quality control and were examined for gender-specific enrichment of risk alleles associated with panic disorder by using logistic regression including a genotype6gender interaction term. The latter was found to be nominally significant for four SNPs (rs1978340, rs3762555, rs3749034, rs2241165) in the discovery sample; of note, the respective minor/risk alleles were associated with panic disorder only in females. These findings were not confirmed in the replication sample; however, the genotype6gender interaction of rs3749034 remained significant in the combined sample. Furthermore, this polymorphism showed a nominally significant association with the Agoraphobic Cognitions Questionnaire sum score. Conclusions/Significance: The present study represents the first systematic evaluation of gender-specific enrichment of risk alleles of the common SNP variation in the panic disorder candidate gene GAD1. Our tentative results provide a possible explanation for the higher susceptibility of females to panic disorder.},
  subject      = {Medizin},
  language  = {en}
}
@article{AhmadWolberEckardtetal.2012,
  author    = {Ahmad, Ruhel and Wolber, Wanja and Eckardt, Sigrid and Koch, Philipp and Schmitt, Jessica and Semechkin, Ruslan and Geis, Christian and Heckmann, Manfred and Br{\"u}stle, Oliver and McLaughlin, John K. and Sir{\´e}n, Anna-Leena and M{\"u}ller, Albrecht M.},
  title     = {Functional Neuronal Cells Generated by Human Parthenogenetic Stem Cells},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {8},
  doi       = {10.1371/journal.pone.0042800},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-130268},
  pages     = {e42800},
  year      = {2012},
  abstract  = {Parent of origin imprints on the genome have been implicated in the regulation of neural cell type differentiation. The ability of human parthenogenetic (PG) embryonic stem cells (hpESCs) to undergo neural lineage and cell type-specific differentiation is undefined. We determined the potential of hpESCs to differentiate into various neural subtypes. Concurrently, we examined DNA methylation and expression status of imprinted genes. Under culture conditions promoting neural differentiation, hpESC-derived neural stem cells (hpNSCs) gave rise to glia and neuron-like cells that expressed subtype-specific markers and generated action potentials. Analysis of imprinting in hpESCs and in hpNSCs revealed that maternal-specific gene expression patterns and imprinting marks were generally maintained in PG cells upon differentiation. Our results demonstrate that despite the lack of a paternal genome, hpESCs generate proliferating NSCs that are capable of differentiation into physiologically functional neuron-like cells and maintain allele-specific expression of imprinted genes. Thus, hpESCs can serve as a model to study the role of maternal and paternal genomes in neural development and to better understand imprinting-associated brain diseases.},
  language  = {en}
}
@article{SturmHessWeibeletal.2012,
  author    = {Sturm, Julia B. and Hess, Michael and Weibel, Stephanie and Chen, Nanhei G. and Yu, Yong A. and Zhang, Quian and Donat, Ulrike and Reiss, Cora and Gambaryan, Stepan and Krohne, Georg and Stritzker, Jochen and Szalay, Aladar A.},
  title     = {Functional hyper-IL-6 from vaccinia virus-colonized tumors triggers platelet formation and helps to alleviate toxicity of mitomycin C enhanced virus therapy},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75224},
  year      = {2012},
  abstract  = {Background: Combination of oncolytic vaccinia virus therapy with conventional chemotherapy has shown promise for tumor therapy. However, side effects of chemotherapy including thrombocytopenia, still remain problematic. Methods: Here, we describe a novel approach to optimize combination therapy of oncolytic virus and chemotherapy utilizing virus-encoding hyper-IL-6, GLV-1h90, to reduce chemotherapy-associated side effects. Results: We showed that the hyper-IL-6 cytokine was successfully produced by GLV-1h90 and was functional both in cell culture as well as in tumor-bearing animals, in which the cytokine-producing vaccinia virus strain was well tolerated. When combined with the chemotherapeutic mitomycin C, the anti-tumor effect of the oncolytic virotherapy was significantly enhanced. Moreover, hyper-IL-6 expression greatly reduced the time interval during which the mice suffered from chemotherapy-induced thrombocytopenia. Conclusion: Therefore, future clinical application would benefit from careful investigation of additional cytokine treatment to reduce chemotherapy-induced side effects.},
  subject      = {Biologie},
  language  = {en}
}
@article{MajounieRentonMoketal.2012,
  author    = {Majounie, Elisa and Renton, Alan E. and Mok, Kin and Dopper, Elise G. P. and Waite, Adrian and Rollinson, Sara and Chi{\`o}, Adriano and Restagno, Gabriella and Nicolaou, Nayia and Simon-Sanchez, Javier and van Swieten, John C. and Abramzon, Yevgeniya and Johnson, Janel O. and Sendtner, Michael and Pamphlett, Roger and Orrell, Richard W. and Mead, Simon and Sidle, Katie C. and Houlden, Henry and Rohrer, Jonathan D. and Morrison, Karen E. and Pall, Hardev and Talbot, Kevin and Ansorge, Olaf and Hernandez, Dena G. and Arepalli, Sampath and Sabatelli, Mario and Mora, Gabriele and Corbo, Massimo and Giannini, Fabio and Calvo, Andrea and Englund, Elisabet and Borghero, Giuseppe and Floris, Gian Luca and Remes, Anne M. and Laaksovirta, Hannu and McCluskey, Leo and Trojanowski, John Q. and Van Deerlin, Vivianna M. and Schellenberg, Gerard D. and Nalls, Michael A. and Drory, Vivian E. and Lu, Chin-Song and Yeh, Tu-Hsueh and Ishiura, Hiroyuki and Takahashi, Yuji and Tsuji, Shoji and Le Ber, Isabelle and Brice, Alexis and Drepper, Carsten and Williams, Nigel and Kirby, Janine and Shaw, Pamela and Hardy, John and Tienari, Pentti J. and Heutink, Peter and Morris, Huw R. and Pickering-Brown, Stuart and Traynor, Bryan J.},
  title     = {Frequency of the C9orf72 hexanucleotide repeat expansion in patients with amyotrophic lateral sclerosis and frontotemporal dementia: a cross-sectional study},
  series = {The Lancet Neurology},
  volume    = {11},
  journal   = {The Lancet Neurology},
  doi       = {10.1016/S1474-4422(12)70043-1},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-154644},
  pages     = {323 -- 330},
  year      = {2012},
  abstract  = {Background We aimed to accurately estimate the frequency of a hexanucleotide repeat expansion in C9orf72 that has been associated with a large proportion of cases of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Methods We screened 4448 patients diagnosed with ALS (El Escorial criteria) and 1425 patients with FTD (Lund-Manchester criteria) from 17 regions worldwide for the GGGGCC hexanucleotide expansion using a repeat-primed PCR assay. We assessed familial disease status on the basis of self-reported family history of similar neurodegenerative diseases at the time of sample collection. We compared haplotype data for 262 patients carrying the expansion with the known Finnish founder risk haplotype across the chromosomal locus. We calculated age-related penetrance using the Kaplan-Meier method with data for 603 individuals with the expansion. Findings In patients with sporadic ALS, we identified the repeat expansion in 236 (7·0\%) of 3377 white individuals from the USA, Europe, and Australia, two (4·1\%) of 49 black individuals from the USA, and six (8·3\%) of 72 Hispanic individuals from the USA. The mutation was present in 217 (39·3\%) of 552 white individuals with familial ALS from Europe and the USA. 59 (6·0\%) of 981 white Europeans with sporadic FTD had the mutation, as did 99 (24·8\%) of 400 white Europeans with familial FTD. Data for other ethnic groups were sparse, but we identified one Asian patient with familial ALS (from 20 assessed) and two with familial FTD (from three assessed) who carried the mutation. The mutation was not carried by the three Native Americans or 360 patients from Asia or the Pacific Islands with sporadic ALS who were tested, or by 41 Asian patients with sporadic FTD. All patients with the repeat expansion had (partly or fully) the founder haplotype, suggesting a one-off expansion occurring about 1500 years ago. The pathogenic expansion was non-penetrant in individuals younger than 35 years, 50\% penetrant by 58 years, and almost fully penetrant by 80 years. Interpretation A common Mendelian genetic lesion in C9orf72 is implicated in many cases of sporadic and familial ALS and FTD. Testing for this pathogenic expansion should be considered in the management and genetic counselling of patients with these fatal neurodegenerative diseases.},
  language  = {en}
}
@article{GuckenbergerHawkinsFlentjeetal.2012,
  author    = {Guckenberger, Matthias and Hawkins, Maria and Flentje, Michael and Sweeney, Reinhart A.},
  title     = {Fractionated radiosurgery for painful spinal metastases: DOSIS - a phase II trial},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75853},
  year      = {2012},
  abstract  = {Background One third of all cancer patients will develop bone metastases and the vertebral column is involved in approximately 70 \% of these patients. Conventional radiotherapy with of 1-10 fractions and total doses of 8-30 Gy is the current standard for painful vertebral metastases; however, the median pain response is short with 3-6 months and local tumor control is limited with these rather low irradiation doses. Recent advances in radiotherapy technology - intensity modulated radiotherapy for generation of highly conformal dose distributions and image-guidance for precise treatment delivery - have made dose-escalated radiosurgery of spinal metastases possible and early results of pain and local tumor control are promising. The current study will investigate efficacy and safety of radiosurgery for painful vertebral metastases and three characteristics will distinguish this study. 1) A prognostic score for overall survival will be used for selection of patients with longer life expectancy to allow for analysis of long-term efficacy and safety. 2) Fractionated radiosurgery will be performed with the number of treatment fractions adjusted to either good (10 fractions) or intermediate (5 fractions) life expectancy. Fractionation will allow inclusion of tumors immediately abutting the spinal cord due to higher biological effective doses at the tumor - spinal cord interface compared to single fraction treatment. 3) Dose intensification will be performed in the involved parts of the vertebrae only, while uninvolved parts are treated with conventional doses using the simultaneous integrated boost concept. Methods / Design It is the study hypothesis that hypo-fractionated image-guided radiosurgery significantly improves pain relief compared to historic data of conventionally fractionated radiotherapy. Primary endpoint is pain response 3 months after radiosurgery, which is defined as pain reduction of ≥2 points at the treated vertebral site on the 0 to 10 Visual Analogue Scale. 60 patients will be included into this two-centre phase II trial. Conclusions Results of this study will refine the methods of patient selection, target volume definition, treatment planning and delivery as well as quality assurance for radiosurgery. It is the intention of this study to form the basis for a future randomized controlled trial comparing conventional radiotherapy with fractionated radiosurgery for palliation of painful vertebral metastases. Trial registration ClinicalTrials.gov Identifier: NCT01594892},
  subject      = {Medizin},
  language  = {en}
}
@article{ReuterSparwasserHuenigetal.2012,
  author    = {Reuter, Dajana and Sparwasser, Tim and H{\"u}nig, Thomas and Schneider-Schaulies, J{\"u}rgen},
  title     = {Foxp3\(^+\) Regulatory T Cells Control Persistence of Viral CNS Infection},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {3},
  doi       = {10.1371/journal.pone.0033989},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134248},
  pages     = {e33989},
  year      = {2012},
  abstract  = {We earlier established a model of a persistent viral CNS infection using two week old immunologically normal (genetically unmodified) mice and recombinant measles virus (MV). Using this model infection we investigated the role of regulatory T cells (Tregs) as regulators of the immune response in the brain, and assessed whether the persistent CNS infection can be modulated by manipulation of Tregs in the periphery. CD4\(^+\) CD25\(^+\) Foxp3\(^+\) Tregs were expanded or depleted during the persistent phase of the CNS infection, and the consequences for the virus-specific immune response and the extent of persistent infection were analyzed. Virus-specific CD8\(^+\) T cells predominantly recognising the H-2D(b)-presented viral hemagglutinin epitope MV-H22-30 (RIVINREHL) were quantified in the brain by pentamer staining. Expansion of Tregs after intraperitoneal (i.p.) application of the superagonistic anti-CD28 antibody D665 inducing transient immunosuppression caused increased virus replication and spread in the CNS. In contrast, depletion of Tregs using diphtheria toxin (DT) in DEREG (depletion of regulatory T cells)-mice induced an increase of virus-specific CD8\(^+\) effector T cells in the brain and caused a reduction of the persistent infection. These data indicate that manipulation of Tregs in the periphery can be utilized to regulate virus persistence in the CNS.},
  language  = {en}
}
@article{AadAbbottAbdallahetal.2012,
  author    = {Aad, G. and Abbott, B. and Abdallah, J. and Abdelalim, A. A. and Abdesselam, A.},
  title     = {Forward-backward correlations and charged-particle azimuthal distributions in pp interactions using the ATLAS detector},
  series = {Journal of High Energy Physics},
  volume    = {7},
  journal   = {Journal of High Energy Physics},
  number    = {19},
  organization    = {ATLAS Collaboration},
  doi       = {10.1007/JHEP07(2012)019},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127336},
  year      = {2012},
  abstract  = {Using inelastic proton-proton interactions at s√=900 GeV and 7 TeV, recorded by the ATLAS detector at the LHC, measurements have been made of the correlations between forward and backward charged-particle multiplicities and, for the first time, between forward and backward charged-particle summed transverse momentum. In addition, jet-like structure in the events is studied by means of azimuthal distributions of charged particles relative to the charged particle with highest transverse momentum in a selected kinematic region of the event. The results are compared with predictions from tunes of the pythia and herwig++ Monte Carlo generators, which in most cases are found to provide a reasonable description of the data.},
  language  = {en}
}
@article{RaslanAlbertWeissenbergerErnestusetal.2012,
  author    = {Raslan, Furat and Albert-Weißenberger, Christiane and Ernestus, Ralf-Ingo and Kleinschnitz, Christoph and Sir{\´e}n, Anna-Leena},
  title     = {Focal brain trauma in the cryogenic lesion model in mice},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75419},
  year      = {2012},
  abstract  = {The method to induce unilateral cryogenic lesions was first described in 1958 by Klatzo. We describe here an adaptation of this model that allows reliable measurement of lesion volume and vasogenic edema by 2, 3, 5-triphenyltetrazolium chloride-staining and Evans blue extravasation in mice. A copper or aluminium cylinder with a tip diameter of 2.5 mm is cooled with liquid nitrogen and placed on the exposed skull bone over the parietal cortex (coordinates from bregma: 1.5 mm posterior, 1.5 mm lateral). The tip diameter and the contact time between the tip and the parietal skull determine the extent of cryolesion. Due to an early damage of the blood brain barrier, the cryogenic cortical injury is characterized by vasogenic edema, marked brain swelling, and inflammation. The lesion grows during the first 24 hours, a process involving complex interactions between endothelial cells, immune cells, cerebral blood flow, and the intracranial pressure. These contribute substantially to the damage from the initial injury. The major advantage of the cryogenic lesion model is the circumscribed and highly reproducible lesion size and location.},
  subject      = {Medizin},
  language  = {en}
}
@article{OwenSauerGaus2012,
  author    = {Owen, Dylan M. and Sauer, Markus and Gaus, Katharina},
  title     = {Fluorescence localization microscopy},
  series = {Communicative \& Integrative Biology},
  volume    = {5},
  journal   = {Communicative \& Integrative Biology},
  number    = {4},
  doi       = {10.4161/cib.20348},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-124416},
  pages     = {345-349},
  year      = {2012},
  abstract  = {Localization microscopy techniques are super-resolution fluorescence imaging methods based on the detection of individual molecules. Despite the relative simplicity of the microscope setups and the availability of commercial instruments, localization microscopy faces unique challenges. While achieving super-resolution is now routine, issues concerning data analysis and interpretation mean that revealing novel biological insights is not. Here, we outline why data analysis and the design of robust test samples may hold the key to harness the full potential of localization microscopy.},
  language  = {en}
}
@article{RakosyStreinzerPaulusetal.2012,
  author    = {Rakosy, Demetra and Streinzer, Martin and Paulus, Hannes F. and Spaethe, Johannes},
  title     = {Floral visual signal increases reproductive success in a sexually deceptive orchid},
  series = {Arthropod-Plant Interactions},
  volume    = {6},
  journal   = {Arthropod-Plant Interactions},
  number    = {4},
  doi       = {10.1007/s11829-012-9217-0},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127209},
  pages     = {671-681},
  year      = {2012},
  abstract  = {Sexually deceptive orchids mimic signals emitted by female insects in order to attract mate-searching males. Specific attraction of the targeted pollinator is achieved by sex pheromone mimicry, which constitutes the major attraction channel. In close vicinity of the flower, visual signals may enhance attraction, as was shown recently in the sexually deceptive orchid Ophrys heldreichii. Here, we conducted an in situ manipulation experiment in two populations of O. heldreichii on Crete to investigate whether the presence/absence of the conspicuous pink perianth affects reproductive success in two natural orchid populations. We estimated reproductive success of three treatment groups (with intact, removed and artificial perianth) throughout the flowering period as pollinaria removal (male reproductive success) and massulae deposition (female reproductive success). Reproductive success was significantly increased by the presence of a strong visual signal—the conspicuous perianth—in one study population, however, not in the second, most likely due to the low pollinator abundance in the latter population. This study provides further evidence that the coloured perianth in O. heldreichii is adaptive and thus adds to the olfactory signal to maximise pollinator attraction and reproductive success.},
  language  = {en}
}
@article{PoppeAndersKneitzetal.2012,
  author    = {Poppe, Lidia Marilia and Anders, Diana and Kneitz, Hermann and Br{\"o}cker, Eva-Bettina and Benoit, Sandrine},
  title     = {Flagellate dermatitis caused by shiitake mushrooms},
  series = {Anais Brasileiros de Dermatologia},
  volume    = {87},
  journal   = {Anais Brasileiros de Dermatologia},
  number    = {3},
  doi       = {10.1590/S0365-05962012000300017 },
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134362},
  pages     = {463-465},
  year      = {2012},
  abstract  = {Shiitake (Lentinus edodes) is the second most consumed mushroom in the world. It has long been known in Asian medicine for its anticarcinogenic, antihypertensive and serum cholesterol level reduction properties. Nevertheless, the consumption of raw or not well-cooked mushrooms may cause skin eruptions which usually occur 24 to 48 hours after ingestion and are characterized by linearly arranged pruritic erythematous papules and plaques. We present a 36-year-old patient that developed typical symptoms 24 hours after consumption of shiitake mushrooms and summarize therapeutic options and particularities of this disease.},
  language  = {en}
}
@article{LikowskiMuehlbergerGerdesetal.2012,
  author    = {Likowski, Katja U. and M{\"u}hlberger, Andreas and Gerdes, Antje B. M. and Wieser, Mattias J. and Pauli, Paul and Weyers, Peter},
  title     = {Facial mimicry and the mirror neuron system: simultaneous acquisition of facial electromyography and functional magnetic resonance imaging},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75813},
  year      = {2012},
  abstract  = {Numerous studies have shown that humans automatically react with congruent facial reactions, i.e., facial mimicry, when seeing a vis-{\´a}-vis' facial expressions. The current experiment is the first investigating the neuronal structures responsible for differences in the occurrence of such facial mimicry reactions by simultaneously measuring BOLD and facial EMG in an MRI scanner. Therefore, 20 female students viewed emotional facial expressions (happy, sad, and angry) of male and female avatar characters. During picture presentation, the BOLD signal as well as M. zygomaticus major and M. corrugator supercilii activity were recorded simultaneously. Results show prototypical patterns of facial mimicry after correction for MR-related artifacts: enhanced M. zygomaticus major activity in response to happy and enhanced M. corrugator supercilii activity in response to sad and angry expressions. Regression analyses show that these congruent facial reactions correlate significantly with activations in the IFG, SMA, and cerebellum. Stronger zygomaticus reactions to happy faces were further associated to increased activities in the caudate, MTG, and PCC. Corrugator reactions to angry expressions were further correlated with the hippocampus, insula, and STS. Results are discussed in relation to core and extended models of the mirror neuron system (MNS).},
  subject      = {Psychologie},
  language  = {en}
}
@article{GrussWieserSchweinbergeretal.2012,
  author    = {Gruss, L. Forest and Wieser, Matthias J. and Schweinberger, Stefan R. and Keil, Andreas},
  title     = {Face-evoked steady-state visual potentials: effects of presentation rate and face inversion},
  series = {Frontiers in Human Neuroscience},
  volume    = {6},
  journal   = {Frontiers in Human Neuroscience},
  number    = {316},
  doi       = {10.3389/fnhum.2012.00316},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134399},
  year      = {2012},
  abstract  = {Face processing can be explored using electrophysiological methods. Research with event-related potentials has demonstrated the so-called face inversion effect, in which the N170 component is enhanced in amplitude and latency to inverted, compared to upright, faces. The present study explored the extent to which repetitive lower-level visual cortical engagement, reflected in flicker steady-state visual evoked potentials (ssVEPs), shows similar amplitude enhancement to face inversion. We also asked if inversion-related ssVEP modulation would be dependent on the stimulation rate at which upright and inverted faces were flickered. To this end, multiple tagging frequencies were used (5, 10, 15, and 20 Hz) across two studies (n=21, n=18). Results showed that amplitude enhancement of the ssVEP for inverted faces was found solely at higher stimulation frequencies (15 and 20 Hz). By contrast, lower frequency ssVEPs did not show this inversion effect. These findings suggest that stimulation frequency affects the sensitivity of ssVEPs to face inversion.},
  language  = {en}
}