@article{AlmadeJongJelusicetal.2016, author = {Alma, Harma and de Jong, Corina and Jelusic, Danijel and Wittmann, Michael and Schuler, Michael and Flokstra-de Blok, Bertine and Kocks, Janwillem and Schultz, Konrad and van der Molen, Thys}, title = {Health status instruments for patients with COPD in pulmonary rehabilitation: defining a minimal clinically important difference}, series = {npj Primary Care Respiration Medicine}, volume = {26}, journal = {npj Primary Care Respiration Medicine}, number = {16041}, doi = {10.1038/npjpcrm.2016.41}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-166327}, year = {2016}, abstract = {The minimal clinically important difference (MCID) defines to what extent change on a health status instrument is clinically relevant, which aids scientists and physicians in measuring therapy effects. This is the first study that aimed to establish the MCID of the Clinical chronic obstructive pulmonary disease (COPD) Questionnaire (CCQ), the COPD Assessment Test (CAT) and the St George's Respiratory Questionnaire (SGRQ) in the same pulmonary rehabilitation population using multiple approaches. In total, 451 COPD patients participated in a 3-week Pulmonary Rehabilitation (PR) programme (58 years, 65\% male, 43 pack-years, GOLD stage II/III/IV 50/39/11\%). Techniques used to assess the MCID were anchor-based approaches, including patient-referencing, criterion-referencing and questionnaire-referencing, and the distribution-based methods standard error of measurement (SEM), 1.96SEM and half standard deviation (0.5s.d.). Patient- and criterion-referencing led to MCID estimates of 0.56 and 0.62 (CCQ); 3.12 and 2.96 (CAT); and 8.40 and 9.28 (SGRQ). Questionnaire-referencing suggested MCID ranges of 0.28-0.61 (CCQ), 1.46-3.08 (CAT) and 6.86-9.47 (SGRQ). The SEM, 1.96SEM and 0.5s.d. were 0.29, 0.56 and 0.46 (CCQ); 3.28, 6.43 and 2.80 (CAT); 5.20, 10.19 and 6.06 (SGRQ). Pooled estimates were 0.52 (CCQ), 3.29 (CAT) and 7.91 (SGRQ) for improvement. MCID estimates differed depending on the method used. Pooled estimates suggest clinically relevant improvements needing to exceed 0.40 on the CCQ, 3.00 on the CAT and 7.00 on the SGRQ for moderate to very severe COPD patients. The MCIDs of the CAT and SGRQ in the literature might be too low, leading to overestimation of treatment effects for patients with COPD.}, language = {en} } @article{RedlichLingnauHolzingeretal.2016, author = {Redlich, Christoph and Lingnau, Benjamin and Holzinger, Steffen and Schlottmann, Elisabeth and Kreinberg, S{\"o}ren and Schneider, Christian and Kamp, Martin and H{\"o}fling, Sven and Wolters, Janik and Reitzenstein, Stephan and L{\"u}dge, Kathy}, title = {Mode-switching induced super-thermal bunching in quantum-dot microlasers}, series = {New Journal of Physics}, volume = {18}, journal = {New Journal of Physics}, number = {063011}, doi = {10.1088/1367-2630/18/6/063011}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-166286}, year = {2016}, abstract = {The super-thermal photon bunching in quantum-dot (QD) micropillar lasers is investigated both experimentally and theoretically via simulations driven by dynamic considerations. Using stochastic multi-mode rate equations we obtain very good agreement between experiment and theory in terms of intensity profiles and intensity-correlation properties of the examined QD micro-laser's emission. Further investigations of the time-dependent emission show that super-thermal photon bunching occurs due to irregular mode-switching events in the bimodal lasers. Our bifurcation analysis reveals that these switchings find their origin in an underlying bistability, such that spontaneous emission noise is able to effectively perturb the two competing modes in a small parameter region. We thus ascribe the observed high photon correlation to dynamical multistabilities rather than quantum mechanical correlations.}, language = {en} } @article{HargartRoyChoudhuryJohnetal.2016, author = {Hargart, F and Roy-Choudhury, K and John, T and Portalupi, S L and Schneider, C and H{\"o}fling, S and Kamp, M and Hughes, S and Michler, P}, title = {Probing different regimes of strong field light-matter interaction with semiconductor quantum dots and few cavity photons}, series = {New Journal of Physics}, volume = {18}, journal = {New Journal of Physics}, doi = {10.1088/1367-2630/aa5198}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-166278}, year = {2016}, abstract = {In this work we present an extensive experimental and theoretical investigation of different regimes of strong field light-matter interaction for cavity-driven quantum dot (QD) cavity systems. The electric field enhancement inside a high-Q micropillar cavity facilitates exceptionally strong interaction with few cavity photons, enabling the simultaneous investigation for a wide range of QD-laser detuning. In case of a resonant drive, the formation of dressed states and a Mollow triplet sideband splitting of up to 45 μeV is measured for amean cavity photon number \(\leq\) 1. In the asymptotic limit of the linear ACStark effect we systematically investigate the power and detuning dependence of more than 400 QDs. Some QD-cavity systems exhibit an unexpected anomalous Stark shift, which can be explained by an extended dressed 4-levelQDmodel.Weprovide a detailed analysis of the QD-cavity systems properties enabling this novel effect. The experimental results are successfully reproduced using a polaron master equation approach for the QD-cavity system, which includes the driving laser field, exciton-cavity and exciton-phonon interactions}, language = {en} } @article{vandeKerkhofFekkesvanderHeijdenetal.2016, author = {van de Kerkhof, Nora WA and Fekkes, Durk and van der Heijden, Frank MMA and Hoogendijk, Witte JG and St{\"o}ber, Gerald and Egger, Jos IM and Verhoeven, Willem MA}, title = {Cycloid psychoses in the psychosis spectrum: evidence for biochemical differences with schizophrenia}, series = {Neuropsychiatric Disease and Treatment}, volume = {12}, journal = {Neuropsychiatric Disease and Treatment}, doi = {10.2147/NDT.S101317}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-166255}, pages = {1927-1933}, year = {2016}, abstract = {Cycloid psychoses (CP) differ from schizophrenia regarding symptom profile, course, and prognosis and over many decades they were thought to be a separate entity within the psychosis spectrum. As to schizophrenia, research into the pathophysiology has focused on dopamine, brain-derived neurotrophic factor, and glutamate signaling in which, concerning the latter, the N-methyl-d-aspartate receptor plays a crucial role. The present study aims to determine whether CP can biochemically be delineated from schizophrenia. Eighty patients referred for psychotic disorders were assessed with the Comprehensive Assessment of Symptoms and History, and (both at inclusion and after 6 weeks of antipsychotic treatment) with the Positive and Negative Syndrome Scale and Clinical Global Impression. From 58 completers, 33 patients were diagnosed with schizophrenia and ten with CP according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, and Leonhard criteria, respectively. Fifteen patients were diagnosed with other disorders within the psychosis spectrum. At both time points, blood levels of the dopamine metabolite homovanillic acid, brain-derived neurotrophic factor, and amino acids related to glutamate neurotransmission were measured and compared with a matched control sample. Patients with CP showed a significantly better response to antipsychotic treatment as compared to patients with schizophrenia. In CP, glycine levels were elevated and tryptophan levels were lowered as compared to schizophrenia. Glutamate levels were increased in both patient groups as compared to controls. These results, showing marked differences in both treatment outcome and glutamate-related variable parameters, may point at better neuroplasticity in CP, necessitating demarcation of this subgroup within the psychosis spectrum.}, language = {en} } @article{StoeckelEsserGameretal.2016, author = {Stoeckel, M. Cornelia and Esser, Roland W. and Gamer, Matthias and B{\"u}chel, Christian and von Leupoldt, Andreas}, title = {Brain Responses during the Anticipation of Dyspnea}, series = {Neural Plasticity}, volume = {2016}, journal = {Neural Plasticity}, number = {6434987}, doi = {10.1155/2016/6434987}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-166238}, year = {2016}, abstract = {Dyspnea is common in many cardiorespiratory diseases. Already the anticipation of this aversive symptom elicits fear in many patients resulting in unfavorable health behaviors such as activity avoidance and sedentary lifestyle. This study investigated brain mechanisms underlying these anticipatory processes. We induced dyspnea using resistive-load breathing in healthy subjects during functional magnetic resonance imaging. Blocks of severe and mild dyspnea alternated, each preceded by anticipation periods. Severe dyspnea activated a network of sensorimotor, cerebellar, and limbic areas. The left insular, parietal opercular, and cerebellar cortices showed increased activation already during dyspnea anticipation. Left insular and parietal opercular cortex showed increased connectivity with right insular and anterior cingulate cortex when severe dyspnea was anticipated, while the cerebellum showed increased connectivity with the amygdala. Notably, insular activation during dyspnea perception was positively correlated with midbrain activation during anticipation. Moreover, anticipatory fear was positively correlated with anticipatory activation in right insular and anterior cingulate cortex. The results demonstrate that dyspnea anticipation activates brain areas involved in dyspnea perception. The involvement of emotion-related areas such as insula, anterior cingulate cortex, and amygdala during dyspnea anticipation most likely reflects anticipatory fear and might underlie the development of unfavorable health behaviors in patients suffering from dyspnea.}, language = {en} } @article{BenoitAdelmanReinhardtetal.2016, author = {Benoit, Joshua B. and Adelman, Zach N. and Reinhardt, Klaus and Dolan, Amanda and Poelchau, Monica and Jennings, Emily C. and Szuter, Elise M. and Hagan, Richard W. and Gujar, Hemant and Shukla, Jayendra Nath and Zhu, Fang and Mohan, M. and Nelson, David R. and Rosendale, Andrew J. and Derst, Christian and Resnik, Valentina and Wernig, Sebastian and Menegazzi, Pamela and Wegener, Christian and Peschel, Nicolai and Hendershot, Jacob M. and Blenau, Wolfgang and Predel, Reinhard and Johnston, Paul R. and Ioannidis, Panagiotis and Waterhouse, Robert M. and Nauen, Ralf and Schorn, Corinna and Ott, Mark-Christoph and Maiwald, Frank and Johnston, J. Spencer and Gondhalekar, Ameya D. and Scharf, Michael E. and Raje, Kapil R. and Hottel, Benjamin A. and Armis{\´e}n, David and Crumi{\`e}re, Antonin Jean Johan and Refki, Peter Nagui and Santos, Maria Emilia and Sghaier, Essia and Viala, S{\`e}verine and Khila, Abderrahman and Ahn, Seung-Joon and Childers, Christopher and Lee, Chien-Yueh and Lin, Han and Hughes, Daniel S.T. and Duncan, Elizabeth J. and Murali, Shwetha C. and Qu, Jiaxin and Dugan, Shannon and Lee, Sandra L. and Chao, Hsu and Dinh, Huyen and Han, Yi and Doddapaneni, Harshavardhan and Worley, Kim C. and Muzny, Donna M. and Wheeler, David and Panfilio, Kristen A. and Jentzsch, Iris M. Vargas and Jentzsch, IMV and Vargo, Edward L. and Booth, Warren and Friedrich, Markus and Weirauch, Matthew T. and Anderson, Michelle A.E. and Jones, Jeffery W. and Mittapalli, Omprakash and Zhao, Chaoyang and Zhou, Jing-Jiang and Evans, Jay D. and Attardo, Geoffrey M. and Robertson, Hugh M. and Zdobnov, Evgeny M. and Ribeiro, Jose M.C. and Gibbs, Richard A. and Werren, John H. and Palli, Subba R. and Schal, Coby and Richards, Stephen}, title = {Unique features of a global human ectoparasite identified through sequencing of the bed bug genome}, series = {Nature Communications}, volume = {7}, journal = {Nature Communications}, number = {10165}, doi = {10.1038/ncomms10165}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-166221}, year = {2016}, abstract = {The bed bug, Cimex lectularius, has re-established itself as a ubiquitous human ectoparasite throughout much of the world during the past two decades. This global resurgence is likely linked to increased international travel and commerce in addition to widespread insecticide resistance. Analyses of the C. lectularius sequenced genome (650 Mb) and 14,220 predicted protein-coding genes provide a comprehensive representation of genes that are linked to traumatic insemination, a reduced chemosensory repertoire of genes related to obligate hematophagy, host-symbiont interactions, and several mechanisms of insecticide resistance. In addition, we document the presence of multiple putative lateral gene transfer events. Genome sequencing and annotation establish a solid foundation for future research on mechanisms of insecticide resistance, human-bed bug and symbiont-bed bug associations, and unique features of bed bug biology that contribute to the unprecedented success of C. lectularius as a human ectoparasite.}, language = {en} } @article{ConradAlbrechtRodriguesdeMeloCostaetal.2016, author = {Conrad, Thomas and Albrecht, Anne-Susann and Rodrigues de Melo Costa, Veronica and Sauer, Sascha and Meierhofer, David and Andersson {\O}rom, Ulf}, title = {Serial interactome capture of the human cell nucleus}, series = {Nature Communications}, volume = {7}, journal = {Nature Communications}, number = {11212}, doi = {10.1038/ncomms11212}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-166172}, year = {2016}, abstract = {Novel RNA-guided cellular functions are paralleled by an increasing number of RNA-binding proteins (RBPs). Here we present 'serial RNA interactome capture' (serIC), a multiple purification procedure of ultraviolet-crosslinked poly(A)-RNA-protein complexes that enables global RBP detection with high specificity. We apply serIC to the nuclei of proliferating K562 cells to obtain the first human nuclear RNA interactome. The domain composition of the 382 identified nuclear RBPs markedly differs from previous IC experiments, including few factors without known RNA-binding domains that are in good agreement with computationally predicted RNA binding. serIC extends the number of DNA-RNA-binding proteins (DRBPs), and reveals a network of RBPs involved in p53 signalling and double-strand break repair. serIC is an effective tool to couple global RBP capture with additional selection or labelling steps for specific detection of highly purified RBPs.}, language = {en} } @article{JahnkeGiesAssmannetal.2016, author = {Jahnke, Frank and Gies, Christopher and Aßmann, Marc and Bayer, Manfred and Leymann, H.A.M. and Foerster, Alexander and Wiersig, Jan and Schneider, Christian and Kamp, Martin and H{\"o}fling, Sven}, title = {Giant photon bunching, superradiant pulse emission and excitation trapping in quantum-dot nanolasers}, series = {Nature Communications}, volume = {7}, journal = {Nature Communications}, number = {11540}, doi = {10.1038/ncomms11540}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-166144}, year = {2016}, abstract = {Light is often characterized only by its classical properties, like intensity or coherence. When looking at its quantum properties, described by photon correlations, new information about the state of the matter generating the radiation can be revealed. In particular the difference between independent and entangled emitters, which is at the heart of quantum mechanics, can be made visible in the photon statistics of the emitted light. The well-studied phenomenon of superradiance occurs when quantum-mechanical correlations between the emitters are present. Notwithstanding, superradiance was previously demonstrated only in terms of classical light properties. Here, we provide the missing link between quantum correlations of the active material and photon correlations in the emitted radiation. We use the superradiance of quantum dots in a cavity-quantum electrodynamics laser to show a direct connection between superradiant pulse emission and distinctive changes in the photon correlation function. This directly demonstrates the importance of quantum-mechanical correlations and their transfer between carriers and photons in novel optoelectronic devices.}, language = {en} } @article{GoebelPankratzAsaridouetal.2016, author = {G{\"o}bel, Kerstin and Pankratz, Susann and Asaridou, Chloi-Magdalini and Herrmann, Alexander M. and Bittner, Stefan and Merker, Monika and Ruck, Tobias and Glumm, Sarah and Langhauser, Friederike and Kraft, Peter and Krug, Thorsten F. and Breuer, Johanna and Herold, Martin and Gross, Catharina C. and Beckmann, Denise and Korb-Pap, Adelheid and Schuhmann, Michael K. and Kuerten, Stefanie and Mitroulis, Ioannis and Ruppert, Clemens and Nolte, Marc W. and Panousis, Con and Klotz, Luisa and Kehrel, Beate and Korn, Thomas and Langer, Harald F. and Pap, Thomas and Nieswandt, Bernhard and Wiendl, Heinz and Chavakis, Triantafyllos and Kleinschnitz, Christoph and Meuth, Sven G.}, title = {Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells}, series = {Nature Communications}, volume = {7}, journal = {Nature Communications}, number = {11626}, doi = {10.1038/ncomms11626}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-165503}, year = {2016}, abstract = {Aberrant immune responses represent the underlying cause of central nervous system (CNS) autoimmunity, including multiple sclerosis (MS). Recent evidence implicated the crosstalk between coagulation and immunity in CNS autoimmunity. Here we identify coagulation factor XII (FXII), the initiator of the intrinsic coagulation cascade and the kallikrein-kinin system, as a specific immune cell modulator. High levels of FXII activity are present in the plasma of MS patients during relapse. Deficiency or pharmacologic blockade of FXII renders mice less susceptible to experimental autoimmune encephalomyelitis (a model of MS) and is accompanied by reduced numbers of interleukin-17A-producing T cells. Immune activation by FXII is mediated by dendritic cells in a CD87-dependent manner and involves alterations in intracellular cyclic AMP formation. Our study demonstrates that a member of the plasmatic coagulation cascade is a key mediator of autoimmunity. FXII inhibition may provide a strategy to combat MS and other immune-related disorders.}, language = {en} } @article{DomschkeZwanzgerRehbeinetal.2016, author = {Domschke, Katharina and Zwanzger, Peter and Rehbein, Maimu A and Steinberg, Christian and Knoke, Kathrin and Dobel, Christian and Klinkenberg, Isabelle and Kugel, Harald and Kersting, Anette and Arolt, Volker and Pantev, Christo and Junghofer, Markus}, title = {Magnetoencephalographic correlates of emotional processing in major depression before and after pharmacological treatment}, series = {International Journal of Neuropsychopharmacology}, volume = {19}, journal = {International Journal of Neuropsychopharmacology}, number = {2}, doi = {10.1093/ijnp/pyv093}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-149873}, pages = {pyv093}, year = {2016}, abstract = {Background: In major depressive disorder (MDD), electrophysiological and imaging studies suggest reduced neural activity in the parietal and dorsolateral prefrontal cortex regions. In the present study, neural correlates of emotional processing in MDD were analyzed for the first time in a pre-/post-treatment design by means of magnetoencephalography (MEG), allowing for detecting temporal dynamics of brain activation. Methods: Twenty-five medication-free Caucasian in-patients with MDD and 25 matched controls underwent a baseline MEG session with passive viewing of pleasant, unpleasant, and neutral pictures. Fifteen patients were followed-up with a second MEG session after 4 weeks of antidepressant monopharmacotherapy with mirtazapine. The corresponding controls received no intervention between the measurements. The clinical course of depression was assessed using the Hamilton Depression scale. Results: Prior to treatment, an overall neocortical hypoactivation during emotional processing, particularly at the parietal regions and areas at the right temporoparietal junction, as well as abnormal valence-specific reactions at the right parietal and bilateral dorsolateral prefrontal cortex (dlPFC) regions were observed in patients compared to controls. These effects occurred <150ms, suggesting dysfunctional processing of emotional stimuli at a preconscious level. Successful antidepressant treatment resulted in a normalization of the hypoactivation at the right parietal and right temporoparietal regions. Accordingly, both dlPFC regions revealed an increase of activity after therapy. Conclusions: The present study provides neurophysiological evidence for dysfunctional emotional processing in a fronto-parieto-temporal network, possibly contributing to the pathogenesis of MDD. These activation patterns might have the potential to serve as biomarkers of treatment success.}, language = {en} }