@article{SchneiderSchneiderScharnagletal.2013,
  author    = {Schneider, Andreas and Schneider, Markus P. and Scharnagl, Hubert and Jardine, Alan G. and Wanner, Christoph and Drechsler, Christiane},
  title     = {Predicting erythropoietin resistance in hemodialysis patients with type 2 diabetes},
  series = {BMC Nephrology},
  volume    = {14},
  journal   = {BMC Nephrology},
  number    = {67},
  doi       = {10.1186/1471-2369-14-67},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-128695},
  year      = {2013},
  abstract  = {Background: Resistance to ESAs (erythropoietin stimulating agents) is highly prevalent in hemodialysis patients with diabetes and associated with an increased mortality. The aim of this study was to identify predictors for ESA resistance and to develop a prediction model for the risk stratification in these patients. Methods: A post-hoc analysis was conducted of the 4D study, including 1015 patients with type 2 diabetes undergoing hemodialysis. Determinants of ESA resistance were identified by univariate logistic regression analyses. Subsequently, multivariate models were performed with stepwise inclusion of significant predictors from clinical parameters, routine laboratory and specific biomarkers. Results: In the model restricted to clinical parameters, male sex, shorter dialysis vintage, lower BMI, history of CHF, use of ACE-inhibitors and a higher heart rate were identified as independent predictors of ESA resistance. In regard to routine laboratory markers, lower albumin, lower iron saturation, higher creatinine and higher potassium levels were independently associated with ESA resistance. With respect to specific biomarkers, higher ADMA and CRP levels as well as lower Osteocalcin levels were predictors of ESA resistance. Conclusions: Easily obtainable clinical parameters and routine laboratory parameters can predict ESA resistance in diabetic hemodialysis patients with good discrimination. Specific biomarkers did not meaningfully further improve the risk prediction of ESA resistance. Routinely assessed data can be used in clinical practice to stratify patients according to the risk of ESA resistance, which may help to assign appropriate treatment strategies.},
  language  = {en}
}
@article{SchneiderSchneiderKrieteretal.2015,
  author    = {Schneider, Andreas and Schneider, Markus P. and Krieter, Detlef H. and Genser, Bernd and Scharnagl, Hubert and Stojakovic, Tatjana and Wanner, Christoph and Drechsler, Christiane},
  title     = {Effect of high-flux dialysis on circulating FGF-23 levels in end-stage renal disease patients: results from a randomized trial},
  series = {PLoS ONE},
  volume    = {10},
  journal   = {PLoS ONE},
  number    = {5},
  doi       = {10.1371/journal.pone.0128079},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-148559},
  pages     = {e0128079},
  year      = {2015},
  abstract  = {Background In patients undergoing maintenance hemodialysis (HD), increased levels of circulating fibroblast growth factor-23 (FGF-23) are independently associated with cardiovascular events and mortality. Interventional strategies aiming to reduce levels of FGF-23 in HD patients are of particular interest. The purpose of the current study was to compare the impact of high-flux versus low-flux HD on circulating FGF-23 levels. Methods We conducted a post-hoc analysis of the MINOXIS study, including 127 dialysis patients randomized to low-flux (n = 62) and high-flux (n = 65) HD for 52 weeks. Patients with valid measures for FGF-23 investigated baseline and after 52 weeks were included. Results Compared to baseline, a significant increase in FGF-23 levels after one year of low-flux HD was observed (Delta plasma FGF-23: +4026 RU/ml; p < 0.001). In contrast, FGF-23 levels remained stable in the high flux group (Delta plasma FGF-23: +373 RU/ml, p = 0.70). The adjusted difference of the absolute change in FGF-23 levels between the two treatment groups was statistically significant (p < 0.01). Conclusions Over a period of 12 months, high-flux HD was associated with stable FGF-23 levels, whereas the low-flux HD group showed an increase of FGF-23. However, the implications of the different FGF 23 time-trends in patients on high flux dialysis, as compared to the control group, remain to be explored in specifically designed clinical trials.},
  language  = {en}
}
@article{MarenholzEsparzaGordilloRueschendorfetal.2015,
  author    = {Marenholz, Ingo and Esparza-Gordillo, Jorge and R{\"u}schendorf, Franz and Bauerfeind, Anja and Strachan, David P. and Spycher, Ben D. and Baurecht, Hansj{\"o}rg and Magaritte-Jeannin, Patricia and S{\"a}{\"a}f, Annika and Kerkhof, Marjan and Ege, Markus and Baltic, Svetlana and Matheson, Melanie C. and Li, Jin and Michel, Sven and Ang, Wei Q. and McArdle, Wendy and Arnold, Andreas and Homuth, Georg and Demenais, Florence and Bouzigon, Emmanuelle and S{\"o}derh{\"a}ll, Cilla and Pershagen, G{\"o}ran and de Jongste, Johan C. and Postma, Dirkje S. and Braun-Fahrl{\"a}nder, Charlotte and Horak, Elisabeth and Ogorodova, Ludmila M. and Puzyrev, Valery P. and Bragina, Elena Yu and Hudson, Thomas J. and Morin, Charles and Duffy, David L. and Marks, Guy B. and Robertson, Colin F. and Montgomery, Grant W. and Musk, Bill and Thompson, Philip J. and Martin, Nicholas G. and James, Alan and Sleiman, Patrick and Toskala, Elina and Rodriguez, Elke and F{\"o}lster-Holst, Regina and Franke, Andre and Lieb, Wolfgang and Gieger, Christian and Heinzmann, Andrea and Rietschel, Ernst and Keil, Thomas and Cichon, Sven and N{\"o}then, Markus M. and Pennel, Craig E. and Sly, Peter D. and Schmidt, Carsten O. and Matanovic, Anja and Schneider, Valentin and Heinig, Matthias and H{\"u}bner, Norbert and Holt, Patrick G. and Lau, Susanne and Kabesch, Michael and Weidinger, Stefan and Hakonarson, Hakon and Ferreira, Manuel A. R. and Laprise, Catherine and Freidin, Maxim B. and Genuneit, Jon and Koppelman, Gerard H. and Mel{\´e}n, Erik and Dizier, Marie-H{\´e}l{\`e}ne and Henderson, A. John and Lee, Young Ae},
  title     = {Meta-analysis identifies seven susceptibility loci involved in the atopic march},
  series = {Nature Communications},
  volume    = {6},
  journal   = {Nature Communications},
  number    = {8804},
  doi       = {10.1038/ncomms9804},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-139835},
  year      = {2015},
  abstract  = {Eczema often precedes the development of asthma in a disease course called the 'atopic march'. To unravel the genes underlying this characteristic pattern of allergic disease, we conduct a multi-stage genome-wide association study on infantile eczema followed by childhood asthma in 12 populations including 2,428 cases and 17,034 controls. Here we report two novel loci specific for the combined eczema plus asthma phenotype, which are associated with allergic disease for the first time; rs9357733 located in EFHC1 on chromosome 6p12.3 (OR 1.27; P = 2.1 x 10(-8)) and rs993226 between TMTC2 and SLC6A15 on chromosome 12q21.3 (OR 1.58; P = 5.3 x 10(-9)). Additional susceptibility loci identified at genome-wide significance are FLG (1q21.3), IL4/KIF3A (5q31.1), AP5B1/OVOL1 (11q13.1), C11orf30/LRRC32 (11q13.5) and IKZF3 (17q21). We show that predominantly eczema loci increase the risk for the atopic march. Our findings suggest that eczema may play an important role in the development of asthma after eczema.},
  language  = {en}
}
@article{SchneiderKleinMielichSuessetal.2015,
  author    = {Schneider, Johannes and Klein, Teresa and Mielich-S{\"u}ss, Benjamin and Koch, Gudrun and Franke, Christian and Kuipers, Oskar P. and Kov{\´a}cs, {\´A}kos T. and Sauer, Markus and Lopez, Daniel},
  title     = {Spatio-temporal Remodeling of Functional Membrane Microdomains Organizes the Signaling Networks of a Bacterium},
  series = {PLoS Genetics},
  volume    = {11},
  journal   = {PLoS Genetics},
  number    = {4},
  doi       = {10.1371/journal.pgen.1005140},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-125577},
  pages     = {e1005140},
  year      = {2015},
  abstract  = {Lipid rafts are membrane microdomains specialized in the regulation of numerous cellular processes related to membrane organization, as diverse as signal transduction, protein sorting, membrane trafficking or pathogen invasion. It has been proposed that this functional diversity would require a heterogeneous population of raft domains with varying compositions. However, a mechanism for such diversification is not known. We recently discovered that bacterial membranes organize their signal transduction pathways in functional membrane microdomains (FMMs) that are structurally and functionally similar to the eukaryotic lipid rafts. In this report, we took advantage of the tractability of the prokaryotic model Bacillus subtilis to provide evidence for the coexistence of two distinct families of FMMs in bacterial membranes, displaying a distinctive distribution of proteins specialized in different biological processes. One family of microdomains harbors the scaffolding flotillin protein FloA that selectively tethers proteins specialized in regulating cell envelope turnover and primary metabolism. A second population of microdomains containing the two scaffolding flotillins, FloA and FloT, arises exclusively at later stages of cell growth and specializes in adaptation of cells to stationary phase. Importantly, the diversification of membrane microdomains does not occur arbitrarily. We discovered that bacterial cells control the spatio-temporal remodeling of microdomains by restricting the activation of FloT expression to stationary phase. This regulation ensures a sequential assembly of functionally specialized membrane microdomains to strategically organize signaling networks at the right time during the lifespan of a bacterium.},
  language  = {en}
}
@article{RauHeindelUnsleberetal.2014,
  author    = {Rau, Markus and Heindel, Tobias and Unsleber, Sebastian and Braun, Tristan and Fischer, Julian and Frick, Stefan and Nauerth, Sebastian and Schneider, Christian and Vest, Gwenaelle and Reitzenstein, Stephan and Kamp, Martin and Forchel, Alfred and H{\"o}fling, Sven and Weinfurter, Harald},
  title     = {Free space quantum key distribution over 500 meters using electrically driven quantum dot single-photon sources-a proof of principle experiment},
  series = {New Journal of Physics},
  volume    = {16},
  journal   = {New Journal of Physics},
  number    = {043003},
  doi       = {10.1088/1367-2630/16/4/043003},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-116760},
  year      = {2014},
  abstract  = {Highly efficient single-photon sources (SPS) can increase the secure key rate of quantum key distribution (QKD) systems compared to conventional attenuated laser systems. Here we report on a free space QKD test using an electrically driven quantum dot single-photon source (QD SPS) that does not require a separate laser setup for optical pumping and thus allows for a simple and compact SPS QKD system. We describe its implementation in our 500 m free space QKD system in downtown Munich. Emulating a BB84 protocol operating at a repetition rate of 125 MHz, we could achieve sifted key rates of 5-17 kHz with error ratios of 6-9\% and g((2))(0)-values of 0.39-0.76.},
  language  = {en}
}
@phdthesis{Schneider2004,
  author    = {Schneider, Markus},
  title     = {Exhalatkondensat bei Gesunden und thorakal bestrahlten Patienten},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-10579},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2004},
  abstract  = {Die thorakale Strahlentherapie birgt stets das Risiko der Entstehung einer Pneumonitis, deren fr{\"u}he Diagnose wichtig ist. Mit der Exhalat-Kondensat-Methode gelingt es, die alveol{\"a}re Oberfl{\"a}che wenig invasiv und beliebig oft wiederholbar untersuchen zu k{\"o}nnen. Methodik, Variabilit{\"a}t der Exhalatparameter bei Gesunden, Unterschiede zwischen diesen und Patienten w{\"a}hrend einer thorakalen Strahlentherapie sollten untersucht, Zusammenh{\"a}nge der Exhalatparameter mit Blutserumkonzentrationen von Total-Protein und TGF-beta; gekl{\"a}rt werden und die Eignung der Methode zur Fr{\"u}herkennung einer Strahlenpneumonitis gepr{\"u}ft werden. 14 gesunde Probanden (an drei aufeinander folgenden Messtagen) und 14 Patienten (bei 0 und 50Gy Gesamt-Energiedosis) wurden untersucht. Jeder atmete 15 Minuten lang am Jaeger ECoScreen; Exhalatmenge und Atemvolumen (V'E) wurden bestimmt. Bei den Probanden wurde am ersten Messtag, bei den Patienten beides Mal Blutserum abgenommen. Exhalat- und Serumproben wurden eingefroren und sp{\"a}ter auf TGF-beta; und Total-Protein untersucht. Die Untersuchungen waren problemlos durchzuf{\"u}hren; die Messung des V'E war allerdings umst{\"a}ndlich. Eine Bestimmung der Masse des Exhalat-Kondensats ist genauer als die des Volumens. TGF-beta; konnte in keiner Kondensatprobe nachgewiesen werden, Total-Protein bei allen. Total-Protein und TGF-beta; ließen sich im Serum messen. Vier Patienten erkrankten an einer Pneumonitis, im Mittel 43,5 ±27 Tage nach Erhalt von 50Gy. Bei Gesunden bedeutet ein h{\"o}heres V'E auch signifikant mehr Exhalat (p = 0,0004***); die Tag-zu-Tag-Variabilit{\"a}t aller Exhalatparameter war betr{\"a}chtlich. {\"U}bungsphasen, weitere Standardisierungen und geeignete „Referenzkollektive" sind f{\"u}r eine Etablierung der Methode unbedingt notwendig. Patienten h{\"o}heren K{\"o}rpergewichts (p = 0,0072**) und mit einem gr{\"o}ßerem Body-Mass-Index (BMI, p = 0,0095**) produzierten vor Therapie signifikant mehr Exhalat-Kondensat. Es fand sich bei den {\"A}lteren am zweiten Messtermin signifikant mehr Protein im Exhalat (p = 0,045*), dies ist als Alters- und / oder Krankheitsfolge zu werten (in beiden Teilkollektiven findet sich kein solcher Zusammenhang). Die Patienten hatten h{\"o}here Ausgangswerte aller drei Exhalatparameter als die Probanden. Bei den Gesunden fand sich infolge „Gew{\"o}hnung" an die Messapparatur am zweiten Messtag weniger Exhalat und ein geringeres V'E. Die Patienten hatten vor Beginn der Therapie mehr Protein im Exhalat, was eine bei vielen vorbestehende alveol{\"a}re Schrankenst{\"o}rung vermuten l{\"a}sst. Die Patienten hatten stets mehr Protein im Exhalat als die Probanden, dieses stieg w{\"a}hrend der Therapie um das 1,7fache an; trotzdem ließ sich kein signifikanter Zusammenhang mit der Entwicklung einer Strahlenpneumonitis finden. Bei den Gesunden fanden sich bei jeweils h{\"o}heren Ausgangswerten auch signifikant st{\"a}rkere Abnahmen der Exhalatmenge (p = 0,025*) und des V'E (p = 0,040*) - es kommt also bei den „Gew{\"o}hnungseffekten" auf die Zeitdauer des Messintervalls an. Mittelwerte aus mehreren Messungen trugen zu einer sch{\"a}rferen Abgrenzung der zwei Kollektive bei; bei jeweils n = 22 Personen pro Kollektiv w{\"a}ren mehr signifikante Unterschiede zu finden gewesen. Die Serumkonzentrationen von Protein und TGF-beta waren von den demographischen Daten unabh{\"a}ngig und hingen niemals voneinander ab. Die TGF-beta-Serumkonzentrationen der an Pneumonitis erkrankten Patienten nahmen im Laufe der Strahlentherapie im Durchschnitt um 32,9\% ab, w{\"a}hrend sie sich bei den {\"u}brigen praktisch nicht {\"a}nderten; wahrscheinlich handelt es sich hier um typische transiente Abf{\"a}lle von TGF-beta. Bei den Probanden waren Serum- und Exhalatparameter unabh{\"a}ngig voneinander. Bei den Patienten war mehr Protein im Exhalat-Kondensat, wenn bei 0Gy mehr Serum-TGF-beta vorhanden war. Nach 50Gy war umso mehr Protein im Kondensat, je niedriger es im Serum war. Bei Patienten, die im Laufe der Therapie mehr Protein im Exhalat hatten, fand sich auch eine signifikant steigende Proteinkonzentration im Serum (p = 0,027*). Sinkt TGF-beta im Serum w{\"a}hrend der Therapie ab (eher steigendes Pneumonitis-Risiko in dieser Studie), dann steigt V'E (p = 0,0100*) und sinkt das Protein im Exhalat (p = 0,043*) signifikant. Bei 0Gy war der Protein-Quotient aus Exhalat und Serum bei den Patienten 1,3mal h{\"o}her und stieg bis 50Gy um das 1,75fache auf das 2,28fache der Probanden-Ausgangswerte an. Ein hohes TGF-beta im Serum bei 0Gy ging mit einem signifikant steigenden V'E (p = 0,0067**) und sinkenden Protein im Exhalat (p = 0,012*) im Laufe der Therapie einher. Steigt Protein im Serum w{\"a}hrend der Therapie an, fand sich ein eher h{\"o}heres V'E vor Beginn der Therapie. Waren Exhalatmenge und V'E vor Therapie eher hoch, stieg TGF-beta im Serum bis 50Gy eher an.},
  language  = {de}
}
@article{LombardiMayerSemleretal.2021,
  author    = {Lombardi, Jolina and Mayer, Benjamin and Semler, Elisa and Anderl-Straub, Sarah and Uttner, Ingo and Kassubek, Jan and Diehl-Schmid, Janine and Danek, Adrian and Levin, Johannes and Fassbender, Klaus and Fliessbach, Klaus and Schneider, Anja and Huppertz, Hans-J{\"u}rgen and Jahn, Holger and Volk, Alexander and Kornhuber, Johannes and Landwehrmeyer, Bernhard and Lauer, Martin and Prudlo, Johannes and Wiltfang, Jens and Schroeter, Matthias L. and Ludolph, Albert and Otto, Markus},
  title     = {Quantifying progression in primary progressive aphasia with structural neuroimaging},
  series = {Alzheimer's \& Dementia},
  volume    = {17},
  journal   = {Alzheimer's \& Dementia},
  number    = {10},
  doi       = {10.1002/alz.12323},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-262605},
  pages     = {1595 -- 1609},
  year      = {2021},
  abstract  = {Introduction The term primary progressive aphasia (PPA) sums up the non-fluent (nfv), the semantic (sv), and the logopenic (lv) variant. Up to now, there is only limited data available concerning magnetic resonance imaging volumetry to monitor disease progression. Methods Structural brain imaging and an extensive assessment were applied at baseline and up to 4-year(s) follow-up in 269 participants. With automated atlas-based volumetry 56 brain regions were assessed. Atrophy progression served to calculate sample sizes for therapeutic trials. Results At baseline highest atrophy appeared in parts of the left frontal lobe for nfvPPA (-17\%) and of the left temporal lobe for svPPA (-34\%) and lvPPA (-24\%). Severest progression within 1-year follow-up occurred in the basal ganglia in nfvPPA (-7\%), in the hippocampus/amygdala in svPPA (-9\%), and in (medial) temporal regions in lvPPA (-6\%). Conclusion PPA presents as a left-dominant, mostly gray matter sensitive disease with considerable atrophy at baseline that proceeds variant-specific.},
  language  = {en}
}
@article{TegtmeyerMoodleyYamaokaetal.2016,
  author    = {Tegtmeyer, Nicole and Moodley, Yoshan and Yamaoka, Yoshio and Pernitzsch, Sandy Ramona and Schmidt, Vanessa and Traverso, Francisco Rivas and Schmidt, Thomas P. and Rad, Roland and Yeoh, Khay Guan and Bow, Ho and Torres, Javier and Gerhard, Markus and Schneider, Gisbert and Wessler, Silja and Backert, Steffen},
  title     = {Characterisation of worldwide Helicobacter pylori strains reveals genetic conservation and essentiality of serine protease HtrA},
  series = {Molecular Microbiology},
  volume    = {99},
  journal   = {Molecular Microbiology},
  number    = {5},
  doi       = {10.1111/mmi.13276},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-190774},
  pages     = {925-944},
  year      = {2016},
  abstract  = {HtrA proteases and chaperones exhibit important roles in periplasmic protein quality control and stress responses. The genetic inactivation of htrA has been described for many bacterial pathogens. However, in some cases such as the gastric pathogen Helicobacter pylori, HtrA is secreted where it cleaves the tumour-suppressor E-cadherin interfering with gastric disease development, but the generation of htrA mutants is still lacking. Here, we show that the htrA gene locus is highly conserved in worldwide strains. HtrA presence was confirmed in 992 H.pylori isolates in gastric biopsy material from infected patients. Differential RNA-sequencing (dRNA-seq) indicated that htrA is encoded in an operon with two subsequent genes, HP1020 and HP1021. Genetic mutagenesis and complementation studies revealed that HP1020 and HP1021, but not htrA, can be mutated. In addition, we demonstrate that suppression of HtrA proteolytic activity with a newly developed inhibitor is sufficient to effectively kill H.pylori, but not other bacteria. We show that Helicobacter htrA is an essential bifunctional gene with crucial intracellular and extracellular functions. Thus, we describe here the first microbe in which htrA is an indispensable gene, a situation unique in the bacterial kingdom. HtrA can therefore be considered a promising new target for anti-bacterial therapy.},
  language  = {en}
}
@article{DerakhshaniKurzJaptoketal.2019,
  author    = {Derakhshani, Shaghayegh and Kurz, Andreas and Japtok, Lukasz and Schumacher, Fabian and Pilgram, Lisa and Steinke, Maria and Kleuser, Burkhard and Sauer, Markus and Schneider-Schaulies, Sibylle and Avota, Elita},
  title     = {Measles virus infection fosters dendritic cell motility in a 3D environment to enhance transmission to target cells in the respiratory epithelium},
  series = {Frontiers in Immunology},
  volume    = {10},
  journal   = {Frontiers in Immunology},
  number    = {1294},
  doi       = {10.3389/fimmu.2019.01294},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-201818},
  year      = {2019},
  abstract  = {Transmission of measles virus (MV) from dendritic to airway epithelial cells is considered as crucial to viral spread late in infection. Therefore, pathways and effectors governing this process are promising targets for intervention. To identify these, we established a 3D respiratory tract model where MV transmission by infected dendritic cells (DCs) relied on the presence of nectin-4 on H358 lung epithelial cells. Access to recipient cells is an important prerequisite for transmission, and we therefore analyzed migration of MV-exposed DC cultures within the model. Surprisingly, enhanced motility toward the epithelial layer was observed for MV-infected DCs as compared to their uninfected siblings. This occurred independently of factors released from H358 cells indicating that MV infection triggered cytoskeletal remodeling associated with DC polarization enforced velocity. Accordingly, the latter was also observed for MV-infected DCs in collagen matrices and was particularly sensitive to ROCK inhibition indicating infected DCs preferentially employed the amoeboid migration mode. This was also implicated by loss of podosomes and reduced filopodial activity both of which were retained in MV-exposed uninfected DCs. Evidently, sphingosine kinase (SphK) and sphingosine-1-phosphate (S1P) as produced in response to virus-infection in DCs contributed to enhanced velocity because this was abrogated upon inhibition of sphingosine kinase activity. These findings indicate that MV infection promotes a push-and-squeeze fast amoeboid migration mode via the SphK/S1P system characterized by loss of filopodia and podosome dissolution. Consequently, this enables rapid trafficking of virus toward epithelial cells during viral exit.},
  language  = {en}
}
@article{MeirKannapinDiefenbacheretal.2021,
  author    = {Meir, Michael and Kannapin, Felix and Diefenbacher, Markus and Ghoreishi, Yalda and Kollmann, Catherine and Flemming, Sven and Germer, Christoph-Thomas and Waschke, Jens and Leven, Patrick and Schneider, Reiner and Wehner, Sven and Burkard, Natalie and Schlegel, Nicolas},
  title     = {Intestinal epithelial barrier maturation by enteric glial cells is GDNF-dependent},
  series = {International Journal of Molecular Sciences},
  volume    = {22},
  journal   = {International Journal of Molecular Sciences},
  number    = {4},
  issn      = {1422-0067},
  doi       = {10.3390/ijms22041887},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-258913},
  year      = {2021},
  abstract  = {Enteric glial cells (EGCs) of the enteric nervous system are critically involved in the maintenance of intestinal epithelial barrier function (IEB). The underlying mechanisms remain undefined. Glial cell line-derived neurotrophic factor (GDNF) contributes to IEB maturation and may therefore be the predominant mediator of this process by EGCs. Using GFAP\(^{cre}\) x Ai14\(^{floxed}\) mice to isolate EGCs by Fluorescence-activated cell sorting (FACS), we confirmed that they synthesize GDNF in vivo as well as in primary cultures demonstrating that EGCs are a rich source of GDNF in vivo and in vitro. Co-culture of EGCs with Caco2 cells resulted in IEB maturation which was abrogated when GDNF was either depleted from EGC supernatants, or knocked down in EGCs or when the GDNF receptor RET was blocked. Further, TNFα-induced loss of IEB function in Caco2 cells and in organoids was attenuated by EGC supernatants or by recombinant GDNF. These barrier-protective effects were blunted when using supernatants from GDNF-deficient EGCs or by RET receptor blockade. Together, our data show that EGCs produce GDNF to maintain IEB function in vitro through the RET receptor.},
  language  = {en}
}
@article{TiwarekarFehrholzSchneiderSchaulies2019,
  author    = {Tiwarekar, Vishakha and Fehrholz, Markus and Schneider-Schaulies, J{\"u}rgen},
  title     = {KDELR2 competes with measles virus envelope proteins for cellular chaperones reducing their chaperone-mediated cell surface transport},
  series = {Viruses},
  volume    = {11},
  journal   = {Viruses},
  number    = {1},
  issn      = {1999-4915},
  doi       = {10.3390/v11010027},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-197468},
  pages     = {27},
  year      = {2019},
  abstract  = {Recently, we found that the cytidine deaminase APOBEC3G (A3G) inhibits measles (MV) replication. Using a microarray, we identified differential regulation of several host genes upon ectopic expression of A3G. One of the up-regulated genes, the endoplasmic reticulum (ER) protein retention receptor KDELR2, reduced MV replication ~5 fold when it was over-expressed individually in Vero and CEM-SS T cells. Silencing of KDELR2 in A3G-expressing Vero cells abrogated the antiviral activity induced by A3G, confirming its role as an A3G-regulated antiviral host factor. Recognition of the KDEL (Lys-Asp-Glu-Leu) motif by KDEL receptors initiates the retrograde transport of soluble proteins that have escaped the ER and play an important role in ER quality control. Although KDELR2 over-expression reduced MV titers in cell cultures, we observed no interaction between KDELR2 and the MV hemagglutinin (H) protein. Instead, KDELR2 retained chaperones in the ER, which are required for the correct folding and transport of the MV envelope glycoproteins H and fusion protein (F) to the cell surface. Our data indicate that KDELR2 competes with MV envelope proteins for binding to calnexin and GRP78/Bip, and that this interaction limits the availability of the chaperones for MV proteins, causing the reduction of virus spread and titers.},
  language  = {en}
}
@article{BoertleinDraegerSchoenaueretal.2018,
  author    = {B{\"o}rtlein, Charlene and Draeger, Annette and Schoenauer, Roman and Kuhlemann, Alexander and Sauer, Markus and Schneider-Schaulies, Sybille and Avota, Elita},
  title     = {The neutral sphingomyelinase 2 is required to polarize and sustain T Cell receptor signaling},
  series = {Frontiers in Immunology},
  volume    = {9},
  journal   = {Frontiers in Immunology},
  number    = {815},
  doi       = {10.3389/fimmu.2018.00815},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-176572},
  year      = {2018},
  abstract  = {By promoting ceramide release at the cytosolic membrane leaflet, the neutral sphingomyelinase 2 (NSM) is capable of organizing receptor and signalosome segregation. Its role in T cell receptor (TCR) signaling remained so far unknown. We now show that TCR-driven NSM activation is dispensable for TCR clustering and initial phosphorylation, but of crucial importance for further signal amplification. In particular, at low doses of TCR stimulatory antibodies, NSM is required for Ca\(^{2+}\) mobilization and T cell proliferation. NSM-deficient T cells lack sustained CD3ζ and ZAP-70 phosphorylation and are unable to polarize and stabilize their microtubular system. We identified PKCζ as the key NSM downstream effector in this second wave of TCR signaling supporting dynamics of microtubule-organizing center (MTOC). Ceramide supplementation rescued PKCζ membrane recruitment and MTOC translocation in NSM-deficient cells. These findings identify the NSM as essential in TCR signaling when dynamic cytoskeletal reorganization promotes continued lateral and vertical supply of TCR signaling components: CD3ζ, Zap70, and PKCζ, and functional immune synapses are organized and stabilized via MTOC polarization.},
  language  = {en}
}
@article{BrennerGeigerSchlegeletal.2023,
  author    = {Brenner, Daniela and Geiger, Nina and Schlegel, Jan and Diesendorf, Viktoria and Kersting, Louise and Fink, Julian and Stelz, Linda and Schneider-Schaulies, Sibylle and Sauer, Markus and Bodem, Jochen and Seibel, J{\"u}rgen},
  title     = {Azido-ceramides, a tool to analyse SARS-CoV-2 replication and inhibition — SARS-CoV-2 is inhibited by ceramides},
  series = {International Journal of Molecular Sciences},
  volume    = {24},
  journal   = {International Journal of Molecular Sciences},
  number    = {8},
  issn      = {1422-0067},
  doi       = {10.3390/ijms24087281},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-313581},
  year      = {2023},
  abstract  = {Recently, we have shown that C6-ceramides efficiently suppress viral replication by trapping the virus in lysosomes. Here, we use antiviral assays to evaluate a synthetic ceramide derivative α-NH2-ω-N3-C6-ceramide (AKS461) and to confirm the biological activity of C6-ceramides inhibiting SARS-CoV-2. Click-labeling with a fluorophore demonstrated that AKS461 accumulates in lysosomes. Previously, it has been shown that suppression of SARS-CoV-2 replication can be cell-type specific. Thus, AKS461 inhibited SARS-CoV-2 replication in Huh-7, Vero, and Calu-3 cells up to 2.5 orders of magnitude. The results were confirmed by CoronaFISH, indicating that AKS461 acts comparable to the unmodified C6-ceramide. Thus, AKS461 serves as a tool to study ceramide-associated cellular and viral pathways, such as SARS-CoV-2 infections, and it helped to identify lysosomes as the central organelle of C6-ceramides to inhibit viral replication.},
  language  = {en}
}
@article{GeigerKerstingSchlegeletal.2022,
  author    = {Geiger, Nina and Kersting, Louise and Schlegel, Jan and Stelz, Linda and F{\"a}hr, Sofie and Diesendorf, Viktoria and Roll, Valeria and Sostmann, Marie and K{\"o}nig, Eva-Maria and Reinhard, Sebastian and Brenner, Daniela and Schneider-Schaulies, Sibylle and Sauer, Markus and Seibel, J{\"u}rgen and Bodem, Jochen},
  title     = {The acid ceramidase is a SARS-CoV-2 host factor},
  series = {Cells},
  volume    = {11},
  journal   = {Cells},
  number    = {16},
  issn      = {2073-4409},
  doi       = {10.3390/cells11162532},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-286105},
  year      = {2022},
  abstract  = {SARS-CoV-2 variants such as the delta or omicron variants, with higher transmission rates, accelerated the global COVID-19 pandemic. Thus, novel therapeutic strategies need to be deployed. The inhibition of acid sphingomyelinase (ASM), interfering with viral entry by fluoxetine was reported. Here, we described the acid ceramidase as an additional target of fluoxetine. To discover these effects, we synthesized an ASM-independent fluoxetine derivative, AKS466. High-resolution SARS-CoV-2-RNA FISH and RTqPCR analyses demonstrate that AKS466 down-regulates viral gene expression. It is shown that SARS-CoV-2 deacidifies the lysosomal pH using the ORF3 protein. However, treatment with AKS488 or fluoxetine lowers the lysosomal pH. Our biochemical results show that AKS466 localizes to the endo-lysosomal replication compartments of infected cells, and demonstrate the enrichment of the viral genomic, minus-stranded RNA and mRNAs there. Both fluoxetine and AKS466 inhibit the acid ceramidase activity, cause endo-lysosomal ceramide elevation, and interfere with viral replication. Furthermore, Ceranib-2, a specific acid ceramidase inhibitor, reduces SARS-CoV-2 replication and, most importantly, the exogenous supplementation of C6-ceramide interferes with viral replication. These results support the hypotheses that the acid ceramidase is a SARS-CoV-2 host factor.},
  language  = {en}
}
@article{MaiwaldBruschkeSchneideretal.2023,
  author    = {Maiwald, Ferdinand and Bruschke, Jonas and Schneider, Danilo and Wacker, Markus and Niebling, Florian},
  title     = {Giving historical photographs a new perspective: introducing camera orientation parameters as new metadata in a large-scale 4D application},
  series = {Remote Sensing},
  volume    = {15},
  journal   = {Remote Sensing},
  number    = {7},
  issn      = {2072-4292},
  doi       = {10.3390/rs15071879},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-311103},
  year      = {2023},
  abstract  = {The ongoing digitization of historical photographs in archives allows investigating the quality, quantity, and distribution of these images. However, the exact interior and exterior camera orientations of these photographs are usually lost during the digitization process. The proposed method uses content-based image retrieval (CBIR) to filter exterior images of single buildings in combination with metadata information. The retrieved photographs are automatically processed in an adapted structure-from-motion (SfM) pipeline to determine the camera parameters. In an interactive georeferencing process, the calculated camera positions are transferred into a global coordinate system. As all image and camera data are efficiently stored in the proposed 4D database, they can be conveniently accessed afterward to georeference newly digitized images by using photogrammetric triangulation and spatial resection. The results show that the CBIR and the subsequent SfM are robust methods for various kinds of buildings and different quantity of data. The absolute accuracy of the camera positions after georeferencing lies in the range of a few meters likely introduced by the inaccurate LOD2 models used for transformation. The proposed photogrammetric method, the database structure, and the 4D visualization interface enable adding historical urban photographs and 3D models from other locations.},
  language  = {en}
}
@article{SemlerAnderlStraubUttneretal.2018,
  author    = {Semler, Elisa and Anderl-Straub, Sarah and Uttner, Ingo and Diehl-Schmid, Janine and Danek, Adrian and Einsiedler, Beate and Fassbender, Klaus and Fliessbach, Klaus and Huppertz, Hans-J{\"u}rgen and Jahn, Holger and Kornhuber, Johannes and Landwehrmeyer, Bernhard and Lauer, Martin and Muche, Rainer and Prudlo, Johannes and Schneider, Anja and Schroeter, Matthias L. and Ludolph, Albert C. and Otto, Markus},
  title     = {A language-based sum score for the course and therapeutic intervention in primary progressive aphasia},
  series = {Alzheimer's Research \& Therapy},
  volume    = {10},
  journal   = {Alzheimer's Research \& Therapy},
  organization    = {FLTD consortium},
  doi       = {10.1186/s13195-018-0345-3},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-236277},
  year      = {2018},
  abstract  = {Background With upcoming therapeutic interventions for patients with primary progressive aphasia (PPA), instruments for the follow-up of patients are needed to describe disease progression and to evaluate potential therapeutic effects. So far, volumetric brain changes have been proposed as clinical endpoints in the literature, but cognitive scores are still lacking. This study followed disease progression predominantly in language-based performance within 1 year and defined a PPA sum score which can be used in therapeutic interventions. Methods We assessed 28 patients with nonfluent variant PPA, 17 with semantic variant PPA, 13 with logopenic variant PPA, and 28 healthy controls in detail for 1 year. The most informative neuropsychological assessments were combined to a sum score, and associations between brain atrophy were investigated followed by a sample size calculation for clinical trials. Results Significant absolute changes up to 20\% in cognitive tests were found after 1 year. Semantic and phonemic word fluency, Boston Naming Test, Digit Span, Token Test, AAT Written language, and Cookie Test were identified as the best markers for disease progression. These tasks provide the basis of a new PPA sum score. Assuming a therapeutic effect of 50\% reduction in cognitive decline for sample size calculations, a number of 56 cases is needed to find a significant treatment effect. Correlations between cognitive decline and atrophy showed a correlation up to r = 0.7 between the sum score and frontal structures, namely the superior and inferior frontal gyrus, as well as with left-sided subcortical structures. Conclusion Our findings support the high performance of the proposed sum score in the follow-up of PPA and recommend it as an outcome measure in intervention studies.},
  language  = {en}
}