@article{BousquetFarrellCrooksetal.2016,
  author    = {Bousquet, J. and Farrell, J. and Crooks, G. and Hellings, P. and Bel, E. H. and Bewick, M. and Chavannes, N. H. and Correia de Sousa, J. and Cruz, A. A. and Haahtela, T. and Joos, G. and Khaltaev, N. and Malva, J. and Muraro, A. and Nogues, M. and Palkonen, S. and Pedersen, S. and Robalo-Cordeiro, C. and Samolinski, B. and Strandberg, T. and Valiulis, A. and Yorgancioglu, A. and Zuberbier, T. and Bedbrook, A. and Aberer, W. and Adachi, M. and Agusti, A. and Akdis, C. A. and Akdis, M. and Ankri, J. and Alonso, A. and Annesi-Maesano, I. and Ansotegui, I. J. and Anto, J. M. and Arnavielhe, S. and Arshad, H. and Bai, C. and Baiardini, I. and Bachert, C. and Baigenzhin, A. K. and Barbara, C. and Bateman, E. D. and Begh{\´e}, B. and Ben Kheder, A. and Bennoor, K. S. and Benson, M. and Bergmann, K. C. and Bieber, T. and Bindslev-Jensen, C. and Bjermer, L. and Blain, H. and Blasi, F. and Boner, A. L. and Bonini, M. and Bonini, S. and Bosnic-Anticevitch, S. and Boulet, L. P. and Bourret, R. and Bousquet, P. J. and Braido, F. and Briggs, A. H. and Brightling, C. E. and Brozek, J. and Buhl, R. and Burney, P. G. and Bush, A. and Caballero-Fonseca, F. and Caimmi, D. and Calderon, M. A. and Calverley, P. M. and Camargos, P. A. M. and Canonica, G. W. and Camuzat, T. and Carlsen, K. H. and Carr, W. and Carriazo, A. and Casale, T. and Cepeda Sarabia, A. M. and Chatzi, L. and Chen, Y. Z. and Chiron, R. and Chkhartishvili, E. and Chuchalin, A. G. and Chung, K. F. and Ciprandi, G. and Cirule, I. and Cox, L. and Costa, D. J. and Custovic, A. and Dahl, R. and Dahlen, S. E. and Darsow, U. and De Carlo, G. and De Blay, F. and Dedeu, T. and Deleanu, D. and De Manuel Keenoy, E. and Demoly, P. and Denburg, J. A. and Devillier, P. and Didier, A. and Dinh-Xuan, A. T. and Djukanovic, R. and Dokic, D. and Douagui, H. and Dray, G. and Dubakiene, R. and Durham, S. R. and Dykewicz, M. S. and El-Gamal, Y. and Emuzyte, R. and Fabbri, L. M. and Fletcher, M. and Fiocchi, A. and Fink Wagner, A. and Fonseca, J. and Fokkens, W. J. and Forastiere, F. and Frith, P. and Gaga, M. and Gamkrelidze, A. and Garces, J. and Garcia-Aymerich, J. and Gemicioğlu, B. and Gereda, J. E. and Gonz{\´a}lez Diaz, S. and Gotua, M. and Grisle, I. and Grouse, L. and Gutter, Z. and Guzm{\´a}n, M. A. and Heaney, L. G. and Hellquist-Dahl, B. and Henderson, D. and Hendry, A. and Heinrich, J. and Heve, D. and Horak, F. and Hourihane, J. O'. B. and Howarth, P. and Humbert, M. and Hyland, M. E. and Illario, M. and Ivancevich, J. C. and Jardim, J. R. and Jares, E. J. and Jeandel, C. and Jenkins, C. and Johnston, S. L. and Jonquet, O. and Julge, K. and Jung, K. S. and Just, J. and Kaidashev, I. and Kaitov, M. R. and Kalayci, O. and Kalyoncu, A. F. and Keil, T. and Keith, P. K. and Klimek, L. and Koffi N'Goran, B. and Kolek, V. and Koppelman, G. H. and Kowalski, M. L. and Kull, I. and Kuna, P. and Kvedariene, V. and Lambrecht, B. and Lau, S. and Larenas‑Linnemann, D. and Laune, D. and Le, L. T. T. and Lieberman, P. and Lipworth, B. and Li, J. and Lodrup Carlsen, K. and Louis, R. and MacNee, W. and Magard, Y. and Magnan, A. and Mahboub, B. and Mair, A. and Majer, I. and Makela, M. J. and Manning, P. and Mara, S. and Marshall, G. D. and Masjedi, M. R. and Matignon, P. and Maurer, M. and Mavale‑Manuel, S. and Mel{\´e}n, E. and Melo‑Gomes, E. and Meltzer, E. O. and Menzies‑Gow, A. and Merk, H. and Michel, J. P. and Miculinic, N. and Mihaltan, F. and Milenkovic, B. and Mohammad, G. M. Y. and Molimard, M. and Momas, I. and Montilla‑Santana, A. and Morais‑Almeida, M. and Morgan, M. and M{\"o}sges, R. and Mullol, J. and Nafti, S. and Namazova‑Baranova, L. and Naclerio, R. and Neou, A. and Neffen, H. and Nekam, K. and Niggemann, B. and Ninot, G. and Nyembue, T. D. and O'Hehir, R. E. and Ohta, K. and Okamoto, Y. and Okubo, K. and Ouedraogo, S. and Paggiaro, P. and Pali‑Sch{\"o}ll, I. and Panzner, P. and Papadopoulos, N. and Papi, A. and Park, H. S. and Passalacqua, G. and Pavord, I. and Pawankar, R. and Pengelly, R. and Pfaar, O. and Picard, R. and Pigearias, B. and Pin, I. and Plavec, D. and Poethig, D. and Pohl, W. and Popov, T. A. and Portejoie, F. and Potter, P. and Postma, D. and Price, D. and Rabe, K. F. and Raciborski, F. and Radier Pontal, F. and Repka‑Ramirez, S. and Reitamo, S. and Rennard, S. and Rodenas, F. and Roberts, J. and Roca, J. and Rodriguez Ma{\~n}as, L. and et al,},
  title     = {Scaling up strategies of the chronic respiratory disease programme of the European Innovation Partnership on Active and Healthy Ageing (Action Plan B3: Area 5)},
  series = {Clinical and Translational Allergy},
  volume    = {6},
  journal   = {Clinical and Translational Allergy},
  number    = {29},
  doi       = {10.1186/s13601-016-0116-9},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-166874},
  year      = {2016},
  abstract  = {Action Plan B3 of the European Innovation Partnership on Active and Healthy Ageing (EIP on AHA) focuses on the integrated care of chronic diseases. Area 5 (Care Pathways) was initiated using chronic respiratory diseases as a model. The chronic respiratory disease action plan includes (1) AIRWAYS integrated care pathways (ICPs), (2) the joint initiative between the Reference site MACVIA-LR (Contre les MAladies Chroniques pour un VIeillissement Actif) and ARIA (Allergic Rhinitis and its Impact on Asthma), (3) Commitments for Action to the European Innovation Partnership on Active and Healthy Ageing and the AIRWAYS ICPs network. It is deployed in collaboration with the World Health Organization Global Alliance against Chronic Respiratory Diseases (GARD). The European Innovation Partnership on Active and Healthy Ageing has proposed a 5-step framework for developing an individual scaling up strategy: (1) what to scale up: (1-a) databases of good practices, (1-b) assessment of viability of the scaling up of good practices, (1-c) classification of good practices for local replication and (2) how to scale up: (2-a) facilitating partnerships for scaling up, (2-b) implementation of key success factors and lessons learnt, including emerging technologies for individualised and predictive medicine. This strategy has already been applied to the chronic respiratory disease action plan of the European Innovation Partnership on Active and Healthy Ageing.},
  language  = {en}
}
@article{GalluzziBravoSanPedroVitaleetal.2015,
  author    = {Galluzzi, L. and Bravo-San Pedro, J. M. and Vitale, I. and Aaronson, S. A. and Abrams, J. M. and Adam, D. and Alnemri, E. S. and Altucci, L. and Andrews, D. and Annicchiarico-Petruzelli, M. and Baehrecke, E. H. and Bazan, N. G. and Bertrand, M. J. and Bianchi, K. and Blagosklonny, M. V. and Blomgren, K. and Borner, C. and Bredesen, D. E. and Brenner, C. and Campanella, M. and Candi, E. and Cecconi, F. and Chan, F. K. and Chandel, N. S. and Cheng, E. H. and Chipuk, J. E. and Cidlowski, J. A. and Ciechanover, A. and Dawson, T. M. and Dawson, V. L. and De Laurenzi, V. and De Maria, R. and Debatin, K. M. and Di Daniele, N. and Dixit, V. M. and Dynlacht, B. D. and El-Deiry, W. S. and Fimia, G. M. and Flavell, R. A. and Fulda, S. and Garrido, C. and Gougeon, M. L. and Green, D. R. and Gronemeyer, H. and Hajnoczky, G. and Hardwick, J. M. and Hengartner, M. O. and Ichijo, H. and Joseph, B. and Jost, P. J. and Kaufmann, T. and Kepp, O. and Klionsky, D. J. and Knight, R. A. and Kumar, S. and Lemasters, J. J. and Levine, B. and Linkermann, A. and Lipton, S. A. and Lockshin, R. A. and L{\´o}pez-Ot{\´i}n, C. and Lugli, E. and Madeo, F. and Malorni, W. and Marine, J. C. and Martin, S. J. and Martinou, J. C. and Medema, J. P. and Meier, P. and Melino, S. and Mizushima, N. and Moll, U. and Mu{\~n}oz-Pinedo, C. and Nu{\~n}ez, G. and Oberst, A. and Panaretakis, T. and Penninger, J. M. and Peter, M. E. and Piacentini, M. and Pinton, P. and Prehn, J. H. and Puthalakath, H. and Rabinovich, G. A. and Ravichandran, K. S. and Rizzuto, R. and Rodrigues, C. M. and Rubinsztein, D. C. and Rudel, T. and Shi, Y. and Simon, H. U. and Stockwell, B. R. and Szabadkai, G. and Tait, S. W. and Tang, H. L. and Tavernarakis, N. and Tsujimoto, Y. and Vanden Berghe, T. and Vandenabeele, P. and Villunger, A. and Wagner, E. F. and Walczak, H. and White, E. and Wood, W. G. and Yuan, J. and Zakeri, Z. and Zhivotovsky, B. and Melino, G. and Kroemer, G.},
  title     = {Essential versus accessory aspects of cell death: recommendations of the NCCD 2015},
  series = {Cell Death and Differentiation},
  volume    = {22},
  journal   = {Cell Death and Differentiation},
  doi       = {10.1038/cdd.2014.137},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-121207},
  pages     = {58-73},
  year      = {2015},
  abstract  = {Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as 'accidental cell death' (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. 'Regulated cell death' (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death.},
  language  = {en}
}
@article{PfefferSchoelGulleetal.1991,
  author    = {Pfeffer, K. and Schoel, H. and Gulle, H. and Moll, Heidrun and Kromer, S. and Kaufmann, S. H. E. and Wagner, H.},
  title     = {Analysis of primary T cell responses to intact and fractionated microbial pathogens},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-46916},
  year      = {1991},
  abstract  = {Freshly isolated human T lymphocytes were tested for their response to mycobacteria, mycobacteriallysates, 2 dimensional (2D) PAGE separated mycobacteriallysates, leishmania and defined leishmanial antigen preparations. While,o T cells proliferated vigourously in the presence of mycobacteria and mycobacteria derived lysates, a significant stimulation from 2 D gel separated lysates was not detected. In addition '10 T cells failed to respond towards leishmania or leishmanial components. In the ab T cell compartment some donors, presumably according to their state of immunity against mycobacteria, responded to mycobacteria, mycobacterial lysates and 2 D gel separated mycobacterial lysates. Neither freshly isolated '10 T cells nor ab T cells from naive donors did mount a significant immune response against leishmania.},
  language  = {en}
}
@article{ElHelouBiegnerBodeetal.2019,
  author    = {El-Helou, Sabine M. and Biegner, Anika-Kerstin and Bode, Sebastian and Ehl, Stephan R. and Heeg, Maximilian and Maccari, Maria E. and Ritterbusch, Henrike and Speckmann, Carsten and Rusch, Stephan and Scheible, Raphael and Warnatz, Klaus and Atschekzei, Faranaz and Beider, Renata and Ernst, Diana and Gerschmann, Stev and Jablonka, Alexandra and Mielke, Gudrun and Schmidt, Reinhold E. and Sch{\"u}rmann, Gesine and Sogkas, Georgios and Baumann, Ulrich H. and Klemann, Christian and Viemann, Dorothee and Bernuth, Horst von and Kr{\"u}ger, Renate and Hanitsch, Leif G. and Scheibenbogen, Carmen M. and Wittke, Kirsten and Albert, Michael H. and Eichinger, Anna and Hauck, Fabian and Klein, Christoph and Rack-Hoch, Anita and Sollinger, Franz M. and Avila, Anne and Borte, Michael and Borte, Stephan and Fasshauer, Maria and Hauenherm, Anja and Kellner, Nils and M{\"u}ller, Anna H. and {\"U}lzen, Anett and Bader, Peter and Bakhtiar, Shahrzad and Lee, Jae-Yun and Heß, Ursula and Schubert, Ralf and W{\"o}lke, Sandra and Zielen, Stefan and Ghosh, Sujal and Laws, Hans-Juergen and Neubert, Jennifer and Oommen, Prasad T. and H{\"o}nig, Manfred and Schulz, Ansgar and Steinmann, Sandra and Klaus, Schwarz and D{\"u}ckers, Gregor and Lamers, Beate and Langemeyer, Vanessa and Niehues, Tim and Shai, Sonu and Graf, Dagmar and M{\"u}glich, Carmen and Schmalzing, Marc T. and Schwaneck, Eva C. and Tony, Hans-Peter and Dirks, Johannes and Haase, Gabriele and Liese, Johannes G. and Morbach, Henner and Foell, Dirk and Hellige, Antje and Wittkowski, Helmut and Masjosthusmann, Katja and Mohr, Michael and Geberzahn, Linda and Hedrich, Christian M. and M{\"u}ller, Christiane and R{\"o}sen-Wolff, Angela and Roesler, Joachim and Zimmermann, Antje and Behrends, Uta and Rieber, Nikolaus and Schauer, Uwe and Handgretinger, Rupert and Holzer, Ursula and Henes, J{\"o}rg and Kanz, Lothar and Boesecke, Christoph and Rockstroh, J{\"u}rgen K. and Schwarze-Zander, Carolynne and Wasmuth, Jan-Christian and Dilloo, Dagmar and H{\"u}lsmann, Brigitte and Sch{\"o}nberger, Stefan and Schreiber, Stefan and Zeuner, Rainald and Ankermann, Tobias and Bismarck, Philipp von and Huppertz, Hans-Iko and Kaiser-Labusch, Petra and Greil, Johann and Jakoby, Donate and Kulozik, Andreas E. and Metzler, Markus and Naumann-Bartsch, Nora and Sobik, Bettina and Graf, Norbert and Heine, Sabine and Kobbe, Robin and Lehmberg, Kai and M{\"u}ller, Ingo and Herrmann, Friedrich and Horneff, Gerd and Klein, Ariane and Peitz, Joachim and Schmidt, Nadine and Bielack, Stefan and Groß-Wieltsch, Ute and Classen, Carl F. and Klasen, Jessica and Deutz, Peter and Kamitz, Dirk and Lassy, Lisa and Tenbrock, Klaus and Wagner, Norbert and Bernbeck, Benedikt and Brummel, Bastian and Lara-Villacanas, Eusebia and M{\"u}nstermann, Esther and Schneider, Dominik T. and Tietsch, Nadine and Westkemper, Marco and Weiß, Michael and Kramm, Christof and K{\"u}hnle, Ingrid and Kullmann, Silke and Girschick, Hermann and Specker, Christof and Vinnemeier-Laubenthal, Elisabeth and Haenicke, Henriette and Schulz, Claudia and Schweigerer, Lothar and M{\"u}ller, Thomas G. and Stiefel, Martina and Belohradsky, Bernd H. and Soetedjo, Veronika and Kindle, Gerhard and Grimbacher, Bodo},
  title     = {The German national registry of primary immunodeficiencies (2012-2017)},
  series = {Frontiers in Immunology},
  volume    = {10},
  journal   = {Frontiers in Immunology},
  doi       = {10.3389/fimmu.2019.01272},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-226629},
  year      = {2019},
  abstract  = {Introduction: The German PID-NET registry was founded in 2009, serving as the first national registry of patients with primary immunodeficiencies (PID) in Germany. It is part of the European Society for Immunodeficiencies (ESID) registry. The primary purpose of the registry is to gather data on the epidemiology, diagnostic delay, diagnosis, and treatment of PIDs. Methods: Clinical and laboratory data was collected from 2,453 patients from 36 German PID centres in an online registry. Data was analysed with the software Stata® and Excel. Results: The minimum prevalence of PID in Germany is 2.72 per 100,000 inhabitants. Among patients aged 1-25, there was a clear predominance of males. The median age of living patients ranged between 7 and 40 years, depending on the respective PID. Predominantly antibody disorders were the most prevalent group with 57\% of all 2,453 PID patients (including 728 CVID patients). A gene defect was identified in 36\% of patients. Familial cases were observed in 21\% of patients. The age of onset for presenting symptoms ranged from birth to late adulthood (range 0-88 years). Presenting symptoms comprised infections (74\%) and immune dysregulation (22\%). Ninety-three patients were diagnosed without prior clinical symptoms. Regarding the general and clinical diagnostic delay, no PID had undergone a slight decrease within the last decade. However, both, SCID and hyper IgE-syndrome showed a substantial improvement in shortening the time between onset of symptoms and genetic diagnosis. Regarding treatment, 49\% of all patients received immunoglobulin G (IgG) substitution (70\%-subcutaneous; 29\%-intravenous; 1\%-unknown). Three-hundred patients underwent at least one hematopoietic stem cell transplantation (HSCT). Five patients had gene therapy. Conclusion: The German PID-NET registry is a precious tool for physicians, researchers, the pharmaceutical industry, politicians, and ultimately the patients, for whom the outcomes will eventually lead to a more timely diagnosis and better treatment.},
  language  = {en}
}
@article{AdrianMartinezAlbertAndreetal.2016,
  author    = {Adri{\´a}n-Mart{\´i}nez, S. and Albert, A. and Andr{\´e}, M. and Anton, G. and Ardid, M. and Aubert, J.-J. and Avgitas, T. and Baret, B. and Barrios-Mart{\´i}, J. and Basa, S. and Bertin, V. and Biagi, S. and Bormuth, R. and Bou-Cabo, M. and Bouwhuis, M.C. and Bruijn, R. and Brunner, J. and Busto, J. and Capone, A. and Caramete, L. and Carr, J. and Celli, S. and Chiarusi, T. and Circella, M. and Coleiro, A. and Coniglione, R. and Costantini, H. and Coyle, P. and Creusot, A. and Deschamps, A. and De Bonis, G. and Distefano, C. and Donzaud, C. and Dornic, D. and Drouhin, D. and Eberl, T. and El Bojaddaini, I. and Els{\"a}sser, D. and Enzenh{\"o}fer, A. and Fehn, K. and Felis, I. and Fusco, L.A. and Galat{\`a}, S. and Gay, P. and Geißels{\"o}der, S. and Geyer, K. and Giordano, V. and Gleixner, A. and Glotin, H. and Gracia-Ruiz, R. and Graf, K. and Hallmann, S. and van Haren, H. and Heijboer, A.J. and Hello, Y. and Hern{\´a}ndez-Rey, J.-J. and H{\"o}ßl, J. and Hofest{\"a}dt, J. and Hugon, C. and Illuminati, G. and James, C.W. and de Jong, M. and Kadler, M. and Kalekin, O. and Katz, U. and Kießling, D. and Kouchner, A. and Kreter, M. and Kreykenbohm, I. and Kulikovskiy, V. and Lachaud, C. and Lahmann, R. and Lef{\`e}vre, D. and Leonora, E. and Loucatos, S. and Marcelin, M. and Margiotta, A. and Marinelli, A. and Mart{\´i}nez-Mora, J.A. and Mathieu, A. and Michael, T. and Migliozzi, P. and Moussa, A. and Mueller, C. and Nezri, E. and Păvălaș, G.E. and Pellegrino, C. and Perrina, C. and Piattelli, P. and Popa, V. and Pradier, T. and Racca, C. and Riccobene, G. and Roensch, K. and Salda{\~n}a, M. and Samtleben, D.F.E. and Sanguineti, M. and Sapienza, P. and Schnabel, J. and Sch{\"u}ssler, F. and Seitz, T. and Sieger, C. and Spurio, M. and Stolarczyk, Th. and S{\´a}nchez-Losa, A. and Taiuti, M. and Trovato, A. and Tselengidou, M. and Turpin, D. and T{\"o}nnis, C. and Vallage, B. and Vall{\´e}e, C. and Van Elewyck, V. and Vivolo, D. and Wagner, S. and Wilms, J. and Zornoza, J.D. and Z{\´u}{\~n}iga, J.},
  title     = {A search for Secluded Dark Matter in the Sun with the ANTARES neutrino telescope},
  series = {Journal of Cosmology and Astroparticle Physics},
  volume    = {2016},
  journal   = {Journal of Cosmology and Astroparticle Physics},
  number    = {5},
  organization    = {The ANTARES collaboration},
  doi       = {10.1088/1475-7516/2016/05/016},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-189035},
  pages     = {12},
  year      = {2016},
  abstract  = {A search for Secluded Dark Matter annihilation in the Sun using 2007-2012 data of the ANTARES neutrino telescope is presented. Three different cases are considered: a) detection of dimuons that result from the decay of the mediator, or neutrino detection from: b) mediator that decays into a dimuon and, in turn, into neutrinos, and c) mediator that decays directly into neutrinos. As no significant excess over background is observed, constraints are derived on the dark matter mass and the lifetime of the mediator.},
  language  = {en}
}
@article{DavisYuKeenanetal.2013,
  author    = {Davis, Lea K. and Yu, Dongmei and Keenan, Clare L. and Gamazon, Eric R. and Konkashbaev, Anuar I. and Derks, Eske M. and Neale, Benjamin M. and Yang, Jian and Lee, S. Hong and Evans, Patrick and Barr, Cathy L. and Bellodi, Laura and Benarroch, Fortu and Berrio, Gabriel Bedoya and Bienvenu, Oscar J. and Bloch, Michael H. and Blom, Rianne M. and Bruun, Ruth D. and Budman, Cathy L. and Camarena, Beatriz and Campbell, Desmond and Cappi, Carolina and Cardona Silgado, Julio C. and Cath, Danielle C. and Cavallini, Maria C. and Chavira, Denise A. and Chouinard, Sylvian and Conti, David V. and Cook, Edwin H. and Coric, Vladimir and Cullen, Bernadette A. and Deforce, Dieter and Delorme, Richard and Dion, Yves and Edlund, Christopher K. and Egberts, Karin and Falkai, Peter and Fernandez, Thomas V. and Gallagher, Patience J. and Garrido, Helena and Geller, Daniel and Girard, Simon L. and Grabe, Hans J. and Grados, Marco A. and Greenberg, Benjamin D. and Gross-Tsur, Varda and Haddad, Stephen and Heiman, Gary A. and Hemmings, Sian M. J. and Hounie, Ana G. and Illmann, Cornelia and Jankovic, Joseph and Jenike, Micheal A. and Kennedy, James L. and King, Robert A. and Kremeyer, Barbara and Kurlan, Roger and Lanzagorta, Nuria and Leboyer, Marion and Leckman, James F. and Lennertz, Leonhard and Liu, Chunyu and Lochner, Christine and Lowe, Thomas L. and Macciardi, Fabio and McCracken, James T. and McGrath, Lauren M. and Restrepo, Sandra C. Mesa and Moessner, Rainald and Morgan, Jubel and Muller, Heike and Murphy, Dennis L. and Naarden, Allan L. and Ochoa, William Cornejo and Ophoff, Roel A. and Osiecki, Lisa and Pakstis, Andrew J. and Pato, Michele T. and Pato, Carlos N. and Piacentini, John and Pittenger, Christopher and Pollak, Yehunda and Rauch, Scott L. and Renner, Tobias J. and Reus, Victor I. and Richter, Margaret A. and Riddle, Mark A. and Robertson, Mary M. and Romero, Roxana and Ros{\`a}rio, Maria C. and Rosenberg, David and Rouleau, Guy A. and Ruhrmann, Stephan and Ruiz-Linares, Andreas and Sampaio, Aline S. and Samuels, Jack and Sandor, Paul and Sheppard, Broke and Singer, Harvey S. and Smit, Jan H. and Stein, Dan J. and Strengman, E. and Tischfield, Jay A. and Valencia Duarte, Ana V. and Vallada, Homero and Van Nieuwerburgh, Flip and Veenstra-VanderWeele, Jeremy and Walitza, Susanne and Wang, Ying and Wendland, Jens R. and Westenberg, Herman G. M. and Shugart, Yin Yao and Miguel, Euripedes C. and McMahon, William and Wagner, Michael and Nicolini, Humberto and Posthuma, Danielle and Hanna, Gregory L. and Heutink, Peter and Denys, Damiaan and Arnold, Paul D. and Oostra, Ben A. and Nestadt, Gerald and Freimer, Nelson B. and Pauls, David L. and Wray, Naomi R. and Stewart, S. Evelyn and Mathews, Carol A. and Knowles, James A. and Cox, Nancy J. and Scharf, Jeremiah M.},
  title     = {Partitioning the Heritability of Tourette Syndrome and Obsessive Compulsive Disorder Reveals Differences in Genetic Architecture},
  series = {PLoS Genetics},
  volume    = {9},
  journal   = {PLoS Genetics},
  number    = {10},
  issn      = {1553-7390},
  doi       = {10.1371/journal.pgen.1003864},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127377},
  pages     = {e1003864},
  year      = {2013},
  abstract  = {The direct estimation of heritability from genome-wide common variant data as implemented in the program Genome-wide Complex Trait Analysis (GCTA) has provided a means to quantify heritability attributable to all interrogated variants. We have quantified the variance in liability to disease explained by all SNPs for two phenotypically-related neurobehavioral disorders, obsessive-compulsive disorder (OCD) and Tourette Syndrome (TS), using GCTA. Our analysis yielded a heritability point estimate of 0.58 (se = 0.09, p = 5.64e-12) for TS, and 0.37 (se = 0.07, p = 1.5e-07) for OCD. In addition, we conducted multiple genomic partitioning analyses to identify genomic elements that concentrate this heritability. We examined genomic architectures of TS and OCD by chromosome, MAF bin, and functional annotations. In addition, we assessed heritability for early onset and adult onset OCD. Among other notable results, we found that SNPs with a minor allele frequency of less than 5\% accounted for 21\% of the TS heritability and 0\% of the OCD heritability. Additionally, we identified a significant contribution to TS and OCD heritability by variants significantly associated with gene expression in two regions of the brain (parietal cortex and cerebellum) for which we had available expression quantitative trait loci (eQTLs). Finally we analyzed the genetic correlation between TS and OCD, revealing a genetic correlation of 0.41 (se = 0.15, p = 0.002). These results are very close to previous heritability estimates for TS and OCD based on twin and family studies, suggesting that very little, if any, heritability is truly missing (i.e., unassayed) from TS and OCD GWAS studies of common variation. The results also indicate that there is some genetic overlap between these two phenotypically-related neuropsychiatric disorders, but suggest that the two disorders have distinct genetic architectures.},
  language  = {en}
}
@article{AdrianMartinezAlbertAndreetal.2016,
  author    = {Adri{\´a}n-Mart{\´i}nez, S. and Albert, A. and Andr{\´e}, M. and Anton, G. and Ardid, M. and Aubert, J.-J. and Avgitas, T. and Baret, B. and Barrios-Mart{\´i}, J. and Basa, S. and Bertin, V. and Biagi, S. and Bormuth, R. and Bouwhuis, M.C. and Bruijn, R. and Brunner, J. and Busto, J. and Capone, A. and Caramete, L. and Carr, J. and Celli, S. and Chiarusi, T. and Circella, M. and Coleiro, A. and Coniglione, R. and Costantini, H. and Coyle, P. and Creusot, A. and Deschamps, A. and De Bonis, G. and Distefano, C. and Donzaud, C. and Dornic, D. and Drouhin, D. and Eberl, T. and El Bojaddaini, I. and Els{\"a}sser, D. and Enzenh{\"o}fer, A. and Fehn, K. and Felis, I. and Fusco, L.A. and Galat{\`a}, S. and Gay, P. and Geißels{\"o}der, S. and Geyer, K. and Giordano, V. and Gleixner, A. and Glotin, H. and Gracia-Ruiz, R. and Graf, K. and Hallmann, S. and van Haren, H. and Heijboer, A.J. and Hello, Y. and Hern{\´a}ndez-Rey, J.J. and H{\"o}ßl, J. and Hofest{\"a}dt, J. and Hugon, C. and Illuminati, G. and James, C.W. and de Jong, M. and Jongen, M. and Kadler, M. and Kalekin, O. and Katz, U. and Kießling, D. and Kouchner, A. and Kreter, M. and Kreykenbohm, I. and Kulikovskiy, V. and Lachaud, C. and Lahmann, R. and Lef{\`e}vre, D. and Leonora, E. and Loucatos, S. and Marcelin, M. and Margiotta, A. and Marinelli, A. and Mart{\´i}nez-Mora, J.A. and Mathieu, A. and Melis, K. and Michael, T. and Migliozzi, P. and Moussa, A. and Mueller, C. and Nezri, E. and Pavalas, G.E. and Pellegrino, C. and Perrina, C. and Piattelli, P. and Popa, V. and Pradier, T. and Racca, C. and Riccobene, G. and Roensch, K. and Salda{\~n}a, M. and Samtleben, D.F.E. and S{\´a}nchez-Losa, A. and Sanguineti, M. and Sapienza, P. and Schnabel, J. and Sch{\"u}ssler, F. and Seitz, T. and Sieger, C. and Spurio, M. and Stolarczyk, Th. and Taiuti, M. and T{\"o}nnis, C. and Trovato, A. and Tselengidou, M. and Turpin, D. and Vallage, B. and Vall{\´e}e, C. and Van Elewyck, V. and Vivolo, D. and Wagner, S. and Wilms, J. and Zornoza, J.D. and Z{\´u}{\~n}iga, J.},
  title     = {Limits on dark matter annihilation in the sun using the ANTARES neutrino telescope},
  series = {Physics Letters B},
  volume    = {759},
  journal   = {Physics Letters B},
  doi       = {10.1016/j.physletb.2016.05.019},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-166642},
  pages     = {69-74},
  year      = {2016},
  abstract  = {A search for muon neutrinos originating from dark matter annihilations in the Sun is performed using the data recorded by the ANTARES neutrino telescope from 2007 to 2012. In order to obtain the best possible sensitivities to dark matter signals, an optimisation of the event selection criteria is performed taking into account the background of atmospheric muons, atmospheric neutrinos and the energy spectra of the expected neutrino signals. No significant excess over the background is observed and 90\% C.L. upper limits on the neutrino flux, the spin-dependent and spin-independent WIMP-nucleon cross-sections are derived for WIMP masses ranging from 50 GeV to 5 TeV for the annihilation channels WIMP + WIMP→ b\(\overline{b}\), W\(^{+}\)W\(^{-}\) and τ\(^{+}\)τ\(^{-}\).},
  language  = {en}
}
@article{AdrianMartinezAlbertAndreetal.2016,
  author    = {Adri{\´a}n-Mart{\´i}nez, S. and Albert, A. and Andr{\´e}, M. and Anghinolfi, M. and Anton, G. and Ardid, M. and Aubert, J.-J. and Avgitas, T. and Baret, B. and Barrios-Mart{\´i}, J. and Basa, S. and Bertin, V. and Biagi, S. and Bormuth, R. and Bouwhuis, M.C. and Bruijn, R. and Brunner, J. and Busto, J. and Capone, A. and Caramete, L. and Carr, J. and Celli, S. and Chiarusi, T. and Circella, M. and Coleiro, A. and Coniglione, R. and Constantini, H. and Coyle, P. and Creusot, A. and Deschamps, A. and De Bonis, G. and Distefano, C. and Donzaud, C. and Dornic, D. and Drouhin, D. and Eberl, T. and El Bojaddaini, I. and Els{\"a}sser, D. and Enzenh{\"o}fer, A. and Fehn, K. and Felis, I. and Fusco, L.A. and Galat{\`a}, S. and Gay, P. and Geißels{\"o}der, S. and Geyer, K. and Giordano, V. and Gleixner, A. and Glotin, H. and Gracia-Ruiz, R. and Graf, K. and Hallmann, S. and van Haren, H. and Heijboer, A.J. and Hello, Y. and Hern{\´a}ndez-Rey, J.J. and H{\"o}ßl, J. and Hofest{\"a}dt, J. and Hugon, C. and Illuminati, G. and James, C.W. and de Jong, M. and Kadler, M. and Kalekin, O. and Katz, U. and Kießling, D. and Kouchner, A. and Kreter, M. and Kreykenbohm, I. and Kulikovskiy, V. and Lachaud, C. and Lahmann, R. and Lef{\`e}vre, D. and Leonora, E. and Loucatos, S. and Marcelin, M. and Margiotta, A. and Marinelli, A. and Mart{\´i}nez-Mora, J.A. and Mathieu, A. and Michael, T. and Migliozzi, P. and Moussa, A. and Mueller, C. and Nezri, E. and Pavalas, G.E. and Pellegrino, C. and Perrina, C. and Piattelli, P. and Popa, V. and Pradier, T. and Racca, C. and Riccobene, G. and Roensch, K. and Salda{\~n}a, M. and Samtleben, D.F.E. and S{\´a}nchez-Losa, A. and Sanguineti, M. and Sapienza, P. and Schnabel, J. and Sch{\"u}ssler, F. and Seitz, T. and Sieger, C. and Spurio, M. and Stolarczyk, Th. and Taiuti, M. and Trovato, A. and Tselengidou, M. and Turpin, D. and T{\"o}nnis, C. and Vallage, B. and Vall{\´e}e, C. and Van Elewyck, V. and Visser, E. and Vivolo, D. and Wagner, S. and Wilms, J. and Zornoza, J.D. and Z{\´u}{\~n}iga, J.},
  title     = {Constraints on the neutrino emission from the Galactic Ridge with the ANTARES telescope},
  series = {Physics Letters B},
  volume    = {760},
  journal   = {Physics Letters B},
  doi       = {10.1016/j.physletb.2016.06.051},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-166608},
  pages     = {143-148},
  year      = {2016},
  abstract  = {A highly significant excess of high-energy astrophysical neutrinos has been reported by the IceCube Collaboration. Some features of the energy and declination distributions of IceCube events hint at a North/South asymmetry of the neutrino flux. This could be due to the presence of the bulk of our Galaxy in the Southern hemisphere. The ANTARES neutrino telescope, located in the Mediterranean Sea, has been taking data since 2007. It offers the best sensitivity to muon neutrinos produced by galactic cosmic ray interactions in this region of the sky. In this letter a search for an extended neutrino flux from the Galactic Ridge region is presented. Different models of neutrino production by cosmic ray propagation are tested. No excess of events is observed and upper limits for different neutrino flux spectral indices Γ are set. For Γ=2.4 the 90\% confidence level flux upper limit at 100 TeV for one neutrino flavour corresponds to Φ\(^{1f}_{0}\) (100 TeV) = 2.0 · 10\(^{-17}\) GeV\(^{-1}\) cm\(^{-2}\)s\(^{-1}\)sr\(^{-1}\). Under this assumption, at most two events of the IceCube cosmic candidates can originate from the Galactic Ridge. A simple power-law extrapolation of the Fermi-LAT flux to account for IceCube High Energy Starting Events is excluded at 90\% confidence level.},
  language  = {en}
}
@article{SyldatkAndreeStoffregenetal.1987,
  author    = {Syldatk, C. and Andree, H. and Stoffregen, A. and Wagner, F. and Stumpf, B. and Ernst, L. and Zilch, H. and Tacke, Reinhold},
  title     = {Enantioselective reduction of acetyldimethylphenylsilane by Trigonopsis variabilis (DSM 70714)},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63836},
  year      = {1987},
  abstract  = {Growing and resting cells of the yeast Trigonapsis variabilis (DSM 70714) can be used for the enantioselective reduction of the organosilicon compound acetyldimethylphenylsilane (J) to give optically active (R)-(1-hydroxyethyl)dimethylphenylsilane [(R)-2] in good yields. The enantiomeric purity of the isolated product was determined tobe 62-86\% ee depending on the substrate concentration used. Both substrate and product caused an inhibition of the reaction at concentrations higher than 0.35 and 0.5 g/1, respectively. Besides, higher substrate and product concentrations led to increased formation of the by-product 1,1,3,3-tetramethyl-1,3-diphenyldisiloxane. Considering the limiting substrate and product concentrations, it was possible to use the same biomass at least 5 times without significant loss of enzyme activity. 3-Methyl-3-phenyl-2-butanone (5) and acetyldimethylphenylgermane (7), which represent carbon and germanium analogues of 1, were also found to be accepted as substrates by Trigonapsis variabilis (DSM 70714). The reduction rates of the silicon {1) and germanium compound {7) were much higher than the transformation rate of the corresponding carbon analogue 5.},
  subject      = {Anorganische Chemie},
  language  = {en}
}
@article{LambrechtFeifelWagnerRoederetal.1989,
  author    = {Lambrecht, G. and Feifel, R. and Wagner-R{\"o}der, M. and Strohmann, C. and Zilch, H. and Tacke, Reinhold and Waelbroeck, M. and Christophe, J. and Boddeke, H. and Mutschler, E.},
  title     = {Affinity profiles of hexahydro-sila-difenidol analogues at muscarinic receptor subtypes},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63979},
  year      = {1989},
  abstract  = {In an attempt to assess the structural requirements of hexahydro-sila-difenidol for potency and selectivity, a series of analogues modified in the amino group and the phenyl ring were investigated for their affinity to muscarinic M1- (rabbit vas deferens), Mr (guinea-pig atria) and Mr (guinea-pig ileum) receptors. All compounds were competitive antagonists in the three tissues. Their affinities to the three muscarinic receptor subtypes differed by more than two orders of magnitude and the observed receptor selectivities were not associated with high affinity. The pyrrolidino and hexamethyleneimino analogues, compounds substituted in the phenylring with a methoxy group or a chlorine atom as weil as p-fluoro-hexahydro-difenidol displayed the same affinity profile as the parent compound, hexahydro-sila-difenidol: M1 = M3 > M2 • A different selectivity patternwas observed for p-fluoro-hexahydro-sila-difenidol: M3 > M1 > M2 • This compound exhibited its highest affinity for M3-receptors in guinea-pig ileum (pA 2 = 7.84), intermediate affinity for M1-receptors in rabbit vas deferens (pA 2 = 6.68) and lowest affinity for the Mrreceptors in guinea-pig atria (pA 2 = 6.01). This receptor selectivity profile of p-fluoro-hexahydro-sila-difenidol was confirmed in ganglia (M1), atria (M2 ) and ileum (M 3 ) of the rat. Furthermore, dose ratios obtained with either pirenzepine (Mt) or hexahydrosila- difenidol (M2 and M3) and the p-fluoro analogue used in combination suggested that the antagonism was additive, implying mutual competition with a single population of muscarinic receptor subtypes. These results indicate that p-fluoro-hexahydro-sila-difenidol represents a valuable tool for characterization of muscarinic receptor subtypes.},
  subject      = {Anorganische Chemie},
  language  = {en}
}
@article{HircheKnoopHebestreitetal.2014,
  author    = {Hirche, T. O. and Knoop, C. and Hebestreit, H. and Shimmin, D. and Sol{\´e}, A. and Elborn, J. S. and Ellemunter, H. and Aurora, P. and Hogardt, M. and Wagner, T. O. F.},
  title     = {Practical Guidelines: Lung Transplantation in Patients with Cystic Fibrosis},
  series = {Pulmonary Medicine},
  volume    = {2014},
  journal   = {Pulmonary Medicine},
  organization    = {ECORN-CF Study Group},
  issn      = {2090-1836},
  doi       = {10.1155/2014/621342},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-121569},
  pages     = {621342},
  year      = {2014},
  abstract  = {There are no European recommendations on issues specifically related to lung transplantation (LTX) in cystic fibrosis (CF). The main goal of this paper is to provide CF care team members with clinically relevant CF-specific information on all aspects of LTX, highlighting areas of consensus and controversy throughout Europe. Bilateral lung transplantation has been shown to be an important therapeutic option for end-stage CF pulmonary disease. Transplant function and patient survival after transplantation are better than in most other indications for this procedure. Attention though has to be paid to pretransplant morbidity, time for referral, evaluation, indication, and contraindication in children and in adults. This review makes extensive use of specific evidence in the field of lung transplantation in CF patients and addresses all issues of practical importance. The requirements of pre-, peri-, and postoperative management are discussed in detail including bridging to transplant and postoperative complications, immune suppression, chronic allograft dysfunction, infection, and malignancies being the most important. Among the contributors to this guiding information are 19 members of the ECORN-CF project and other experts. The document is endorsed by the European Cystic Fibrosis Society and sponsored by the Christiane Herzog Foundation.},
  language  = {en}
}
@inproceedings{ClarkeWagnerEllgring1981,
  author    = {Clarke, A. H. and Wagner, H. and Ellgring, Johann Heinrich},
  title     = {Eine syntaktische Analyse von Sprechen und Blickverhalten bei dyadischer Interaktion},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42093},
  year      = {1981},
  abstract  = {No abstract available},
  language  = {de}
}
@article{WagnerClarkeEllgring1983,
  author    = {Wagner, H. and Clarke, A. H. and Ellgring, Johann Heinrich},
  title     = {Eye-contact and individual looking - The role of chance},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42078},
  year      = {1983},
  abstract  = {No abstract available},
  language  = {de}
}
@article{FritscheSyldatkWagneretal.1989,
  author    = {Fritsche, K. and Syldatk, C. and Wagner, F. and Hengelsberg, H. and Tacke, Reinhold},
  title     = {Enzymatic resolution of rac-1,1-dimethyl-1-sila-cyclohexan-2-ol by ester hydrolysis or transesterification using a crude lipase preparation of Candida cylindracea},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63967},
  year      = {1989},
  abstract  = {No abstract available},
  subject      = {Anorganische Chemie},
  language  = {en}
}
@article{HengelsbergTackeFritscheetal.1991,
  author    = {Hengelsberg, H. and Tacke, Reinhold and Fritsche, K. and Syldatk, C. and Wagner, F.},
  title     = {Synthesis and enantioselective enzymatic hydrolysis of rac-dimethylphenyl[1-(phenylacetamido)- ethyl]silane},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-64153},
  year      = {1991},
  abstract  = {Racemic dimethylphenyl(l-(phenylacetamido)ethyl)silane [rac-5) has been made by a four-step synthesis starting from (chloromethyl)dimethylphenylsilane [PhMe\(_2\)SiCH2Cl (1) ~ PhMe\(_2\)SiCH(Cl)Me (rac-2) - PhMe\(_2\)SiCH(l)Me (rac-3) - PhMe2SiCH(NH2)Me (rac-4) ~ PhMe\(_2\)SiCH[N(H)C(O)CH\(_2\)Ph]Me ( rac-5); total yield 41\% ). Enantioselective enzymatic hydrolysis of rac-5, catalyzed by immobilized penicillin G acylase (E.C. 3.5.1.11) from Escherichia coli 5K (pHM 12), gave (R)-(1- aminoethyl)dimethylphenylsilane [( R )-4] in 40\% yield with an enantiomeric purity of 92\% ee.},
  subject      = {Anorganische Chemie},
  language  = {en}
}
@article{WagnerVolkmerSharanetal.2014,
  author    = {Wagner, Ines and Volkmer, Michael and Sharan, Malvika and Villaveces, Jose M. and Oswald, Felix and Surendranath, Vineeth and Habermann, Bianca H.},
  title     = {morFeus: a web-based program to detect remotely conserved orthologs using symmetrical best hits and orthology network scoring},
  series = {BMC Bioinformatics},
  volume    = {15},
  journal   = {BMC Bioinformatics},
  number    = {263},
  doi       = {10.1186/1471-2105-15-263},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-115590},
  year      = {2014},
  abstract  = {Background: Searching the orthologs of a given protein or DNA sequence is one of the most important and most commonly used Bioinformatics methods in Biology. Programs like BLAST or the orthology search engine Inparanoid can be used to find orthologs when the similarity between two sequences is sufficiently high. They however fail when the level of conservation is low. The detection of remotely conserved proteins oftentimes involves sophisticated manual intervention that is difficult to automate. Results: Here, we introduce morFeus, a search program to find remotely conserved orthologs. Based on relaxed sequence similarity searches, morFeus selects sequences based on the similarity of their alignments to the query, tests for orthology by iterative reciprocal BLAST searches and calculates a network score for the resulting network of orthologs that is a measure of orthology independent of the E-value. Detecting remotely conserved orthologs of a protein using morFeus thus requires no manual intervention. We demonstrate the performance of morFeus by comparing it to state-of-the-art orthology resources and methods. We provide an example of remotely conserved orthologs, which were experimentally shown to be functionally equivalent in the respective organisms and therefore meet the criteria of the orthology-function conjecture. Conclusions: Based on our results, we conclude that morFeus is a powerful and specific search method for detecting remotely conserved orthologs.},
  language  = {en}
}
@article{BousquetAntoBachertetal.2021,
  author    = {Bousquet, Jean and Anto, Josep M. and Bachert, Claus and Haahtela, Tari and Zuberbier, Torsten and Czarlewski, Wienczyslawa and Bedbrook, Anna and Bosnic-Anticevich, Sinthia and Walter Canonica, G. and Cardona, Victoria and Costa, Elisio and Cruz, Alvaro A. and Erhola, Marina and Fokkens, Wytske J. and Fonseca, Joao A. and Illario, Maddalena and Ivancevich, Juan-Carlos and Jutel, Marek and Klimek, Ludger and Kuna, Piotr and Kvedariene, Violeta and Le, LTT and Larenas-Linnemann, D{\´e}sir{\´e}e E. and Laune, Daniel and Louren{\c{c}}o, Olga M. and Mel{\´e}n, Erik and Mullol, Joaquim and Niedoszytko, Marek and Odemyr, Mika{\"e}la and Okamoto, Yoshitaka and Papadopoulos, Nikos G. and Patella, Vincenzo and Pfaar, Oliver and Pham-Thi, Nh{\^a}n and Rolland, Christine and Samolinski, Boleslaw and Sheikh, Aziz and Sofiev, Mikhail and Suppli Ulrik, Charlotte and Todo-Bom, Ana and Tomazic, Peter-Valentin and Toppila-Salmi, Sanna and Tsiligianni, Ioanna and Valiulis, Arunas and Valovirta, Erkka and Ventura, Maria-Teresa and Walker, Samantha and Williams, Sian and Yorgancioglu, Arzu and Agache, Ioana and Akdis, Cezmi A. and Almeida, Rute and Ansotegui, Ignacio J. and Annesi-Maesano, Isabella and Arnavielhe, Sylvie and Basaga{\~n}a, Xavier and D. Bateman, Eric and B{\´e}dard, Annabelle and Bedolla-Barajas, Martin and Becker, Sven and Bennoor, Kazi S. and Benveniste, Samuel and Bergmann, Karl C. and Bewick, Michael and Bialek, Slawomir and E. Billo, Nils and Bindslev-Jensen, Carsten and Bjermer, Leif and Blain, Hubert and Bonini, Matteo and Bonniaud, Philippe and Bosse, Isabelle and Bouchard, Jacques and Boulet, Louis-Philippe and Bourret, Rodolphe and Boussery, Koen and Braido, Fluvio and Briedis, Vitalis and Briggs, Andrew and Brightling, Christopher E. and Brozek, Jan and Brusselle, Guy and Brussino, Luisa and Buhl, Roland and Buonaiuto, Roland and Calderon, Moises A. and Camargos, Paulo and Camuzat, Thierry and Caraballo, Luis and Carriazo, Ana-Maria and Carr, Warner and Cartier, Christine and Casale, Thomas and Cecchi, Lorenzo and Cepeda Sarabia, Alfonso M. and H. Chavannes, Niels and Chkhartishvili, Ekaterine and Chu, Derek K. and Cingi, Cemal and Correia de Sousa, Jaime and Costa, David J. and Courbis, Anne-Lise and Custovic, Adnan and Cvetkosvki, Biljana and D'Amato, Gennaro and da Silva, Jane and Dantas, Carina and Dokic, Dejan and Dauvilliers, Yves and De Feo, Giulia and De Vries, Govert and Devillier, Philippe and Di Capua, Stefania and Dray, Gerard and Dubakiene, Ruta and Durham, Stephen R. and Dykewicz, Mark and Ebisawa, Motohiro and Gaga, Mina and El-Gamal, Yehia and Heffler, Enrico and Emuzyte, Regina and Farrell, John and Fauquert, Jean-Luc and Fiocchi, Alessandro and Fink-Wagner, Antje and Fontaine, Jean-Fran{\c{c}}ois and Fuentes Perez, Jos{\´e} M. and Gemicioğlu, Bilun and Gamkrelidze, Amiran and Garcia-Aymerich, Judith and Gevaert, Philippe and Gomez, Ren{\´e} Maximiliano and Gonz{\´a}lez Diaz, Sandra and Gotua, Maia and Guldemond, Nick A. and Guzm{\´a}n, Maria-Antonieta and Hajjam, Jawad and Huerta Villalobos, Yunuen R. and Humbert, Marc and Iaccarino, Guido and Ierodiakonou, Despo and Iinuma, Tomohisa and Jassem, Ewa and Joos, Guy and Jung, Ki-Suck and Kaidashev, Igor and Kalayci, Omer and Kardas, Przemyslaw and Keil, Thomas and Khaitov, Musa and Khaltaev, Nikolai and Kleine-Tebbe, Jorg and Kouznetsov, Rostislav and Kowalski, Marek L. and Kritikos, Vicky and Kull, Inger and La Grutta, Stefania and Leonardini, Lisa and Ljungberg, Henrik and Lieberman, Philip and Lipworth, Brian and Lodrup Carlsen, Karin C. and Lopes-Pereira, Catarina and Loureiro, Claudia C. and Louis, Renaud and Mair, Alpana and Mahboub, Bassam and Makris, Micha{\"e}l and Malva, Joao and Manning, Patrick and Marshall, Gailen D. and Masjedi, Mohamed R. and Maspero, Jorge F. and Carreiro-Martins, Pedro and Makela, Mika and Mathieu-Dupas, Eve and Maurer, Marcus and De Manuel Keenoy, Esteban and Melo-Gomes, Elisabete and Meltzer, Eli O. and Menditto, Enrica and Mercier, Jacques and Micheli, Yann and Miculinic, Neven and Mihaltan, Florin and Milenkovic, Branislava and Mitsias, Dimitirios I. and Moda, Giuliana and Mogica-Martinez, Maria-Dolores and Mohammad, Yousser and Montefort, Steve and Monti, Ricardo and Morais-Almeida, Mario and M{\"o}sges, Ralph and M{\"u}nter, Lars and Muraro, Antonella and Murray, Ruth and Naclerio, Robert and Napoli, Luigi and Namazova-Baranova, Leyla and Neffen, Hugo and Nekam, Kristoff and Neou, Angelo and Nordlund, Bj{\"o}rn and Novellino, Ettore and Nyembue, Dieudonn{\´e} and O'Hehir, Robyn and Ohta, Ken and Okubo, Kimi and Onorato, Gabrielle L. and Orlando, Valentina and Ouedraogo, Solange and Palamarchuk, Julia and Pali-Sch{\"o}ll, Isabella and Panzner, Peter and Park, Hae-Sim and Passalacqua, Gianni and P{\´e}pin, Jean-Louis and Paulino, Ema and Pawankar, Ruby and Phillips, Jim and Picard, Robert and Pinnock, Hilary and Plavec, Davor and Popov, Todor A. and Portejoie, Fabienne and Price, David and Prokopakis, Emmanuel P. and Psarros, Fotis and Pugin, Benoit and Puggioni, Francesca and Quinones-Delgado, Pablo and Raciborski, Filip and Rajabian-S{\"o}derlund, Rojin and Regateiro, Frederico S. and Reitsma, Sietze and Rivero-Yeverino, Daniela and Roberts, Graham and Roche, Nicolas and Rodriguez-Zagal, Erendira and Rolland, Christine and Roller-Wirnsberger, Regina E. and Rosario, Nelson and Romano, Antonino and Rottem, Menachem and Ryan, Dermot and Salim{\"a}ki, Johanna and Sanchez-Borges, Mario M. and Sastre, Joaquin and Scadding, Glenis K. and Scheire, Sophie and Schmid-Grendelmeier, Peter and Sch{\"u}nemann, Holger J. and Sarquis Serpa, Faradiba and Shamji, Mohamed and Sisul, Juan-Carlos and Sofiev, Mikhail and Sol{\´e}, Dirceu and Somekh, David and Sooronbaev, Talant and Sova, Milan and Spertini, Fran{\c{c}}ois and Spranger, Otto and Stellato, Cristiana and Stelmach, Rafael and Thibaudon, Michel and To, Teresa and Toumi, Mondher and Usmani, Omar and Valero, Antonio A. and Valenta, Rudolph and Valentin-Rostan, Marylin and Pereira, Marilyn Urrutia and van der Kleij, Rianne and Van Eerd, Michiel and Vandenplas, Olivier and Vasankari, Tuula and Vaz Carneiro, Antonio and Vezzani, Giorgio and Viart, Fr{\´e}d{\´e}ric and Viegi, Giovanni and Wallace, Dana and Wagenmann, Martin and Wang, De Yun and Waserman, Susan and Wickman, Magnus and Williams, Dennis M. and Wong, Gary and Wroczynski, Piotr and Yiallouros, Panayiotis K. and Yusuf, Osman M. and Zar, Heather J. and Zeng, St{\´e}phane and Zernotti, Mario E. and Zhang, Luo and Shan Zhong, Nan and Zidarn, Mihaela},
  title     = {ARIA digital anamorphosis: Digital transformation of health and care in airway diseases from research to practice},
  series = {Allergy},
  volume    = {76},
  journal   = {Allergy},
  number    = {1},
  doi       = {10.1111/all.14422},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-228339},
  pages     = {168 -- 190},
  year      = {2021},
  abstract  = {Digital anamorphosis is used to define a distorted image of health and care that may be viewed correctly using digital tools and strategies. MASK digital anamorphosis represents the process used by MASK to develop the digital transformation of health and care in rhinitis. It strengthens the ARIA change management strategy in the prevention and management of airway disease. The MASK strategy is based on validated digital tools. Using the MASK digital tool and the CARAT online enhanced clinical framework, solutions for practical steps of digital enhancement of care are proposed.},
  language  = {en}
}
@incollection{ClarkeEllgringWagner1980,
  author    = {Clarke, AH and Ellgring, Johann Heinrich and Wagner, H.},
  title     = {Situational effects on the syntax of speech and gaze behaviour in dyads},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-50316},
  publisher      = {Universit{\"a}t W{\"u}rzburg},
  year      = {1980},
  abstract  = {A substantial literature exists on the coordination of speaking and looking behaviour and their significance as indicators for the production and reception of social information. Within this framework, the temporal organisation of such behaviour has been 'shown to reflect both the coordination within the individual and between participants in a situation. In this paper, it is proposed that observed behavioural sequences may be formally described by rules of syntax, thus implying the likelihood of structural organisation as opposed to, for example, linear time dependence between behavioural states. This being the case, differing sets of rules and grammars respectively can be expected for various social situations. Clinical interviews and discu~sions between couples on a topic of marital conflict were analysed, the on-off patterns of speech and gaze being taken as data. The resulting behavioural repertoire was regarded, in the sense of a formal grammar, as the terminal vocabulary. A set of rewriting rules was determined and their associated probabilities inferred. The situational conditions were found to be reflectedin the syntactic features of the grammatical model - the terminal vocabulary, the production rules and the production probabilities.},
  subject      = {Psychologie},
  language  = {en}
}
@incollection{ClarkeEllgringWagner1981,
  author    = {Clarke, Andrew H. and Ellgring, Johann Heinrich and Wagner, Helmut},
  title     = {Analyse des Blickverhaltens in sozialen Situationen},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-43012},
  publisher      = {Universit{\"a}t W{\"u}rzburg},
  year      = {1981},
  abstract  = {Der vorliegende Beitrag behandelt inhaltliche und methodische Probleme einer L{\"a}ngsschnittstudie, die derzeit am MPI f{\"u}r Psychiatrie in M{\"u}nchen an depressiven Patienten durchgef{\"u}hrt wird. Diese Untersuchung hat einen diagnostischen und einen kommunikationstheoretischen Aspekt. Von diagnostischem Interesse sind die depressionsspezifischen Ver{\"a}nderungen des kommunikativen Verhaltens. Kommunikationstheoretisch gewendet lautet die Frage, wie sich der interne Zustand einer Person in ihrem Verhalten reflektiert. In diesem Beitrag wird die Fragestellung konzentriert auf tonische Eigenschaften des Blickverhaltens im Interaktionsprozeß und deren Stabilit{\"a}t im Krankheitsverlauf. Zun{\"a}chst wird die theoretische Grundlage referiert, die wir f{\"u}r das Blickverhalten entwickelt haben. Im zweiten Abschnitt wird auf Datenerhebung und Reliabilit{\"a}tskontrolle eingegangen. Die Struktur der Daten bestimmt die Auswertungsmethoden. Einige der Methoden, mit denen wir derzeit arbeiten, werden im Zusammenhang mit umschriebenen Problemstellungen erl{\"a}utert: Deskription und Interpretation des tonischen Blickverhaltens depressiver Patienten im Krankheitsverlauf (Abschnitt 3). Zusammenhang der individuellen Blickniveaus von Interaktionspartnern (Abschnitt 4) Deskription eines Dialogs (Interviews) als Sequenz von distinkten Zust{\"a}nden. In den Zust{\"a}nden werden Sprech- und Blickverhalten beider Interaktionspartner miteinander kombiniert (Abschnitt 5) Analyse der intraindividuellen Wechselwirkung zwischen Blick- und Sprechverhalten (Abschnitt 6). Die Abschnitte 3 mit 6 werden durch vorl{\"a}ufige Ergebnisse illustriert.},
  language  = {de}
}
@article{EllgringWagnerClarke1980,
  author    = {Ellgring, Johann Heinrich and Wagner, Helmut and Clarke, Andrew H.},
  title     = {Bin{\"a}re Kodierung von Sprechen und Blicken: Validit{\"a}t, Reliabilit{\"a}t und ihre Abh{\"a}ngigkeit von der zeitlichen Aufl{\"o}sung},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-43163},
  year      = {1980},
  abstract  = {Validit{\"a}t und Reliabilit{\"a}t der Sprechkodierung einer Beobachtergruppe wurden in Abh{\"a}ngigkeit von der zeitlichen Aufl{\"o}sung untersucht. Die Validit{\"a}t wurde anhand der {\"U}bereinstimmung der Beobachter mit einem automatischen Sprachdetektor berechnet. Die Reliabilit{\"a}tswerte f{\"u}r die Kodierung von Sprechen und Blikken ergaben sich aus der {\"U}bereinstimmung der Beobachter untereinander. Im wesentlichen zeigten sich folgende Ergebnisse: 1. Die Validit{\"a}t/Reliabilit{\"a}t der Sprechkodierung ist eine monotone, nichtlineare Funktion der gew{\"a}hlten Aufl{\"o}sung. Die systematischen Fehler, die auf Latenz und Tr{\"a}gheit der menschlichen Beobachter zur{\"u}ckgehen, werden bei einer Aufl{\"o}sung von 400 msec nahezu vollst{\"a}ndig unterdr{\"u}ckt. 2. Weder bei der Erfassung des Sprech- noch des Blickverhaltens lassen sich Anzeichen f{\"u}r Observer-Drift feststellen. Trainierte und untrainierte Beobachter unterscheiden sich nicht signifikant. 3. Die Kodierung des Sprechverhaltens ist geringf{\"u}gig reliabler als die des Blickverhaltens. Dieser Unterschied kann in der Praxis vernachl{\"a}ssigt werden.},
  language  = {de}
}
@incollection{EllgringWagnerClarke1980,
  author    = {Ellgring, Johann Heinrich and Wagner, H. and Clarke, AH},
  title     = {Psychopathological states and their effects on speech and gaze behaviour},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-50323},
  publisher      = {Universit{\"a}t W{\"u}rzburg},
  year      = {1980},
  abstract  = {Internal characteristics such as depressed mood, anxiety and general negative emotions are accompanied, particularly during depressive illness, by changes in observable behaviour. Accordingly, the following questions may be examined: are intra-individual changes in speech and gaze behaviour related to changes in the internal psychopathological state? Further, do these changes occur synchronously to changes in the state of subjective well-being? A longitudinal study was made on depressed patients. Their behaviour was observed during standardised interviews and diagnostic-therapeutic discussions held at regu~ lar intervals. Various speech and gaze parameters were examined with respect to their coordination and their relationship to the subjective state of well-being. Considerable variation was found in the temporal relationship amongst these variables. The results are discussed with respect to the relevance of speech parameters and the coordination of verbal and nonverbal behaviour as indicators of the psychopathological condition.},
  subject      = {Psychologie},
  language  = {en}
}
@incollection{EllgringClarkeWagner1983,
  author    = {Ellgring, Johann Heinrich and Clarke, AH and Wagner, H.},
  title     = {A syntactic approach to the analysis of nonverbal behaviour},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-52403},
  publisher      = {Universit{\"a}t W{\"u}rzburg},
  year      = {1983},
  abstract  = {No abstract available},
  subject      = {Psychologie},
  language  = {en}
}
@article{DumontWeberLassalleJolyBeauparlantetal.2022,
  author    = {Dumont, Martine and Weber-Lassalle, Nana and Joly-Beauparlant, Charles and Ernst, Corinna and Droit, Arnaud and Feng, Bing-Jian and Dubois, St{\´e}phane and Collin-Deschesnes, Annie-Claude and Soucy, Penny and Vall{\´e}e, Maxime and Fournier, Fr{\´e}d{\´e}ric and Lema{\c{c}}on, Audrey and Adank, Muriel A. and Allen, Jamie and Altm{\"u}ller, Janine and Arnold, Norbert and Ausems, Margreet G. E. M. and Berutti, Riccardo and Bolla, Manjeet K. and Bull, Shelley and Carvalho, Sara and Cornelissen, Sten and Dufault, Michael R. and Dunning, Alison M. and Engel, Christoph and Gehrig, Andrea and Geurts-Giele, Willemina R. R. and Gieger, Christian and Green, Jessica and Hackmann, Karl and Helmy, Mohamed and Hentschel, Julia and Hogervorst, Frans B. L. and Hollestelle, Antoinette and Hooning, Maartje J. and Horv{\´a}th, Judit and Ikram, M. Arfan and Kaulfuß, Silke and Keeman, Renske and Kuang, Da and Luccarini, Craig and Maier, Wolfgang and Martens, John W. M. and Niederacher, Dieter and N{\"u}rnberg, Peter and Ott, Claus-Eric and Peters, Annette and Pharoah, Paul D. P. and Ramirez, Alfredo and Ramser, Juliane and Riedel-Heller, Steffi and Schmidt, Gunnar and Shah, Mitul and Scherer, Martin and St{\"a}bler, Antje and Strom, Tim M. and Sutter, Christian and Thiele, Holger and van Asperen, Christi J. and van der Kolk, Lizet and van der Luijt, Rob B. and Volk, Alexander E. and Wagner, Michael and Waisfisz, Quinten and Wang, Qin and Wang-Gohrke, Shan and Weber, Bernhard H. F. and Devilee, Peter and Tavtigian, Sean and Bader, Gary D. and Meindl, Alfons and Goldgar, David E. and Andrulis, Irene L. and Schmutzler, Rita K. and Easton, Douglas F. and Schmidt, Marjanka K. and Hahnen, Eric and Simard, Jacques},
  title     = {Uncovering the contribution of moderate-penetrance susceptibility genes to breast cancer by whole-exome sequencing and targeted enrichment sequencing of candidate genes in women of European ancestry},
  series = {Cancers},
  volume    = {14},
  journal   = {Cancers},
  number    = {14},
  issn      = {2072-6694},
  doi       = {10.3390/cancers14143363},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-281768},
  year      = {2022},
  abstract  = {Rare variants in at least 10 genes, including BRCA1, BRCA2, PALB2, ATM, and CHEK2, are associated with increased risk of breast cancer; however, these variants, in combination with common variants identified through genome-wide association studies, explain only a fraction of the familial aggregation of the disease. To identify further susceptibility genes, we performed a two-stage whole-exome sequencing study. In the discovery stage, samples from 1528 breast cancer cases enriched for breast cancer susceptibility and 3733 geographically matched unaffected controls were sequenced. Using five different filtering and gene prioritization strategies, 198 genes were selected for further validation. These genes, and a panel of 32 known or suspected breast cancer susceptibility genes, were assessed in a validation set of 6211 cases and 6019 controls for their association with risk of breast cancer overall, and by estrogen receptor (ER) disease subtypes, using gene burden tests applied to loss-of-function and rare missense variants. Twenty genes showed nominal evidence of association (p-value < 0.05) with either overall or subtype-specific breast cancer. Our study had the statistical power to detect susceptibility genes with effect sizes similar to ATM, CHEK2, and PALB2, however, it was underpowered to identify genes in which susceptibility variants are rarer or confer smaller effect sizes. Larger sample sizes would be required in order to identify such genes.},
  language  = {en}
}
@article{DiersWagnerBaumetal.2020,
  author    = {Diers, J. and Wagner, J. and Baum, P. and Lichthardt, S. and Kastner, C. and Matthes, N. and Matthes, H. and Germer, C.-T. and L{\"o}b, S. and Wiegering, A.},
  title     = {Nationwide in-hospital mortality rate following rectal resection for rectal cancer according to annual hospital volume in Germany},
  series = {BJS Open},
  volume    = {4},
  journal   = {BJS Open},
  number    = {2},
  doi       = {10.1002/bjs5.50254},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-212878},
  pages     = {310 -- 319},
  year      = {2020},
  abstract  = {Background The impact of hospital volume after rectal cancer surgery is seldom investigated. This study aimed to analyse the impact of annual rectal cancer surgery cases per hospital on postoperative mortality and failure to rescue. Methods All patients diagnosed with rectal cancer and who had a rectal resection procedure code from 2012 to 2015 were identified from nationwide administrative hospital data. Hospitals were grouped into five quintiles according to caseload. The absolute number of patients, postoperative deaths and failure to rescue (defined as in-hospital mortality after a documented postoperative complication) for severe postoperative complications were determined. Results Some 64 349 patients were identified. The overall in-house mortality rate was 3·9 per cent. The crude in-hospital mortality rate ranged from 5·3 per cent in very low-volume hospitals to 2·6 per cent in very high-volume centres, with a distinct trend between volume categories (P < 0·001). In multivariable logistic regression analysis using hospital volume as random effect, very high-volume hospitals (53 interventions/year) had a risk-adjusted odds ratio of 0·58 (95 per cent c.i. 0·47 to 0·73), compared with the baseline in-house mortality rate in very low-volume hospitals (6 interventions per year) (P < 0·001). The overall postoperative complication rate was comparable between different volume quintiles, but failure to rescue decreased significantly with increasing caseload (15·6 per cent after pulmonary embolism in the highest volume quintile versus 38 per cent in the lowest quintile; P = 0·010). Conclusion Patients who had rectal cancer surgery in high-volume hospitals showed better outcomes and reduced failure to rescue rates for severe complications than those treated in low-volume hospitals.},
  language  = {en}
}
@article{LiuHanBlairetal.2021,
  author    = {Liu, Fengming and Han, Kun and Blair, Robert and Kenst, Kornelia and Qin, Zhongnan and Upcin, Berin and W{\"o}rsd{\"o}rfer, Philipp and Midkiff, Cecily C. and Mudd, Joseph and Belyaeva, Elizaveta and Milligan, Nicholas S. and Rorison, Tyler D. and Wagner, Nicole and Bodem, Jochen and D{\"o}lken, Lars and Aktas, Bertal H. and Vander Heide, Richard S. and Yin, Xiao-Ming and Kolls, Jay K. and Roy, Chad J. and Rappaport, Jay and Erg{\"u}n, S{\"u}leyman and Qin, Xuebin},
  title     = {SARS-CoV-2 Infects Endothelial Cells In Vivo and In Vitro},
  series = {Frontiers in Cellular and Infection Microbiology},
  volume    = {11},
  journal   = {Frontiers in Cellular and Infection Microbiology},
  issn      = {2235-2988},
  doi       = {10.3389/fcimb.2021.701278},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-241948},
  year      = {2021},
  abstract  = {SARS-CoV-2 infection can cause fatal inflammatory lung pathology, including thrombosis and increased pulmonary vascular permeability leading to edema and hemorrhage. In addition to the lung, cytokine storm-induced inflammatory cascade also affects other organs. SARS-CoV-2 infection-related vascular inflammation is characterized by endotheliopathy in the lung and other organs. Whether SARS-CoV-2 causes endotheliopathy by directly infecting endothelial cells is not known and is the focus of the present study. We observed 1) the co-localization of SARS-CoV-2 with the endothelial cell marker CD31 in the lungs of SARS-CoV-2-infected mice expressing hACE2 in the lung by intranasal delivery of adenovirus 5-hACE2 (Ad5-hACE2 mice) and non-human primates at both the protein and RNA levels, and 2) SARS-CoV-2 proteins in endothelial cells by immunogold labeling and electron microscopic analysis. We also detected the co-localization of SARS-CoV-2 with CD31 in autopsied lung tissue obtained from patients who died from severe COVID-19. Comparative analysis of RNA sequencing data of the lungs of infected Ad5-hACE2 and Ad5-empty (control) mice revealed upregulated KRAS signaling pathway, a well-known pathway for cellular activation and dysfunction. Further, we showed that SARS-CoV-2 directly infects mature mouse aortic endothelial cells (AoECs) that were activated by performing an aortic sprouting assay prior to exposure to SARS-CoV-2. This was demonstrated by co-localization of SARS-CoV-2 and CD34 by immunostaining and detection of viral particles in electron microscopic studies. Moreover, the activated AoECs became positive for ACE-2 but not quiescent AoECs. Together, our results indicate that in addition to pneumocytes, SARS-CoV-2 also directly infects mature vascular endothelial cells in vivo and ex vivo, which may contribute to cardiovascular complications in SARS-CoV-2 infection, including multipleorgan failure.},
  language  = {en}
}
@article{DiersWagnerBaumetal.2019,
  author    = {Diers, J. and Wagner, J. and Baum, P. and Lichthardt, S. and Kastner, C. and Matthes, N. and L{\"o}b, S. and Matthes, H. and Germer, C.-T. and Wiegering, A.},
  title     = {Nationwide in-hospital mortality following colonic cancer resection according to hospital volume in Germany},
  series = {BJS Open},
  volume    = {3},
  journal   = {BJS Open},
  number    = {5},
  doi       = {10.1002/bjs5.50173},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-204385},
  pages     = {672-677},
  year      = {2019},
  abstract  = {Background: Colonic cancer is the most common cancer of the gastrointestinal tract. The aim of this study was to determine mortality rates following colonic cancer resection and the effect of hospital caseload on in-hospital mortality in Germany. Methods: Patients admitted with a diagnosis of colonic cancer undergoing colonic resection from 2012 to 2015 were identifed from a nationwide registry using procedure codes. The outcome measure was in-hospital mortality. Hospitals were ranked according to their caseload for colonic cancer resection, and patients were categorized into five subgroups on the basis of hospital volume. Results: Some 129 196 colonic cancer resections were reviewed. The overall in-house mortality rate was 5⋅8 per cent, ranging from 6⋅9 per cent (1775 of 25 657 patients) in very low-volume hospitals to 4⋅8 per cent (1239 of 25 825) in very high-volume centres (P < 0⋅001). In multivariable logistic regression analysis the risk-adjusted odds ratio for in-house mortality was 0⋅75 (95 per cent c.i. 0⋅66 to 0⋅84) in very high-volume hospitals performing a mean of 85⋅0 interventions per year, compared with that in very low-volume hospitals performing a mean of only 12⋅7 interventions annually, after adjustment for sex, age, co-morbidity, emergency procedures, prolonged mechanical ventilation and transfusion. Conclusion: In Germany, patients undergoing colonic cancer resections in high-volume hospitals had with improved outcomes compared with patients treated in low-volume hospitals},
  language  = {en}
}
@article{MeierMoebusHeigletal.2023,
  author    = {Meier, Johannes P. and M{\"o}bus, Selina and Heigl, Florian and Asbach-Nitzsche, Alexandra and Niller, Hans Helmut and Plentz, Annelie and Avsar, Korkut and Heiß-Neumann, Marion and Schaaf, Bernhard and Cassens, Uwe and Seese, Bernd and Teschner, Daniel and Handzhiev, Sabin and Graf, Uwe and L{\"u}bbert, Christoph and Steinmaurer, Monika and Kontogianni, Konstantina and Berg, Christoph and Maieron, Andreas and Blaas, Stefan H. and Wagner, Ralf and Deml, Ludwig and Barabas, Sascha},
  title     = {Performance of T-Track\(^®\) TB, a novel dual marker RT-qPCR-based whole-blood test for improved detection of active tuberculosis},
  series = {Diagnostics},
  volume    = {13},
  journal   = {Diagnostics},
  number    = {4},
  issn      = {2075-4418},
  doi       = {10.3390/diagnostics13040758},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-304113},
  year      = {2023},
  abstract  = {Tuberculosis (TB) is one of the leading causes of death by an infectious disease. It remains a major health burden worldwide, in part due to misdiagnosis. Therefore, improved diagnostic tests allowing the faster and more reliable diagnosis of patients with active TB are urgently needed. This prospective study examined the performance of the new molecular whole-blood test T-Track\(^®\) TB, which relies on the combined evaluation of IFNG and CXCL10 mRNA levels, and compared it to that of the QuantiFERON\(^®\)-TB Gold Plus (QFT-Plus) enzyme-linked immunosorbent assay (ELISA). Diagnostic accuracy and agreement analyses were conducted on the whole blood of 181 active TB patients and 163 non-TB controls. T-Track\(^®\) TB presented sensitivity of 94.9\% and specificity of 93.8\% for the detection of active TB vs. non-TB controls. In comparison, the QFT-Plus ELISA showed sensitivity of 84.3\%. The sensitivity of T-Track\(^®\) TB was significantly higher (p < 0.001) than that of QFT-Plus. The overall agreement of T-Track\(^®\) TB with QFT-Plus to diagnose active TB was 87.9\%. Out of 21 samples with discordant results, 19 were correctly classified by T-Track\(^®\) TB while misclassified by QFT-Plus (T-Track\(^®\) TB-positive/QFT-Plus-negative), and two samples were misclassified by T-Track\(^®\) TB while correctly classified by QFT-Plus (T-Track\(^®\) TB-negative/QFT-Plus-positive). Our results demonstrate the excellent performance of the T-Track\(^®\) TB molecular assay and its suitability to accurately detect TB infection and discriminate active TB patients from non-infected controls.},
  language  = {en}
}
@article{HaakeHaackSchaeferetal.2023,
  author    = {Haake, Markus and Haack, Beatrice and Sch{\"a}fer, Tina and Harter, Patrick N. and Mattavelli, Greta and Eiring, Patrick and Vashist, Neha and Wedekink, Florian and Genssler, Sabrina and Fischer, Birgitt and Dahlhoff, Julia and Mokhtari, Fatemeh and Kuzkina, Anastasia and Welters, Marij J. P. and Benz, Tamara M. and Sorger, Lena and Thiemann, Vincent and Almanzar, Giovanni and Selle, Martina and Thein, Klara and Sp{\"a}th, Jacob and Gonzalez, Maria Cecilia and Reitinger, Carmen and Ipsen-Escobedo, Andrea and Wistuba-Hamprecht, Kilian and Eichler, Kristin and Filipski, Katharina and Zeiner, Pia S. and Beschorner, Rudi and Goedemans, Renske and Gogolla, Falk Hagen and Hackl, Hubert and Rooswinkel, Rogier W. and Thiem, Alexander and Romer Roche, Paula and Joshi, Hemant and P{\"u}hringer, Dirk and W{\"o}ckel, Achim and Diessner, Joachim E. and R{\"u}diger, Manfred and Leo, Eugen and Cheng, Phil F. and Levesque, Mitchell P. and Goebeler, Matthias and Sauer, Markus and Nimmerjahn, Falk and Schuberth-Wagner, Christine and Felten, Stefanie von and Mittelbronn, Michel and Mehling, Matthias and Beilhack, Andreas and van der Burg, Sjoerd H. and Riedel, Angela and Weide, Benjamin and Dummer, Reinhard and Wischhusen, J{\"o}rg},
  title     = {Tumor-derived GDF-15 blocks LFA-1 dependent T cell recruitment and suppresses responses to anti-PD-1 treatment},
  series = {Nature Communications},
  volume    = {14},
  journal   = {Nature Communications},
  doi       = {10.1038/s41467-023-39817-3},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-357333},
  year      = {2023},
  abstract  = {Immune checkpoint blockade therapy is beneficial and even curative for some cancer patients. However, the majority don't respond to immune therapy. Across different tumor types, pre-existing T cell infiltrates predict response to checkpoint-based immunotherapy. Based on in vitro pharmacological studies, mouse models and analyses of human melanoma patients, we show that the cytokine GDF-15 impairs LFA-1/β2-integrin-mediated adhesion of T cells to activated endothelial cells, which is a pre-requisite of T cell extravasation. In melanoma patients, GDF-15 serum levels strongly correlate with failure of PD-1-based immune checkpoint blockade therapy. Neutralization of GDF-15 improves both T cell trafficking and therapy efficiency in murine tumor models. Thus GDF-15, beside its known role in cancer-related anorexia and cachexia, emerges as a regulator of T cell extravasation into the tumor microenvironment, which provides an even stronger rationale for therapeutic anti-GDF-15 antibody development.},
  language  = {en}
}
@article{SteuerCostaVanderAuweraGlocketal.2019,
  author    = {Steuer Costa, Wagner and Van der Auwera, Petrus and Glock, Caspar and Liewald, Jana F. and Bach, Maximilian and Sch{\"u}ler, Christina and Wabnig, Sebastian and Oranth, Alexandra and Masurat, Florentin and Bringmann, Henrik and Schoofs, Liliane and Stelzer, Ernst H. K. and Fischer, Sabine C. and Gottschalk, Alexander},
  title     = {A GABAergic and peptidergic sleep neuron as a locomotion stop neuron with compartmentalized Ca2+ dynamics},
  series = {Nature Communications},
  volume    = {10},
  journal   = {Nature Communications},
  doi       = {10.1038/s41467-019-12098-5},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-223273},
  year      = {2019},
  abstract  = {Animals must slow or halt locomotion to integrate sensory inputs or to change direction. In Caenorhabditis elegans, the GABAergic and peptidergic neuron RIS mediates developmentally timed quiescence. Here, we show RIS functions additionally as a locomotion stop neuron. RIS optogenetic stimulation caused acute and persistent inhibition of locomotion and pharyngeal pumping, phenotypes requiring FLP-11 neuropeptides and GABA. RIS photoactivation allows the animal to maintain its body posture by sustaining muscle tone, yet inactivating motor neuron oscillatory activity. During locomotion, RIS axonal Ca2+ signals revealed functional compartmentalization: Activity in the nerve ring process correlated with locomotion stop, while activity in a branch correlated with induced reversals. GABA was required to induce, and FLP-11 neuropeptides were required to sustain locomotion stop. RIS attenuates neuronal activity and inhibits movement, possibly enabling sensory integration and decision making, and exemplifies dual use of one cell across development in a compact nervous system.},
  language  = {en}
}