@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{BousquetAntoAkdisetal.2016,
  author    = {Bousquet, J. and Anto, J. M. and Akdis, M. and Auffray, C. and Keil, T. and Momas, I. and Postma, D. S. and Valenta, R. and Wickman, M. and Cambon-Thomsen, A. and Haahtela, T. and Lambrecht, B. N. and Lodrup Carlsen, K. C. and Koppelman, G. H. and Sunyer, J. and Zuberbier, T. and Annesi-Maesano, I. and Arno, A. and Bindslev-Jensen, C. and De Carlo, G. and Forastiere, F. and Heinrich, J. and Kowalski, M. L. and Maier, D. and Melen, E. and Palkonen, S. and Smit, H. A. and Standl, M. and Wright, J. and Asarnoj, A. and Benet, M. and Ballardini, N. and Garcia-Aymerich, J. and Gehring, U. and Guerra, S. and Hohman, C. and Kull, I. and Lupinek, C. and Pinart, M. and Skrindo, I. and Westman, M. and Smagghe, D. and Akdis, C. and Albang, R. and Anastasova, V. and Anderson, N. and Bachert, C. and Ballereau, S. and Ballester, F. and Basagana, X. and Bedbrook, A. and Bergstrom, A. and von Berg, A. and Brunekreef, B. and Burte, E. and Carlsen, K.H. and Chatzi, L. and Coquet, J.M. and Curin, M. and Demoly, P. and Eller, E. and Fantini, M.P. and Gerhard, B. and Hammad, H. and von Hertzen, L. and Hovland, V. and Jacquemin, B. and Just, J. and Keller, T. and Kerkhof, M. and Kiss, R. and Kogevinas, M. and Koletzko, S. and Lau, S. and Lehmann, I. and Lemonnier, N. and McEachan, R. and Makela, M. and Mestres, J. and Minina, E. and Mowinckel, P. and Nadif, R. and Nawijn, M. and Oddie, S. and Pellet, J. and Pin, I. and Porta, D. and Ranci{\`e}re, F. and Rial-Sebbag, A. and Schuijs, M.J. and Siroux, V. and Tischer, C.G. and Torrent, M. and Varraso, R. and De Vocht, J. and Wenger, K. and Wieser, S. and Xu, C.},
  title     = {Paving the way of systems biology and precision medicine in allergic diseases: the MeDALL success story Mechanisms of the Development of ALLergy; EUFP7-CP-IP; Project No: 261357; 2010-2015},
  series = {Allergy},
  volume    = {71},
  journal   = {Allergy},
  number    = {11},
  doi       = {10.1111/all.12880},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-186858},
  pages     = {1513-1525},
  year      = {2016},
  abstract  = {MeDALL (Mechanisms of the Development of ALLergy; EU FP7-CP-IP; Project No: 261357; 2010-2015) has proposed an innovative approach to develop early indicators for the prediction, diagnosis, prevention and targets for therapy. MeDALL has linked epidemiological, clinical and basic research using a stepwise, large-scale and integrative approach: MeDALL data of precisely phenotyped children followed in 14 birth cohorts spread across Europe were combined with systems biology (omics, IgE measurement using microarrays) and environmental data. Multimorbidity in the same child is more common than expected by chance alone, suggesting that these diseases share causal mechanisms irrespective of IgE sensitization. IgE sensitization should be considered differently in monosensitized and polysensitized individuals. Allergic multimorbidities and IgE polysensitization are often associated with the persistence or severity of allergic diseases. Environmental exposures are relevant for the development of allergy-related diseases. To complement the population-based studies in children, MeDALL included mechanistic experimental animal studies and in vitro studies in humans. The integration of multimorbidities and polysensitization has resulted in a new classification framework of allergic diseases that could help to improve the understanding of genetic and epigenetic mechanisms of allergy as well as to better manage allergic diseases. Ethics and gender were considered. MeDALL has deployed translational activities within the EU agenda.},
  language  = {en}
}
@article{EmmertWitzelHeinrich2016,
  author    = {Emmert, M. and Witzel, P. and Heinrich, D.},
  title     = {Challenges in tissue engineering - towards cell control inside artificial scaffolds},
  series = {Soft Matter},
  volume    = {12},
  journal   = {Soft Matter},
  number    = {19},
  doi       = {10.1039/c5sm02844b},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-191341},
  pages     = {4287-4294},
  year      = {2016},
  abstract  = {Control of living cells is vital for the survival of organisms. Each cell inside an organism is exposed to diverse external mechano-chemical cues, all coordinated in a spatio-temporal pattern triggering individual cell functions. This complex interplay between external chemical cues and mechanical 3D environments is translated into intracellular signaling loops. Here, we describe how external mechano-chemical cues control cell functions, especially cell migration, and influence intracellular information transport. In particular, this work focuses on the quantitative analysis of (1) intracellular vesicle transport to understand intracellular state changes in response to external cues, (2) cellular sensing of external chemotactic cues, and (3) the cells' ability to migrate in 3D structured environments, artificially fabricated to mimic the 3D environment of tissue in the human body.},
  language  = {en}
}
@article{MitchellMacarthurGanetal.2014,
  author    = {Mitchell, Anna L. and Macarthur, Katie D. R. and Gan, Earn H. and Baggott, Lucy E. and Wolff, Anette S. B. and Skinningsrud, Beate and Platt, Hazel and Short, Andrea and Lobell, Anna and Kampe, Olle and Bensing, Sophie and Betterle, Corrado and Kasperlik-Zaluska, Anna and Zurawek, Magdalena and Fichna, Marta and Kockum, Ingrid and Eriksson, Gabriel Nordling and Ekwall, Olov and Wahlberg, Jeanette and Dahlqvist, Per and Hulting, Anna-Lena and Penna-Martinez, Marissa and Meyer, Gesine and Kahles, Heinrich and Badenhoop, Klaus and Hahner, Stephanie and Quinkler, Marcus and Falorni, Alberto and Phipps-Green, Amanda and Merriman, Tony R. and Ollier, William and Cordell, Heather J. and Undlien, Dag and Czarnocka, Barbara and Husebye, Eystein and Pearce, Simon H. S.},
  title     = {Association of Autoimmune Addison's Disease with Alleles of STAT4 and GATA3 in European Cohorts},
  series = {PLOS ONE},
  volume    = {9},
  journal   = {PLOS ONE},
  number    = {3},
  doi       = {10.1371/journal.pone.0088991},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-117105},
  pages     = {e88991},
  year      = {2014},
  abstract  = {Background: Gene variants known to contribute to Autoimmune Addison's disease (AAD) susceptibility include those at the MHC, MICA, CIITA, CTLA4, PTPN22, CYP27B1, NLRP-1 and CD274 loci. The majority of the genetic component to disease susceptibility has yet to be accounted for. Aim: To investigate the role of 19 candidate genes in AAD susceptibility in six European case-control cohorts. Methods: A sequential association study design was employed with genotyping using Sequenom iPlex technology. In phase one, 85 SNPs in 19 genes were genotyped in UK and Norwegian AAD cohorts (691 AAD, 715 controls). In phase two, 21 SNPs in 11 genes were genotyped in German, Swedish, Italian and Polish cohorts (1264 AAD, 1221 controls). In phase three, to explore association of GATA3 polymorphisms with AAD and to determine if this association extended to other autoimmune conditions, 15 SNPs in GATA3 were studied in UK and Norwegian AAD cohorts, 1195 type 1 diabetes patients from Norway, 650 rheumatoid arthritis patients from New Zealand and in 283 UK Graves' disease patients. Meta-analysis was used to compare genotype frequencies between the participating centres, allowing for heterogeneity. Results: We report significant association with alleles of two STAT4 markers in AAD cohorts (rs4274624: P = 0.00016; rs10931481: P = 0.0007). In addition, nominal association of AAD with alleles at GATA3 was found in 3 patient cohorts and supported by meta-analysis. Association of AAD with CYP27B1 alleles was also confirmed, which replicates previous published data. Finally, nominal association was found at SNPs in both the NF-kappa B1 and IL23A genes in the UK and Italian cohorts respectively. Conclusions: Variants in the STAT4 gene, previously associated with other autoimmune conditions, confer susceptibility to AAD. Additionally, we report association of GATA3 variants with AAD: this adds to the recent report of association of GATA3 variants with rheumatoid arthritis.},
  language  = {en}
}
@incollection{EllgringPloog1985,
  author    = {Ellgring, Johann Heinrich and Ploog, D.},
  title     = {Sozialkommunikatives Verhalten in klinischer Perspektive},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42107},
  publisher      = {Universit{\"a}t W{\"u}rzburg},
  year      = {1985},
  abstract  = {No abstract available},
  language  = {de}
}