@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{HoppAlbertWeissenbergerMencletal.2016,
  author    = {Hopp, Sarah and Albert-Weissenberger, Christiane and Mencl, Stine and Bieber, Michael and Schuhmann, Michael K. and Stetter, Christian and Nieswandt, Bernhard and Schmidt, Peter M. and Monoranu, Camelia-Maria and Alafuzoff, Irina and Marklund, Niklas and Nolte, Marc W. and Sir{\´e}n, Anna-Leena and Kleinschnitz, Christoph},
  title     = {Targeting coagulation factor XII as a novel therapeutic option in brain trauma},
  series = {Annals of Neurology},
  volume    = {79},
  journal   = {Annals of Neurology},
  number    = {6},
  doi       = {10.1002/ana.24655},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-188800},
  pages     = {970-982},
  year      = {2016},
  abstract  = {Objective: Traumatic brain injury is a major global public health problem for which specific therapeutic interventions are lacking. There is, therefore, a pressing need to identify innovative pathomechanism-based effective therapies for this condition. Thrombus formation in the cerebral microcirculation has been proposed to contribute to secondary brain damage by causing pericontusional ischemia, but previous studies have failed to harness this finding for therapeutic use. The aim of this study was to obtain preclinical evidence supporting the hypothesis that targeting factor XII prevents thrombus formation and has a beneficial effect on outcome after traumatic brain injury. Methods: We investigated the impact of genetic deficiency of factor XII and acute inhibition of activated factor XII with a single bolus injection of recombinant human albumin-fused infestin-4 (rHA-Infestin-4) on trauma-induced microvascular thrombus formation and the subsequent outcome in 2 mouse models of traumatic brain injury. Results: Our study showed that both genetic deficiency of factor XII and an inhibition of activated factor XII in mice minimize trauma-induced microvascular thrombus formation and improve outcome, as reflected by better motor function, reduced brain lesion volume, and diminished neurodegeneration. Administration of human factor XII in factor XII-deficient mice fully restored injury-induced microvascular thrombus formation and brain damage. Interpretation: The robust protective effect of rHA-Infestin-4 points to a novel treatment option that can decrease ischemic injury after traumatic brain injury without increasing bleeding tendencies.},
  language  = {en}
}
@article{CarstenAGorskiLietal.2011,
  author    = {Carsten A., B{\"o}ger and Gorski, Mathias and Li, Man and Hoffmann, Michael M. and Huang, Chunmei and Yang, Qiong and Teumer, Alexander and Krane, Vera and O'Seaghdha, Conall M. and Kutalik, Zolt{\´a}n and Wichmann, H.-Erich and Haak, Thomas and Boes, Eva and Coassin, Stefan and Coresh, Josef and Kollerits, Barbara and Haun, Margot and Paulweber, Bernhard and K{\"o}ttgen, Anna and Li, Guo and Shlipak, Michael G. and Powe, Neil and Hwang, Shih-Jen and Dehghan, Abbas and Rivadeneira, Fernando and Uitterlinden, Andr{\´e} and Hofman, Albert and Beckmann, Jacques S. and Kr{\"a}mer, Bernhard K. and Witteman, Jacqueline and Bochud, Murielle and Siscovick, David and Rettig, Rainer and Kronenberg, Florian and Wanner, Christoph and Thadhani, Ravi I. and Heid, Iris M. and Fox, Caroline S. and Kao, W.H.},
  title     = {Association of eGFR-Related Loci Identified by GWAS with Incident CKD and ESRD},
  series = {PLoS Genetics},
  volume    = {7},
  journal   = {PLoS Genetics},
  number    = {9},
  doi       = {10.1371/journal.pgen.1002292},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-133758},
  pages     = {e1002292},
  year      = {2011},
  abstract  = {Family studies suggest a genetic component to the etiology of chronic kidney disease (CKD) and end stage renal disease (ESRD). Previously, we identified 16 loci for eGFR in genome-wide association studies, but the associations of these single nucleotide polymorphisms (SNPs) for incident CKD or ESRD are unknown. We thus investigated the association of these loci with incident CKD in 26,308 individuals of European ancestry free of CKD at baseline drawn from eight population-based cohorts followed for a median of 7.2 years (including 2,122 incident CKD cases defined as eGFR < 60ml/min/1.73m(2) at follow-up) and with ESRD in four case-control studies in subjects of European ancestry (3,775 cases, 4,577 controls). SNPs at 11 of the 16 loci (UMOD, PRKAG2, ANXA9, DAB2, SHROOM3, DACH1, STC1, SLC34A1, ALMS1/NAT8, UBE2Q2, and GCKR) were associated with incident CKD; p-values ranged from p = 4.1e-9 in UMOD to p = 0.03 in GCKR. After adjusting for baseline eGFR, six of these loci remained significantly associated with incident CKD (UMOD, PRKAG2, ANXA9, DAB2, DACH1, and STC1). SNPs in UMOD (OR = 0.92, p = 0.04) and GCKR (OR = 0.93, p = 0.03) were nominally associated with ESRD. In summary, the majority of eGFR-related loci are either associated or show a strong trend towards association with incident CKD, but have modest associations with ESRD in individuals of European descent. Additional work is required to characterize the association of genetic determinants of CKD and ESRD at different stages of disease progression.},
  language  = {en}
}
@article{AdrianMartinezAgeronAharonianetal.2016,
  author    = {Adri{\´a}n-Mart{\´i}nez, S. and Ageron, M. and Aharonian, F. and Aiello, S. and Albert, A. and Ameli, F. and Annasontzis, E. and Andre, M. and Androulakis, G. and Anghinolfi, M. and Anton, G. and Ardid, M. and Avgitas, T. and Barbarino, G. and Baret, B. and Barrios-Mart{\´i}, J. and Belhorma, B. and Belias, A. and Berbee, A. and van den Berg, A. and Bertin, V. and Beurthey, S. and van Beeveren, V. and Beverini, N. and Biagi, S. and Biagioni, A. and Billault, M. and Bond{\`i}, M. and Bormuth, R. and Bouhadef, B. and Bourlis, G. and Bourret, S. and Boutonnet, C. and Bouwhuis, M. and Bozza, C. and Bruijn, R. and Brunner, J. and Buis, E. and Busto, J. and Cacopardo, G. and Caillat, L. and Calmai, M. and Calvo, D. and Capone, A. and Caramete, L. and Cecchini, S. and Celli, S. and Champion, C. and Cherkaoui El Moursli, R. and Cherubini, S. and Chiarusi, T. and Circella, M. and Classen, L. and Cocimano, R. and Coelho, J. A. B. and Coleiro, A. and Colonges, S. and Coniglione, R. and Cordelli, M. and Cosquer, A. and Coyle, P. and Creusot, A. and Cuttone, G. and D'Amico, A. and De Bonis, G. and De Rosa, G. and De Sio, C. and Di Capua, F. and Di Palma, I. and D{\´i}az Garc{\´i}a, A. F. and Distefano, C. and Donzaud, C. and Dornic, D. and Dorosti-Hasankiadeh, Q. and Drakopoulou, E. and Drouhin, D. and Drury, L. and Durocher, M. and Eberl, T. and Eichie, S. and van Eijk, D. and El Bojaddaini, I. and El Khayati, N. and Elsaesser, D. and Enzenh{\"o}fer, A. and Fassi, F. and Favali, P. and Fermani, P. and Ferrara, G. and Filippidis, C. and Frascadore, G. and Fusco, L. A. and Gal, T. and Galat{\`a}, S. and Garufi, F. and Gay, P. and Gebyehu, M. and Giordano, V. and Gizani, N. and Gracia, R. and Graf, K. and Gr{\´e}goire, T. and Grella, G. and Habel, R. and Hallmann, S. and van Haren, H. and Harissopulos, S. and Heid, T. and Heijboer, A. and Heine, E. and Henry, S. and Hern{\´a}ndez-Rey, J. J. and Hevinga, M. and Hofest{\"a}dt, J. and Hugon, C. M. F. and Illuminati, G. and James, C. W. and Jansweijer, P. and Jongen, M. and de Jong, M. and Kadler, M. and Kalekin, O. and Kappes, A. and Katz, U. F. and Keller, P. and Kieft, G. and Kießling, D. and Koffeman, E. N. and Kooijman, P. and Kouchner, A. and Kulikovskiy, V. and Lahmann, R. and Lamare, P. and Leisos, A. and Leonora, E. and Lindsey Clark, M. and Liolios, A. and Llorenz Alvarez, C. D. and Lo Presti, D. and L{\"o}hner, H. and Lonardo, A. and Lotze, M. and Loucatos, S. and Maccioni, E. and Mannheim, K. and Margiotta, A. and Marinelli, A. and Mari{\c{s}}, O. and Markou, C. and Mart{\´i}nez-Mora, J. A. and Martini, A. and Mele, R. and Melis, K. W. and Michael, T. and Migliozzi, P. and Migneco, E. and Mijakowski, P. and Miraglia, A. and Mollo, C. M. and Mongelli, M. and Morganti, M. and Moussa, A. and Musico, P. and Musumeci, M. and Navas, S. and Nicoleau, C. A. and Olcina, I. and Olivetto, C. and Orlando, A. and Papaikonomou, A. and Papaleo, R. and Păvăla{\c{s}}, G. E. and Peek, H. and Pellegrino, C. and Perrina, C. and Pfutzner, M. and Piattelli, P. and Pikounis, K. and Poma, G. E. and Popa, V. and Pradier, T. and Pratolongo, F. and P{\"u}hlhofer, G. and Pulvirenti, S. and Quinn, L. and Racca, C. and Raffaelli, F. and Randazzo, N. and Rapidis, P. and Razis, P. and Real, D. and Resvanis, L. and Reubelt, J. and Riccobene, G. and Rossi, C. and Rovelli, A. and Salda{\~n}a, M. and Salvadori, I. and Samtleben, D. F. E. and S{\´a}nchez Garc{\´i}a, A. and S{\´a}nchez Losa, A. and Sanguineti, M. and Santangelo, A. and Santonocito, D. and Sapienza, P. and Schimmel, F. and Schmelling, J. and Sciacca, V. and Sedita, M. and Seitz, T. and Sgura, I. and Simeone, F. and Siotis, I. and Sipala, V. and Spisso, B. and Spurio, M. and Stavropoulos, G. and Steijger, J. and Stellacci, S. M. and Stransky, D. and Taiuti, M. and Tayalati, Y. and T{\´e}zier, D. and Theraube, S. and Thompson, L. and Timmer, P. and T{\"o}nnis, C. and Trasatti, L. and Trovato, A. and Tsirigotis, A. and Tzamarias, S. and Tzamariudaki, E. and Vallage, B. and Van Elewyk, V. and Vermeulen, J. and Vicini, P. and Viola, S. and Vivolo, D. and Volkert, M. and Voulgaris, G. and Wiggers, L. and Wilms, J. and de Wolf, E. and Zachariadou, K. and Zornoza, J. D. and Z{\´u}{\~n}iga, J.},
  title     = {Letter of intent for KM3NeT 2.0},
  series = {Journal of Physics G-Nuclear and Particle Physics},
  volume    = {43},
  journal   = {Journal of Physics G-Nuclear and Particle Physics},
  number    = {8},
  doi       = {10.1088/0954-3899/43/8/084001},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-188050},
  pages     = {84001},
  year      = {2016},
  abstract  = {The main objectives of the KM3NeT Collaboration are (i) the discovery and subsequent observation of high-energy neutrino sources in the Universe and (ii) the determination of the mass hierarchy of neutrinos. These objectives are strongly motivated by two recent important discoveries, namely: (1) the high-energy astrophysical neutrino signal reported by IceCube and (2) the sizable contribution of electron neutrinos to the third neutrino mass eigenstate as reported by Daya Bay, Reno and others. To meet these objectives, the KM3NeT Collaboration plans to build a new Research Infrastructure consisting of a network of deep-sea neutrino telescopes in the Mediterranean Sea. A phased and distributed implementation is pursued which maximises the access to regional funds, the availability of human resources and the synergistic opportunities for the Earth and sea sciences community. Three suitable deep-sea sites are selected, namely off-shore Toulon (France), Capo Passero (Sicily, Italy) and Pylos (Peloponnese, Greece). The infrastructure will consist of three so-called building blocks. A building block comprises 115 strings, each string comprises 18 optical modules and each optical module comprises 31 photo-multiplier tubes. Each building block thus constitutes a three-dimensional array of photo sensors that can be used to detect the Cherenkov light produced by relativistic particles emerging from neutrino interactions. Two building blocks will be sparsely configured to fully explore the IceCube signal with similar instrumented volume, different methodology, improved resolution and},
  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}
}
@phdthesis{Albert2019,
  author    = {Albert, Michael},
  title     = {Intelligent analysis of medical data in a generic telemedicine infrastructure},
  isbn      = {978-3-945459-26-3 (Online)},
  doi       = {10.25972/OPUS-17421},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-174213},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2019},
  abstract  = {Telemedicine uses telecommunication and information technology to provide health care services over spatial distances. In the upcoming demographic changes towards an older average population age, especially rural areas suffer from a decreasing doctor to patient ratio as well as a limited amount of available medical specialists in acceptable distance. These areas could benefit the most from telemedicine applications as they are known to improve access to medical services, medical expertise and can also help to mitigate critical or emergency situations. Although the possibilities of telemedicine applications exist in the entire range of healthcare, current systems focus on one specific disease while using dedicated hardware to connect the patient with the supervising telemedicine center. This thesis describes the development of a telemedical system which follows a new generic design approach. This bridges the gap of existing approaches that only tackle one specific application. The proposed system on the contrary aims at supporting as many diseases and use cases as possible by taking all the stakeholders into account at the same time. To address the usability and acceptance of the system it is designed to use standardized hardware like commercial medical sensors and smartphones for collecting medical data of the patients and transmitting them to the telemedical center. The smartphone can also act as interface to the patient for health questionnaires or feedback. The system can handle the collection and transport of medical data, analysis and visualization of the data as well as providing a real time communication with video and audio between the users. On top of the generic telemedical framework the issue of scalability is addressed by integrating a rule-based analysis tool for the medical data. Rules can be easily created by medical personnel via a visual editor and can be personalized for each patient. The rule-based analysis tool is extended by multiple options for visualization of the data, mechanisms to handle complex rules and options for performing actions like raising alarms or sending automated messages. It is sometimes hard for the medical experts to formulate their knowledge into rules and there may be information in the medical data that is not yet known. This is why a machine learning module was integrated into the system. It uses the incoming medical data of the patients to learn new rules that are then presented to the medical personnel for inspection. This is in line with European legislation where the human still needs to be in charge of such decisions. Overall, we were able to show the benefit of the generic approach by evaluating it in three completely different medical use cases derived from specific application needs: monitoring of COPD (chronic obstructive pulmonary disease) patients, support of patients performing dialysis at home and councils of intensive-care experts. In addition the system was used for a non-medical use case: monitoring and optimization of industrial machines and robots. In all of the mentioned cases, we were able to prove the robustness of the generic approach with real users of the corresponding domain. This is why we can propose this approach for future development of telemedical systems.},
  subject      = {Telemedizin},
  language  = {en}
}
@article{AlbertWeissenbergerMenclSchuhmannetal.2014,
  author    = {Albert-Weissenberger, Christiane and Mencl, Stine and Schuhmann, Michael K. and Salur, Irmak and G{\"o}b, Eva and Langhauser, Friederike and Hopp, Sarah and Hennig, Nelli and Meuth, Sven G. and Nolte, Marc W. and Sir{\´e}n, Anna-Leena and Kleinschnitz, Christoph},
  title     = {C1-Inhibitor protects from focal brain trauma in a cortical cryolesion mice model by reducing thrombo-inflammation},
  series = {Frontiers in Cellular Neuroscience},
  volume    = {8},
  journal   = {Frontiers in Cellular Neuroscience},
  issn      = {1662-5102},
  doi       = {10.3389/fncel.2014.00269},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-119263},
  pages     = {269},
  year      = {2014},
  abstract  = {Traumatic brain injury (TBI) induces a strong inflammatory response which includes blood-brain barrier damage, edema formation and infiltration of different immune cell subsets. More recently, microvascular thrombosis has been identified as another pathophysiological feature of TBI. The contact-kinin system represents an interface between inflammatory and thrombotic circuits and is activated in different neurological diseases. C1-Inhibitor counteracts activation of the contact-kinin system at multiple levels. We investigated the therapeutic potential of C1-Inhibitor in a model of TBI. Male and female C57BL/6 mice were subjected to cortical cryolesion and treated with C1-Inhibitor after 1 h. Lesion volumes were assessed between day 1 and day 5 and blood-brain barrier damage, thrombus formation as well as the local inflammatory response were determined post TBI. Treatment of male mice with 15.0 IU C1-Inhibitor, but not 7.5 IU, 1 h after cryolesion reduced lesion volumes by ~75\% on day 1. This protective effect was preserved in female mice and at later stages of trauma. Mechanistically, C1-Inhibitor stabilized the blood-brain barrier and decreased the invasion of immune cells into the brain parenchyma. Moreover, C1-Inhibitor had strong antithrombotic effects. C1-Inhibitor represents a multifaceted anti-inflammatory and antithrombotic compound that prevents traumatic neurodegeneration in clinically meaningful settings.},
  language  = {en}
}
@article{AlbertWeissenbergerStetterMeuthetal.2012,
  author    = {Albert-Weissenberger, Christiane and Stetter, Christian and Meuth, Sven G. and G{\"o}bel, Kerstin and Bader, Michael and Sir{\´e}n, Anna-Leena and Kleinschnitz, Christoph},
  title     = {Blocking of Bradykinin Receptor B1 Protects from Focal Closed Head Injury in Mice by Reducing Axonal Damage and Astroglia Activation},
  series = {Journal of Cerebral Blood Flow and Metabolism},
  volume    = {32},
  journal   = {Journal of Cerebral Blood Flow and Metabolism},
  number    = {9},
  doi       = {10.1038/jcbfm.2012.62},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-125903},
  pages     = {1747-1756},
  year      = {2012},
  abstract  = {The two bradykinin receptors B1R and B2R are central components of the kallikrein-kinin system with different expression kinetics and binding characteristics. Activation of these receptors by kinins triggers inflammatory responses in the target organ and in most situations enhances tissue damage. We could recently show that blocking of B1R, but not B2R, protects from cortical cryolesion by reducing inflammation and edema formation. In the present study, we investigated the role of B1R and B2R in a closed head model of focal traumatic brain injury (TBI; weight drop). Increased expression of B1R in the injured hemispheres of wild-type mice was restricted to the later stages after brain trauma, i.e. day 7 (P<0.05), whereas no significant induction could be observed for the B2R (P>0.05). Mice lacking the B1R, but not the B2R, showed less functional deficits on day 3 (P<0.001) and day 7 (P<0.001) compared with controls. Pharmacological blocking of B1R in wild-type mice had similar effects. Reduced axonal injury and astroglia activation could be identified as underlying mechanisms, while inhibition of B1R had only little influence on the local inflammatory response in this model. Inhibition of B1R may become a novel strategy to counteract trauma-induced neurodegeneration.},
  language  = {en}
}
@article{DupuisDenglerHenekaetal.2012,
  author    = {Dupuis, Luc and Dengler, Reinhard and Heneka, Michael T. and Meyer, Thomas and Zierz, Stephan and Kassubek, Jan and Fischer, Wilhelm and Steiner, Franziska and Lindauer, Eva and Otto, Markus and Dreyhaupt, Jens and Grehl, Torsten and Hermann, Andreas and Winkler, Andrea S. and Bogdahn, Ulrich and Benecke, Reiner and Schrank, Bertold and Wessig, Carsten and Grosskreutz, Julian and Ludolph, Albert C.},
  title     = {A Randomized, Double Blind, Placebo-Controlled Trial of Pioglitazone in Combination with Riluzole in Amyotrophic Lateral Sclerosis},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {6},
  doi       = {10.1371/journal.pone.0037885},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-130255},
  pages     = {e37885},
  year      = {2012},
  abstract  = {Background: Pioglitazone, an oral anti-diabetic that stimulates the PPAR-gamma transcription factor, increased survival of mice with amyotrophic lateral sclerosis (ALS). Methods/Principal Findings: We performed a phase II, double blind, multicentre, placebo controlled trial of pioglitazone in ALS patients under riluzole. 219 patients were randomly assigned to receive 45 mg/day of pioglitazone or placebo (one: one allocation ratio). The primary endpoint was survival. Secondary endpoints included incidence of non-invasive ventilation and tracheotomy, and slopes of ALS-FRS, slow vital capacity, and quality of life as assessed using EUROQoL EQ-5D. The study was conducted under a two-stage group sequential test, allowing to stop for futility or superiority after interim analysis. Shortly after interim analysis, 30 patients under pioglitazone and 24 patients under placebo had died. The trial was stopped for futility; the hazard ratio for primary endpoint was 1.21 (95\% CI: 0.71-2.07, p = 0.48). Secondary endpoints were not modified by pioglitazone treatment. Pioglitazone was well tolerated. Conclusion/Significance: Pioglitazone has no beneficial effects on the survival of ALS patients as add-on therapy to riluzole.},
  language  = {en}
}
@article{StetterLopezCaperuchipiHoppKraemeretal.2021,
  author    = {Stetter, Christian and Lopez-Caperuchipi, Simon and Hopp-Kr{\"a}mer, Sarah and Bieber, Michael and Kleinschnitz, Christoph and Sir{\´e}n, Anna-Leena and Albert-Weißenberger, Christiane},
  title     = {Amelioration of cognitive and behavioral deficits after traumatic brain injury in coagulation factor XII deficient mice},
  series = {International Journal of Molecular Sciences},
  volume    = {22},
  journal   = {International Journal of Molecular Sciences},
  number    = {9},
  issn      = {1422-0067},
  doi       = {10.3390/ijms22094855},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-284959},
  year      = {2021},
  abstract  = {Based on recent findings that show that depletion of factor XII (FXII) leads to better posttraumatic neurological recovery, we studied the effect of FXII-deficiency on post-traumatic cognitive and behavioral outcomes in female and male mice. In agreement with our previous findings, neurological deficits on day 7 after weight-drop traumatic brain injury (TBI) were significantly reduced in FXII\(^{-/-}\) mice compared to wild type (WT) mice. Also, glycoprotein Ib (GPIb)-positive platelet aggregates were more frequent in brain microvasculature of WT than FXII\(^{-/-}\) mice 3 months after TBI. Six weeks after TBI, memory for novel object was significantly reduced in both female and male WT but not in FXII\(^{-/-}\) mice compared to sham-operated mice. In the setting of automated home-cage monitoring of socially housed mice in IntelliCages, female WT mice but not FXII\(^{-/-}\) mice showed decreased exploration and reacted negatively to reward extinction one month after TBI. Since neuroendocrine stress after TBI might contribute to trauma-induced cognitive dysfunction and negative emotional contrast reactions, we measured peripheral corticosterone levels and the ration of heart, lung, and spleen weight to bodyweight. Three months after TBI, plasma corticosterone levels were significantly suppressed in both female and male WT but not in FXII\(^{-/-}\) mice, while the relative heart weight increased in males but not in females of both phenotypes when compared to sham-operated mice. Our results indicate that FXII deficiency is associated with efficient post-traumatic behavioral and neuroendocrine recovery.},
  language  = {en}
}