@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{WallmannSperlichDuekingMuelleretal.2022,
  author    = {Wallmann-Sperlich, Birgit and D{\"u}king, Peter and M{\"u}ller, Miriam and Frob{\"o}se, Ingo and Sperlich, Billy},
  title     = {Type and intensity distribution of structured and incidental lifestyle physical activity of students and office workers: a retrospective content analysis},
  series = {BMC Public Health},
  volume    = {22},
  journal   = {BMC Public Health},
  doi       = {10.1186/s12889-022-12999-z},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-301217},
  year      = {2022},
  abstract  = {Background Physical activity (PA) guidelines acknowledge the health benefits of regular moderate-to-vigorous physical activity (MVPA) regardless of bout duration. However, little knowledge exists concerning the type and intensity distribution of structured and incidental lifestyle PA of students and office workers. The present study aimed to i) assess the duration and distribution of intensity of MVPAs during waking hours ≥50\% of heart rate reserve (HRR), ii) to identify the type of PA through diary assessment, iii) to assign these activities into structured and lifestyle incidental PA, and iv) to compare this information between students and office workers. Methods Twenty-three healthy participants (11 students, 12 office workers) recorded heart rate (HR) with a wrist-worn HR monitor (Polar M600) and filled out a PA diary throughout seven consecutive days (i.e. ≥ 8 waking h/day). Relative HR zones were calculated, and PA diary information was coded using the Compendium of PA. We matched HR data with the reported PA and identified PA bouts during waking time ≥ 50\% HRR concerning duration, HRR zone, type of PA, and assigned each activity to incidental and structured PA. Descriptive measures for time spend in different HRR zones and differences between students and office workers were calculated. Results In total, we analyzed 276.894 s (76 h 54 min 54 s) of waking time in HRR zones ≥50\% and identified 169 different types of PA. The participants spend 31.9 ± 27.1 min/day or 3.9 ± 3.2\% of their waking time in zones of ≥50\% HRR with no difference between students and office workers (p > 0.01). The proportion of assigned incidental lifestyle PA was 76.9 ± 22.5\%. Conclusions The present study provides initial insights regarding the type, amount, and distribution of intensity of structured and incidental lifestyle PA ≥ 50\% HRR. Findings show a substantial amount of incidental lifestyle PA during waking hours and display the importance of promoting a physically active lifestyle. Future research could employ ambulatory assessments with integrated electronic diaries to detect information on the type and context of MVPA during the day.},
  language  = {en}
}
@article{BaurOttoStegeretal.2018,
  author    = {Baur, Johannes and Otto, Christoph and Steger, Ulrich and Klein-Hessling, Stefan and Muhammad, Khalid and Pusch, Tobias and Murti, Krisna and Wismer, Rhoda and Germer, Christoph-Thomas and Klein, Ingo and M{\"u}ller, Nora and Serfling, Edgar and Avots, Andris},
  title     = {The transcription factor NFaTc1 supports the rejection of heterotopic heart allografts},
  series = {Frontiers in Immunology},
  volume    = {9},
  journal   = {Frontiers in Immunology},
  doi       = {10.3389/fimmu.2018.01338},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-221530},
  year      = {2018},
  abstract  = {The immune suppressants cyclosporin A (CsA) and tacrolimus (FK506) are used worldwide in transplantation medicine to suppress graft rejection. Both CsA and FK506 inhibit the phosphatase calcineurin (CN) whose activity controls the immune receptor-mediated activation of lymphocytes. Downstream targets of CN in lymphocytes are the nuclear factors of activated T cells (NFATs). We show here that the activity of NFATc1, the most prominent NFAT factor in activated lymphocytes supports the acute rejection of heterotopic heart allografts. While ablation of NFATc1 in T cells prevented graft rejection, ectopic expression of inducible NFATc1/αA isoform led to rejection of heart allografts in recipient mice. Acceptance of transplanted hearts in mice bearing NFATc1-deficient T cells was accompanied by a reduction in number and cytotoxicity of graft infiltrating cells. In CD8\(^+\) T cells, NFATc1 controls numerous intracellular signaling pathways that lead to the metabolic switch to aerobic glycolysis and the expression of numerous lymphokines, chemokines, and their receptors, including Cxcr3 that supports the rejection of allogeneic heart transplants. These findings favors NFATc1 as a molecular target for the development of new strategies to control the cytotoxicity of T cells upon organ transplantation.},
  language  = {en}
}