@article{BhavsarSinghSharmaetal.2016,
  author    = {Bhavsar, Shefalee K. and Singh, Yogesh and Sharma, Piyush and Khairnar, Vishal and Hosseinzadeh, Zohreh and Zhang, Shaqiu and Palmada, Monica and Sabolic, Ivan and Koepsell, Hermann and Lang, Karl S. and Lang, Philipp A. and Lang, Florian},
  title     = {Expression of JAK3 Sensitive Na\(^+\) Coupled Glucose Carrier SGLT1 in Activated Cytotoxic T Lymphocytes},
  series = {Cellular Physiology and Biochemistry},
  volume    = {39},
  journal   = {Cellular Physiology and Biochemistry},
  number    = {3},
  doi       = {10.1159/000447827},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-164900},
  pages     = {1209-1228},
  year      = {2016},
  abstract  = {Background: Similar to tumor cells, activated T-lymphocytes generate ATP mainly by glycolytic degradation of glucose. Lymphocyte glucose uptake involves non-concentrative glucose carriers of the GLUT family. In contrast to GLUT isoforms, Na+-coupled glucose-carrier SGLT1 accumulates glucose against glucose gradients and is effective at low extracellular glucose concentrations. The present study explored expression and regulation of SGLT1 in activated murine splenic cytotoxic T cells (CTLs) and human Jurkat T cells. Methods: FACS analysis, immunofluorescence, confocal microscopy, chemiluminescence and Western blotting were employed to estimate SGLT1 expression, function and regulation in lymphocytes, as well as dual electrode voltage clamp in SGLT1 ± JAK3 expressing Xenopus oocytes to quantify the effect of janus kinase3 (JAK3) on SGLT1 function. Results: SGLT1 is expressed in murine CTLs and also in human Jurkat T cells. 2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose uptake was significantly decreased by SGLT1-blocker phloridzin (0.2 mM) and by pharmacological inhibition of JAK3 with WHI-P131 (156 µM), WHI-P154 (11.2 µM) and JAK3 inhibitor VI (0.5 µM). Electrogenic glucose transport (Iglucose) in Xenopus oocytes expressing human SGLT1 was increased by additional expression of human wild type JAK3, active A568VJAK3 but not inactive K851AJAK3. Coexpression of JAK3 enhanced the maximal transport rate without significantly modifying affinity of the carrier. Iglucose in SGLT1+JAK3 expressing oocytes was significantly decreased by WHI-P154 (11.2 µM). JAK3 increased the SGLT1 protein abundance in the cell membrane. Inhibition of carrier insertion by brefeldin A (5 µM) in SGLT1+JAK3 expressing oocytes resulted in a decline of Iglucose, which was similar in presence and absence of JAK3. Conclusions: SGLT1 is expressed in murine cytotoxic T cells and human Jurkat T cells and significantly contributes to glucose uptake in those cells post activation. JAK3 up-regulates SGLT1 activity by increasing the carrier protein abundance in the cell membrane, an effect enforcing cellular glucose uptake into activated lymphocytes and thus contributing to the immune response.},
  language  = {en}
}
@article{SchleicherPaduchDebusetal.2016,
  author    = {Schleicher, Ulrike and Paduch, Katrin and Debus, Andrea and Obermeyer, Stephanie and K{\"o}nig, Till and Kling, Jessica C. and Ribechini, Eliana and Dudziak, Diana and Mougiakakos, Dimitrios and Murray, Peter J. and Ostuni, Renato and K{\"o}rner, Heinrich and Bogdan, Christian},
  title     = {TNF-Mediated Restriction of Arginase 1 Expression in Myeloid Cells Triggers Type 2 NO Synthase Activity at the Site of Infection},
  series = {Cell Reports},
  volume    = {15},
  journal   = {Cell Reports},
  number    = {5},
  doi       = {10.1016/j.celrep.2016.04.001},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-164897},
  pages     = {1062-1075},
  year      = {2016},
  abstract  = {Neutralization or deletion of tumor necrosis factor (TNF) causes loss of control of intracellular pathogens in mice and humans, but the underlying mechanisms are incompletely understood. Here, we found that TNF antagonized alternative activation of macrophages and dendritic cells by IL-4. TNF inhibited IL-4-induced arginase 1 (Arg1) expression by decreasing histone acetylation, without affecting STAT6 phosphorylation and nuclear translocation. In Leishmania major-infected C57BL/6 wild-type mice, type 2 nitric oxide (NO) synthase (NOS2) was detected in inflammatory dendritic cells or macrophages, some of which co-expressed Arg1. In TNF-deficient mice, Arg1 was hyperexpressed, causing an impaired production of NO in situ. A similar phenotype was seen in L. major-infected BALB/c mice. Arg1 deletion in hematopoietic cells protected these mice from an otherwise lethal disease, although their disease-mediating T cell response (Th2, Treg) was maintained. Thus, deletion or TNF-mediated restriction of Arg1 unleashes the production of NO by NOS2, which is critical for pathogen control.},
  language  = {en}
}
@article{GattoSchulzeNielsen2016,
  author    = {Gatto, Francesco and Schulze, Almut and Nielsen, Jens},
  title     = {Systematic Analysis Reveals that Cancer Mutations Converge on Deregulated Metabolism of Arachidonate and Xenobiotics},
  series = {Cell Reports},
  volume    = {16},
  journal   = {Cell Reports},
  number    = {3},
  doi       = {10.1016/j.celrep.2016.06.038},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-164814},
  pages     = {878-895},
  year      = {2016},
  abstract  = {Mutations are the basis of the clonal evolution of most cancers. Nevertheless, a systematic analysis of whether mutations are selected in cancer because they lead to the deregulation of specific biological processes independent of the type of cancer is still lacking. In this study, we correlated the genome and transcriptome of 1,082 tumors. We found that nine commonly mutated genes correlated with substantial changes in gene expression, which primarily converged on metabolism. Further network analyses circumscribed the convergence to a network of reactions, termed AraX, that involves the glutathione- and oxygen-mediated metabolism of arachidonic acid and xenobiotics. In an independent cohort of 4,462 samples, all nine mutated genes were consistently correlated with the deregulation of AraX. Among all of the metabolic pathways, AraX deregulation represented the strongest predictor of patient survival. These findings suggest that oncogenic mutations drive a selection process that converges on the deregulation of the AraX network.},
  language  = {en}
}
@article{ChilloKleinertLautzetal.2016,
  author    = {Chillo, Omary and Kleinert, Eike Christian and Lautz, Thomas and Lasch, Manuel and Pagel, Judith-Irina and Heun, Yvonn and Troidl, Kerstin and Fischer, Silvia and Caballero-Martinez, Amelia and Mauer, Annika and Kurz, Angela R. M. and Assmann, Gerald and Rehberg, Markus and Kanse, Sandip M. and Nieswandt, Bernhard and Walzog, Barbara and Reichel, Christoph A. and Mannell, Hanna and Preissner, Klaus T. and Deindl, Elisabeth},
  title     = {Perivascular Mast Cells Govern Shear Stress-Induced Arteriogenesis by Orchestrating Leukocyte Function},
  series = {Cell Reports},
  volume    = {16},
  journal   = {Cell Reports},
  number    = {8},
  doi       = {10.1016/j.celrep.2016.07.040},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-164800},
  pages     = {2197-2207},
  year      = {2016},
  abstract  = {The body has the capacity to compensate for an occluded artery by creating a natural bypass upon increased fluid shear stress. How this mechanical force is translated into collateral artery growth (arteriogenesis) is unresolved. We show that extravasation of neutrophils mediated by the platelet receptor GPIbα and uPA results in Nox2-derived reactive oxygen radicals, which activate perivascular mast cells. These c-kit+/CXCR-4+ cells stimulate arteriogenesis by recruiting additional neutrophils as well as growth-promoting monocytes and T cells. Additionally, mast cells may directly contribute to vascular remodeling and vascular cell proliferation through increased MMP activity and by supplying growth-promoting factors. Boosting mast cell recruitment and activation effectively promotes arteriogenesis, thereby protecting tissue from severe ischemic damage. We thus find that perivascular mast cells are central regulators of shear stress-induced arteriogenesis by orchestrating leukocyte function and growth factor/cytokine release, thus providing a therapeutic target for treatment of vascular occlusive diseases.},
  language  = {en}
}
@article{BartelheimNemesSeeringeretal.2016,
  author    = {Bartelheim, Kerstin and Nemes, Karolina and Seeringer, Angela and Kerl, Kornelius and Buechner, Jochen and Boos, Joachim and Graf, Norbert and D{\"u}rken, Matthias and Gerss, Joachim and Hasselblatt, Martin and Kortmann, Rolf-Dieter and Teichert von Luettichau, Irene and Nagel, Inga and Nygaard, Randi and Oyen, Florian and Quiroga, Eduardo and Schlegel, Paul-Gerhardt and Schmid, Irene and Schneppenheim, Reinhard and Siebert, Reiner and Solano-Paez, Palma and Timmermann, Beate and Warmuth-Metz, Monika and Fr{\"u}hwald, Michael Christoph},
  title     = {Improved 6-year overall survival in AT/RT - results of the registry study Rhabdoid 2007},
  series = {Cancer Medicine},
  volume    = {5},
  journal   = {Cancer Medicine},
  number    = {8},
  doi       = {10.1002/cam4.741},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-164799},
  pages     = {1765-1775},
  year      = {2016},
  abstract  = {Atypical teratoid rhabdoid tumors (AT/RT) are characterized by mutations and subsequent inactivation of SMARCB1 (INI1, hSNF5), a predilection for very young children and an unfavorable outcome. The European Registry for rhabdoid tumors (EU-RHAB) was established to generate a common European database and to establish a standardized treatment regimen as the basis for phase I/II trials. Thus, genetic analyses, neuropathologic and radiologic diagnoses, and a consensus treatment regimen were prospectively evaluated. From 2005 to 2009, 31 patients with AT/RT from four countries were recruited into the registry study Rhabdoid 2007 and treated with systemic and intraventricular chemotherapy. Eight patients received high-dose chemotherapy, 23 radiotherapy, and 17 maintenance therapy. Reference evaluations were performed in 64\% (genetic analyses, FISH, MLPA, sequencing) up to 97\% (neuropathology, INI1 stain). Germ-line mutations (GLM) were detected in 6/21 patients. Prolonged overall survival was associated with age above 3 years, radiotherapy and achievement of a complete remission. 6-year overall and event-free survival rates were 46\% (±0.10) and 45\% (±0.09), respectively. Serious adverse events and one treatment-related death due to insufficiency of a ventriculo peritoneal shunt (VP-shunt) and consecutive herniation were noted. Acquisition of standardized data including reference diagnosis and a standard treatment schedule improved data quality along with a survival benefit. Treatment was feasible with significant but manageable toxicity. Although our analysis is biased due to heterogeneous adherence to therapy, EU-RHAB provides the best available basis for phase I/II clinical trials.},
  language  = {en}
}
@article{SilvestriBarrowdaleMulliganetal.2016,
  author    = {Silvestri, Valentina and Barrowdale, Daniel and Mulligan, Anna Marie and Neuhausen, Susan L. and Fox, Stephen and Karlan, Beth Y. and Mitchell, Gillian and James, Paul and Thull, Darcy L. and Zorn, Kristin K. and Carter, Natalie J. and Nathanson, Katherine L. and Domchek, Susan M. and Rebbeck, Timothy R. and Ramus, Susan J. and Nussbaum, Robert L. and Olopade, Olufunmilayo I. and Rantala, Johanna and Yoon, Sook-Yee and Caligo, Maria A. and Spugnesi, Laura and Bojesen, Anders and Pedersen, Inge Sokilde and Thomassen, Mads and Jensen, Uffe Birk and Toland, Amanda Ewart and Senter, Leigha and Andrulis, Irene L. and Glendon, Gord and Hulick, Peter J. and Imyanitov, Evgeny N. and Greene, Mark H. and Mai, Phuong L. and Singer, Christian F. and Rappaport-Fuerhauser, Christine and Kramer, Gero and Vijai, Joseph and Offit, Kenneth and Robson, Mark and Lincoln, Anne and Jacobs, Lauren and Machackova, Eva and Foretova, Lenka and Navratilova, Marie and Vasickova, Petra and Couch, Fergus J. and Hallberg, Emily and Ruddy, Kathryn J. and Sharma, Priyanka and Kim, Sung-Won and Teixeira, Manuel R. and Pinto, Pedro and Montagna, Marco and Matricardi, Laura and Arason, Adalgeir and Johannsson, Oskar Th and Barkardottir, Rosa B. and Jakubowska, Anna and Lubinski, Jan and Izquierdo, Angel and Pujana, Miguel Angel and Balma{\~n}a, Judith and Diez, Orland and Ivady, Gabriella and Papp, Janos and Olah, Edith and Kwong, Ava and Nevanlinna, Heli and Aittom{\"a}ki, Kristiina and Segura, Pedro Perez and Caldes, Trinidad and Van Maerken, Tom and Poppe, Bruce and Claes, Kathleen B. M. and Isaacs, Claudine and Elan, Camille and Lasset, Christine and Stoppa-Lyonnet, Dominique and Barjhoux, Laure and Belotti, Muriel and Meindl, Alfons and Gehrig, Andrea and Sutter, Christian and Engel, Christoph and Niederacher, Dieter and Steinemann, Doris and Hahnen, Eric and Kast, Karin and Arnold, Norbert and Varon-Mateeva, Raymonda and Wand, Dorothea and Godwin, Andrew K. and Evans, D. Gareth and Frost, Debra and Perkins, Jo and Adlard, Julian and Izatt, Louise and Platte, Radka and Eeles, Ros and Ellis, Steve and Hamann, Ute and Garber, Judy and Fostira, Florentia and Fountzilas, George and Pasini, Barbara and Giannini, Giuseppe and Rizzolo, Piera and Russo, Antonio and Cortesi, Laura and Papi, Laura and Varesco, Liliana and Palli, Domenico and Zanna, Ines and Savarese, Antonella and Radice, Paolo and Manoukian, Siranoush and Peissel, Bernard and Barile, Monica and Bonanni, Bernardo and Viel, Alessandra and Pensotti, Valeria and Tommasi, Stefania and Peterlongo, Paolo and Weitzel, Jeffrey N. and Osorio, Ana and Benitez, Javier and McGuffog, Lesley and Healey, Sue and Gerdes, Anne-Marie and Ejlertsen, Bent and Hansen, Thomas V. O. and Steele, Linda and Ding, Yuan Chun and Tung, Nadine and Janavicius, Ramunas and Goldgar, David E. and Buys, Saundra S. and Daly, Mary B. and Bane, Anita and Terry, Mary Beth and John, Esther M. and Southey, Melissa and Easton, Douglas F. and Chenevix-Trench, Georgia and Antoniou, Antonis C. and Ottini, Laura},
  title     = {Male breast cancer in BRCA1 and BRCA2 mutation carriers: pathology data from the Consortium of Investigators of Modifiers of BRCA1/2},
  series = {Breast Cancer Research},
  volume    = {18},
  journal   = {Breast Cancer Research},
  number    = {15},
  doi       = {10.1186/s13058-016-0671-y},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-164769},
  year      = {2016},
  abstract  = {Background BRCA1 and, more commonly, BRCA2 mutations are associated with increased risk of male breast cancer (MBC). However, only a paucity of data exists on the pathology of breast cancers (BCs) in men with BRCA1/2 mutations. Using the largest available dataset, we determined whether MBCs arising in BRCA1/2 mutation carriers display specific pathologic features and whether these features differ from those of BRCA1/2 female BCs (FBCs). Methods We characterised the pathologic features of 419 BRCA1/2 MBCs and, using logistic regression analysis, contrasted those with data from 9675 BRCA1/2 FBCs and with population-based data from 6351 MBCs in the Surveillance, Epidemiology, and End Results (SEER) database. Results Among BRCA2 MBCs, grade significantly decreased with increasing age at diagnosis (P = 0.005). Compared with BRCA2 FBCs, BRCA2 MBCs were of significantly higher stage (P for trend = 2 × 10-5) and higher grade (P for trend = 0.005) and were more likely to be oestrogen receptor-positive [odds ratio (OR) 10.59; 95 \% confidence interval (CI) 5.15-21.80] and progesterone receptor-positive (OR 5.04; 95 \% CI 3.17-8.04). With the exception of grade, similar patterns of associations emerged when we compared BRCA1 MBCs and FBCs. BRCA2 MBCs also presented with higher grade than MBCs from the SEER database (P for trend = 4 × 10-12). Conclusions On the basis of the largest series analysed to date, our results show that BRCA1/2 MBCs display distinct pathologic characteristics compared with BRCA1/2 FBCs, and we identified a specific BRCA2-associated MBC phenotype characterised by a variable suggesting greater biological aggressiveness (i.e., high histologic grade). These findings could lead to the development of gender-specific risk prediction models and guide clinical strategies appropriate for MBC management.},
  language  = {en}
}
@article{WeigandBoosTasbihietal.2016,
  author    = {Weigand, Annika and Boos, Anja M. and Tasbihi, Kereshmeh and Beier, Justus P. and Dalton, Paul D. and Schrauder, Michael and Horch, Raymund E. and Beckmann, Matthias W. and Strissel, Pamela L. and Strick, Reiner},
  title     = {Selective isolation and characterization of primary cells from normal breast and tumors reveal plasticity of adipose derived stem cells},
  series = {Breast Cancer Research},
  volume    = {18},
  journal   = {Breast Cancer Research},
  number    = {32},
  doi       = {10.1186/s13058-016-0688-2},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-164759},
  year      = {2016},
  abstract  = {Background There is a need to establish more cell lines from breast tumors in contrast to immortalized cell lines from metastatic effusions in order to represent the primary tumor and not principally metastatic biology of breast cancer. This investigation describes the simultaneous isolation, characterization, growth and function of primary mammary epithelial cells (MEC), mesenchymal cells (MES) and adipose derived stem cells (ADSC) from four normal breasts, one inflammatory and one triple-negative ductal breast tumors. Methods A total of 17 cell lines were established and gene expression was analyzed for MEC and MES (n = 42) and ADSC (n = 48) and MUC1, pan-KRT, CD90 and GATA-3 by immunofluorescence. DNA fingerprinting to track cell line identity was performed between original primary tissues and isolates. Functional studies included ADSC differentiation, tumor MES and MEC invasion co-cultured with ADSC-conditioned media (CM) and MES adhesion and growth on 3D-printed scaffolds. Results Comparative analysis showed higher gene expression of EPCAM, CD49f, CDH1 and KRTs for normal MEC lines; MES lines e.g. Vimentin, CD10, ACTA2 and MMP9; and ADSC lines e.g. CD105, CD90, CDH2 and CDH11. Compared to the mean of all four normal breast cell lines, both breast tumor cell lines demonstrated significantly lower ADSC marker gene expression, but higher expression of mesenchymal and invasion gene markers like SNAI1 and MMP2. When compared with four normal ADSC differentiated lineages, both tumor ADSC showed impaired osteogenic and chondrogenic but enhanced adipogenic differentiation and endothelial-like structures, possibly due to high PDGFRB and CD34. Addressing a functional role for overproduction of adipocytes, we initiated 3D-invasion studies including different cell types from the same patient. CM from ADSC differentiating into adipocytes induced tumor MEC 3D-invasion via EMT and amoeboid phenotypes. Normal MES breast cells adhered and proliferated on 3D-printed scaffolds containing 20 fibers, but not on 2.5D-printed scaffolds with single fiber layers, important for tissue engineering. Conclusion Expression analyses confirmed successful simultaneous cell isolations of three different phenotypes from normal and tumor primary breast tissues. Our cell culture studies support that breast-tumor environment differentially regulates tumor ADSC plasticity as well as cell invasion and demonstrates applications for regenerative medicine.},
  language  = {en}
}
@article{DuenasEspinVelaPauwsetal.2016,
  author    = {Due{\~n}as-Esp{\´i}n, Ivan and Vela, Emili and Pauws, Steffen and Bescos, Cristina and Cano, Isaac and Cleries, Montserrat and Contel, Joan Carles and Keenoy, Esteban de Manuel and Garcia-Aymerich, Judith and Gomez-Cabrero, David and Kaye, Rachelle and Lahr, Maarten M. H. and Lluch-Ariet, Mag{\´i} and Moharra, Montserrat and Monterde, David and Mora, Joana and Nalin, Marco and Pavlickova, Andrea and Piera, Jordi and Ponce, Sara and Santaeugenia, Sebasti{\`a} and Schonenberg, Helen and St{\"o}rk, Stefan and Tegner, Jesper and Velickovski, Filip and Westerteicher, Christoph and Roca, Josep},
  title     = {Proposals for enhanced health risk assessment and stratification in an integrated care scenario},
  series = {BMJ Open},
  volume    = {6},
  journal   = {BMJ Open},
  number    = {e010301},
  doi       = {10.1136/bmjopen-2015-010301},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-164743},
  year      = {2016},
  abstract  = {Objectives Population-based health risk assessment and stratification are considered highly relevant for large-scale implementation of integrated care by facilitating services design and case identification. The principal objective of the study was to analyse five health-risk assessment strategies and health indicators used in the five regions participating in the Advancing Care Coordination and Telehealth Deployment (ACT) programme (http://www.act-programme.eu). The second purpose was to elaborate on strategies toward enhanced health risk predictive modelling in the clinical scenario. Settings The five ACT regions: Scotland (UK), Basque Country (ES), Catalonia (ES), Lombardy (I) and Groningen (NL). Participants Responsible teams for regional data management in the five ACT regions. Primary and secondary outcome measures We characterised and compared risk assessment strategies among ACT regions by analysing operational health risk predictive modelling tools for population-based stratification, as well as available health indicators at regional level. The analysis of the risk assessment tool deployed in Catalonia in 2015 (GMAs, Adjusted Morbidity Groups) was used as a basis to propose how population-based analytics could contribute to clinical risk prediction. Results There was consensus on the need for a population health approach to generate health risk predictive modelling. However, this strategy was fully in place only in two ACT regions: Basque Country and Catalonia. We found marked differences among regions in health risk predictive modelling tools and health indicators, and identified key factors constraining their comparability. The research proposes means to overcome current limitations and the use of population-based health risk prediction for enhanced clinical risk assessment. Conclusions The results indicate the need for further efforts to improve both comparability and flexibility of current population-based health risk predictive modelling approaches. Applicability and impact of the proposals for enhanced clinical risk assessment require prospective evaluation.},
  language  = {en}
}
@article{HammerleHussErnstetal.2016,
  author    = {Hammerle, Florian and Huss, Michael and Ernst, Verena and B{\"u}rger, Arne},
  title     = {Thinking dimensional: prevalence of DSM-5 early adolescent full syndrome, partial and subthreshold eating disorders in a cross-sectional survey in German schools},
  series = {BMJ Open},
  volume    = {6},
  journal   = {BMJ Open},
  number    = {e010843},
  doi       = {10.1136/bmjopen-2015-010843},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-164734},
  year      = {2016},
  abstract  = {Objectives Investigating for the first time in Germany Diagnostic and Statistical Manual Fifth Edition (DSM-5) prevalences of adolescent full syndrome, Other Specified Feeding or Eating Disorder (OSFED), partial and subthreshold anorexia nervosa (AN), bulimia nervosa (BN) and binge eating disorder (BED). Method A national school-based cross-sectional survey with nine schools in Germany was undertaken that was aimed at students from grades 7 and 8. Of the 1775 students who were contacted to participate in the study, 1654 participated (participation rate: 93.2\%). The sample consisted of 873 female and 781 male adolescents (mean age=13.4 years). Prevalence rates were established using direct symptom criteria with a structured inventory (SIAB-S) and an additional self-report questionnaire (Eating Disorder Inventory 2 (EDI-2)). Results Prevalences for full syndrome were 0.3\% for AN, 0.4\% for BN, 0.5\% for BED and 3.6\% for OSFED-atypical AN, 0\% for BN (low frequency/limited duration), 0\% for BED (low frequency/limited duration) and 1.9\% for purging disorder (PD). Prevalences of partial syndrome were 10.9\% for AN (7.1\% established with cognitive symptoms only, excluding weight criteria), 0.2\% for BN and 2.1\% for BED, and of subthreshold syndrome were 0.8\% for AN, 0.3\% for BN and 0.2\% for BED. Cases on EDI-2 scales were much more pronounced with 12.6-21.1\% of the participants with significant sex differences. Conclusions The findings were in accordance with corresponding international studies but were in contrast to other German studies showing much higher prevalence rates. The study provides, for the first time, estimates for DSM-5 prevalences of eating disorders in adolescents for Germany, and evidence in favour of using valid measures for improving prevalence estimates."},
  language  = {en}
}
@article{KolarHammerleJenetzkyetal.2016,
  author    = {Kolar, David R. and Hammerle, Florian and Jenetzky, Ekkehart and Huss, Michael and B{\"u}rger, Arne},
  title     = {Aversive tension in female adolescents with Anorexia Nervosa: a controlled ecological momentary assessment using smartphones},
  series = {BMC Psychiatry},
  volume    = {16},
  journal   = {BMC Psychiatry},
  number    = {97},
  doi       = {10.1186/s12888-016-0807-8},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-164720},
  year      = {2016},
  abstract  = {Background Current models of Anorexia Nervosa (AN) emphasize the role of emotion regulation. Aversive tension, described as a state of intense arousal and negative valence, is considered to be a link between emotional events and disordered eating. Recent research focused only on adult patients, and mainly general emotion regulation traits were studied. However, the momentary occurrence of aversive tension, particularly in adolescents with AN, has not been previously studied. Method 20 female adolescents with AN in outpatient treatment and 20 healthy adolescents aged 12 to 19 years participated in an ecological momentary assessment using their smartphones. Current states of aversive tension and events were assessed hourly for two consecutive weekdays. Mean and maximum values of aversive tension were compared. Multilevel analyses were computed to test the influence of time and reported events on aversive tension. The effect of reported events on subsequent changes of aversive tension in patients with AN were additionally tested in a multilevel model. Results AN patients showed higher mean and maximum levels of aversive tension. In a multilevel model, reported food intake was associated with higher levels of aversive tension in the AN group, whereas reported school or sport-related events were not linked to specific states of aversive tension. After food intake, subsequent increases of aversive tension were diminished and decreases of aversive tension were induced in adolescents with AN. Conclusions Aversive tension may play a substantial role in the psychopathology of AN, particular in relation with food intake. Therefore, treatment should consider aversive tension as a possible intervening variable during refeeding. Our findings encourage further research on aversive tension and its link to disordered eating.},
  language  = {en}
}