@phdthesis{Schaefer2019,
  author    = {Sch{\"a}fer, Christina},
  title     = {Erich Welter - Der Mann hinter der F.A.Z.},
  edition   = {1. Auflage},
  doi       = {10.25972/OPUS-19211},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-192117},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2019},
  abstract  = {Wer war Erich Welter? Geboren 1900 in Straßburg, gelebt in Berlin, Frankfurt am Main und Mainz, gestorben 1982 in Frankfurt am Main. Sohn eines preußischen Beamten, Weltkriegsveteran des Ersten und Zweiten Weltkriegs, Wirtschaftsredakteur, wissenschaftlicher Autor, Politikberater, Professor f{\"u}r Volkswirtschaftslehre und Gr{\"u}ndungsherausgeber der Frankfurter Allgemeinen Zeitung. Erich Welter war vieles, vor allem war er jedoch ein anpackender Unternehmer. {\"U}ber 30 Jahre pr{\"a}gte er die Geschicke der F.A.Z. Sein Name findet sich mit der Betitelung Gr{\"u}ndungsherausgeber bis heute im t{\"a}glichen Impressum der F.A.Z., trotzdem ist er selbst langj{\"a}hrigen Lesern der Zeitung nicht gel{\"a}ufig. Erich Welter agierte nicht gerne im grellen Licht der {\"O}ffentlichkeit, er stand im Hintergrund. In der vorliegenden Biografie werden die vielf{\"a}ltigen Facetten des Mannes hinter der F.A.Z. verfolgt und in ihrer Gesamtheit beschrieben.},
  subject      = {Welter, Erich},
  language  = {de}
}
@article{DonatRotherSchaeferetal.2014,
  author    = {Donat, Ulrike and Rother, Juliane and Sch{\"a}fer, Simon and Hess, Michael and H{\"a}rtl, Barbara and Kober, Christina and Langbein-Laugwitz, Johanna and Stritzker, Jochen and Chen, Nanhai G. and Aguilar, Richard J. and Weibel, Stephanie and Szalay, Alandar A.},
  title     = {Characterization of Metastasis Formation and Virotherapy in the Human C33A Cervical Cancer Model},
  series = {PLoS ONE},
  volume    = {9},
  journal   = {PLoS ONE},
  number    = {6},
  issn      = {1932-6203},
  doi       = {10.1371/journal.pone.0098533},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-119674},
  pages     = {e98533},
  year      = {2014},
  abstract  = {More than 90\% of cancer mortalities are due to cancer that has metastasized. Therefore, it is crucial to intensify research on metastasis formation and therapy. Here, we describe for the first time the metastasizing ability of the human cervical cancer cell line C33A in athymic nude mice after subcutaneous implantation of tumor cells. In this model, we demonstrated a steady progression of lumbar and renal lymph node metastases during tumor development. Besides predominantly occurring lymphatic metastases, we visualized the formation of hematogenous metastases utilizing red fluorescent protein (RFP) expressing C33A-RFP cells. RFP positive cancer cells were found migrating in blood vessels and forming micrometastases in lungs of tumor-bearing mice. Next, we set out to analyze the influence of oncolytic virotherapy in the C33A-RFP model and demonstrated an efficient virus-mediated reduction of tumor size and metastatic burden. These results suggest the C33A-RFP cervical cancer model as a new platform to analyze cancer metastases as well as to test novel treatment options to combat metastases.},
  language  = {en}
}
@article{ChopraLangSalzmannetal.2013,
  author    = {Chopra, Martin and Lang, Isabell and Salzmann, Steffen and Pachel, Christina and Kraus, Sabrina and B{\"a}uerlein, Carina A. and Brede, Christian and Jord{\´a}n Garrote, Ana-Laura and Mattenheimer, Katharina and Ritz, Miriam and Schwinn, Stefanie and Graf, Carolin and Sch{\"a}fer, Viktoria and Frantz, Stefan and Einsele, Hermann and Wajant, Harald and Beilhack, Andreas},
  title     = {Tumor Necrosis Factor Induces Tumor Promoting and Anti-Tumoral Effects on Pancreatic Cancer via TNFR1},
  series = {PLoS ONE},
  journal   = {PLoS ONE},
  doi       = {10.1371/journal.pone.0075737},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-97246},
  year      = {2013},
  abstract  = {Multiple activities are ascribed to the cytokine tumor necrosis factor (TNF) in health and disease. In particular, TNF was shown to affect carcinogenesis in multiple ways. This cytokine acts via the activation of two cell surface receptors, TNFR1, which is associated with inflammation, and TNFR2, which was shown to cause anti-inflammatory signaling. We assessed the effects of TNF and its two receptors on the progression of pancreatic cancer by in vivo bioluminescence imaging in a syngeneic orthotopic tumor mouse model with Panc02 cells. Mice deficient for TNFR1 were unable to spontaneously reject Panc02 tumors and furthermore displayed enhanced tumor progression. In contrast, a fraction of wild type (37.5\%), TNF deficient (12.5\%), and TNFR2 deficient mice (22.2\%) were able to fully reject the tumor within two weeks. Pancreatic tumors in TNFR1 deficient mice displayed increased vascular density, enhanced infiltration of CD4+ T cells and CD4+ forkhead box P3 (FoxP3)+ regulatory T cells (Treg) but reduced numbers of CD8+ T cells. These alterations were further accompanied by transcriptional upregulation of IL4. Thus, TNF and TNFR1 are required in pancreatic ductal carcinoma to ensure optimal CD8+ T cell-mediated immunosurveillance and tumor rejection. Exogenous systemic administration of human TNF, however, which only interacts with murine TNFR1, accelerated tumor progression. This suggests that TNFR1 has basically the capability in the Panc02 model to trigger pro-and anti-tumoral effects but the spatiotemporal availability of TNF seems to determine finally the overall outcome.},
  language  = {en}
}
@phdthesis{Schaefer2014,
  author    = {Sch{\"a}fer, Christina},
  title     = {Berechnung des Verh{\"a}ltnisses k der Mutationsraten von Spermatogenese zu Oogenese bei Muskeldystrophie Duchenne},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-109160},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2014},
  abstract  = {Muskeldystrophie Duchenne (DMD) (Xp21.2) und geh{\"o}rt mit 1:3500 m{\"a}nnlichen Geburten zu den h{\"a}ufigsten genetisch-determinierten Erkrankungen. DMD ist bis heute nicht heilbar. Die genetische Beratung ist Teil der Betreuung dieser Patienten und bezieht auch die heterozygotenwahrscheinlichkeit weiblicher Angeh{\"o}riger mit ein. F{\"u}r die Risikoberechnung zum {\"U}bertr{\"a}gerstatus weiblicher Angeh{\"o}riger von DMD-Patienten sind neben Stammbauminformationen und Enzymwerten Verh{\"a}ltnisse der Mutationsraten ( k -Werte) essentiell, welche die unterschiedliche Entstehungswahrscheinlichkeit der einzelnen Mutationstypen (Deletion, Duplikation, Punktmutation) in Spermatogenese oder Oogenese beschreiben.Die Bestimmung des Verh{\"a}ltnisses k der Mutationsraten zeigte, dass einerseits Deletionen im Dystrophin-Gen viel h{\"a}ufiger großm{\"u}tterlichen Ursprungs (k Deletion ≈ 0,26) und andererseits Punktmutationen im Dystrophin-Gen meist großv{\"a}terlichen Ursprungs (k Punktmutation ≈ 2,8) sind.},
  subject      = {Duchenne-Syndrom},
  language  = {de}
}
@article{GriemertSchwarzmaierHummeletal.2019,
  author    = {Griemert, Eva-Verena and Schwarzmaier, Susanne M. and Hummel, Regina and G{\"o}lz, Christina and Yang, Dong and Neuhaus, Winfried and Burek, Malgorzata and F{\"o}rster, Carola Y. and Petkovic, Ivan and Trabold, Raimund and Plesnila, Nikolaus and Engelhard, Kristin and Sch{\"a}fer, Michael K. and Thal, Serge C.},
  title     = {Plasminogen activator inhibitor-1 augments damage by impairing fibrinolysis after traumatic brain injury},
  series = {Annals of Neurology},
  volume    = {85},
  journal   = {Annals of Neurology},
  doi       = {10.1002/ana.25458},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-228682},
  pages     = {667-680},
  year      = {2019},
  abstract  = {Objective Plasminogen activator inhibitor-1 (PAI-1) is the key endogenous inhibitor of fibrinolysis, and enhances clot formation after injury. In traumatic brain injury, dysregulation of fibrinolysis may lead to sustained microthrombosis and accelerated lesion expansion. In the present study, we hypothesized that PAI-1 mediates post-traumatic malfunction of coagulation, with inhibition or genetic depletion of PAI-1 attenuating clot formation and lesion expansion after brain trauma. Methods We evaluated PAI-1 as a possible new target in a mouse controlled cortical impact (CCI) model of traumatic brain injury. We performed the pharmacological inhibition of PAI-1 with PAI-039 and stimulation by tranexamic acid, and we confirmed our results in PAI-1-deficient animals. Results PAI-1 mRNA was time-dependently upregulated, with a 305-fold peak 12 hours after CCI, which effectively counteracted the 2- to 3-fold increase in cerebral tissue-type/urokinase plasminogen activator expression. PAI-039 reduced brain lesion volume by 26\% at 24 hours and 43\% at 5 days after insult. This treatment also attenuated neuronal apoptosis and improved neurofunctional outcome. Moreover, intravital microscopy demonstrated reduced post-traumatic thrombus formation in the pericontusional cortical microvasculature. In PAI-1-deficient mice, the therapeutic effect of PAI-039 was absent. These mice also displayed 13\% reduced brain damage compared with wild type. In contrast, inhibition of fibrinolysis with tranexamic acid increased lesion volume by 25\% compared with vehicle. Interpretation This study identifies impaired fibrinolysis as a critical process in post-traumatic secondary brain damage and suggests that PAI-1 may be a central endogenous inhibitor of the fibrinolytic pathway, promoting a procoagulatory state and clot formation in the cerebral microvasculature. Ann Neurol 2019;85:667-680},
  language  = {en}
}