@article{MuellerKrennSchindleretal.1993,
  author    = {M{\"u}ller, J. G. and Krenn, V. and Schindler, C. and Czub, S. and Stahl-Henning, C. and Coulibaly, C. and Hunsmann, G. and Kneitz, C. and Kerkau, T. and Rethwilm, A. and ter Meulen, V. and M{\"u}ller-Hermelink, H. K.},
  title     = {Alterations of Thymus Cortical Epithelium and Interdigitating Dendritic Cells but No Increase of Thymocyte Cell Death in the Early Course of Simian Immunodeficiency Virus Infection},
  series = {American Journal of Pathology},
  volume    = {143},
  journal   = {American Journal of Pathology},
  number    = {3},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-128250},
  pages     = {699-713},
  year      = {1993},
  abstract  = {The role of the thymus in the pathogenesis of simian acquired immunodeficiency syndrome was investigated in 18 juvenile rhesus monkeys (Macaca mulatta). The thymus was infected from the first week post-SIVmac inoculation, but the amount of virus-positive cells was very low « 1 in 1 04 T cells) as demonstrated by polymerase chain reaction and in situ hybridization. First morphological alteration was a narrowing of the cortex at 12 and 24 wpi. Morphometry revealed no increase of pyknotic T cells but a decrease of the proliferation rate andflow cytometry showed a reduction of the immature \(CD4^+/CD8^+\) double-positive T cells. Ultrastructural analysis revealed vacuolization, shrinkage, andfinally cytolysis of the cortical epithelial cells and the interdigitating dendritic cells. Immunofluorescence staining exhibited a widespread loss of cortical epithelial cells. This damage to the thymic microenvironment could explain the breakdown of the intrathymic T cell proliferation. It preceded fully developed simian acquired immunodeficiency syndrome and is therefore considered to play a major role in its pathogenesis.},
  language  = {en}
}
@article{MuellerKrennSchindleretal.1993,
  author    = {M{\"u}ller, J. G. and Krenn, V. and Schindler, C. and Czub, S. and Stahl-Henning, C. and Coulibaly, C. and Hunsmann, G. and Kneitz, C. and Kerkau, Thomas and Rethwilm, Axel and terMeulen, Volker},
  title     = {Alterations of thymus cortical epithelium and interdigitating dendritic cells but no increase of thymocyte cell death in the early course of simian immunodeficiency virus infection},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-32583},
  year      = {1993},
  abstract  = {No abstract available},
  language  = {en}
}
@article{MuellerKrennCzubetal.1993,
  author    = {M{\"u}ller, J. and Krenn, V. and Czub, S. and Schindler, C. and Kneitz, C. and Kerkau, T. and Stahl-Henning, C. and Coulibaly, C. and Hunsmann, G. and Rethwilm, Axel and ter Meulen, Volker and M{\"u}ller-Hermelink, H. K.},
  title     = {The thymus in SIV infection},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-80265},
  year      = {1993},
  abstract  = {no abstract available},
  subject      = {HIV-Infektion},
  language  = {en}
}
@article{MuellerStahlHennigRethwilmetal.1991,
  author    = {M{\"u}ller, JG and Stahl-Hennig, C. and Rethwilm, Axel and Kneitz, C. and Kerkau, T. and Schmauser, B. and Schindler, C. and Krenn, V. and terMeulen, V. and M{\"u}ller-Hermelink, HK},
  title     = {Morphologische Untersuchungen von Lymphknoten und Thymusin der Fr{\"u}hphase der SIV-Infektion bei Rhesus-Affen},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-80210},
  year      = {1991},
  abstract  = {Rhesus monkeys (M. mulatta) were i.v. infected with SIV mac251. Three phases of lymph node changes were observed. 1: physiological follicular hyperplasia (3 and 6 weeks p.i.). 2: Alterations of germinal centers: loss of follicular mande zone, fragmentation or sclerosis (12 and 24 weeks p.i.). 3: Partial depletion of T-lymphocytes, accumulation of plasma cells, increased numbers of syncytial giant cells, hemophgocytosis in the sinuses (ab out 1 year p.i.). The thymus of the juvenile animals showed first changes 12 and 24 weeks after infection with focalloss of immature (and Ki-67 positive) cortical thymocytes, leading to severe accidental involution of the thymuses one year after infection and reduced numbers of Hassalls corpuscles. These investigations show the value of this animal model for the study of morphology and pathogenesis of AIDS.},
  subject      = {Virologie},
  language  = {de}
}
@article{MuellerStahlHennigRethwilmetal.1991,
  author    = {M{\"u}ller, J. G. and Stahl-Hennig, Christiane and Rethwilm, Axel and Kneitz, C. and Kerkau, Thomas and Schmauser, B. and Schindler, C and Krenn, V. and terMeulen, V. and M{\"u}ller-Hermelink, H.K.},
  title     = {Morphologische Untersuchungen von Lymphknoten und Thymusin der Fr{\"u}hphase der SIV-Infektion bei Rhesus-Affen},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47183},
  year      = {1991},
  abstract  = {Rhesus monkeys (M. mulatta) were i. v. infected with SIV mac251. Three phases of lymph node changes were observed. 1: physiological follicular hyperplasia (3 and 6 weeks p.i.). 2: Alterations of germinal centers: loss of follicular mantle zone, fragmentation or sclerosis (12 and 24 weeks p.i.). 3: Partial depletion of T-lymphocytes, accumulation of plasma cells, increased numbers of syncytial giant cells, hemophgocytosis in the sinuses (about 1 year p.i.). The thymus of the juvenile animals showed first changes 12 and 24 weeks after infection with focalloss of immature (and Ki-67 positive) cortical thymocytes, leading to severe accidental involution of the thymuses one year after infection and reduced numbers of Hassalls corpuscles. These investigations show the value of this animal model for the study of morphology and pathogenesis of AIDS.},
  subject      = {Affenimmundefizienzvirus},
  language  = {de}
}
@techreport{LuettickenWegenkaYuanetal.1994,
  author    = {L{\"u}tticken, Claudia and Wegenka, Ursula M. and Yuan, Juping and Buschmann, Jan and Schindler, Chris and Ziemiecki, Andrew and Harpur, Alisa G. and Wilks, Andrew F. and Yasukawa, Kiyoshi and Taga, Tetsuya and Kishimoto, Tadamitsu and Barbieri, Giovanna and Sendtner, Michael and Pellegrini, Sandra and Heinrich, Peter C. and Horn, Friedemann},
  title     = {Association of transcription factor APRF and protein kinase JAK1 with the IL-6 signal transducer gp130},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42577},
  year      = {1994},
  abstract  = {Interleukin-6, leukemia inhibitory factor, oncostatin M. Interleukin-11, and cilialy neurotrophic factor bind to receptor complexes that share the signal transducer gp130. Upon binding, the ligands rapidly activate DNA binding of acute-phase response factor (APRF), a protein antigenicaly relaled to the p91 subunit of the interferon-stimulated gene factor-(ISGF-3a). These cytokines caused tyrosine phosphorylation of APRF and ISGF-3a p91. Protein kinases of the Jak family were also rapidly tyrosine phosphorylated, and both APRF and Jak1 associated with gp130. These data indicate that Jak family protein kinases may participate in IL-6 signaling and that APRF may be activated in a complex with gp130.},
  language  = {en}
}
@article{HebestreitLandsAlarieetal.2018,
  author    = {Hebestreit, Helge and Lands, Larry C. and Alarie, Nancy and Schaeff, Jonathan and Karila, Chantal and Orenstein, David M. and Urquhart, Don S. and Hulzebos, Erik H. J. and Stein, Lothar and Schindler, Christian and Kriemler, Susi and Radtke, Thomas},
  title     = {Effects of a partially supervised conditioning programme in cystic fibrosis: an international multi-centre randomised controlled trial (ACTIVATE-CF): study protocol},
  series = {BMC Pulmonary Medicine},
  volume    = {18},
  journal   = {BMC Pulmonary Medicine},
  doi       = {10.1186/s12890-018-0596-6},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-227960},
  year      = {2018},
  abstract  = {Background Physical activity (PA) and exercise have become an accepted and valued component of cystic fibrosis (CF) care. Regular PA and exercise can positively impact pulmonary function, improve physical fitness, and enhance health-related quality of life (HRQoL). However, motivating people to be more active is challenging. Supervised exercise programs are expensive and labour intensive, and adherence falls off significantly once supervision ends. Unsupervised or partially supervised programs are less costly and more flexible, but compliance can be more problematic. The primary objective of this study is to evaluate the effects of a partially supervised exercise intervention along with regular motivation on forced expiratory volume in 1 s (FEV1) at 6 months in a large international group of CF patients. Secondary endpoints include patient reported HRQoL, as well as levels of anxiety and depression, and control of blood sugar. Methods/design It is planned that a total of 292 patients with CF 12 years and older with a FEV1 ≥ 35\% predicted shall be randomised. Following baseline assessments (2 visits) patients are randomised into an intervention and a control group. Thereafter, they will be seen every 3 months for assessments in their centre for one year (4 follow-up visits). Along with individual counselling to increase vigorous PA by at least 3 h per week on each clinic visit, the intervention group documents daily PA and inactivity time and receives a step counter to record their progress within a web-based diary. They also receive monthly phone calls from the study staff during the first 6 months of the study. After 6 months, they continue with the step counter and web-based programme for a further 6 months. The control group receives standard care and keeps their PA level constant during the study period. Thereafter, they receive the intervention as well. Discussion This is the first large, international multi-centre study to investigate the effects of a PA intervention in CF with motivational feedback on several health outcomes using modern technology. Should this relatively simple programme prove successful, it will be made available on a wider scale internationally. Trial registration ClinicalTrials.gov Identifier: NCT01744561; Registration date: December 6, 2012.},
  language  = {en}
}
@article{RickmanLachAbhyankaretal.2015,
  author    = {Rickman, Kimberly A. and Lach, Francis P. and Abhyankar, Avinash and Donovan, Frank X. and Sanborn, Erica M. and Kennedy, Jennifer A. and Sougnez, Carrie and Gabriel, Stacey B. and Elemento, Olivier and Chandrasekharappa, Settara C. and Schindler, Detlev and Auerbach, Arleen D. and Smogorzewska, Agata},
  title     = {Deficiency of UBE2T, the E2 Ubiquitin Ligase Necessary for FANCD2 and FANCI Ubiquitination, Causes FA-T Subtype of Fanconi Anemia},
  series = {Cell Reports},
  volume    = {12},
  journal   = {Cell Reports},
  doi       = {10.1016/j.celrep.2015.06.014},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-151525},
  pages     = {35 -- 41},
  year      = {2015},
  abstract  = {Fanconi anemia (FA) is a rare bone marrow failure and cancer predisposition syndrome resulting from pathogenic mutations in genes encoding proteins participating in the repair of DNA interstrand crosslinks (ICLs). Mutations in 17 genes (FANCA-FANCS) have been identified in FA patients, defining 17 complementation groups. Here, we describe an individual presenting with typical FA features who is deficient for the ubiquitin-conjugating enzyme (E2), UBE2T. UBE2T is known to interact with FANCL, the E3 ubiquitin-ligase component of the multiprotein FA core complex, and is necessary for the monoubiquitination of FANCD2 and FANCI. Proband fibroblasts do not display FANCD2 and FANCI monoubiquitination, do not form FANCD2 foci following treatment with mitomycin C, and are hypersensitive to crosslinking agents. These cellular defects are complemented by expression of wild-type UBE2T, demonstrating that deficiency of the protein UBE2T can lead to Fanconi anemia. UBE2T gene gains an alias of FANCT.},
  language  = {en}
}