@article{MayerRabindranathBoerneretal.2013,
  author    = {Mayer, Matthias and Rabindranath, Raman and B{\"o}rner, Juliane and H{\"o}rner, Eva and Bentz, Alexander and Salgado, Josefina and Han, Hong and B{\"o}se, Holger and Probst, J{\"o}rn and Shamonin, Mikhail and Monkman, Gereth J. and Schlunck, G{\"u}nther},
  title     = {Ultra-Soft PDMS-Based Magnetoactive Elastomers as Dynamic Cell Culture Substrata},
  series = {PLOS ONE},
  volume    = {8},
  journal   = {PLOS ONE},
  number    = {10},
  issn      = {1932-6203},
  doi       = {10.1371/journal.pone.0076196},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-128246},
  pages     = {e76196},
  year      = {2013},
  abstract  = {Mechanical cues such as extracellular matrix stiffness and movement have a major impact on cell differentiation and function. To replicate these biological features in vitro, soft substrata with tunable elasticity and the possibility for controlled surface translocation are desirable. Here we report on the use of ultra-soft (Young's modulus <100 kPa) PDMS-based magnetoactive elastomers (MAE) as suitable cell culture substrata. Soft non-viscous PDMS (<18 kPa) is produced using a modified extended crosslinker. MAEs are generated by embedding magnetic microparticles into a soft PDMS matrix. Both substrata yield an elasticity-dependent (14 vs. 100 kPa) modulation of alpha-smooth muscle actin expression in primary human fibroblasts. To allow for static or dynamic control of MAE material properties, we devise low magnetic field (approximate to 40 mT) stimulation systems compatible with cell-culture environments. Magnetic field-instigated stiffening (14 to 200 kPa) of soft MAE enhances the spreading of primary human fibroblasts and decreases PAX-7 transcription in human mesenchymal stem cells. Pulsatile MAE movements are generated using oscillating magnetic fields and are well tolerated by adherent human fibroblasts. This MAE system provides spatial and temporal control of substratum material characteristics and permits novel designs when used as dynamic cell culture substrata or cell culture-coated actuator in tissue engineering applications or biomedical devices.},
  language  = {en}
}
@article{KochHoernerMuenchetal.2020,
  author    = {Koch, Rebecca-Diana and H{\"o}rner, Eva-Maria and M{\"u}nch, Nadine and Maier, Elke and Kozjak-Pavlovic, Vera},
  title     = {Modulation of Host Cell Death and Lysis Are Required for the Release of Simkania negevensis},
  series = {Frontiers in Cellular and Infection Microbiology},
  volume    = {10},
  journal   = {Frontiers in Cellular and Infection Microbiology},
  issn      = {2235-2988},
  doi       = {10.3389/fcimb.2020.594932},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-215158},
  year      = {2020},
  abstract  = {Simkania negevensis is a Chlamydia-like bacterium and emerging pathogen of the respiratory tract. It is an obligate intracellular bacterium with a biphasic developmental cycle, which replicates in a wide range of host cells. The life cycle of S. negevensis has been shown to proceed for more than 12 days, but little is known about the mechanisms that mediate the cellular release of these bacteria. This study focuses on the investigation of host cell exit by S. negevensis and its connection to host cell death modulation. We show that Simkania-infected epithelial HeLa as well as macrophage-like THP-1 cells reduce in number during the course of infection. At the same time, the infectivity of the cell culture supernatant increases, starting at the day 3 for HeLa and day 4 for THP-1 cells and reaching maximum at day 5 post infection. This correlates with the ability of S. negevensis to block TNFα-, but not staurosporin-induced cell death up to 3 days post infection, after which cell death is boosted by the presence of bacteria. Mitochondrial permeabilization through Bax and Bak is not essential for host cell lysis and release of S. negevensis. The inhibition of caspases by Z-VAD-FMK, caspase 1 by Ac-YVAD-CMK, and proteases significantly reduces the number of released infectious particles. In addition, the inhibition of myosin II by blebbistatin also strongly affects Simkania release, pointing to a possible double mechanism of exit through host cell lysis and potentially extrusion.},
  language  = {en}
}
@article{MahyeraSchneiderHalligerKelleretal.2018,
  author    = {Mahyera, Alexis S. and Schneider, Tamara and Halliger-Keller, Birgit and Schrooten, Katja and H{\"o}rner, Eva-Maria and Rost, Simone and Kress, Wolfram},
  title     = {Distribution and Structure of DM2 Repeat Tract Alleles in the German Population},
  series = {Frontiers in Neurology},
  volume    = {9},
  journal   = {Frontiers in Neurology},
  number    = {463},
  issn      = {1664-2295},
  doi       = {10.3389/fneur.2018.00463},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-196252},
  year      = {2018},
  abstract  = {Autosomal dominant inherited Myotonic dystrophy type 1 and 2 (DM1 and DM2) are the most frequent muscle dystrophies in the European population and are caused by repeat expansion mutations. For Germany cumulative empiric evidence suggests an estimated prevalence of DM2 of roughly 9 in 100,000, therefore being as prevalent as DM1. In DM2, a (CCTG)n repeat tract located in the first intron of the CNBP gene is expanded. The CCTG repeat tract is part of a complex repeat structure comprising not only CCTG tetraplets but also repeated TG dinucleotides and TCTG tetraplet elements as well as NCTG interruptions. Here, we provide the distribution of normal sized alleles in the German population, which was found to be highly similar to the Slovak population. Sequencing of 34 unexpanded healthy range alleles in DM2 positive patients (heterozygous for a full expansion) revealed that the CCTG repeat tract is usually interrupted by at least three tetraplets which according to current opinion is supposed to render it stable against expansion. Interestingly, only the largest analyzed normal allele had 23 uninterrupted CCTGs and consequently could represent an instable early premutation allele. In our diagnostic history of DM2 cases, a total of 18 premutations were detected in 16 independent cases. Here, we describe two premutation families, one with an expansion from a premutation allele and the other with a contraction of a full expansion down to a premutation allele. Our diagnostic results support the general assumption that the premutation range of unstable CCTG stretches lies obviously between 25 and 75 CCTGs. However, the clinical significance of premutation alleles is still unclear. In the light of the two described families we suggest incomplete penetrance. Thus, as it was proposed for other repeat expansion diseases (e.g., Huntington's disease), a fluid transition of penetrance is more likely rather than a clear cut CCTG number threshold.},
  language  = {en}
}