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@ARTICLE{Schroeder:889139,
      author       = {Schroeder, Daniel C. and Popp, Erik and Rohleder, Cathrin
                      and Vus, Stefanie and Bethencourt, David de la Puente and
                      Finke, Simon R. and Zlatopolskiy, Boris and Zischler,
                      Johannes and Drzezga, Alexander and Herff, Holger and
                      Annecke, Thorsten and Hucho, Tim and Neumaier, Bernd and
                      Böttiger, Bernd W. and Endepols, Heike},
      title        = {{P}ositron-{E}mission-{T}omography {I}maging of
                      {L}ong-{T}erm {E}xpression of the 18k{D}a {T}ranslocator
                      {P}rotein {A}fter {S}udden {C}ardiac {A}rrest in {R}ats},
      journal      = {Shock},
      volume       = {55},
      number       = {5},
      issn         = {1073-2322},
      address      = {Augusta, Ga.},
      publisher    = {Biomedical Press},
      reportid     = {FZJ-2021-00064},
      pages        = {620-629},
      year         = {2021},
      note         = {PostPrint liegt leider nicht vor und kann zeitnah auch
                      nicht eingeholt werden; wird nachgetragen.},
      abstract     = {Background: Knowledge about the neuroinflammatory state
                      during months after sudden cardiac arrest is scarce.
                      Neuroinflammation is mediated by cells that express the
                      18kDa translocator protein (TSPO). We determined the time
                      course of TSPO-expressing cells in a rat model of sudden
                      cardiac arrest using longitudinal in vivo positron emission
                      tomography (PET) imaging with the TSPO-specific tracer
                      [F]DAA1106 over a period of 6 months.Methods: Five male
                      Sprague Dawley rats were resuscitated from 6 minutes sudden
                      cardiac arrest due to ventricular fibrillation, 3 animals
                      served as shams. PET measurements were performed on day 5,
                      8, 14, 90 and 180 after intervention. Magnetic resonance
                      imaging was performed on day 140. Imaging was preceded by
                      Barnes Maze spatial memory testing on day 3, 13, 90 and 180.
                      Specificity of [F]DAA1106 binding was confirmed by Iba-1
                      immunohistochemistry.Results: [F]DAA1106 accumulated
                      bilaterally in the dorsal hippocampus of all sudden cardiac
                      arrest animals on all measured time points.
                      Immunohistochemistry confirmed Iba-1 expressing cells in the
                      hippocampal CA1 region. The number of Iba-1-immunoreactive
                      objects per mm was significantly correlated with [F]DAA1106
                      uptake. Additionally, two of the five sudden cardiac arrest
                      rats showed bilateral TSPO-expression in the striatum that
                      persisted until day 180. In Barnes Maze, the relative time
                      spent in the target quadrant negatively correlates with
                      dorsal hippocampal [F]DAA1106 uptake on day 14 and
                      180.Conclusions: After sudden cardiac arrest, TSPO remains
                      expressed over the long-term. Sustainable treatment options
                      for neuroinflammation may be considered to improve cognitive
                      functions after sudden cardiac arrest.},
      cin          = {INM-2 / INM-5},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-2-20090406 / I:(DE-Juel1)INM-5-20090406},
      pnm          = {5253 - Neuroimaging (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5253},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {32433203},
      UT           = {WOS:000663739200008},
      doi          = {10.1097/SHK.0000000000001546},
      url          = {https://juser.fz-juelich.de/record/889139},
}