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@ARTICLE{Boy:61611,
      author       = {Boy, C. and Meyer, P. T. and Kircheis, G. and Holschbach,
                      M. H. and Herzog, H. and Elmenhorst, D. and Kaiser, H. J.
                      and Coenen, H. H. and Häussinger, D. and Zilles, K. and
                      Bauer, A.},
      title        = {{C}erebral {A}(1) adenosine receptors ({A}(1){AR}) in liver
                      cirrhosis},
      journal      = {European Journal of Nuclear Medicine and Molecular Imaging},
      volume       = {35},
      issn         = {1619-7070},
      address      = {Heidelberg [u.a.]},
      publisher    = {Springer-Verl.},
      reportid     = {PreJuSER-61611},
      pages        = {589 - 597},
      year         = {2008},
      note         = {Record converted from VDB: 12.11.2012},
      abstract     = {The cerebral mechanisms underlying hepatic encephalopathy
                      (HE) are poorly understood. Adenosine, a neuromodulator that
                      pre- and postsynaptically modulates neuronal excitability
                      and release of classical neurotransmitters via A(1)
                      adenosine receptors (A(1)AR), is likely to be involved. The
                      present study investigates changes of cerebral A(1)AR
                      binding in cirrhotic patients by means of positron emission
                      tomography (PET) and [(18)F]CPFPX, a novel selective A(1)AR
                      antagonist.PET was performed in cirrhotic patients (n = 10)
                      and healthy volunteers (n = 10). Quantification of in vivo
                      receptor density was done by Logan's non-invasive graphical
                      analysis (pons as reference region). The outcome parameter
                      was the apparent binding potential (aBP, proportional to B
                      (max)/K (D)).Cortical and subcortical regions showed lower
                      A(1)AR binding in cirrhotic patients than in controls. The
                      aBP changes reached statistical significance vs healthy
                      controls (p < 0.05, U test with Bonferroni-Holm adjustment
                      for multiple comparisons) in cingulate cortex $(-50.0\%),$
                      precentral gyrus $(-40.9\%),$ postcentral gyrus $(-38.6\%),$
                      insular cortex $(-38.6\%),$ thalamus $(-32.9\%),$ parietal
                      cortex $(-31.7\%),$ frontal cortex (-28.6), lateral temporal
                      cortex $(-28.2\%),$ orbitofrontal cortex $(-27.9\%),$
                      occipital cortex (-24.6), putamen $(-22.7\%)$ and mesial
                      temporal lobe $(-22.4\%).Regional$ cerebral adenosinergic
                      neuromodulation is heterogeneously altered in cirrhotic
                      patients. The decrease of cerebral A(1)AR binding may
                      further aggravate neurotransmitter imbalance at the synaptic
                      cleft in cirrhosis and hepatic encephalopathy. Different
                      pathomechanisms may account for these alterations including
                      decrease of A(1)AR density or affinity, as well as blockade
                      of the A(1)AR by endogenous adenosine or exogenous
                      xanthines.},
      keywords     = {Adult / Aged / Brain: metabolism / Brain: radionuclide
                      imaging / Female / Humans / Liver Cirrhosis: metabolism /
                      Liver Cirrhosis: radionuclide imaging / Male / Middle Aged /
                      Radiopharmaceuticals: diagnostic use / Radiopharmaceuticals:
                      pharmacokinetics / Receptor, Adenosine A1: metabolism /
                      Tissue Distribution / Xanthines: diagnostic use / Xanthines:
                      pharmacokinetics /
                      8-cyclopenta-3-(3-fluoropropyl)-1-propylxanthine (NLM
                      Chemicals) / Radiopharmaceuticals (NLM Chemicals) /
                      Receptor, Adenosine A1 (NLM Chemicals) / Xanthines (NLM
                      Chemicals) / J (WoSType)},
      cin          = {INB-3 / INB-4 / JARA-BRAIN},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INB-3-20090406 / I:(DE-Juel1)VDB807 /
                      $I:(DE-82)080010_20140620$},
      pnm          = {Funktion und Dysfunktion des Nervensystems},
      pid          = {G:(DE-Juel1)FUEK409},
      shelfmark    = {Radiology, Nuclear Medicine $\&$ Medical Imaging},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:18000666},
      UT           = {WOS:000254402800018},
      doi          = {10.1007/s00259-007-0586-z},
      url          = {https://juser.fz-juelich.de/record/61611},
}