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001     61611
005     20180211174426.0
024 7 _ |2 pmid
|a pmid:18000666
024 7 _ |2 DOI
|a 10.1007/s00259-007-0586-z
024 7 _ |2 WOS
|a WOS:000254402800018
024 7 _ |2 ISSN
|a 1432-105X
037 _ _ |a PreJuSER-61611
041 _ _ |a eng
082 _ _ |a 610
084 _ _ |2 WoS
|a Radiology, Nuclear Medicine & Medical Imaging
100 1 _ |a Boy, C.
|b 0
|0 P:(DE-HGF)0
245 _ _ |a Cerebral A(1) adenosine receptors (A(1)AR) in liver cirrhosis
260 _ _ |c 2008
|a Heidelberg [u.a.]
|b Springer-Verl.
300 _ _ |a 589 - 597
336 7 _ |a Journal Article
|0 PUB:(DE-HGF)16
|2 PUB:(DE-HGF)
336 7 _ |a Output Types/Journal article
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336 7 _ |a Journal Article
|0 0
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336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a article
|2 DRIVER
440 _ 0 |a European Journal of Nuclear Medicine and Molecular Imaging
|x 1619-7070
|0 9906
|v 35
500 _ _ |a Record converted from VDB: 12.11.2012
520 _ _ |a 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.
536 _ _ |a Funktion und Dysfunktion des Nervensystems
|c P33
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588 _ _ |a Dataset connected to Web of Science, Pubmed
650 _ 2 |2 MeSH
|a Adult
650 _ 2 |2 MeSH
|a Aged
650 _ 2 |2 MeSH
|a Brain: metabolism
650 _ 2 |2 MeSH
|a Brain: radionuclide imaging
650 _ 2 |2 MeSH
|a Female
650 _ 2 |2 MeSH
|a Humans
650 _ 2 |2 MeSH
|a Liver Cirrhosis: metabolism
650 _ 2 |2 MeSH
|a Liver Cirrhosis: radionuclide imaging
650 _ 2 |2 MeSH
|a Male
650 _ 2 |2 MeSH
|a Middle Aged
650 _ 2 |2 MeSH
|a Radiopharmaceuticals: diagnostic use
650 _ 2 |2 MeSH
|a Radiopharmaceuticals: pharmacokinetics
650 _ 2 |2 MeSH
|a Receptor, Adenosine A1: metabolism
650 _ 2 |2 MeSH
|a Tissue Distribution
650 _ 2 |2 MeSH
|a Xanthines: diagnostic use
650 _ 2 |2 MeSH
|a Xanthines: pharmacokinetics
650 _ 7 |0 0
|2 NLM Chemicals
|a 8-cyclopenta-3-(3-fluoropropyl)-1-propylxanthine
650 _ 7 |0 0
|2 NLM Chemicals
|a Radiopharmaceuticals
650 _ 7 |0 0
|2 NLM Chemicals
|a Receptor, Adenosine A1
650 _ 7 |0 0
|2 NLM Chemicals
|a Xanthines
650 _ 7 |a J
|2 WoSType
653 2 0 |2 Author
|a cirrhosis
653 2 0 |2 Author
|a brain receptors and neurotransmitters
653 2 0 |2 Author
|a positron emission tomography
653 2 0 |2 Author
|a adenosine
653 2 0 |2 Author
|a [F-18]CPFPX
700 1 _ |a Meyer, P. T.
|b 1
|0 P:(DE-HGF)0
700 1 _ |a Kircheis, G.
|b 2
|0 P:(DE-HGF)0
700 1 _ |a Holschbach, M. H.
|b 3
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700 1 _ |a Herzog, H.
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700 1 _ |a Elmenhorst, D.
|b 5
|u FZJ
|0 P:(DE-Juel1)131679
700 1 _ |a Kaiser, H. J.
|b 6
|0 P:(DE-HGF)0
700 1 _ |a Coenen, H. H.
|b 7
|u FZJ
|0 P:(DE-Juel1)131816
700 1 _ |a Häussinger, D.
|b 8
|0 P:(DE-HGF)0
700 1 _ |a Zilles, K.
|b 9
|u FZJ
|0 P:(DE-Juel1)131714
700 1 _ |a Bauer, A.
|b 10
|u FZJ
|0 P:(DE-Juel1)131672
773 _ _ |0 PERI:(DE-600)2098375-X
|a 10.1007/s00259-007-0586-z
|g Vol. 35, p. 589 - 597
|p 589 - 597
|q 35<589 - 597
|t European Journal of Nuclear Medicine and Molecular Imaging
|v 35
|x 1619-7070
|y 2008
856 7 _ |u http://dx.doi.org/10.1007/s00259-007-0586-z
909 C O |o oai:juser.fz-juelich.de:61611
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