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000061611 084__ $$2WoS$$aRadiology, Nuclear Medicine & Medical Imaging
000061611 1001_ $$0P:(DE-HGF)0$$aBoy, C.$$b0
000061611 245__ $$aCerebral A(1) adenosine receptors (A(1)AR) in liver cirrhosis
000061611 260__ $$aHeidelberg [u.a.]$$bSpringer-Verl.$$c2008
000061611 300__ $$a589 - 597
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000061611 440_0 $$09906$$aEuropean Journal of Nuclear Medicine and Molecular Imaging$$v35$$x1619-7070
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000061611 520__ $$aThe cerebral mechanisms underlying hepatic encephalopathy (HE) are poorly understood. Adenosine, a neuromodulator that pre- and postsynaptically modulates neuronal excitability and release of classical neurotransmitters via A(1) adenosine receptors (A(1)AR), is likely to be involved. The present study investigates changes of cerebral A(1)AR binding in cirrhotic patients by means of positron emission tomography (PET) and [(18)F]CPFPX, a novel selective A(1)AR antagonist.PET was performed in cirrhotic patients (n = 10) and healthy volunteers (n = 10). Quantification of in vivo receptor density was done by Logan's non-invasive graphical analysis (pons as reference region). The outcome parameter was the apparent binding potential (aBP, proportional to B (max)/K (D)).Cortical and subcortical regions showed lower A(1)AR binding in cirrhotic patients than in controls. The aBP changes reached statistical significance vs healthy controls (p < 0.05, U test with Bonferroni-Holm adjustment for multiple comparisons) in cingulate cortex (-50.0%), precentral gyrus (-40.9%), postcentral gyrus (-38.6%), insular cortex (-38.6%), thalamus (-32.9%), parietal cortex (-31.7%), frontal cortex (-28.6), lateral temporal cortex (-28.2%), orbitofrontal cortex (-27.9%), occipital cortex (-24.6), putamen (-22.7%) and mesial temporal lobe (-22.4%).Regional cerebral adenosinergic neuromodulation is heterogeneously altered in cirrhotic patients. The decrease of cerebral A(1)AR binding may further aggravate neurotransmitter imbalance at the synaptic cleft in cirrhosis and hepatic encephalopathy. Different pathomechanisms may account for these alterations including decrease of A(1)AR density or affinity, as well as blockade of the A(1)AR by endogenous adenosine or exogenous xanthines.
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000061611 65320 $$2Author$$acirrhosis
000061611 65320 $$2Author$$abrain receptors and neurotransmitters
000061611 65320 $$2Author$$apositron emission tomography
000061611 65320 $$2Author$$aadenosine
000061611 65320 $$2Author$$a[F-18]CPFPX
000061611 650_2 $$2MeSH$$aAdult
000061611 650_2 $$2MeSH$$aAged
000061611 650_2 $$2MeSH$$aBrain: metabolism
000061611 650_2 $$2MeSH$$aBrain: radionuclide imaging
000061611 650_2 $$2MeSH$$aFemale
000061611 650_2 $$2MeSH$$aHumans
000061611 650_2 $$2MeSH$$aLiver Cirrhosis: metabolism
000061611 650_2 $$2MeSH$$aLiver Cirrhosis: radionuclide imaging
000061611 650_2 $$2MeSH$$aMale
000061611 650_2 $$2MeSH$$aMiddle Aged
000061611 650_2 $$2MeSH$$aRadiopharmaceuticals: diagnostic use
000061611 650_2 $$2MeSH$$aRadiopharmaceuticals: pharmacokinetics
000061611 650_2 $$2MeSH$$aReceptor, Adenosine A1: metabolism
000061611 650_2 $$2MeSH$$aTissue Distribution
000061611 650_2 $$2MeSH$$aXanthines: diagnostic use
000061611 650_2 $$2MeSH$$aXanthines: pharmacokinetics
000061611 650_7 $$00$$2NLM Chemicals$$a8-cyclopenta-3-(3-fluoropropyl)-1-propylxanthine
000061611 650_7 $$00$$2NLM Chemicals$$aRadiopharmaceuticals
000061611 650_7 $$00$$2NLM Chemicals$$aReceptor, Adenosine A1
000061611 650_7 $$00$$2NLM Chemicals$$aXanthines
000061611 650_7 $$2WoSType$$aJ
000061611 7001_ $$0P:(DE-HGF)0$$aMeyer, P. T.$$b1
000061611 7001_ $$0P:(DE-HGF)0$$aKircheis, G.$$b2
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000061611 7001_ $$0P:(DE-Juel1)VDB612$$aHerzog, H.$$b4$$uFZJ
000061611 7001_ $$0P:(DE-Juel1)131679$$aElmenhorst, D.$$b5$$uFZJ
000061611 7001_ $$0P:(DE-HGF)0$$aKaiser, H. J.$$b6
000061611 7001_ $$0P:(DE-Juel1)131816$$aCoenen, H. H.$$b7$$uFZJ
000061611 7001_ $$0P:(DE-HGF)0$$aHäussinger, D.$$b8
000061611 7001_ $$0P:(DE-Juel1)131714$$aZilles, K.$$b9$$uFZJ
000061611 7001_ $$0P:(DE-Juel1)131672$$aBauer, A.$$b10$$uFZJ
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000061611 8567_ $$uhttp://dx.doi.org/10.1007/s00259-007-0586-z
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