001     10219
005     20210129210517.0
024 7 _ |2 pmid
|a pmid:20583283
024 7 _ |2 pmc
|a pmc:PMC3395472
024 7 _ |2 DOI
|a 10.1002/hep.23656
024 7 _ |2 WOS
|a WOS:000279409200028
037 _ _ |a PreJuSER-10219
041 _ _ |a eng
082 _ _ |a 610
084 _ _ |2 WoS
|a Gastroenterology & Hepatology
100 1 _ |0 P:(DE-HGF)0
|a Görg, B.
|b 0
245 _ _ |a Oxidative stress markers in the brain of patients with cirrhosis and hepatic encephalopathy
260 _ _ |a New York [u.a.]
|b Wiley Interscience
|c 2010
300 _ _ |a 256 - 265
336 7 _ |a Journal Article
|0 PUB:(DE-HGF)16
|2 PUB:(DE-HGF)
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|0 0
|2 EndNote
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a article
|2 DRIVER
440 _ 0 |0 11862
|a Hepatology
|v 52
|x 0270-9139
|y 1
500 _ _ |a This Study was Supported by Deutsche Forschungsgemeinschaft through Sonderforschungsbereich 575 "Experimentelle Hepatologle" (Dusseldorf).
520 _ _ |a Cell culture studies and animal models point to an important role of oxidative/nitrosative stress in the pathogenesis of cerebral ammonia toxicity. However, it is unknown whether oxidative/nitrosative stress in the brain is also characteristic of hepatic encephalopathy (HE) in humans. We therefore analyzed post mortem cortical brain tissue samples from patients with cirrhosis dying with or without HE in comparison with brains from patients without liver disease. Significantly elevated levels of protein tyrosine-nitrated proteins, heat shock protein-27, and 8-hydroxyguanosine as a marker for RNA oxidation were found in the cerebral cortex of HE patients, but not of patients with cirrhosis but without HE. Glutamine synthetase (GS) activity was significantly decreased, whereas GS protein expression was not significantly affected. Protein expression of the glutamate/aspartate cotransporter was up-regulated in HE, whereas protein expression of neuronal and inducible nitric oxide synthases, manganese-dependent and copper/zinc-dependent superoxide dismutase, and glial glutamate transporter-1 were not significantly increased. CONCLUSION: These data indicate that HE in patients with cirrhosis is associated with oxidative/nitrosative stress, protein tyrosine nitration, and RNA oxidation, suggesting a role of oxidative stress in the pathogenesis of HE in patients with cirrhosis.
536 _ _ |0 G:(DE-Juel1)FUEK409
|2 G:(DE-HGF)
|x 0
|c FUEK409
|a Funktion und Dysfunktion des Nervensystems (FUEK409)
536 _ _ |0 G:(DE-HGF)POF2-89571
|a 89571 - Connectivity and Activity (POF2-89571)
|c POF2-89571
|f POF II T
|x 1
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 Amino Acid Transport System X-AG: analysis
650 _ 2 |2 MeSH
|a Amino Acid Transport System X-AG: metabolism
650 _ 2 |2 MeSH
|a Biological Markers: analysis
650 _ 2 |2 MeSH
|a Biological Markers: metabolism
650 _ 2 |2 MeSH
|a Cerebral Cortex: chemistry
650 _ 2 |2 MeSH
|a Cerebral Cortex: metabolism
650 _ 2 |2 MeSH
|a Excitatory Amino Acid Transporter 2: analysis
650 _ 2 |2 MeSH
|a Excitatory Amino Acid Transporter 2: metabolism
650 _ 2 |2 MeSH
|a Female
650 _ 2 |2 MeSH
|a Glutamate-Ammonia Ligase: analysis
650 _ 2 |2 MeSH
|a Glutamate-Ammonia Ligase: metabolism
650 _ 2 |2 MeSH
|a Guanosine: analogs & derivatives
650 _ 2 |2 MeSH
|a Guanosine: analysis
650 _ 2 |2 MeSH
|a Guanosine: metabolism
650 _ 2 |2 MeSH
|a HSP27 Heat-Shock Proteins: analysis
650 _ 2 |2 MeSH
|a HSP27 Heat-Shock Proteins: metabolism
650 _ 2 |2 MeSH
|a Hepatic Encephalopathy: etiology
650 _ 2 |2 MeSH
|a Hepatic Encephalopathy: metabolism
650 _ 2 |2 MeSH
|a Humans
650 _ 2 |2 MeSH
|a Liver Cirrhosis: complications
650 _ 2 |2 MeSH
|a Male
650 _ 2 |2 MeSH
|a Middle Aged
650 _ 2 |2 MeSH
|a Nitrates: analysis
650 _ 2 |2 MeSH
|a Nitrates: metabolism
650 _ 2 |2 MeSH
|a Oxidative Stress
650 _ 2 |2 MeSH
|a RNA: analysis
650 _ 2 |2 MeSH
|a RNA: metabolism
650 _ 2 |2 MeSH
|a Tyrosine: analysis
650 _ 2 |2 MeSH
|a Tyrosine: metabolism
650 _ 7 |0 0
|2 NLM Chemicals
|a Amino Acid Transport System X-AG
650 _ 7 |0 0
|2 NLM Chemicals
|a Biological Markers
650 _ 7 |0 0
|2 NLM Chemicals
|a Excitatory Amino Acid Transporter 2
650 _ 7 |0 0
|2 NLM Chemicals
|a HSP27 Heat-Shock Proteins
650 _ 7 |0 0
|2 NLM Chemicals
|a Nitrates
650 _ 7 |0 118-00-3
|2 NLM Chemicals
|a Guanosine
650 _ 7 |0 3868-31-3
|2 NLM Chemicals
|a 8-hydroxyguanosine
650 _ 7 |0 55520-40-6
|2 NLM Chemicals
|a Tyrosine
650 _ 7 |0 63231-63-0
|2 NLM Chemicals
|a RNA
650 _ 7 |0 EC 6.3.1.2
|2 NLM Chemicals
|a Glutamate-Ammonia Ligase
650 _ 7 |2 WoSType
|a J
700 1 _ |0 P:(DE-HGF)0
|a Qvartskhava, N.
|b 1
700 1 _ |0 P:(DE-HGF)0
|a Bidmon, H.-J.
|b 2
700 1 _ |0 P:(DE-Juel1)VDB1208
|a Palomero-Gallagher, N.
|b 3
|u FZJ
700 1 _ |0 P:(DE-HGF)0
|a Kircheis, G.
|b 4
700 1 _ |0 P:(DE-Juel1)131714
|a Zilles, K.
|b 5
|u FZJ
700 1 _ |0 P:(DE-HGF)0
|a Häussinger, D.
|b 6
773 _ _ |0 PERI:(DE-600)1472120-x
|a 10.1002/hep.23656
|g Vol. 52, p. 256 - 265
|p 256 - 265
|q 52<256 - 265
|t Hepatology
|v 52
|x 0270-9139
|y 2010
856 7 _ |2 Pubmed Central
|u http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3395472
909 C O |o oai:juser.fz-juelich.de:10219
|p VDB
913 2 _ |0 G:(DE-HGF)POF3-571
|1 G:(DE-HGF)POF3-570
|2 G:(DE-HGF)POF3-500
|a DE-HGF
|b Key Technologies
|l Decoding the Human Brain
|v Connectivity and Activity
|x 0
913 1 _ |0 G:(DE-HGF)POF2-89571
|a DE-HGF
|v Connectivity and Activity
|x 1
|4 G:(DE-HGF)POF
|1 G:(DE-HGF)POF3-890
|3 G:(DE-HGF)POF3
|2 G:(DE-HGF)POF3-800
|b Programmungebundene Forschung
|l ohne Programm
914 1 _ |y 2010
915 _ _ |0 StatID:(DE-HGF)0010
|a JCR/ISI refereed
920 1 _ |0 I:(DE-Juel1)INM-2-20090406
|k INM-2
|l Molekulare Organisation des Gehirns
|g INM
|x 0
920 1 _ |0 I:(DE-82)080010_20140620
|k JARA-BRAIN
|l Jülich-Aachen Research Alliance - Translational Brain Medicine
|g JARA
|x 1
970 _ _ |a VDB:(DE-Juel1)120466
980 _ _ |a VDB
980 _ _ |a ConvertedRecord
980 _ _ |a journal
980 _ _ |a I:(DE-Juel1)INM-2-20090406
980 _ _ |a I:(DE-82)080010_20140620
980 _ _ |a UNRESTRICTED
981 _ _ |a I:(DE-Juel1)VDB1046


LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21