FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2062786251> ?p ?o ?g. }

• W2062786251 endingPage "1160" @default.
• W2062786251 startingPage "1154" @default.
• W2062786251 abstract "Background & Aims Hepatic encephalopathy (HE) is now thought to be caused by cerebral oedema although the precise pathogenesis is uncertain. We hypothesised that if ammonia is a key factor, induced hyperammonaemia would lead to transient changes in brain water distribution and metabolite concentration, detectable by diffusion tensor imaging (DTI) and magnetic resonance spectroscopy (MRS). Methods Thirteen cirrhotic patients being evaluated for liver transplantation were challenged with 54 g of equal parts of threonine, serine, and glycine. Conventional magnetic resonance imaging was performed to exclude structural lesions and localise regions of interest. DTI was used to generate white matter apparent diffusion coefficient (ADC) maps and proton MRS to measure brain metabolite concentrations before and after the challenge. Results The challenge caused a mean (±SD) rise in blood ammonia of 58 (±41) μmol/L, which was accompanied by a significant 9% increase in ADC (p = 0.004). Increased ADC significantly correlated with blood ammonia (r = 0.58, p = 0.04). The change in ammonia levels also correlated with the increase in glutamine levels (r = 0.78, p = 0.002). Myo-inositol concentration decreased significantly by 0.7 (±0.7) mMol/L between scans and this correlated with the mean difference in ADC (r = 0.59, p <0.04). Conclusions These results show that ammonia can directly drive changes in brain water distribution as a mechanism for cerebral oedema development. Since cerebral astrocytes contain glutamine synthetase, our MRS data suggest intracerebral formation of glutamine from ammonia. The rapid decrease in myo-inositol indicates that this organic osmolyte plays a protective role in HE by release from astrocytes in order to maintain cell volume. Hepatic encephalopathy (HE) is now thought to be caused by cerebral oedema although the precise pathogenesis is uncertain. We hypothesised that if ammonia is a key factor, induced hyperammonaemia would lead to transient changes in brain water distribution and metabolite concentration, detectable by diffusion tensor imaging (DTI) and magnetic resonance spectroscopy (MRS). Thirteen cirrhotic patients being evaluated for liver transplantation were challenged with 54 g of equal parts of threonine, serine, and glycine. Conventional magnetic resonance imaging was performed to exclude structural lesions and localise regions of interest. DTI was used to generate white matter apparent diffusion coefficient (ADC) maps and proton MRS to measure brain metabolite concentrations before and after the challenge. The challenge caused a mean (±SD) rise in blood ammonia of 58 (±41) μmol/L, which was accompanied by a significant 9% increase in ADC (p = 0.004). Increased ADC significantly correlated with blood ammonia (r = 0.58, p = 0.04). The change in ammonia levels also correlated with the increase in glutamine levels (r = 0.78, p = 0.002). Myo-inositol concentration decreased significantly by 0.7 (±0.7) mMol/L between scans and this correlated with the mean difference in ADC (r = 0.59, p <0.04). These results show that ammonia can directly drive changes in brain water distribution as a mechanism for cerebral oedema development. Since cerebral astrocytes contain glutamine synthetase, our MRS data suggest intracerebral formation of glutamine from ammonia. The rapid decrease in myo-inositol indicates that this organic osmolyte plays a protective role in HE by release from astrocytes in order to maintain cell volume." @default.
• W2062786251 created "2016-06-24" @default.
• W2062786251 creator A5011894973 @default.
• W2062786251 creator A5068951739 @default.
• W2062786251 creator A5082054783 @default.
• W2062786251 creator A5082915677 @default.
• W2062786251 date "2011-06-01" @default.
• W2062786251 modified "2023-09-25" @default.
• W2062786251 title "Magnetic resonance quantification of water and metabolites in the brain of cirrhotics following induced hyperammonaemia" @default.
• W2062786251 cites W170445198 @default.
• W2062786251 cites W1967871721 @default.
• W2062786251 cites W1968445631 @default.
• W2062786251 cites W1973386884 @default.
• W2062786251 cites W1981636233 @default.
• W2062786251 cites W1983906125 @default.
• W2062786251 cites W1992107615 @default.
• W2062786251 cites W1995653322 @default.
• W2062786251 cites W2017557941 @default.
• W2062786251 cites W2019347611 @default.
• W2062786251 cites W2023798788 @default.
• W2062786251 cites W2030219424 @default.
• W2062786251 cites W2032137489 @default.
• W2062786251 cites W2032724842 @default.
• W2062786251 cites W2035634412 @default.
• W2062786251 cites W2048052925 @default.
• W2062786251 cites W2055719070 @default.
• W2062786251 cites W2058027749 @default.
• W2062786251 cites W2060123467 @default.
• W2062786251 cites W2063001897 @default.
• W2062786251 cites W2067764012 @default.
• W2062786251 cites W2083754290 @default.
• W2062786251 cites W2084630199 @default.
• W2062786251 cites W2085091329 @default.
• W2062786251 cites W2088846188 @default.
• W2062786251 cites W2093298383 @default.
• W2062786251 cites W2095597591 @default.
• W2062786251 cites W2102854066 @default.
• W2062786251 cites W2107739856 @default.
• W2062786251 cites W2109628321 @default.
• W2062786251 cites W2115438979 @default.
• W2062786251 cites W2133179125 @default.
• W2062786251 cites W2135285816 @default.
• W2062786251 cites W2136573752 @default.
• W2062786251 cites W2148726987 @default.
• W2062786251 cites W2152521775 @default.
• W2062786251 cites W2154082725 @default.
• W2062786251 cites W2160453061 @default.
• W2062786251 cites W2165981364 @default.
• W2062786251 cites W2344218612 @default.
• W2062786251 cites W4232870623 @default.
• W2062786251 doi "https://doi.org/10.1016/j.jhep.2010.09.030" @default.
• W2062786251 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21145802" @default.
• W2062786251 hasPublicationYear "2011" @default.
• W2062786251 type Work @default.
• W2062786251 sameAs 2062786251 @default.
• W2062786251 citedByCount "45" @default.
• W2062786251 countsByYear W20627862512012 @default.
• W2062786251 countsByYear W20627862512013 @default.
• W2062786251 countsByYear W20627862512014 @default.
• W2062786251 countsByYear W20627862512015 @default.
• W2062786251 countsByYear W20627862512016 @default.
• W2062786251 countsByYear W20627862512017 @default.
• W2062786251 countsByYear W20627862512018 @default.
• W2062786251 countsByYear W20627862512019 @default.
• W2062786251 countsByYear W20627862512021 @default.
• W2062786251 countsByYear W20627862512022 @default.
• W2062786251 countsByYear W20627862512023 @default.
• W2062786251 crossrefType "journal-article" @default.
• W2062786251 hasAuthorship W2062786251A5011894973 @default.
• W2062786251 hasAuthorship W2062786251A5068951739 @default.
• W2062786251 hasAuthorship W2062786251A5082054783 @default.
• W2062786251 hasAuthorship W2062786251A5082915677 @default.
• W2062786251 hasConcept C121332964 @default.
• W2062786251 hasConcept C126322002 @default.
• W2062786251 hasConcept C126838900 @default.
• W2062786251 hasConcept C134018914 @default.
• W2062786251 hasConcept C143409427 @default.
• W2062786251 hasConcept C149550507 @default.
• W2062786251 hasConcept C185592680 @default.
• W2062786251 hasConcept C2777214474 @default.
• W2062786251 hasConcept C2777477808 @default.
• W2062786251 hasConcept C2779289688 @default.
• W2062786251 hasConcept C2779349466 @default.
• W2062786251 hasConcept C2780325230 @default.
• W2062786251 hasConcept C2781099255 @default.
• W2062786251 hasConcept C2781192897 @default.
• W2062786251 hasConcept C46141821 @default.
• W2062786251 hasConcept C515207424 @default.
• W2062786251 hasConcept C55493867 @default.
• W2062786251 hasConcept C70816921 @default.
• W2062786251 hasConcept C71924100 @default.
• W2062786251 hasConceptScore W2062786251C121332964 @default.
• W2062786251 hasConceptScore W2062786251C126322002 @default.
• W2062786251 hasConceptScore W2062786251C126838900 @default.
• W2062786251 hasConceptScore W2062786251C134018914 @default.
• W2062786251 hasConceptScore W2062786251C143409427 @default.
• W2062786251 hasConceptScore W2062786251C149550507 @default.
• W2062786251 hasConceptScore W2062786251C185592680 @default.

• next