FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4387041330> ?p ?o ?g. }

• W4387041330 endingPage "S23" @default.
• W4387041330 startingPage "S23" @default.
• W4387041330 abstract "Background: Hepatic encephalopathy (HE) is a major complication of chronic liver disease (CLD). This neurological disorder is known to be reversible following liver transplantation (LT). Retrospective studies have demonstrated an association between a history of HE episodes and poor neurological outcome following LT. However, the impact of HE episodes on the brain remains unknown. Our aim was to evaluate the impact of multiple episodes on neurological status and brain injury in rats with CLD. Method: Five-week BDL rats and Sham-operated controls were used. BDL rats were injected with ammonium acetate, precipitating an overt episode of HE every 4 days from week 3 post-surgery (total; 4 episodes). Sham rats also received ammonia and control rats received saline. Three days after the last episode, short- and long-term memory (LTM) were assessed. Upon sacrifice, plasma and brains were collected for oxidative stress measurements and western blot used to investigate neuronal integrity in frontal cortex, hippocampus, and cerebellum. Proteomic analysis was performed on hippocampal tissue samples. Results: LTM was found to be impaired in both BDL-Vehicle and BDL-Ammonia groups vs respective Sham. However, LTM impairment was further aggravated in BDL-Ammonia rats. In BDL-Ammonia, GFAP and apoptotic markers (cleaved caspase-3 and Bax/Bcl2) were increased in the hippocampus, whereas neuronal markers (NeuN and SMI311) were reduced compared to all other experimental groups. Plasma oxidative stress was increased in BDL-Ammonia compared to respective Sham and BDL rats. Decreased total antioxidant capacity and increased 4-HNE levels were found in the hippocampus of the BDL-Ammonia group compared to respective sham and BDL rats. These differences observed in the multiple episodic BDL rats were not demonstrated following one episode. Proteomic analysis revealed 2 proteins which significantly altered in BDL-Ammonia compared to BDL-Vehicle and respective Sham. Conclusion: Multiple episodes of overt HE exacerbated the neurological impairments in BDL rats. LTM impairment in the BDL-Ammonia rats was associated with increased oxidative stress, apoptotic markers and decreased neuronal markers in the hippocampus, suggesting neuronal injury/loss. Elevated levels of GFAP in the hippocampus insinuate gliosis. These results suggest that cumulative HE episodes may cause permanent cell damage and, therefore, will less likely reversible following LT." @default.
• W4387041330 created "2023-09-27" @default.
• W4387041330 creator A5011231374 @default.
• W4387041330 creator A5020889426 @default.
• W4387041330 creator A5029941278 @default.
• W4387041330 creator A5083061422 @default.
• W4387041330 creator A5084688823 @default.
• W4387041330 date "2023-09-01" @default.
• W4387041330 modified "2023-10-18" @default.
• W4387041330 title "P32 Multiple Ammonia-Induced Episodes of Hepatic Encephalopathy Provoke Neuronal Cell Loss in Bile-Duct Ligated Rats" @default.
• W4387041330 doi "https://doi.org/10.14309/01.ajg.0000948412.20698.0f" @default.
• W4387041330 hasPublicationYear "2023" @default.
• W4387041330 type Work @default.
• W4387041330 citedByCount "0" @default.
• W4387041330 crossrefType "journal-article" @default.
• W4387041330 hasAuthorship W4387041330A5011231374 @default.
• W4387041330 hasAuthorship W4387041330A5020889426 @default.
• W4387041330 hasAuthorship W4387041330A5029941278 @default.
• W4387041330 hasAuthorship W4387041330A5083061422 @default.
• W4387041330 hasAuthorship W4387041330A5084688823 @default.
• W4387041330 hasBestOaLocation W43870413301 @default.
• W4387041330 hasConcept C126322002 @default.
• W4387041330 hasConcept C134018914 @default.
• W4387041330 hasConcept C142724271 @default.
• W4387041330 hasConcept C148762608 @default.
• W4387041330 hasConcept C2776151105 @default.
• W4387041330 hasConcept C2777214474 @default.
• W4387041330 hasConcept C2778621155 @default.
• W4387041330 hasConcept C2780325230 @default.
• W4387041330 hasConcept C2781099255 @default.
• W4387041330 hasConcept C2781161787 @default.
• W4387041330 hasConcept C71924100 @default.
• W4387041330 hasConceptScore W4387041330C126322002 @default.
• W4387041330 hasConceptScore W4387041330C134018914 @default.
• W4387041330 hasConceptScore W4387041330C142724271 @default.
• W4387041330 hasConceptScore W4387041330C148762608 @default.
• W4387041330 hasConceptScore W4387041330C2776151105 @default.
• W4387041330 hasConceptScore W4387041330C2777214474 @default.
• W4387041330 hasConceptScore W4387041330C2778621155 @default.
• W4387041330 hasConceptScore W4387041330C2780325230 @default.
• W4387041330 hasConceptScore W4387041330C2781099255 @default.
• W4387041330 hasConceptScore W4387041330C2781161787 @default.
• W4387041330 hasConceptScore W4387041330C71924100 @default.
• W4387041330 hasIssue "9S" @default.
• W4387041330 hasLocation W43870413301 @default.
• W4387041330 hasOpenAccess W4387041330 @default.
• W4387041330 hasPrimaryLocation W43870413301 @default.
• W4387041330 hasRelatedWork W2011193344 @default.
• W4387041330 hasRelatedWork W2018406010 @default.
• W4387041330 hasRelatedWork W2020106132 @default.
• W4387041330 hasRelatedWork W2104703549 @default.
• W4387041330 hasRelatedWork W2322192584 @default.
• W4387041330 hasRelatedWork W2808917216 @default.
• W4387041330 hasRelatedWork W3165353807 @default.
• W4387041330 hasRelatedWork W4200444976 @default.
• W4387041330 hasRelatedWork W4312552381 @default.
• W4387041330 hasRelatedWork W4387038131 @default.
• W4387041330 hasVolume "118" @default.
• W4387041330 isParatext "false" @default.
• W4387041330 isRetracted "false" @default.
• W4387041330 workType "article" @default.