Purpose: Hepatocellular carcinoma (HCC) is the fourth commonest cause of cancer-related mortality; it is associated with various genetic alterations, some involved in metabolic reprogramming. This study aimed to explore the potential metabolic impact of Carbamoyl Phosphate Synthase I (CPS1) and carbamoyl phosphate synthetase/aspartate transcarbamoylase/dihydroorotase (CAD) dysregulation through the reconstruction of a network that integrates information from the Kyoto Encyclopedia of Genes and Genomes (KEGG) database, Human Metabolome Database (HMDB) and Human Protein Atlas (HPA). Methods and results: Existing literature was used to determine the roles of CPS1 and CAD in HCC. CPS1 downregulation is thought to play a role in hepatocarcinogenesis through an increased glutamine availability for de novo pyrimidine biosynthesis, which CAD catalyzes the first three steps for. KEGG, HMDB and HPA were used to reconstruct a network of relevant pathways, demonstrating the relationships between genes and metabolites using the MetaboSignal package in R. The network was filtered to exclude any duplicates, and those greater than three steps away from CPS1 or CAD. Consequently, a network of 18 metabolites, 28 metabolic genes and 1 signaling gene was obtained, which indicated expression profiles and prognostic information of each gene in the network. Conclusion: Information from different databases was collated to form an informative network that integrated different "-omics" approaches, demonstrating the relationships between genetic and metabolic components of urea cycle and the de novo pyrimidine biosynthesis pathway. This study paves the way for further research by acting as a template to investigate the relationships between genes and metabolites, explore their potential roles in various diseases and aid the development of new screening and treatment methods through network reconstruction.
Objectives Sinistral portal hypertension (SPH) is caused by increased pressure on the left portal system secondary to splenic vein stenosis or occlusion and may lead to gastric varices. The definitive management of SPH is splenectomy, but this is associated with significant mortality and morbidity in the acute setting. In this systematic review, we investigated the efficacy and safety of splenic artery embolisation (SAE) in managing refractory variceal bleeding in patients with SPH. Methods A comprehensive literature search was conducted using MEDLINE and Embase databases. A qualitative analysis was chosen due to heterogeneity of the studies. Results Our search yielded 339 articles, 278 of which were unique. After initial screening, 16 articles relevant to our search remained for full text review. Of these, 7 were included in the systematic review. All 7 papers were observational, 6 were retrospective. Between them they described 29 SAE procedures to control variceal bleeding. The technical success rate was 100% and there were no cases of rebleeding during follow up. The most common complication was post-embolisation syndrome. Four major complications occurred, two resulting in death. These deaths were the only 30-day mortalities recorded and were in patients with extensive comorbidities. Conclusions Although there is a distinct lack of randomized controlled studies comparing SAE to other treatment modalities, it appears to be safe and effective in treating hemorrhage secondary to SPH.
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