Objective:To investigate the differential expression and methylation level of tripartite-motif protein 59(TRIM59)in hepatocellular carcinoma(HCC)tissues and its clinical significance.Methods:The expression of TRIM59 in HCC tissue and normal liver tissue was analyzed using the TIMER2.0 and University of ALabama at Birmingham CANcer(UALCAN)databases.The prognostic correlation between TRIM59 and HCC patients was investigated through the TIMER2.0 and Kaplan-Meier Plotter databases.The cBioPortal database was utilized to explore the genetic mutations of TRIM59 in HCC and its co-expressed genes.Gene Ontology(GO)analysis and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis of TRIM59 co-expressed genes were conducted using the DAVID database.The CpG sites of TRIM59 were searched in the University of California Santa Cruz(UCSU)database,and the methylation level of TRIM59 and its correlation with HCC patient prognosis were analyzed in the Shiny Methylation Analysis Resource Tool(SMART)database.Results:TRIM59 was highly expressed in HCC tissue and lowly expressed in normal liver tissue.This differential expression was closely related to the prognosis of HCC patients.Based on GO and KEGG enrichment analyses,TRIM59 co-expressed genes were primarily involved in biological processes such as cell cycle regulation and cytoskeletal organization,as well as signaling pathways including TNF signaling,Hippo signaling,and cytoskeletal regulation.In HCC tissues,the expression of TRIM59 was positively correlated with the infiltration of immune cells such as B lymphocytes,CD8+T lymphocytes,and CD4+T lymphocytes.Additionally,the methylation level of TRIM59 was significantly reduced in HCC tissues,and its expression level was inversely correlated with methylation status.HCC patients with high methylation of TRIM59 had a significantly longer prognosis than those with low methylation.Conclusions:TRIM59 exhibits high expression and low methylation levels in HCC tissues,which are closely associated with the prognosis of HCC patients.Furthermore,differential expression of TRIM59 regulated by methylation plays a crucial role in the development and progression of HCC.

Objective:To investigate the differential expression and methylation level of tripartite-motif protein 59(TRIM59)in hepatocellular carcinoma(HCC)tissues and its clinical significance.Methods:The expression of TRIM59 in HCC tissue and normal liver tissue was analyzed using the TIMER2.0 and University of ALabama at Birmingham CANcer(UALCAN)databases.The prognostic correlation between TRIM59 and HCC patients was investigated through the TIMER2.0 and Kaplan-Meier Plotter databases.The cBioPortal database was utilized to explore the genetic mutations of TRIM59 in HCC and its co-expressed genes.Gene Ontology(GO)analysis and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis of TRIM59 co-expressed genes were conducted using the DAVID database.The CpG sites of TRIM59 were searched in the University of California Santa Cruz(UCSU)database,and the methylation level of TRIM59 and its correlation with HCC patient prognosis were analyzed in the Shiny Methylation Analysis Resource Tool(SMART)database.Results:TRIM59 was highly expressed in HCC tissue and lowly expressed in normal liver tissue.This differential expression was closely related to the prognosis of HCC patients.Based on GO and KEGG enrichment analyses,TRIM59 co-expressed genes were primarily involved in biological processes such as cell cycle regulation and cytoskeletal organization,as well as signaling pathways including TNF signaling,Hippo signaling,and cytoskeletal regulation.In HCC tissues,the expression of TRIM59 was positively correlated with the infiltration of immune cells such as B lymphocytes,CD8+T lymphocytes,and CD4+T lymphocytes.Additionally,the methylation level of TRIM59 was significantly reduced in HCC tissues,and its expression level was inversely correlated with methylation status.HCC patients with high methylation of TRIM59 had a significantly longer prognosis than those with low methylation.Conclusions:TRIM59 exhibits high expression and low methylation levels in HCC tissues,which are closely associated with the prognosis of HCC patients.Furthermore,differential expression of TRIM59 regulated by methylation plays a crucial role in the development and progression of HCC.

Objective To analyse the differential metabolites and related metabolic pathways in stable angina pectoris of coronary artery heart disease with spleen deficiency and phlegm turbidity syndrome by serum metabolomics.Methods This study observed 60 patients with stable angina pectoris of coronary artery heart disease with spleen deficiency and phlegm turbidity syndrome and 60 healthy volunteers in the same period.Liquid chromatography-mass spectrometry(LC-MS)was performed on the serum metabonomics.The differential metabolites were identified by multivariate statistical analysis of the original spectrogram and original data,and enrichment analysis of KEGG metabolic pathway was analyzed.Results A total of 60 patients in the group of stable angina pectoris of coronary artery heart disease with spleen deficiency and phlegm turbidity syndrome participated in the study,and a total of 60 healthy volunteers in the control group participated in the study.There was no statistical difference in general information and biochemical indicators between the two groups(P>0.05);Eighteen differential metabolites were found respectively,including phenylacetaldehyde,orthophosphate,guanosine,diethyl phosphate,2-dehydro-d-gluconate,guanine and 5-(2-hydroxyethyl)-4-methylthiazole down-regulated expression,taurocholate,2-propylglutaric acid,8-amino-7-oxononanoate,l-tyrosine,s-sulfo-l-cysteine,cyclohexanecarboxylic acid,porphobilinogen,(r)-acetoin,octanoylglucuronide,melatonin and solanine up-regulated expression,involving phenylalanine metabolism,thiamine metabolism,purine metabolism.Conclusion The differential metabolites reveal the metabolic essence of stable angina pectoris of coronary artery heart disease with spleen deficiency and phlegm turbidity syndrome from the micro level,and can provide clues for clinical early warning of patients with stable angina pectoris of coronary artery heart disease with spleen deficiency and phlegm turbidity syndromet.

Objective To clone the fragment of hepatitis C virus(HCV) core gene and express it in E.coli.Methods The fragment of HCV core gene(approximate 366bp) was amplified by PCR and inserted into the pMD18-T vector.The cloned HCV core gene,which was confirmed by the digestion with EcoRⅠ/BamHⅠ,was subcloned into the expression vector pBV220 to construct recombinant plasmid pBV220/HCV-C.The expressed gene product was identified by SDS-PAGE and Western blotting.Results The fragment of HCV core gene was expressed successfully after temperature induction and a protein of 14 000 u was resulted.Conclusion Expression of the HCV-C gene in E.coli was achieved,which may be helpful for further studies on characterizations of HCV-C gene.