Artifacts in two-dimensional shear wave elastography of liver

BACKGROUND Artifacts are common when using two-dimensional shear wave elastography(2-D SWE)to measure liver stiffness(LS),but they are poorly recognized.AIM To investigate the presence and influence of artifacts in 2-D SWE of liver.METHODS We included 158 patients with chronic liver disease,who underwent 2-D SWE examination by a novice and an expert.A cross line at the center of the elastogram was drawn and was divided it into four locations:top-left,top-right,bottom-left,and bottom-right.The occurrence frequency of artifacts in different locations was compared.The influence of artifacts on the LS measurements was evaluated by comparing the elastogram with the most artifacts(EMA)and the elastogram with the least artifacts(ELA).RESULTS The percentage of elastograms with artifacts in the novice(51.7%)was significantly higher than that of the expert(19.6%)(P<0.001).It was found that both operators had the highest frequency of artifacts at bottom-left,followed by top-left and bottom-right,and top-right had the lowest frequency.The LS values(LSVs)and standard deviation values of EMAs were significantly higher than those of ELAs for both operators.An intraclass correlation coefficient value of 0.96 was found in the LSVs of EMAs of the two operators,and it increased to 0.98 when the LSVs of the ELAs were used.Both operators had lower stability index values for EMAs than ELAs,but the difference was only statistically significant for the novice.CONCLUSION Artifacts are common when using 2-D SWE to measure LS,especially for the novice.Artifacts may lead to the overestimation of LS and reduce the repeatability and reliability of LS measurements.

Bioinformatics analysis of aberrantly methylated-differentially expressed genes and pathways in hepatocellular carcinoma

AIM To discover methylated-differentially expressed genes(MDEGs) in hepatocellular carcinoma(HCC) and to explore relevant hub genes and potential pathways. METHODS The data of expression profiling GSE25097 and methylation profiling GSE57956 were gained from GEO Datasets. We analyzed the differentially methylated genes and differentially expressed genes online using GEO2 R. Functional and enrichment analyses of MDEGs were conducted using the DAVID database. A protein-protein interaction(PPI) network was performed by STRING and then visualized in Cytoscape. Hub genes were ranked by cytoH ubba, and a module analysis of the PPI network was conducted by MCODE in Cytoscape software. RESULTS In total, we categorized 266 genes as hypermethylated, lowly expressed genes(Hyper-LGs) referring to endogenous and hormone stimulus, cell surface receptor linked signal transduction and behavior. In addition, 161 genes were labelled as hypomethylated, highly expressed genes(Hypo-HGs) referring to DNA replication and metabolic process, cell cycle and division. Pathway analysis illustrated that Hyper-LGs were enriched in cancer, Wnt, and chemokine signalling pathways, while Hypo-HGs were related to cell cycle and steroid hormone biosynthesis pathways. Based on PPI networks, PTGS2, PIK3 CD, CXCL1, ESR1, and MMP2 were identified as hub genes for Hyper-LGs, and CDC45, DTL, AURKB, CDKN3, MCM2, and MCM10 were hub genes for Hypo-HGs by combining six ranked methods of cytoH ubba. CONCLUSION In the study, we disclose numerous novel genetic and epigenetic regulations and offer a vital molecular groundwork to understand the pathogenesis of HCC. Hub genes, including PTGS2, PIK3 CD, CXCL1, ESR1, MMP2, CDC45, DTL, AURKB, CDKN3, MCM2, and MCM10, can be used as biomarkers based on aberrant methylation for the accurate diagnosis and treatment of HCC.

Morin enhances hepatic Nrf2 expression in a liver fibrosis rat model

AIM To investigate whether morin can reduce hepatic fibrosis by activating the NF-E2-related factor 2(Nrf2) signaling pathway.METHODS Twenty male Sprague-Dawley rats were randomly divided into four groups: control group, morin group, carbon tetrachloride(CCl4) group, and morin + CCl4 group. Rats in both the CCl4 and morin + CCl4 groups were injected intraperitoneally with CCl4 at a dose of 2 mL/kg twice a week. Rats in both the morin and morin + CCl4 groups were treated orally with morin at a dose of 50 mg/kg twice a week. Control rats were treated with vehicle only twice a week. At the end-point of the 8 wk of the experimental period, serum AST, ALT, and ALP were measured, and the liver specimenswere obtained for pathological assessment. Real-time PCR and Western blot methods were used to analyze the expression of α-smooth muscle actin(α-SMA), collagen Ⅰ, collagen Ⅲ, Nrf2, heme oxygenase(HO-1), and quinone oxidoreductase 1(NQO1) using frozen liver specimens.RESULTS Morin-treated rats in the morin + CCl4 group had less hyperplasia of fiber tissue, minimal inflammatory cells, and less body weight loss with favorable liver enzyme measurements compared to rats treated with CCl4 only. Additionally, morin-treated rats had significantly lower m RNA and protein expression of α-SMA, collagen Ⅰ, and collagen Ⅲ, but significantly higher m RNA and protein expression of Nrf2, HO-1, and NQO1 compared to rats treated with CCl4 only(P < 0.05).CONCLUSION Morin could play a protective role by inducing the expression of Nrf2 and its downstream antioxidant factors(HO-1 and NQO1) and reducing the expression of α-SMA, collagen Ⅰ, and collagen Ⅲ in CCl4-induced liver fibrosis rats.

Impact of SNP-SNP interactions of DNA repair gene ERCC5 and metabolic gene GSTP1 on gastric cancer/atrophic gastritis risk in a Chinese population

AIM To investigate the interactions of the DNA repair gene excision repair cross complementing group 5(ERCC5) and the metabolic gene glutathione S-transferase pi 1(GSTP1) and their effects on atrophic gastritis(AG) and gastric cancer(GC) risk.METHODS Seven ERCC5 single nucleotide polymorphisms(SNPs)(rs1047768, rs2094258, rs2228959, rs4150291, rs4150383, rs751402, and rs873601) and GSTP1 SNP rs1695 were detected using the Sequenom MassA RRAY platform in 450 GC patients, 634 AG cases, and 621 healthy control subjects in a Chinese population.RESULTS Two pairwise combinations(ERCC5 rs2094258 and rs873601 with GSTP1 rs1695) influenced AG risk(P_(interaction) = 0.008 and 0.043, respectively), and the ERCC5 rs2094258-GSTP1 rs1695 SNP pair demonstrated an antagonistic effect, while ERCC5 rs873601-GSTP1 rs1695 showed a synergistic effect on AG risk OR = 0.51 and 1.79, respectively). No pairwise combinations were observed in relation to GC risk. There were no cumulative effects among the pairwise interactions(ERCC5 rs2094258 and rs873601 with GSTP1 rs1695) on AG susceptibility(P_(trend) > 0.05). When the modification effect of Helicobacter pylori(H. pylori) infection was evaluated, the cumulative effect of one of the aforementioned pairwise interactions(ERCC5 rs873601-GSTP1 rs1695) was associated with an increased AG risk in the case of negative H. pylori status(P_(trend)= 0.043).CONCLUSION There is a multifarious interaction between the DNA repair gene ERCC5 SNPs(rs2094258 and rs873601) and the metabolic gene GSTP1 rs1695, which may form the basis for various inter-individual susceptibilities to AG.

突发公共卫生事件、定向增发与市场反应

突发公共卫生事件给中国上市企业带来极大的生存发展压力。运用双重差分方法,探究突发公共卫生事件发生当期上市企业采取定向增发策略对上市企业超额收益率的影响,以此评估突发公共事件发生期间,上市企业是否应该采取定向增发策略以及采取定向增发策略后的市场反应。结果表明,突发公共卫生事件发生当期采取定向增发策略的上市企业,其未来一期的超额收益率要显著高于未采取定向增发策略的上市企业的超额收益率。进一步研究发现,政府推行的定向增发政策也会对上市企业市场反应造成显著影响。异质性检验发现,非国有上市企业在面对突发公共卫生事件时更偏向采用定向增发策略。此结论对于上市企业应对突发公共卫生事件带来的资金短缺问题,具有重要的实践意义。