Comparison of endoscopic submucosal dissection with surgical gastrectomy for early gastric cancer: An updated meta-analysis

BACKGROUND There are several surgical options for treating early gastric cancers(EGCs), such as endoscopic resection, laparoscopic or open gastrectomy with D1 or D2 lymphadenectomy. Endoscopic resection for EGC with low risk of lymph node metastasis has been widely accepted as a therapeutic alternative. The role of endoscopic submucosal dissection(ESD) in treating EGC is not well established,especially when compared with resection surgery cases in a long-term follow-up scope.AIM To compare the safety and efficacy of the short-and long-term outcomes between ESD and resection surgery.METHODS We searched the databases of PubMed, EMBASE, Web of Science, and the Cochrane Library from January 1990 to June 2018, enrolling studies reporting short-or long-term outcomes of ESD in comparison with resection surgery for EGC. The quality of the studies was assessed by the Newcastle-Ottawa Quality Assessment Scale. Stata software(version 12.0) was used for the analysis. Pooling analysis was conducted using either fixed-or random-effects models depending on heterogeneity across studies.RESULTS Fourteen studies comprising 5112 patients were eligible for analysis(2402 for EGC and 2710 for radical surgery). Our meta-analysis demonstrated that the ESD approach showed advantages through decreased operation time [weighted mean difference(WMD):-140.02 min, 95%CI:-254.23 to-34.82 min, P = 0.009], shorter hospital stay(WMD:-5.41 d, 95% CI:-5.93 to-4.89 d, P < 0.001), and lowerpostoperative complication rate [Odds ratio(OR) = 0.39, 95%CI: 0.28-0.55, P <0.001). Meanwhile, EGC patients who underwent ESD had higher recurrence rate(OR = 9.24, 95%CI: 5.94-14.36, P < 0.001) than resection surgery patients.However, the long-term survival including overall survival [Hazard ratio(HR) =0.51, 95%CI: 0.26-1.00, P = 0.05] and event-free survival(HR = 1.59, 95%CI: 0.66-9.81, P = 0.300) showed no significant differences between these two groups.CONCLUSION In the treatment of EGC, ESD was safe and feasible in comparison with resection surgery, with advantages in several surgical and post-operative recovery parameters. Although the recurrence rate was higher in ESD group, the longterm survival was still comparable in these two groups, suggesting ESD could be recommended as standard treatment for EGC with indications.

Identification of candidate biomarkers correlated with pathogenesis of postoperative peritoneal adhesion by using microarray analysis

BACKGROUND Postoperative peritoneal adhesion(PPA),characterized by abdominal pain,female infertility,and even bowel obstruction after surgery,has always been a major concern.The occurrence and formation of adhesion are from complex biological processes.However,the molecular mechanisms underlying the basis of microarray data profile,followed by peritoneal adhesion formation,are largely unknown.AIM To reveal the underlying pathogenesis of PPA at the molecular level.METHODS The gene expression profile was retrieved from the Gene Expression Omnibus database for our analysis.We identified a panel of key genes and related pathways involved in adhesion formation using bioinformatics analysis methods.We performed quantitative PCR and western blotting in vivo to validate the results preliminarily.RESULTS In total,446 expressed genes were altered in peritoneal adhesion.We found that several hub genes(e.g.,tumor necrosis factor,interleukin 1 beta,interleukin 6,CX-C motif chemokine ligand 1,C-X-C motif chemokine ligand 2)were marked as significant biomarkers.Functional analysis suggested that these genes were enriched in the Toll-like receptor signaling pathway.According to the Kyoto Encyclopedia of Genes and Genomes pathway and published studies,TLR4,myeloid differentiation primary response protein 88(MyD88),and nuclear factor kappa B(NF-κB)played essential roles in Toll-like signaling transduction.Here,we obtained a regulatory evidence chain of TLR4/MyD88/NF-κB/inflammatory cytokines/peritoneal adhesion involved in the pathogenesis of postoperative adhesion.The results of the microarray analysis were verified by the animal experiments.These findings may extend our understanding of the molecular mechanisms of PPA.CONCLUSION The regulatory evidence chain of TLR4/MyD88/NF-κB/inflammatory cytokines/peritoneal adhesion may play key roles in the pathogenesis of PPA.Future studies are required to validate our findings.

Identification of key genes involved in post-traumatic stress disorder:Evidence from bioinformatics analysis

BACKGROUND Post-traumatic stress disorder(PTSD)is a serious stress-related disorder.AIM To identify the key genes and pathways to uncover the potential mechanisms of PTSD using bioinformatics methods.METHODS Gene expression profiles were obtained from the Gene Expression Omnibus database.The differentially expressed genes(DEGs)were identified by using GEO2R.Gene functional annotation and pathway enrichment were then conducted.The gene-pathway network was constructed with Cytoscape software.Quantitative real-time polymerase chain reaction(qRT-PCR)analysis was applied for validation,and text mining by Coremine Medical was used to confirm the connections among genes and pathways.RESULTS We identified 973 DEGs including 358 upregulated genes and 615 downregulated genes in PTSD.A group of centrality hub genes and significantly enriched pathways(MAPK,Ras,and ErbB signaling pathways)were identified by using gene functional assignment and enrichment analyses.Six genes(KRAS,EGFR,NFKB1,FGF12,PRKCA,and RAF1)were selected to validate using qRT-PCR.The results of text mining further confirmed the correlation among hub genes and the enriched pathways.It indicated that these altered genes displayed functional roles in PTSD via these pathways,which might serve as key signatures in the pathogenesis of PTSD.CONCLUSION The current study identified a panel of candidate genes and important pathways,which might help us deepen our understanding of the underlying mechanism of PTSD at the molecular level.However,further studies are warranted to discover the critical regulatory mechanism of these genes via relevant pathways in PTSD.