Background:Many studies on long chain non-coding RNAs (lncRNAs) are published in recent years. But the roles of lncRNAs in diarrhea irritable bowel syndrome (IBS-D) are still unclear and should be further examined. The present work focused on determining the molecular mechanisms underlying lncRNAs regulation in IBS-D on the basis of the lncRNA-miRNA-mRNA competing endogenous RNA (ceRNA) network.Methods:This study collected the mRNAs (GSE36701) expression data within human tissue samples with IBS-D group and normal group based on Gene Expression Omnibus (GEO) database and collected the differentially expressed lncRNAs (DELs) and differentially expressed miRNAs (DEmiRs) based on PubMed.Functional enrichment analysis of DEGs was performed on the DAVID database. Then the interaction network was constructed and visualized using STRING database and Cytoscape.Results: This study identified 3192 DEmRNAs (1437 with up-regulation and 1755 with down-regulation),29 DEmiRs (18 upregulated and 11 downregulated)and 2 DELs(one upregulated and one downregulated) between IBS-D and control samples.Furthermore,we constructed a lncRNA-miRNA-mRNA network through two DELs (lncRNA TUG1 with up-regulation and lncRNA H19 with down-regulation), four DemiRs (hsa-miR-148a-3p,hsa-miR-342-3p,hsa-miR-149-5p with up-regulation and hsa-miR-219a-5p with down-regulation)and 24 DEGs (4 with up-regulation and 20 with down-regulation) with 42 axes. Simultaneously, we conducted functional enrichment and pathway analyses on genes within the as-constructed ceRNA network. According to our PPI/ceRNA network and functional enrichment analysis results, two critical genes were found (BCL2L11 and QKI). Conclusion:In conclusion, the ceRNA interaction axis we identified is a potentially critical target for treating IBS-D.BCL2L11 axis(LncH19-hsa-miR-148a-3p-BCL2L11) may via interaction with PI3K/AKT pathways in IBS-D.Our results shed more lights on the possible pathogenic mechanism in IBS-D using a lncRNA-associated ceRNA network.
Background Continuous bladder irrigation (CBI) and proper adjustment of saline irrigation speed are important to avoid CBI failure in hemorrhagic cystitis (HC) patients after allogeneic hematopoietic stem cell transplantation (HSCT). Nevertheless, too fast irrigation speed could take away the patient's much heat, contribute to blood coagulopathy, and increase the nursing workload. Evaluation of risk for CBI failure remains an unmet clinical need. Methods The general information, clinical characteristics, and consultation records of HC patients in 1380 patients with hematopoietic stem cell transplantation in our center from 2017 to 2019 were analyzed retrospectively. The receiver operating characteristic (ROC) curve was used to calculate the cutoff point of the continuous variable, and multivariate logistic regression was used to analyze the risk factors affecting CBI failure in HC patients. Results The incidence of HC after HSCT was 23%. A total of 227 patients with HC above grade 2 were included. Univariate analysis showed that CRP, age, platelet counts, onset time after transplantation, albumin, and hemoglobin were associated with CBI failure in the short-term (P < 0.05). ROC curve and multivariate logistic regression analysis showed that CRP > 8.89 ng/ml (RR = 7.828, 95% CI 2.885–21.244), age < 14.5 years (RR = 9.940, 95% CI 3.219–30.697), and onset time of HC༞37d after transplantation (RR = 7.021, 95% CI 2.204–22.364), were independent risk factors for failure of CBI (P < 0.05). Conclusions The study identified CRP > 8.89 ng/ml, age < 14.5 years, and onset time of HC after HSCT > 37d are independent factors for failure of CBI, which could be combined to allow stratification of HC after HSCT patients into low-, intermediate- and high-risk subgroups of CBI failure.
Background:Chronic atrophic gastritis (CAG) is an established pre-cancerous lesion of intestinal type gastric cancer(GC),H pylori infection is the main pathogenic cause,this study intends to study the pathogenesis of atrophic gastritis(Hp+) from the lncRNA-miRNA-mRNA ceRNA regulatory network, in order to provide the oretical basis and data support for the treatment of atrophic gastritis.Results:GSE111762 downloaded from GEO database was used to analyze the differentially expressed lncRNAs and mRNAs(DEGs).A total of 395 differentially expressed lncRNA (225 upregulated,170 downregulated) and 1093 DEGs ( 674 upregulated, 419 downregulated) are obtained. Through the cross-mapping of miRcode, starBase, Sponescan,miRTarBase and miRBase databases,16 miRNAs were predicted,and the lncRNA-miRNA-mRNA ceRNA regulatory network consisting of 71 IncRNAs,16 miRNAs and 597 mRNAs was constructed.597 DEGs were analyzed by David database for functional enrichment. A total of 250 GO enrichment items were obtained, including 160 BP entries, 48 CC entries and 42 MF entries,29 signal pathways were obtained by enrichment analysis of KEGG pathways, mainly p53 signaling pathway, PI3K-Akt signaling pathway and MAPK signaling pathway. Using Cytoscape plug-in CytoHubba to filter 597 DEGs with "MCC, MNC, Degree" top20 as screening conditions, Eleven key hub targets are obtained from the intersection of jvenn.Protein interaction analysis of key hub targets through Cytoscape plug-in GeneMania, it was found that 87.65% displayed similar co-expression characteristics.Construct ceRNA regulatory network of the key hub targets,11 mRNAs(such as BRCA1, RAD54L),12 miRNAs(such as hsa-miR-340-5p,hsa-miR-182-5p) and 58 lncRNAs(such as PCGEM1,FTX) were predicted. Conclusions:Clarify the complex reticular regulation of atrophicgastritis with multi-targets, multi-pathways and multi-pathways.Which provides a new idea for the study of the mechanism of action of atrophicgastritis (Hp+) and a potential target for its treatment,thus to further early diagnosis and reversal of gastric cancer.
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