PSS-GO:NH3 layer, and partially to the better matched energy-level-alignment at the perovskite interface. Furthermore, the device was shown to be more stable in the ambient condition, which is clearly associated with the improved peovskite structure stability by the GO:NH3 layer observed by the GIXRD measurements. All these achievements will promote more applications of chemically modified graphene oxide interfacial layer in the PSCs as well as other organic multilayer devices.

Background Circular RNAs (circRNAs) are involved in regulating tumor pathogenesis. The mechanism of circRNAs in gastric cancer (GC) is still unknown. Our study aimed to identify differentially expressed circRNAs and assess a novel circRNA (hsa_circ_0000144) in the proliferation, migration, and invasion in GC. Methods Gene ontology (GO) enrichment and analyses of Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, pathway network, and the ceRNA regulatory network of hsa_circ_0000144 targeting miRNAs and mRNAs were performed with the help of bioinformatics using R language and Perl software. hsa_circ_0000144 expression and circRNA knockdown in GC cell lines were detected using quantitative PCR (qPCR) in vitro. Cell proliferation, migration, and invasion after circRNA knockdown were measured using the cell counting kit-8 assay and Transwell assay. Results The circRNA expression profile GSE78092 downloaded from the Gene Expression Omnibus database included three GC patients and three normal tissues. Thirty-two differentially expressed circRNAs comprised six upregulated circRNAs and 26 downregulated circRNAs. In particular, the ErbB signaling pathway, neurotrophin signaling pathway, cellular senescence, and pathways in bladder cancer and GC played the most important roles in the pathway network. The expression of hsa_circ_0000144 was upregulated in GC cell lines. Hsa_circ_0000144 knockdown suppressed tumor growth in vitro. Conclusions Hsa_circ_0000144 promotes GC cell proliferation, migration, and invasion, and the ceRNA regulatory network of hsa_circ_0000144 targeting miRNAs and mRNAs might be biomarkers for GC diagnosis and targeted therapy.

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Strong inflammatory indicators such as C-reactive protein (CRP), high-sensitivity CRP (hsCRP), and hematological indices, including platelet to lymphocyte ratio (PLR), neutrophil to lymphocyte ratio (NLR), hematocrit (HCT), and red blood cell distribution width (RDW), may be related with contrast-induced nephropathy (CIN). Our meta-analysis aimed at exploring the relationship between these indicators and CIN incidence among patients undergoing coronary intervention. Clinical studies were retrieved from the electronic databases of PubMed, EMBASE, Google Scholar, Clinical Trials, and Science Direct from their inception to June 3, 2020. Meta-analysis was performed on pooled eligible studies. Finally, 26 studies involving 29 454 patients were included. Pooled analysis revealed that patients with higher CRP (odds ratio [OR] = 1.06, 95% CI: 1.01-1.12, P = .02), hsCRP (OR = 1.03, 95% CI: 1.01-1.06, P = .004), NLR (OR = 1.11, 95% CI: 1.01-1.20, P = .02), RDW (OR = 1.35, 95% CI: 1.19-1.53, P < .001), and lower HCT (OR = 0.94, 95% CI: 0.92-0.97, P = .003) all exhibited significantly higher CIN rates, but there was no significant association between PLR and CIN risk (OR = 1.12, 95% CI: 0.99-1.26, P = .07). Pre-angiography CRP/hsCRP and some hematological indices are associated with CIN.

The present study investigated the role of the Twist gene in epithelial-mesenchymal transition (EMT) and its effects on the invasion and metastasis of malignant tumors. In vitro, we transfected SW480, HCT116 and HT29 cells with recombinant plasmids, pTracer-CMV/BSD-Twist and pGenesil1.2-Twist-shRNA, to influence expression of Twist. The transfection efficacy of the plasmids in the cell lines was confirmed by flow cytometry. The relative mRNA and protein expression levels of Twist, E-cadherin and vimentin in the transfected cells were detected by RT-PCR and western blotting, respectively. In addition, migration and invasion were assessed by Transwell assays. In vivo, we established a xenogenic liver metastasis mouse model by intrasplenic injection with transfected SW480, HCT116 or HT29 human colon cancer cells and used hematoxylin and eosin (H&E) staining to demonstrate the effective establishment of the model. The relative mRNA levels of Twist and vimentin were detected by RT-PCR. In vitro, RT-PCR and western blotting showed higher relative mRNA and protein expression levels of Twist and vimentin in cell lines transfected with the recombinant, highly expressed Twist plasmid than in non-transfected cell lines (P<0.05), while E-cadherin was inhibited (P<0.05). After transfection with the plasmid pGenesil1.2-Twist-shRNA, the relative mRNA and protein levels of Twist and vimentin were markedly inhibited in the HCT116 cells (P<0.05), and the levels of E-cadherin were not changed (P>0.05), along with inhibition of the migration and invasion abilities of the cell line (P<0.01). In vivo, relative mRNA levels of Twist and vimentin in both the liver and spleen of the mouse model were higher in the groups that were injected with one of the three cell lines transfected with pTracer-CMV/BSD-Twist than in the groups injected with cells transfected with pGenesil1.2-Twist-shRNA (P<0.05). In conclusion, upregulation of Twist gene expression can promote EMT molecular events. Interfering with the Twist gene can effectively silence Twist gene expression in HCT116 cells and consequently inhibit colon cancer cell migration and invasion.