ABSTRACT
Metal foam flow field suffers serious corrosion issues in proton exchange membrane fuel cells due to its large surface area. Ni and Ni/graphene coatings are prepared under constant and gradient current modes, respectively, to improve the corrosion resistance. The effect of the electrodeposition current mode and the deposition mechanism is studied. Compared with Ni coating, Ni/graphene coating brings low corrosion current density and high coating resistance, effectively enhancing the stability of Ni foam in an acidic environment. Different from Ni coating with a single layer, Ni/graphene deposits have core-shell structure, with graphene coated on the surface of Ni nanoparticles. It is shown that graphene deposits cover the Ni particles during the electrodeposition, which protects nickel particles from agglomeration and forms an inert film on the surface of the porous structure. After an 8 h constant potential test, no significant pitting is observed on the surface of Ni/graphene coating, showing excellent anticorrosion performance. As to the effect of the deposition current mode, it is shown that more composite particles deposit on the upper layer under the gradient current mode, which brings denser protective film and fewer surface defects on the surface. Ni/graphene coating electrodeposited under a gradient current mode between 0 and 10 mA·cm-2 exhibits the lowest corrosion current densities. The values at 50 and 80 °C are only 62.9 and 26.0% of those of uncoated Ni foam, respectively.
ABSTRACT
BACKGROUND: Differentiation of induced pluripotent stem cells (iPSCs)-derived ß-like cells is a novel strategy for treatment of type 1 diabetes. Elucidation of the regulatory mechanisms of long noncoding RNAs (lncRNAs) in ß-like cells derived from iPSCs is important for understanding the development of the pancreas and pancreatic ß-cells and may improve the quality of ß-like cells for stem cell therapy. METHODS: ß-like cells were derived from iPSCs in a three-step protocol. RNA sequencing and bioinformatics analysis were carried out to screen the differentially expressed lncRNAs and identify the putative target genes separately. LncRNA Malat1 was chosen for further research. Series of loss and gain of functions experiments were performed to study the biological function of LncRNA Malat1. Quantitative real-time PCR (qRT-PCR), Western blot (WB) analysis and immunofluorescence (IF) staining were carried out to separately detect the functions of pancreatic ß-cells at the mRNA and protein levels. Cytoplasmic and nuclear RNA fractionation and fluorescence in situ hybridization (FISH) were used to determine the subcellar location of lncRNA Malat1 in ß-like cells. Enzyme-linked immunosorbent assays (ELISAs) were performed to examine the differentiation and insulin secretion of ß-like cells after stimulation with different glucose concentrations. Structural interactions between lncRNA Malat1 and miR-15b-5p and between miR-15b-5p/Ihh were detected by dual luciferase reporter assays (LRAs). RESULTS: We found that the expression of lncRNA Malat1 declined during differentiation, and overexpression (OE) of lncRNA Malat1 notably impaired the differentiation and maturation of ß-like cells derived from iPSCs in vitro and in vivo. Most importantly, lncRNA Malat1 could function as a competing endogenous RNA (ceRNA) of miR-15b-5p to regulate the expression of Ihh according to bioinformatics prediction, mechanistic analysis and downstream experiments. CONCLUSION: This study established an unreported regulatory network of lncRNA Malat1 and the miR-15b-5p/Ihh axis during the differentiation of iPSCs into ß-like cells. In addition to acting as an oncogene promoting tumorigenesis, lncRNA Malat1 may be an effective and novel target for treatment of diabetes in the future.
