The first example of amorphous CoFe hydroxide based on the electrospinning process was developed, which was used as an efficient OER catalyst.

Type 1 diabetes is an autoimmune disease which is due to the lack of β cells. The ideal therapy to cure the disease is pancreas transplantation, but its application is confined to a limited number of people due to the shortage of organ and the need for life-long immunosuppression. Regenerative medicine methods such as a tissue engineered pancreas seem to provide a useful method. In order to construct a microenvironment similar to the native pancreas that is suitable for not only cell growth but also cellular function exertion, a decellularized mouse pancreas was used as a natural 3D scaffold in this experiment. MIN-6 β cells were planted in the bioscaffold. The cell engraftment was verified by HE staining and SEM. Immunostaining procedures were performed to confirm the normal function of the engrafted cells. qRT-PCR demonstrated that insulin gene expression of the recellularized pancreas was upregulated compared with conventional plate-cultured cells. In vivo experiment was also accomplished to further evaluate the function of the recellularized bioscaffold and the result was inspiring. And beyond doubt this will bring new hope for type 1 diabetic patients.

Diabetes mellitus is a disease which has affected 415 million patients in 2015. In an effort to replace the significant demands on transplantation and morbidity associated with transplantation, the production of β-like cells differentiated from induced pluripotent stem cells (iPSCs) was evaluated. This approach is associated with promising decellularized scaffolds with natural extracellular matrix (ECM) and ideal cubic environment that will promote cell growth in vivo. Our efforts focused on combining decellularized rat pancreatic scaffolds with mouse GFP+-iPSCs-derived pancreatic β-like cells, to evaluate whether decellularized scaffolds could facilitate the growth and function of β-like cells. β-like cells were differentiated from GFP+-iPSCs and evaluated via cultivating in the dynamic circulation perfusion device. Our results demonstrated that decellularized pancreatic scaffolds display favorable biochemical properties. Furthermore, not only could the scaffolds support the survival of β-like cells, but they also accelerated the expression of the insulin as compared to plate-based cell culture. In conclusion, these results suggest that decellularized pancreatic scaffolds could provide a suitable platform for cellular activities of β-like cells including survival and insulin secretion. This study provides preliminary support for regenerating insulin-secreting organs from the decellularized scaffolds combined with iPSCs derived β-like cells as a potential clinical application.

Background The regulatory mechanism of insulin-producing cells (IPCs) differentiation from induced pluripotent stem cells (iPSCs) in vitro is very important in the phylogenetics of pancreatic islets, the molecular pathogenesis of diabetes, and the acquisition of high-quality pancreatic β-cells derived from stem cells for cell therapy. Methods miPSCs were induced for IPCs differentiation. miRNA microarray assays were performed by using total RNA from our iPCs-derived IPCs containing undifferentiated iPSCs and iPSCs-derived IPCSs at day 4, day 14, and day 21 during step 3 to screen the differentially expressed miRNAs (DEmiRNAs) related to IPCs differentiation, and putative target genes of DEmiRNAs were predicted by bioinformatics analysis. miR-690 was selected for further research, and MPCs were transfected by miR-690-agomir to confirm whether it was involved in the regulation of IPCs differentiation in iPSCs. Quantitative Real-Time PCR (qRT-PCR), Western blotting, and immunostaining assays were performed to examine the pancreatic function of IPCs at mRNA and protein level respectively. Flow cytometry and ELISA were performed to detect differentiation efficiency and insulin content and secretion from iPSCs-derived IPCs in response to stimulation at different concentration of glucose. The targeting of the 3′-untranslated region of Sox9 by miR-690 was examined by luciferase assay. Results We found that miR-690 was expressed dynamically during IPCs differentiation according to the miRNA array results and that overexpression of miR-690 significantly impaired the maturation and insulinogenesis of IPCs derived from iPSCs both in vitro and in vivo. Bioinformatic prediction and mechanistic analysis revealed that miR-690 plays a pivotal role during the differentiation of IPCs by directly targeting the transcription factor sex-determining region Y (SRY)-box9. Furthermore, downstream experiments indicated that miR-690 is likely to act as an inactivated regulator of the Wnt signaling pathway in this process. Conclusions We discovered a previously unknown interaction between miR-690 and sox9 but also revealed a new regulatory signaling pathway of the miR-690/Sox9 axis during iPSCs-induced IPCs differentiation. Electronic supplementary material The online version of this article (10.1186/s13287-019-1154-8) contains supplementary material, which is available to authorized users.

The growth of barrier-type anodic films on amorphous Al-Mo alloys, containing 16 to 40 atom percent Mo, in borate electolyte was investigated by analytical transmission electron microscopy, Rutherford backscattering spectroscopy, secondary ion mass spectrometry, and extended x-ray absorption spectroscopy. During growth at 1 and 5 mA cm, two-layered amorphous oxide films formed at high efficiency by outward migration of cations and inward migration of oxygen ions; the outer layer is composed of units of alumina contaminated by boron species derived from the electrolyte and the inner layer contains units of both Al303 and MoO3 distributed uniformly at the resolution of the analyses. At 0.1 mA cm, the films form at reduced faradaic efficiency, which results in a decreased thickness of the outer alumina layer. The twolayered films develop as a consequence of faster migration of Al3 ions than Mo6 ions within the inner layers of the films. New film material forms at the alloy/film and film/electrolyte interfaces and at the interface between the inner and outer layers. At the alloy/film interface, a thin layer of alloy is highly enriched in molybdenum as a consequence of anodic oxidation. Due to the mechanism of film growth, a high concentration of boron accumulates in a sublayer of film material just above the inner/outer layer interface. Infroduction The formation of barrier-type anodic films, composed mainly of amorphous alumina, on aluminum occurs by migration of Al3 and 02/OW ions through the film thickness under an electric field of about io V cm'. The inward migration of 02_/OH_ ions causes growth of film material at the metal/film interface, while the outward migration of Al3 ions results in film growth at the film/electrolyte interface, and if under the conditions of anodizing growth of film material occurs at less than 100% faradaic efficiency, to direct ejection of A]/ ions to the electrolyte.2 Experiments employing an inert immobile marker have shown that during highly efficient film growth, about 40 and 60% of the film thickness is developed at the film/electrolyte and metal/film interfaces, respectively.3 At reduced efficiency, less than 40% of the film thickness is formed at the former interface, and hence, the marker lies relatively closer to the film surface.2In section, the barrier-type films are highly uniform in thickness and have flat and parallel metal/film and film/electrolyte interfaces.4 The high uniformity is a consequence of smoothing of initial substrate roughness due to film growth by high-field ionic conduction across the labile amorphous film.5 Barrier-type films are formed over an efficiency range from 100 to about 60%. At the latter efficiency, all Al ions migrating to the film/electrolyte interface are ejected under the field to the electrolyte, without formation of film material at the interface; the film then grows exclusively by formation of new film material at the metal/film interface, and the flat film/electrolyte interface is unstable, leading to the development of a porous anodi...

Background: Constructing tissue-engineered kidneys using decellularized kidney scaffolds (DKS) has attracted widespread attention as it is expected to be the key to solving the shortage of donor kidneys.However, thrombosis and the host inflammatory response are unfavorable factors that hider the reendothelialization and vascularization of the decellularized scaffolds.Methods: Heparin was immobilized into the DKS using the method of 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide/N-hydroxysuccinimide (EDC/NHS) activation. Fourier-transform infrared (FTIR) spectra were used to verify the heparinization of DKS. Human umbilical vein endothelial cells (HUVECs) were seeded and cultured in the DKS, then the sliced scaffolds were transplanted subcutaneously into nude mouse. Scanning electron microscopy and a series of histochemical stains including hematoxylin and eosin (H&E), elastic Verhöeff-Van Gieson (EVG), Sirius red, Masson's trichrome, and toluidine blue (TB) staining were used for morphological characterization. The qRT-PCR analysis, immunohistochemistry (IHC), and immunofluorescence (IF) staining were used to determine the expression of related molecular markers. Results:The rat DKS completely retained the extracellular matrix and heparinized modification. The H&E staining results showed there were more HUVECs covering the internal surfaces of tubular structures in the HEP-DKS group compared with the DKS group. The IF analysis results revealed that CD31, Ki67, and CD206 had higher positive rates in HUVECs in the HEP-DKS group compared to the DKS group. Both groups of scaffolds showed blood vessel formation via H&E staining, and there were more blood vessels in the HEP-DKS group compared with the native DKS group (P<0.05). The qRT-PCR results showed that the levels of IL-1β, IL-6, and TNF-α in the HEP-DKS group were significantly lower than those of the native DKS group, while the expression level of IL-10 was significantly higher than that in the native DKS group (P<0.05).Conclusions: Heparin modification improves the re-endothelialization and vascular regeneration of the DKS through anticoagulation in vitro and in vivo. The anti-inflammatory effect of heparin on the transplanted host was initially confirmed, and it is considered that this effect may play a non-negligible role in promoting DKS re-endothelialization and angiogenesis. Heparinized DKS is therefore a promising candidate for kidney tissue engineering.

Diabetes affects millions of people worldwide, and β-cell replacement is one of the promising new strategies for treatment. Induced pluripotent stem cells (iPSCs) can differentiate into any cell type, including pancreatic β cells, providing a potential treatment for diabetes. However, the molecular mechanisms underlying the differentiation of iPSC-derived β cells have not yet been fully elucidated. Here, we generated pancreatic β-like cells from mouse iPSCs using a 3-step protocol and performed deep RNA sequencing to get a transcriptional landscape of iPSC-derived pancreatic β-like cells during the selective differentiation period. We then focused on the differentially expressed genes (DEGs) during the time course of the differentiation period, and these genes underwent Gene Ontology annotation and Kyoto Encyclopedia of Genes and Genomes pathway analysis. In addition, gene-act networks were constructed for these DEGs, and the expression of pivotal genes detected by quantitative real-time polymerase chain reaction was well correlated with RNA sequence (RNA-seq). Overall, our study provides valuable information regarding the transcriptome changes in β cells derived from iPSCs during differentiation, elucidates the biological process and pathways underlying β-cell differentiation, and promotes the identification and functional analysis of potential genes that could be used for improving functional β-cell generation from iPSCs.

Engineering of functional vascularized pancreatic tissues offers an alternative way to solve the perpetual shortage of organs for transplantation. However, revascularization remains a major bottleneck in biological engineering, which limited the further clinical applications of this strategy. In this study, an efficient approach for enhancing re‐endothelialization of rat decellularized pancreatic scaffolds (DPS) was presented, by conjugating with GRGDSPC peptide to maximize coverage of the vessel walls with human umbilical vein endothelial cells (HUVECs). First, pancreas was perfused with 1% Triton X‐100 and 0.1% ammonium hydroxide to remove the cellular components. Subsequently, GRGDSPC was covalently coupled to the vasculature of DPS and re‐seeded with HUVECs via perfusion of the portal vein in the bioreactor. After the re‐endothelialized scaffolds were created, in vitro and in vivo experiments were undertaken to evaluate the angiogenesis. Our results demonstrated that GRGDSPC‐conjugated scaffolds could support the survival and accelerated the proliferation of HUVECs; angiogenesis was also significantly improved over untreated scaffolds. In conclusion, GRGDSPC‐conjugated scaffolds showed great potential for the generation of functional bioengineered pancreatic tissue suitable for long‐term transplantation.