Carbon-Doped Nickle Via a Fast Decarbonization Route for Enhanced Hydrogen Oxidation Reaction in Alkaline Media.

Nickel (Ni) based materials with non-metal heteroatom doping are competitive substitutes for platinum group catalyst toward alkaline hydrogen oxidation reaction (HOR). However, the incorporation of non-metal atom into the lattice of conventional fcc phase Ni can easily trigger a structural phase transformation, forming hcp phase nonmetallic intermetallic compounds. Such tangle phenomenon makes it difficult to uncover the relationship between HOR catalytic activity and doping effect on fcc phase Ni. Herein, taking trace carbon doped Ni (C-Ni) nanoparticles as an example, a new nonmetal doped Ni nanoparticles synthesized by a simple fast decarbonization route using Ni3 C as precursor is presented, which provides an ideal platform to study the structure-activity relationship between alkaline HOR performance and non-metal doping effect toward fcc phase Ni. The obtained C-Ni exhibits an enhanced alkaline HOR catalytic activity compared with pure Ni, approaching to commercial Pt/C. X-ray absorption spectroscopy confirms that the trace carbon doping can modulate the electronic structure of conventional fcc phase nickel. Besides, theoretical calculations suggest that the introducing of C atoms can effectively regulate the d-band center of Ni atoms, resulting in the optimized hydrogen absorption, thereby improving the HOR activity.

LncRNA BANCR promotes oral squamous cell carcinoma progression via regulating Rab1A signaling.

BACKGROUND: Long non-coding RNA BRAF-activated non-protein coding RNA plays bidirectional roles in human cancers. However, function and molecular mechanism of BRAF-activated non-protein coding RNA in oral squamous cell carcinoma still need to clarify further. METHODS: Long non-coding RNA microarray assay, in situ hybridization staining, clinicopathological data analysis were performed to investigate expression pattern of BRAF-activated non-protein coding RNA in oral squamous cell carcinoma tissue samples. Constructing ectopically expressed BRAF-activated non-protein coding RNA in oral squamous cell carcinoma cells via plasmids or siRNAs, then changeable abilities of proliferation and motility of these cells were observed in vitro and in vivo. RNA-protein pulldown, RNA immunoprecipitation, and bioinformatics analyses were performed to explore potential pathways involved in BRAF-activated non-protein coding RNA-based regulation of malignant progression in oral squamous cell carcinoma. RESULTS: BRAF-activated non-protein coding RNA was identified upregulated in oral squamous cell carcinoma tissue and correlated with nodal metastasis and clinical severity of patients. Overexpressed BRAF-activated non-protein coding RNA increased percentage of 5-ethynyl-2'-deoxyuridine-positive cells, viability, migration, and invasion rates of oral squamous cell carcinoma cells, while silenced BRAF-activated non-protein coding RNA could observe weakened effects in vitro. Xenograft tumor formed by BRAF-activated non-protein coding RNA-overexpressed cells had bigger volume, faster growth rates, higher weight, and more Ki67+ cells. Pulmonary metastasis induced by BRAF-activated non-protein coding RNA-silenced cells had fewer colony nodes, Ki67+ cells, and CD31+ blood vessels. Furthermore, BRAF-activated non-protein coding RNA was mainly localized in nucleus of oral squamous cell carcinoma cells and bound Ras-associated binding 1A. Silencing Ras-associated binding 1A could damage mobile ability and phosphorylation levels of nuclear factor-κB in oral squamous cell carcinoma cells induced by overexpressing BRAF-activated non-protein coding RNA. Opposite trend was also observed. CONCLUSION: Acting as a promoter in oral squamous cell carcinoma metastasis, BRAF-activated non-protein coding RNA promotes oral squamous cell carcinoma cells proliferation and motility by regulating the BRAF-activated non-protein coding RNA/Ras-associated binding 1A complex, which activates nuclear factor-κB signaling pathway.

Role of alpha smooth muscle actin in odontogenic differentiation of dental pulp stem cells.

Pulpotomy is an effective treatment for retaining vital pulp after pulp exposure caused by caries removal and/or trauma. The expression of alpha smooth muscle actin (α-SMA) is increased during the wound-healing process, and α-SMA-positive fibroblasts accelerate tissue repair. However, it remains largely unknown whether α-SMA-positive fibroblasts influence pulpal repair. In this study, we established an experimental rat pulpotomy model and found that the expression of α-SMA was increased in dental pulp after pulpotomy relative to that in normal dental pulp. In vitro results showed that the expression of α-SMA was increased during the induction of odontogenic differentiation in dental pulp stem cells (DPSCs) compared with untreated DPSCs. Moreover, α-SMA overexpression promoted the odontogenic differentiation of DPSCs via increasing mitochondrial function. Mechanistically, α-SMA overexpression activated the mammalian target of rapamycin (mTOR) signaling pathway. Inhibition of the mTOR signaling pathway by rapamycin decreased the mitochondrial function in α-SMA-overexpressing DPSCs and suppressed the odontogenic differentiation of DPSCs. Furthermore, we found that α-SMA overexpression increased the secretion of transforming growth factor beta-1 (TGF-ß1). In sum, our present study demonstrates a novel mechanism by which α-SMA promotes odontogenic differentiation of DPSCs by increasing mitochondrial respiratory activity via the mTOR signaling pathway.

Ru Colloidosome Catalysts for the Hydrogen Oxidation Reaction in Alkaline Media.

Developing efficient hydrogen oxidation reaction (HOR) electrocatalysts in alkaline media is of great significance for anion exchange membrane fuel cells. Herein, we report the synthesis of hollow colloidosomes composed of Ru nanocrystals based on a novel gas/liquid interface self-assembly strategy. Structural characterizations reveal that much defects are present in the building block (Ru nanocrystals) of Ru colloidosomes. Theoretical calculations suggest that the defects in the Ru structure can optimize the adsorption binding energy of reaction intermediates for the HOR. Benefiting from the assembled colloidosome and optimized electronic structure, the Ru colloidosomes exhibit remarkable HOR catalytic performance in alkaline media with a mass activity higher than that of benchmark Pt/C. Our work may shed new light on the rational design of advanced electrocatalysts with an assembled structure for energy-related applications.

Dual Mg-Reinforced PCL Membrane with a Janus Structure for Vascularized Bone Regeneration and Bacterial Elimination.

Commercially available guided bone regeneration (GBR) membranes often exhibit limited mechanical properties or bioactivity, leading to poor performance in repairing bone defects. To surmount this limitation, we developed a Janus structural composite membrane (Mg-MgO/PCL) reinforced by dual Mg (Mg sheets and MgO NPs) by using a combined processing technique involving casting and electrospinning. Results showed that the addition of Mg sheets and MgO NPs enhanced the mechanical properties of the composite membrane for osteogenic space maintenance, specifically tensile strength (from 10.2 ± 1.2 to 50.3 ± 4.5 MPa) and compression force (from 0 to 0.94 ± 0.09 N mm-1), through Mg sheet reinforcement and improved crystallization. The dense cast side of the Janus structure membrane displayed better fibroblast barrier capacity than a single fiber structure; meanwhile, the PCL matrix protected the Mg sheet from severe corrosion due to predeformation. The porous microfibers side supported preosteoblast cell adhesion, enhanced osteogenesis, and angiogenesis in vitro, through the biomimetic extracellular matrix and sustainable Mg2+ release. Furthermore, the Mg-MgO/PCL membrane incorporating 2 wt % MgO NPs exhibited remarkable antimicrobial properties, inducing over 88.75% apoptosis in Staphylococcus aureus. An in vivo experiment using the rat skull defect model (Φ = 5 mm) confirmed that the Mg-MgO/PCL membrane significantly improved new bone formation postsurgery. Collectively, our investigation provides valuable insights into the design of multifunctional membranes for clinical oral GBR application.

PDPN+ CAFs facilitate the motility of OSCC cells by inhibiting ferroptosis via transferring exosomal lncRNA FTX.

Cancer-associated fibroblasts (CAFs) are abundant and heterogeneous in tumor microenvironment (TME). Cross-talk between cancer cells and CAFs results in cancer progression. Here, we demonstrated that a distinct cancer-associated fibroblasts subset with podoplanin (PDPN) positive expression (PDPN+ CAFs) was correlated with poor survival in oral squamous cell carcinoma (OSCC). PDPN+ CAFs promoted the progression of OSCC by transferring exosomal lncRNA FTX to OSCC cells. Mechanically, FTX bound to flap endonuclease-1 (FEN1), forming an RNA‒protein complex. FTX enhanced promoter demethylation of FEN1 by recruiting ten-eleven translocation-2 (TET2). In addition, FTX/FEN1 axis promoted OSCC cells motility by inhibiting ferroptosis. In xenograft experiments, RSL-3, a ferroptosis-inducing agent, suppressed the tumorigenesis potential of FEN1-overexpressed OSCC cells. Furthermore, Acyl-CoA synthetase long-chain family member 4 (ACSL4) was confirmed to participate in the motility promotion induced by FEN1 overexpression. FEN1 could bind to promoter region of ACSL4 and then inhibit ferroptosis in OSCC cells. Our study reveals that PDPN+ CAFs promote the invasiveness of OSCC cells by inhibiting ferroptosis through FTX/FEN1/ACSL4 signaling cascade. PDPN+ CAFs may serve as a novel potential therapeutic target for OSCC.

Preparation of 4D printed peripheral vascular stent and its degradation behavior under fluid shear stress after deployment.

Shape memory stents are mild intervention devices for vascular diseases as compared to balloon-dilated ones; however, their degradation behavior under blood shear stress after deployment also deserves further attention. To understand the degradation behavior, we first prepared 4D printed poly(lactic acid) (PLA) stents via 3D printing technology and studied their failure behavior in a dynamic condition after self-expandable deployment. Mechanical property tests showed that the 4D printed stents had a compression force of 0.06-0.39 N mm-1 and a recovery ratio of 85.3-93.4%, respectively, which was verified to be wall thickness dependent. The stents were then implanted in simulated blood vessels with minimal microstructural damage at 60 °C followed by 8-week degradation tests. The results showed the microstructure damage caused by deployment could accelerate the degradation of stents faster than fluid shear stress. Furthermore, we conducted microstructural analysis and numerical simulation on the stent by finite element analysis (FEA) to explain the relationship between stent injury, vascular injury, and stent deployment temperature. A physical model derived from micro-morphologies on the degradation mechanism of PLA was also proposed. These results may provide new insights for the examination of the degradation behavior of 4D printed stents and minimize medical risk.