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We report an in situ electrophoretic anodization process to realize a binary semiconductor heterojunction photocatalyst comprising green-emitting, water-soluble carbon nitride (CN) nanoparticles (NPs) embedded in TiO₂ nanotube (TNT) arrays. Embedding CN inside a TiO₂ matrix eliminates the possibility of the CNNPs leaching away during photocatalysis or photoelectrochemistry. The synthesized CN exhibits visible light absorption down to 600 nm and an unusually redshifted green emission peak at 527 nm, which are attributed to a carbon rich g-C₃N₄ composition with a C:N ratio of ∼ 1.9 at the surface. Spectroscopy revealed the excess carbon to be both amorphous and graphitic while the structural features characteristic of g-C₃N₄ were preserved. Raman spectroscopy, transmission electron microscopy (TEM), electron energy-loss spectroscopy (EELS) and X-ray photoelectron spectroscopy (XPS) analysis verified the formation of the heterostructure as well as indicated strong interaction between the CN and TiO₂ in the hybrid. The CNNP@TNT hybrid demonstrated superior performance in sunlight driven photocatalytic CO₂ reduction without the need for a sacrificial agent. The CO yield of photoreduction showed a more than threefold improvement for the CNNP@TNT hybrid compared to the stand-alone TNT photocatalyst. The synergistic enhancement of photocatalytic performance emerged due to the formation of a high-quality interface between the constituent semiconductors (TiO₂ and CN) that facilitated efficient charge carrier separation. Density functional theory (DFT) calculations showed the feasibility of efficient photogenerated electron-hole pair separation at the heterointerface. Molecular dynamics (MD) simulations validated the facile dispersibility of CNNPs in water and polar solvents.

International audience; Background: Although >150,000 mitral TEER procedures have been performed worldwide, the impact of MR etiology on MV surgery after TEER remains unknown.Objectives: The authors sought to compare outcomes of mitral valve (MV) surgery after failed transcatheter edge-to-edge repair (TEER) stratified by mitral regurgitation (MR) etiology.Methods: Data from the CUTTING-EDGE registry were retrospectively analyzed. Surgeries were stratified by MR etiology: primary (PMR) and secondary (SMR). MVARC (Mitral Valve Academic Research Consortium) outcomes at 30 days and 1 year were evaluated. Median follow-up was 9.1 months (IQR: 1.1-25.8 months) after surgery.Results: From July 2009 to July 2020, 330 patients underwent MV surgery after TEER, of which 47% had PMR and 53.0% had SMR. Mean age was 73.8 ± 10.1 years, median STS risk at initial TEER was 4.0% (IQR: 2.2%-7.3%). Compared with PMR, SMR had a higher EuroSCORE, more comorbidities, lower LVEF pre-TEER and presurgery (all P < 0.05). SMR patients had more aborted TEER (25.7% vs 16.3%; P = 0.043), more surgery for mitral stenosis after TEER (19.4% vs 9.0%; P = 0.008), and fewer MV repairs (4.0% vs 11.0%; P = 0.019). Thirty-day mortality was numerically higher in SMR (20.4% vs 12.7%; P = 0.072), with an observed-to-expected ratio of 3.6 (95% CI: 1.9-5.3) overall, 2.6 (95% CI: 1.2-4.0) in PMR, and 4.6 (95% CI: 2.6-6.6) in SMR. SMR had significantly higher 1-year mortality (38.3% vs 23.2%; P = 0.019). On Kaplan-Meier analysis, the actuarial estimates of cumulative survival were significantly lower in SMR at 1 and 3 years.Conclusions: The risk of MV surgery after TEER is nontrivial, with higher mortality after surgery, especially in SMR patients. These findings provide valuable data for further research to improve these outcomes.

Objectives:: The nuclear factor-κB (NF-κB) signaling pathway plays an important role in regulating tubular epithelial-mesenchymal transition (EMT), an indispensable cellular programme for driving organ fibrosis and tumor progression. Liuwei Dihuang Decoction (LWD) is an effective Chinese formula for treating chronic renal failure. Methods:: First, by using morphological examination, immunofluorescence staining assay, RTqPCR, and Western blot analysis, in vitro experiments were designed to analyze NF-κB and EMT markers (including Snail, α-SMA, and E-cadherin) in transforming growth factor-β1 (TGF-β1) induced renal tubular epithelial cells (HK-2) and to detect the expression levels of LWD-CS cotreatment. Then, the recombinant lentiviral vector was overexpressed and knocked down by NF- κB and transfected into HK-2 cells. Cells were treated with TGF-β1 (10 ng/ml) with blank serum or LWD-containing serum, respectively, and the expression of these molecules in the NF-κB/Snail signaling pathway was further evaluated. Results:: Our results confirmed that TGF-β1 could induce EMT, nuclear translocation of NF-κB p65, and activate the NF-κB/Snail signaling pathway in HK-2 cells. Furthermore, NF-κB knocked-down dramatically increases the TGF-β1-induced mRNA and protein expression level of E-cadherin and reduces the level of Snail and α-SMA; this is reversed by NF-κB overexpression. LWD can decrease the EMT levels through the NF-κB/Snail signaling activation in TGF-β1-induced EMT of HK-2 cells. Conclusion:: The present study provides evidence suggesting a novel mechanism that LWD exerts anti-fibrosis effects through inhibiting activation of the NF-κB/Snail signaling pathway and consequently downregulating the TGF-β1-induced EMT in renal tubular epithelial cells.

Three-dimensional (3D) conductive frameworks have been studied extensively in lithium (Li) metal anodes for their good electronic conductivities and superior structural integrity. In this work, we demonstrated a carbon fiber cloth (CFC) framework coated with SnO2 nanoparticles through a hydrothermal process combined with a carbonization method, which served as a reliable host for pouring molten Li to produce a CFC@SnO2@Li composite anode with dendritic suppression and long-life cycling performances. XRD, TEM, HRTEM, XPS and different electrochemical characterizations were carried out. Compared with the routine bare Li||LiFePO4 cells, the CFC@SnO2@Li||LiFePO4 cells had a strong specific ability, excellent rate performance, and stability for a long time, which confirm its great potential as lithium metal anodes in practical battery applications.

Background: Nasopharyngeal carcinoma (NPC) is a usual head and neck malignancy. Guggulsterone (GS) has potential in cancer chemoprophylaxis and treatment, but its therapeutic effect on NPC is unknown. We aimed to explore whether GS could promote the secretion of exosomal circFIP1L1 from NPC cells and its regulatory mechanism. Methods: NPC tissues and adjacent tissues were collected from NPC patients. Human nasopharyngeal epithelial cell lines (NP69) and NPC lines (5-8F, CNE1, and HNE1) were used for in vitro experiments. HNE1 cells were treated with GS (20, 40, 60 μmol/L). The expressions of miR-125a-5p and circFIP1L1 were evaluated by qRT-PCR. Cell proliferation and apoptosis abilities were measured by CCK-8 and flow cytometry. HNE1 cell exosomes were extracted and identified, and the levels of VEGFA and VEGFR2 were detected by ELISA. Then miR-125a-5p was knocked down and overexpressed. HUVECs angiogenesis was determined by the tube formation assay. qRT-PCR and Western blot were utilized to evaluate the expressions of VEGFA, MMP-2, MMP-9, and ICAM-1 in HUVECs. Results: miR-125a-5p was highly expressed in NPC tissues and cells. GS promoted the secretion of exosomal circFIP1L1 from HNE1 cells to affect HUVECs proliferation and angiogenesis. Overexpression of miR-125a-5p accelerated HUVECs proliferation and angiogenesis. Knocking down miR-125a- 5p inhibited VEGFA expression. In addition, exosomal circFIP1L1 sponged miR-125a-5p, inhibiting the VEGFA pathway to repress HUVECs angiogenesis. Conclusions: GS promoted exosomal circFIP1L1 in NPC cells to mediate miR-125a-5p/VEGFA axis affecting tumor angiogenesis.

Sintering behavior of micron-sized combusted iron powder is studied in a packed bed reactor, at various temperatures under inert (nitrogen) and reducing (hydrogen) conditions. Compression tests are subsequently used to quantify the degree of sintering. A sintering model, based on the formation of a solid bridge through solid state surface diffusion of iron atoms, matches the experimental results. Sintering of combusted iron occurs at temperatures C in both nitrogen and hydrogen atmospheres and increases exponentially with temperature. The observed decrease in reduction rate at high temperatures is not caused by the sintering process but by the formation of wüstite as an intermediate species, leading to the formation of a dense iron layer. Iron whiskers form at high temperatures (C) in combination with low reduction rates (vol% H2), leading to the production of sub-micron fines., Sintering behavior of micron-sized combusted iron powder is studied in a packed bed reactor, at various temperatures under inert (nitrogen) and reducing (hydrogen) conditions. Compression tests are subsequently used to quantify the degree of sintering. A sintering model, based on the formation of a solid bridge through solid state surface diffusion of iron atoms, matches the experimental results. Sintering of combusted iron occurs at temperatures ≥575°C in both nitrogen and hydrogen atmospheres and increases exponentially with temperature. The observed decrease in reduction rate at high temperatures is not caused by the sintering process but by the formation of wüstite as an intermediate species, leading to the formation of a dense iron layer. Iron whiskers form at high temperatures (≥700°C) in combination with low reduction rates (≤25 vol% H 2), leading to the production of sub-micron fines.

Background: Acute lymphoblastic leukemia with MLL/AF4 rearrangement remains a major hurdle to improving outcomes. Gene network and circRNAs have been found to participate in tumorigenesis, while their roles in leukemia still need to be explored. Recent patents have shown that circRNAs exhibit the markers for the children ALL, although the target and related mechanism remain to be elucidated. Objective: This study aims to explore the possible targets and mechanisms of ALL with MLLAF4 rearrangement. Methods: We first generated a gene network focusing on MLL-AF4 rearrangement. Cell viability was determined with Cell Counting Kit-8 assay. The cell apoptosis was tested by the Annexin V/PI assay. The RNA-protein complexes were analyzed by qRT-PCR, and the pathway proteins were analyzed by western blot. Results: This gene network was associated with biological processes, such as nucleic acid metabolism and immunity, indicating its key role in inflammation. We found that circ_0008012 was upregulated in MLL/AF4 ALL cells and regulated cell proliferation and apoptosis. Further computed simulation and RIP showed that IKKβ was the strongest protein in the NF-κB pathway binding with circ_0008012. As a result, possible regulation of circ_0008012 is suggested by binding IKKβ in the IKKα:IKKβ:IKKγ compound, which then phosphorylates IκB and activates NF- κB:p65:p300 compound in cell nucleus, thereby leading to leukemia. Conclusion: We identified a gene network for MLL/AF4 ALL. Moreover, circ_0008012 may be a therapeutic target for this subtype of ALL.