Regulating Phase Distribution of Dion-Jacobson Perovskite Colloidal Multiple Quantum Wells Toward Highly Stable Deep-Blue Emission.

Metal halide perovskite colloidal quantum wells (CQWs) hold great promise for modern photonics and optoelectronics. However, current studies focus on Ruddlesden-Popper (R-P) phase perovskite CQWs that contain bilayers of monovalent long-chain alkylamomoniums between the separated perovskite octahedra layers. The bilayers are packed back-to-back via weak van der Waals interaction, resulting in inferior charge carrier transport and easier decomposition of perovskite. This report first creates a new type of perovskite colloidal multiple QWs (CMQWs) in the form of Dion-Jacobson (D-J) structure by introducing an asymmetric diammonium cation. Furthermore, the phase distribution is optimized by the synergistic effect of valeric acid and zwitterionic lecithin, finally achieving pure deep-blue emission at 435 nm with narrow full width at half maximum. The diammonium layer in D-J perovskite CMQWs features extremely short width of only ≈0.6 nm, thereby contributing to more effective charge carrier transport and higher stability. Through the continuous photoluminescence (PL) measurement and corresponding theoretical calculation, the higher stability of D-J perovskite CMQWs than that of R-P structural CMQWs is confirmed. This work reveals the inherent superior stability of D-J structural CMQWs, which opens a new direction for fabricating stable perovskite optoelectronics.

BNTA attenuates temporomandibular joint osteoarthritis progression by directly targeting ALDH3A1: An in vivo and in vitro study.

BNTA is known to have a therapeutic effect on knee osteoarthritis and inflammatory osteoclastogenesis. However, the protective effect of BNTA regarding temporomandibular mandibular joint osteoarthritis (TMJOA) and its underlying mechanism and physiological target remains unclear. In the present study, BNTA ameliorated cartilage degradation and inflammation responses in monosodium iodoacetate (MIA)-induced TMJOA in vivo. In IL-1ß-induced condylar chondrocytes, BNTA prevents oxidative stress, inflammatory responses and increasing synthesis of cartilage extracellular matrix through activating nuclear factor-E2-related factor 2 (NRF2) signaling. Suppression of NRF2 signaling abolishes the protective effect of BNTA in TMJOA. Notably, BNTA may bind directly to ALDH3A1 and act as a stabilizer, as evidenced by drug affinity responsive target stability assay (DARTS), cellular thermal shift assay (CETSA) and molecular docking results. Further investigation of the underlying molecular and cellular mechanism infers a positive correlation of ALDH3A1 regulating NRF2 signaling. In conclusion, BNTA may attenuate TMJOA progression via the ALDH3A1/NRF2 axis, inferring that BNTA is a therapeutic target for treating temporomandibular mandibular joint osteoarthritis.

Prolonged release of an antimicrobial peptide GL13K-loaded thermosensitive hydrogel on a titanium surface improves its antibacterial and anti-inflammatory properties.

The application of titanium in the orthopedic and dental fields is associated with bacterial infection and chronic inflammation, especially in the early stages after its implantation. In the present study, we investigated the antibacterial and anti-inflammatory activities of a titanium surface that was immobilized in a thermosensitive PLGA-PEG-PLGA hydrogel containing the antimicrobial peptide GL13K. The FTIR results confirmed the successful loading of GL13K. The degradation of the hydrogel and release of GL13K persisted for two weeks. The modified titanium surface exhibited a significant inhibitory effect on Porphyromonas gingivalis in contact with its surface, as well as an inhibitory effect on P.g in the surrounding environment by releasing GL13K antimicrobial peptides. The modified titanium surfaces were biocompatible with RAW264.7. Furthermore, the expression of pro-inflammatory cytokines IL-1ß, TNF-α and iNOS was down-regulated, whereas anti-inflammatory cytokines Arg-1, IL-10 and VEGF-A were up-regulated on the modified titanium surfaces on days 3 and 5. This effect was attributed to the polarization of macrophages from the M1 to M2 phenotype, which was confirmed by the detection of macrophage M1/M2 biomarkers via immunofluorescence staining and flow cytometry. Thus, the thermosensitive PLGA-PEG-PLGA hydrogel release system carrying the antimicrobial peptide GL13K on a titanium surface exhibited antibacterial and anti-inflammatory properties and promoted macrophage polarization from the M1 to M2 phenotype, which may help create a favourable niche for bone formation under infective condition.

Osteogenic effects of rapamycin on bone marrow mesenchymal stem cells via inducing autophagy.

BACKGROUND: While autophagy is essential for stem cells' self-renewal and differentiation, its effect on bone marrow mesenchymal stem cells (BMSCs) remains unclear. This study aimed to investigate the interaction between autophagy and osteogenic differentiation using rapamycin (RAPA), a classical autophagy agonist with osteo-regulatory effects. METHODS: Rat BMSC's autophagy was analyzed after osteoinduction (0, 7, 14, and 21 d) by western blotting, immunofluorescence, and real-time quantitative polymerase chain reaction (RT-qPCR). In addition, we evaluated osteogenic differentiation using alizarin red staining, alkaline phosphatase assays, and RT-qPCR/Western blotting quantification of bone sialoprotein, type 1 collagen, alkaline phosphatase, osteopontin, and Runt-related transcription factor 2 mRNA and protein levels. RESULTS: The BMSC's basal autophagy level gradually decreased during osteogenic differentiation with a decrease in BECN1 level and the lipidated (LC3-II) to unlipidated (LC3-I) microtubule-associated protein 1 light chain 3 ratio and an increase in the expression of selective autophagic target p62. In contrast, it increased with increasing RAPA concentration. Furthermore, while 2 nM RAPA promoted BMSC osteogenic differentiation on days 7 and 14, 5 nM RAPA inhibited osteogenesis on days 14 and 21. Inhibition of autophagy by the inhibitor 3-methyladenine could impair RAPA's osteogenesis-enhancing effect on BMSCs. CONCLUSIONS: The BMSC's basal autophagy level decreased over time during osteogenic differentiation. However, an appropriate RAPA concentration promoted BMSC osteogenic differentiation via autophagy activation.

Identification and validation of autophagy-related genes during osteogenic differentiation of bone marrow mesenchymal stem cells.

Objectives: Osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) is an essential stage in bone formation. Autophagy plays a pivotal role in the self-renewal potential and pluripotency of stem cells. This study aimed to explore the function of autophagy-related genes during osteogenic differentiation of BMSCs. Materials and Methods: The differentially expressed autophagy-related genes (ARGs) were obtained from the GEO and HADb databases. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed using R software. The PPI and hub gene mining networks were constructed using the STRING database and Cytoscape. Finally, the RT-qPCR was conducted to validate the expression level of ARGs in BMSCs. Results: Thirty-seven differentially expressed ARGs were finally obtained, including 12 upregulated and 25 downregulated genes. GO and KEGG enrichment analysis showed that most of these genes were enriched in apoptosis and autophagy. The PPI network revealed strong interactions between differentially expressed ARGs. The expression level of differentially expressed ARGs tested by RT-qPCR showed 6 upregulated ARGs, including FOXO1, MAP1LC3C, CTSB, FOXO3, CALCOCO2, FKBP1A, and 4 downregulated ARGs, including MAPK8IP1, NRG1, VEGFA, and ITGA6 were consistent with the expression of high-throughput sequencing data. Conclusion: We identified 37 ARGs during osteogenic differentiation using bioinformatics analysis. FOXO1, MAP1LC3C, CTSB, FOXO3, CALCOCO2, FKBP1A, MAPK8IP1, NRG1, VEGFA, and ITGA6 may regulate osteogenic differentiation of hBMSCs by involving autophagy pathway. This study provides new insight into the osteogenic differentiation of hBMSCs and may be available in developing therapeutic strategies for maxillofacial bone defects.

Bone quality effect on short implants in the edentulous mandible: a finite element study.

INTRODUCTION: The aim of this study was to verify whether the use of short implants could optimize stress distribution of bone surrounding implants in atrophic mandibles with different bone qualities. METHODS: A three-dimensional model of the atrophic mandible with three levels of bone quality was made using computer software. Short implants (6 mm) and standard implants (10 mm) were used in four designs: Design 1 "All-On four", Design 2 "All-On-four" with two short implants, Design 3 four vertical implants with two short implants, and Design 4 six short implants. The distal short implants were placed at the first molar position. All twelve models were imported into finite element analysis software, and 110 N oblique force was loaded on the left second premolar. Maximum principal stress values of peri-implant bone and the volumes of bone with over 3000 microstrians (overload)were analyzed. RESULT: Stress values and volumes of overload bone increased in all four groups with the decline of bone quality. The highest stress values were found in the cortical bone surrounding the Design 1 inclined implant in two lower bone quality mandibles, and the lowest in Design 3. However, Design 1 had less overload bone tissue than all three designs with short implants. CONCLUSION: Short implants placed posteriorly helped decrease stress values in peri-implant bone, while bone surrounding short implants had a high resorption risk in low bone quality mandible.