A new series of chiral N-heterocyclic carbene (NHC) palladium complexes were synthesized from a relatively inexpensive amino acid, l-phenylalanine. All these compounds were fully characterized by (1)H-NMR, (13)C-NMR and elemental analysis. The X-ray molecular structures of two of the complexes were reported. The catalytic activity of the four palladium complexes was successfully tested in the Sonogashira reaction under copper free conditions in air. The palladium complex 3a provided good activity in the Sonogashira coupling reaction.

A sulfur-mediated electrophilic cyclization reaction of aryl-tethered internal alkynes has been developed. Triflic anhydride-activated sulfoxides induced the electrophilic cyclization and then demethylation with triethylamine in one pot, affording 3-sulfenyl-1,2-dihydronaphthalenes and related types of products in yields of ≤96%.

Bone marrow mesenchymal stem cell (BMSC)-derived exosomes have been found to enhance fracture healing. In addition, microRNAs contributing to the healing of various bone fractures have attracted widespread attention in recent years, but knowledge of the mechanisms by which they act is still very limited. In this study, we clarified the function of altered microRNA-19b (miR-19b) expression in BMSCs in fracture healing. We modulated miR-19b expression via mimics/inhibitors in BMSCs and via agomirs in mice to explore the effects of these changes on osteogenic factors, bone cell mineralization and the healing status of modeled fractures. Through gain- and loss-of function assays, the binding affinity between miR-19b and WWP1/Smurf2 was identified and characterized to explain the underlying mechanism involving the KLF5/β-catenin signaling pathway. miR-19b promoted the differentiation of human BMSCs into osteoblasts by targeting WWP1 and Smurf2. Overexpression of WWP1 or Smurf2 degraded the target protein KLF5 in BMSCs through ubiquitination to inhibit fracture healing. KLF5 knockdown delayed fracture healing by modulating the Wnt/β-catenin signaling pathway. Furthermore, miR-19b enhanced fracture healing via the KLF5/β-catenin signaling pathway by targeting WWP1 or Smurf2. Moreover, miR-19b was found to be enriched in BMSC-derived exosomes, and treatment with exosomes promoted fracture healing in vivo. Collectively, these results indicate that mesenchymal stem cell-derived exosomal miR-19b represses the expression of WWP1 or Smurf2 and elevates KLF5 expression through the Wnt/β-catenin signaling pathway, thereby facilitating fracture healing.

What is known and objective: Propofol and esketamine are routine anaesthetics used in sedation or general anaesthesia for paediatric procedures. Coadministration could reduce the dose of either propofol or esketamine required and lower the incidence of drug-related adverse events. We designed a four-arm randomized controlled trial in children undergoing diagnostic upper gastrointestinal endoscopy to investigate the dose of propofol with different doses of esketamine inducing appropriate depth of anaesthesia in 50% patients (median effective dose, ED 50 ).Methods: After getting the approval of the research ethics committee and informed consent, 92 paediatric patients planning for upper gastrointestinal endoscopy were divided into four groups randomly: esketamine 0, 0.25, 0.5 and 1 mg/kg groups (n = 23/group). Propofol doses followed the Dixon and Massey up-and-down method with different starting and interval doses between groups. During the first attempt of endoscope insertion, if patients' reactions prevented the insertion, it would be considered as a failure. The awakening time, total propofol doses, as well as the perioperative and post-procedure adverse events were evaluated and recorded for each patient. Results and discussion:The ED 50 (median, 95% confidence interval) of propofol was significantly greater in esketamine 0 and 0.25 mg/kg groups in comparison with the esketamine 0.5 and 1 mg/kg groups (4.

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Background: This study aimed to investigate the roles of lncRNA SNHG10 (SNHG10) and miR-218 in osteosarcoma (OS). Methods: Paired OS and non-tumor tissues were collected from 58 OS patients. The expression of SNHG10 and miR-218 in tissue samples were determined by RT-qPCR. The interaction between SNHG10 and miR-218 was evaluated by overexpression experiment. Methylation-specific PCR was performed to assess the methylation status of miR-218. Glucose uptake in OS cells was analyzed by glucose uptake assay. Cell proliferation was detected by cell proliferation assay. Results: SNHG10 was upregulated in OS, while miR-218 was downregulated in OS. The expression of SNHG10 and miR-218 were inversely correlated. In OS cells, high glucose induced the upregulation of SNHG10 and downregulation of miR-218. In OS cells, SNHG10 positively, and miR-218 negatively regulated glucose uptake. Overexpression of SNHG10 increased miR-218 gene methylation and decreased the expression of miR-218. In addition, overexpression of SNHG10 also suppressed the inhibitory effects of overexpression of miR-218 on cell proliferation. Conclusions: SNHG10 increases the methylation of miR-218 gene to promote glucose uptake and cell proliferation in OS.

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