Colloidal Phenol-Amine Coating on Implants for Improved Anti-Inflammation and Osteogenesis.

Phenol-amine coatings have attracted significant attention in recent years owing to their adjustable composition and multifaceted biological functionalities. The current preparation of phenol-amine coatings, however, involves a chemical reaction within the solution or interface, resulting in lengthy preparation times and necessitating specific reaction conditions, such as alkaline environments and oxygen presence. The facile, rapid, and eco-friendly preparation of phenol-amine coatings under mild conditions continues to pose a challenge. In this study, we use a macromolecular phenol-amine, Tanfloc, to form a stable colloid under neutral conditions, which was then rapidly adsorbed on the titanium surface by electrostatic action and then spread and fused to form a continuous coating within several minutes. This nonchemical preparation process was rapid, mild, and free of chemical additives. The in vitro and in vivo results showed that the Tanfloc colloid fusion coating inhibited destructive inflammation, promoted osteogenesis, and enhanced osteointegration. These remarkable advantages of the colloidal phenol-amine fusion coating highlight the suitability of its future application in clinical practice.

Network Pharmacology and Molecular Docking Analysis Exploring the Mechanism of Tripterygium wilfordii in the Treatment of Oral Lichen Planus.

Background: Oral lichen planus (OLP) is an infrequent autoimmune disease of the oral mucosa, which affects up to 2% of the world population. An investigation of Tripterygium wilfordii's mechanism of action for treating OLP was conducted, and a theoretical basis was provided for improving current treatment regimens. Materials and Methods: We used a network pharmacological approach to gain insight into the molecular mechanism of Tripterygium wilfordii in the treatment of OLP. Then, potential protein targets between Tripterygium wilfordii and OLP were analyzed through a drug-target network. This was followed by KEGG enrichment analysis and Gene Ontology (GO) classification. Finally, for molecular docking, AutoDock Vina was used. Results: A protein-protein interaction (PPI) network was constructed by analyzing the common targets of a total of 51 wilfordii-OLP interactions from different databases. The GO and KEGG enrichment analyses showed that the treatment of OLP with Tripterygium wilfordii mainly involves lipopolysaccharide response, bacterial molecular response, positive regulation of cytokine production, and leukocyte proliferation, and the signaling pathways mainly include the AGE-RAGE, NF-κB, Toll-like receptor, IL-17, HIF-1, and TNF signaling pathways. The molecular docking results showed that ß-sitosterol, kaempferol, hederagenin, and triptolide have a higher affinity for AKT1, TNF, CASP3, and PTGS2, respectively. Based on the CytoNCA analysis of common targets, 19 key targets, including AKT1, TNF, VEGFA, STAT3, CXCL8, PTGS2, TP53, and CASP3, and their connections were identified. Conclusions: Preliminarily, this study reveals that Tripterygium wilfordii interferes with OLP by interacting with multiple targets through multiple accesses, as validated by molecular docking.

CRISPR-Cas13-Mediated Knockdown of lncRNA-GACAT3 Inhibited Cell Proliferation and Motility, and Induced Apoptosis by Increasing p21, Bax, and E-Cadherin Expression in Bladder Cancer.

The current study is to investigate the expression pattern and biological function of long non-coding RNA Focally gastric cancer-associated transcript3 (GACAT3) in bladder cancer. Real-time quantitative qPCR was used to detect the expression level of GACAT-3 in tumor tissues and paired normal tissues. Human bladder cancer T24 and 5637 cell lines were transiently transfected with specific CRISPR-Cas13 or negative control CRISPR-Cas13. Cell migration, proliferation, and apoptosis were measured by using wound healing assay CCK-8 assay and Caspase-3 ELISA assay, respectively. The expression changes of p21, Bax, and E-cadherin after knockdown of GACAT3 were detected by using Western blot. The results demonstrated that GACAT3 was up-regulated in bladder cancer tissues than that in the paired normal tissues. Inhibition of cell proliferation, increased apoptosis, and decreased motility were observed in T24 and 5637 cell lines transfected by CRISPR-Cas13 targeting GACAT3. Downregulation of GACAT3 increased p21, Bax, and E-cadherin expression and silencing these genes could eliminate the phenotypic changes induced by knockdown of GACAT3. A ceRNA mechanism for GACAT3 was also revealed. By using CRISPR-Cas13 biotechnology, we suggested that GACAT3 may be a novel target for diagnosis and treatment of bladder cancer.

Amplifications of NCOA3 gene in colorectal cancers in a Chinese population.

AIM: To investigate the copy number variation of NACO3 gene in colorectal cancer (CRC) and its correlation with tumor progression. METHODS: A total of 142 samples of case-matched CRC tissues and adjacent normal tissues were obtained from patients undergoing bowel resection. Quantitative real-time polymerase chain reaction method was used to investigate the copy number variations of NCOA3 as well as gene expression in the collected tissues. RESULTS: Copy number gains of NCOA3 were detected in 39 CRC samples (27.5%) and were correlated with tumor progression (χ2 = 6.42, P = 0.0112). Moreover, there was a positive correlation between copy number gain and mRNA over-expression of NCOA3 in CRCs (P = 0.0023). Expression level of NCOA3 mRNA was also enhanced in the CRC samples with unaltered copy numbers (3.85 ± 1.23 vs. 2.71 ± 0.64, P < 0.01). CONCLUSION: Sporadic colorectal cancers exhibit different mechanisms of NCOA3 regulation.