Preparation and performance study of a reactive polyurethane hot-melt adhesive/CS-Fe3O4 magnetic nanocomposite film/fabric.

Magnetic nanoparticles are attracting significant attention for their wide application as biomaterials and magnetic storage materials. As an environmentally friendly adhesive, reactive polyurethane hot-melt adhesive (PUR) is a biocompatible polymer with a wide range of applications. In this paper, chitosan (CS)-surface-modified magnetic Fe3O4 nanoparticles were synthesized by the sol-gel method. Surface modification of the Fe3O4 nanoparticles with CS enhanced their mechanical properties in PUR. The nanoparticles were characterized by Fourier transform infrared (FTIR) and X-ray diffraction (XRD) analyses, while their surface morphology was elucidated using scanning electron microscopy (SEM) and projection electron microscopy (TEM) techniques. Subsequently, PUR/CS-Fe3O4 magnetic nanocomposite films were prepared using an in situ method, wherein different amounts of CS-surface-modified magnetic Fe3O4 nanoparticles were doped into the PUR and coated on the films. The thermal, UV resistance and mechanical properties of the PUR/CS-Fe3O4 magnetic nanocomposite films were investigated by TGA, UV spectrometer and tensile testing. CS-Fe3O4 nanoparticles were successfully prepared using the sol-gel method and CS to modify the surface of the Fe3O4 nanoparticles. The results show that the mechanical properties and UV resistance of PUR/CS-Fe3O4 magnetic nanocomposites are improved by almost 50%, so the constructed PUR/CS-Fe3O4 magnetic nanocomposites have good UV-resistant properties and mechanical properties. The as-synthesized CS-Fe3O4 magnetic nanocomposites show great potential for application to mechanical and textile development.

Preparation of ultra-high mechanical strength wear-resistant carbon fiber textiles with a PVA/PEG coating.

Polyvinyl alcohol (PVA) is an organic polymer that is non-toxic, harmless to the human body, and has good biocompatibility. Polyethylene glycol (PEG) is a polymer that has good lubricity and compatibility. The unique graphite structure of carbon fibers can promote the potential application of carbon-fiber composites in tribology. This study explores the relationship between two kinds of organic polymer compounds and carbon fiber cloth (CFC), specifically a PVA/PEG composite coating that is impregnated on the CFC surface. The CFC is synthesized by chemical cross-linking, and the CFC composites (PVA/PEG/CFC) were synthesized. The tribological properties of PVA/PEG/CFC were tested under different concentrations, loads, and velocities. The effects of the different lubricants, surface morphologies, and tensile strengths on the mechanical and tribological properties of PVA/PEG/CFC were studied. In comparison to the original CFC, the friction coefficient and wear morphology of the composite material were reduced and the friction coefficient trend was stable. The addition of PVA/PEG improved the surface lubrication performance of the composite material and reduced the average friction coefficient. In addition, under the different lubrication mechanisms, oil as a lubricant can significantly reduce the friction coefficient and surface wear. In summary, the biocompatible coating process that is proposed in this study can effectively improve the tribological properties of the surface of the CFC.

MiR-137-3p Inhibits Colorectal Cancer Cell Migration by Regulating a KDM1A-Dependent Epithelial-Mesenchymal Transition.

BACKGROUND: In colorectal cancer (CRC), miR-137-3p downregulation is associated with disease progression, but the mechanism is not fully understood. KDM1A, also known as LSD1, is upregulated in various cancer and promotes tumor metastasis. Interestingly, miR-137-3p is downregulated by hypoxia, which plays critical roles in tumor metastasis, and KDM1A is a miR-137-3p target gene in brain tumors. AIMS: To study if CRC metastasis is regulated by a hypoxia/miR-137-3p/KDM1A axis and if the epithelial-mesenchymal transition (EMT) process is involved. METHODS: We measured the levels of miR-137-3p, KDM1A, and some EMT markers in CRC biopsy tissues and cell lines. We also investigated the regulation of KDM1A by miR-137-3p and the effects of KDM1A inhibition on the EMT process and cell migration. RESULTS: We verified the low miR-137-3p and high KDM1A levels in CRC tumors. Inhibiting miR-137-3p upregulated KDM1A expression and promoted the invasiveness of CRC cells. KDM1A knockdown, or treatment with tranylcypromine, a specific KDM1A inhibitor, reduced the migration and invasion of CRC cells by inhibiting the EMT process. CRC cells cultured under hypoxic conditions expressed less miR-137-3p but more KDM1A than cells cultured under normal conditions, implying the involvement of miR-137-3p and KDM1A in hypoxia-induced tumor metastasis. CONCLUSIONS: We conclude that MiR-137-3p inhibits CRC cell migration by regulating a KDM1A-dependent EMT process. Our study suggests that restoring the expression of miR-137-3p or targeting KDM1A might be potential therapeutic strategies for CRC.

DRP1 promotes lactate utilization in KRAS-mutant non-small-cell lung cancer cells.

Metabolic alterations are well documented in various cancers. Non-small-cell lung cancers (NSCLCs) preferentially use lactate as the primary carbon source, but the underlying mechanisms are not well understood. We developed a lactate-dependent cell proliferation assay and found that dynamin-related protein (DRP1), which is highly expressed in KRAS-mutant NSCLC, is required for tumor cells to proliferate and uses lactate as fuel, demonstrating the critical role of DRP1 in the metabolic reprogramming of NSCLC. Metabolic and transcriptional profiling suggests that DRP1 orchestrates a supportive metabolic network to promote lactate utilization and redox homeostasis in lung cancer cells. DRP1 suppresses the production of reactive oxygen species (ROS) and protects cells against oxidative damage by enhancing lactate utilization. Moreover, targeting DRP1 not only reduces HSP90 expression but also enhances ROS-induced HSP90 cleavage, thus inhibiting activation of mitogen activated protein kinase and PI3K pathways and leading to suppressed lactate utilization and increased ROS-induced cell death. Taken together, these results suggest that DRP1 is a crucial regulator of lactate metabolism and redox homeostasis in KRAS-mutant lung cancer, and that targeting lactate utilization by modulating DRP1 activity might be an effective treatment for lung cancer.