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Biodegradable magnesium (Mg)-based vascular stents can overcome the limitations of conventional permanent metallic stents, such as late in-stent restenosis and thrombosis, but still have difficulty retarding degradation while providing adequate mechanical support to the blood vessel. We incorporated silica nanoparticles surface-functionalized with hexadecyltrimethoxysilane (mSiNP) into a poly (l-lactic acid) (PLLA) coating as a physical barrier to disturb the penetration of the corrosive medium as well as a bioactive source that releases silicon ions capable of stimulating endothelial cells. The corrosion resistance and biocompatibility of this bifunctional PLLA/mSiNP nanocomposite coating were investigated using different weight ratios of mSiNP. The nanocomposite coating containing more than 10 wt% of the mSiNP (PLLA/10mSiNP and PLLA/20mSiNP) significantly delayed the corrosion of the Mg substrate and exhibited favorable endothelial cell responses, compared to the pure PLLA coating. Specifically, the calculated corrosion rates of PLLA/10mSiNP and PLLA/20mSiNP decreased by half, indicating the durability of the coating after immersion in simulated body fluid for 12 days. Based on the in vitro cellular response, the incorporation of the mSiNPs into the PLLA coating significantly improved the endothelial cell responses to the Mg substrate, showing better initial cell surface coverage, migration, and proliferation rate than those of pure PLLA. These results indicate that the PLLA/mSiNP nanocomposite coatings have significant potential to improve the corrosion resistance and vascular compatibility of biodegradable Mg-based vascular stents.Fenton-based therapy is emerging as an effective and selective strategy against cancer. However, a low concentration of transition metal ions, insufficient endogenous H2O2, and a high level of antioxidant activity within the cancer cells have hindered the therapeutic efficacy of this strategy. To address these issues, in this study, the Fenton reagent (magnetic hydroxyapatite, mHAP) was accompanied with chemotherapy drugs (cisplatin (CDDP) and methotrexate (MTX)) and static magnetic field (SMF), in such a way to be a pH-, redox-, and magnetic-responsive nanoplatform. In vitro and in vivo experiments revealed higher toxicity of the final construct, MTX.CDDP@mHAP, toward colon cancer cells, as compared with that of free drugs. The most effective antitumor activity was observed as MTX.CDDP@mHAP-treated tumor cells were exposed to SMF (0.9 T) and no noticeable damage was observed in the normal cells and tissues. Active targeting by MTX and magnetic targeting by mHAP under magnetic field increased the tumor selectivity and enhanced the tumor site accumulation and cellular uptake of MTX.CDDP@mHAPs. The released iron ions within the cancer cells trigger the Fenton reaction while the release of chemotherapy drugs, reduction of intracellular glutathione, and application of SMF aggravated the Fenton reaction, subsequently leading to the generation of reactive oxygen species (ROS) and induction of apoptosis. Therefore, Fenton magnetic-based therapy-mediated by MTX.CDDP@mHAP could be considered as a promising strategy against colon cancer with high therapeutic efficiency and biosafety.For developing electrochemical plant sensors, in-situ detection of hormone levels in living plants is worth attempting. A microneedle array sensor based on Au@SnO2-vertical graphene (VG)/Ta microelectrodes was constructed for analyzing abscisic acid (ABA) in plants. Graphene was vertically grown on Ta wires with a diameter of 0.6 mm by direct current arc plasma jet chemical vapor deposition with SnO2 as the Au catalyst carrier. Selleckchem Bcl2 inhibitor These VG nanosheets were embedded with core-shell Au@SnO2 nanoparticles, and the formation mechanism of the sensing layer was investigated. Three Au@SnO2-VG microelectrodes, one Ti wire, and one Pt wire were packed into a microneedle array sensor with a three-electrode system. ABA was then quantitatively detected by direct electrocatalytic oxidation, which involves the synergistic catalytic effects of the abundant catalytic active sites of the Au@SnO2 nanoparticles and the excellent conductivity of the VG nanosheets. The microneedle array sensor responds to ABA in the pH range 4-7, the response concentration range was 0.012 (or 0.024)-495.2 μM, and the detection limit varied between 0.002 and 0.005 μM. The small size, wide pH range, low detection limit, and wide linear concentration range allow the microneedle array sensor to be inserted into plants for in-situ detection of ABA.Tailored electrospun meshes have been increasingly explored for abdominal wall defect repair in preclinical and clinical studies. However, the fabrication of a bioengineered mesh adapts to the intraperitoneal repair for a compliant remodeling remains a great challenge. In this study, we fabricated a functional mesh by combining polycaprolactone (PCL) with silk fibroin (SF) and decellularized human amniotic membrane (HAM) proportionally via electrospinning. SF was integrated with PCL (4060 w/w) to regulate the structural flexibility. Micronized HAM was incorporated to PCL/SF (1090 w/w) to provide a biocompatible milieu with functions being conferred to facilitate intraperitoneal repair. After the blend electrospinning, the PCL/SF/HAM mesh was characterized in vitro and implanted into the rat model with a full-thickness defect for a comprehensive evaluation in comparison to the PCL and PCL/SF meshes. The results demonstrated that electrospinning fabricated PCL stabilized the mechanical elongation toward approxiremodeling in the repair of abdominal wall defects.Osteoarthritis (OA) is a degenerative joint disease which is highly prevalent worldwide. However, no therapy for blocking OA pathogenesis is available currently. In this study, chondroitin sulfate (CS) E oligosaccharides were prepared and we identified disaccharide as the functional unit showing the strongest anti-complement activity and screened out complement C5 as its target in the complement system. We determined that CS-E disaccharide produced anti-inflammatory effects to treat OA by regulating the complement system it inhibited the formation of complement-dependent complexes such as the membrane-attack complex (MAC) by targeting C5 and suppressed MAC-induced protein expression and the activation of downstream MAPK and NF-κB signaling pathways accordingly. By identifying CS-E disaccharide which could be regarded as a complement regulator or inhibitor exhibiting high anti-complement activity and revealing its OA-alleviating mechanism, this study not only provides a new strategy for OA treatment and drug development, but also potentially offers a promising C5 target therapy for other associated diseases.

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