A Healable Quasi-Solid Polymer Electrolyte with Balanced Toughness and Ionic Conductivity.

Solid polymer electrolytes (SPEs) have garnered extensive attention as potential alternatives to traditional liquid electrolytes, primarily due to their prowess in curbing lithium dendrite formation and preventing electrolyte leaks. The quest for SPEs that are both mechanically robust and exhibit superior ionic conductivity has been vigorous. However, achieving a harmonious balance between these two attributes remains a significant challenge. In this study, we introduce a novel quasi-solid electrolyte, ingeniously crafted from a poly(urethane-urea) network, enriched with lithium salts and plasticizers. This innovative composition not only boasts remarkable toughness but also ensures commendable ionic conductivity. Our post-gelation method yields gel polymer electrolytes that undergo rigorous evaluation, leading to an optimized version that stands out with its exceptional room-temperature ionic conductivity (2.94×10-4 S cm-1) and outstanding toughness (11.9 MJ m-3). Moreover, it demonstrates a broad electrochemical window (4.73 V), remarkable stability across a 600-hour cycle test, a high capacity retention exceeding 80 % after 100 cycles at 0.2 C, and a noteworthy self-healing capability. This quasi-solid polymer electrolyte emerges as a promising contender to replace current liquid electrolyte solutions.

miR-497-5p promoted neuronal injury in ischemic stroke by inhibiting the BDNF/TrkB/PI3K/Akt pathway.

The aim of this study was to investigate the molecular mechanism by which miR-497-5p regulates neuronal injury after ischemic stroke through the BDNF/TrkB/Akt signaling pathway. PC12 cells were used to construct a stroke injury model by oxygen-glucose deprivation/reoxygenation (OGD/R). The expression level of miR-497-5p was measured by RT-qPCR. CCK-8 kit was used to detect cell viability. Cell apoptosis and reactive oxygen species (ROS) were detected by flow cytometry. MDA and SOD detection kits were used to detect MDA content and SOD activity. A double luciferase reporter system was used to verify the targeting relationship between miR-497-5p and BDNF. The expression of BDNF, TrkB, p-TrkB, Akt and p-Akt was detected by Western blot. We have found that miR-497-5p expression was inhibited after treatment with OGD/R. Simultaneously, cell apoptosis, MDA content and ROS were upregulated, while cell viability and SOD were significantly decreased in PC12 cells. The effects of OGD/R on PC12 cells were reversed with the downregulation of miR-497-5p. A double luciferase reporter assay demonstrated that miR-497-5p negatively targets BDNF. BDNF inhibited cell apoptosis and oxidative stress injury in PC12 cells. These findings suggest that miR-497-5p aggravates neuronal injury in experimental model of ischemic stroke by inhibiting the BDNF/TrkB/PI3K/Akt signaling pathway.

Astrocyte-Derived Exosomal miR-148a-3p Suppresses Neuroinflammation and Restores Neurological Function in Traumatic Brain Injury by Regulating the Microglial Phenotype.

Interactions between astrocytes and microglia play an important role in the regeneration and repair of traumatic brain injury (TBI), and exosomes are involved in cell-cell interactions. A TBI model was constructed in rats. Brain extract (Ext) was isolated 1 d after TBI. Astrocyte-derived exosomes were obtained by coculturing Ext with primary astrocytes, and the morphology of exosomes was observed by electron microscopy. The isolated exosomes were cocultured with microglia to observe phenotypic changes in M1 and M2 markers. Aberrant RNA expression was detected in necrotic brain tissue and edematous brain tissue. The role of miR-148a-3p in regulating microglial phenotype was explored by knocking down or overexpressing miR-148a-3p. Finally, the effect of miR-148a-3p on TBI was studied in a rat TBI model. Astrocyte-derived exosomes stimulated by Ext promoted the transition of microglia from the M1 phenotype to the M2 phenotype. MiR-148a-3p was highly expressed in TBI. Transfecting miR-148a-3p promoted the transition of microglia from the M1 phenotype to the M2 phenotype and inhibited the lipopolysaccharide-induced inflammatory response in pre-microglia. In a rat TBI model, miR-148a-3p significantly improved the modified neurological severity score and attenuated brain injury, which promoted the transition of microglia from the M1 phenotype to the M2 phenotype. MiR-148a-3p alleviated TBI by inhibiting the nuclear factor κB pathway. Astrocyte-derived exosomal miR-148a-3p regulates the microglial phenotype, inhibits neuroinflammation, and restores neurological function in TBI. These results provide new potential targets for the treatment of TBI.

MiR-10b-5p Regulates Neuronal Autophagy and Apoptosis Induced by Spinal Cord Injury Through UBR7.

This study aimed to explore the effects of miR-10b-5p on autophagy and apoptosis in neuronal cells after spinal cord injury (SCI) and the molecular mechanism. Bioinformatics was used to analyze the differentially expressed miRNAs. The expression of related genes and proteins were detected by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) and Western blot, respectively. Cell proliferation was detected by 5-ethynyl-2'-deoxyuridine (EdU), and apoptosis was detected by flow cytometry or terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL). Coimmunoprecipitation confirmed the interaction between UBR7 and Wnt1 or Beclin1. Autophagy was detected by the dansylcadaverine (MDC). The Basso Beattie Bresnahan (BBB) score was used to evaluate motor function, and hematoxylin-eosin (H&E) and Nissl staining were used to detect spinal cord tissue repair and neuronal changes. The result shows that the expression of miR-10b-5p was downregulated in the SCI models, and transfection of a miR-10b-5p mimic inhibited neuronal cell apoptosis. MiR-10b-5p negatively regulated the expression of UBR7, and the inhibitory effect of the miR-10b-5p mimic on neuronal cell apoptosis was reversed by overexpressing UBR7. In addition, UBR7 can regulate apoptosis by affecting the Wnt/ß-catenin pathway by promoting Wnt1 ubiquitination. Treatment with the miR-10b-5p mimic effectively improved motor function, inhibited neuronal cell apoptosis, and promoted spinal cord tissue repair in SCI rats. Overall, miR-10b-5p can alleviate SCI by downregulating UBR7 expression, inhibiting Wnt/ß-catenin signaling pathway ubiquitination to reduce neuronal apoptosis, or inhibiting Beclin 1 ubiquitination to promote autophagy.

Anticoagulation polyvinyl chloride extracorporeal circulation catheters for heparin-free treatment.

Extracorporeal circulation (ECC) catheters have potential to be blood compatible and could be used to prevent thrombotic occlusion. Here, we produced heparin-mimicking anticoagulation PVC tubing on a large scale by synthesizing a heparin-mimicking polymer (HMP) and co-extruding. The PVC@HMP catheter was evaluated using whole human blood in vitro, which indicated it could prevent plasma protein attachment, reduce platelet adhesion and activation, and inhibit coagulation factors (XII, XI, IX, and VIII). Moreover, the anticoagulation PVC tubing was assembled into extracorporeal circulation with a New Zealand rabbit model, manifesting excellent real-time antithrombogenic properties without systemic heparin anticoagulation in vivo. The rapid recovery of coagulation factors after operation further confirmed its superiority over heparin, which would not completely inactivate the activity of those coagulation factors (XII, XI, IX and VIII). In addition, the PVC@HMP-1 catheters remain patent after being implanted in rats for 28 days without apparent inflammation and mortality complications. The anticoagulation PVC tubes could be used to construct various systemic and integrative anticlotting biomedical devices, which would dramatically reduce the introduction of heparin into blood circulation, thus preventing side effects and promoting the development of heparin-free treatment.

Graphene Oxide Modified Polyamide 66 Ultrafiltration Membranes with Enhanced Anti-Fouling Performance.

Improving the contamination resistance of membranes is one of the most effective ways to address the short service life of membranes. While preparing the membrane system structure, doping nanoparticles into the polymer matrix is beneficial to the preparation of high-performance membranes. To develop a new structure for membrane contamination protection, in this study, a novel asymmetric polyamide 66 composite ultrafiltration (UF) membrane was fabricated by incorporating different masses (ranging from zero to 0.5 wt.%) of graphene oxide (GO) into the polyamide 66 microporous substrate, using formic acid and propylene carbonate as solvents. The effects of GO doping on the morphology, microporous structure and surface of ultrafiltration membranes were investigated by atomic force microscopy (AFM), scanning electron microscopy (SEM), integrated thermal analysis (DSC) and contact angle (CA). In addition, pure water flux, bovine serum albumin (BSA) rejection and contamination resistance were measured to evaluate the filtration performance of different membranes. The overall performance of all the modified membranes was improved compared to pure membranes. The results of contact angle and permeation experiments showed that the addition of GO improved the hydrophilicity of the membrane, but reduced the permeability of the membrane. The minimum flux was only 3.5 L/m2·h, but the rejection rate was 92.5%. Most noteworthy was the fact that GO further enhanced the anti-pollution performance of the membranes and achieved a remarkable performance of 91.32% when the GO content was 0.5 wt.%, which was 1.36 times higher than that of the pure membrane. Therefore, optimal performance was achieved. Furthermore, the UF membrane made of composite substrate offers a promising solution for the development of long-life ultrafiltration membranes with better stability, high-cost efficiency and adequate chemical durability.

Axial Crystal Growth Evolution and Crystallization Characteristics of Bi-Continuous Polyamide 66 Membranes Prepared via the Cold Non-Solvent-Induced Phase Separation Technique.

Polyamide 66 microporous membranes were prepared by cold non-solvent-induced phase separation using polyamide 66-formic acid-propylene carbonate as a ternary membrane-forming system. The formed membranes exhibited a special bicontinuous structure consisting of interglued spherical crystals or interlocked bundles of microcrystalline aggregates. The variation of the microporous structure under the influence of preparation conditions, solvent, aging time, and polymer concentration affects the comprehensive performance of the membranes. For example, the cold-induced operation and the use of different membrane-forming solvents contributed to the crystallization of polyamide 66, resulting in an increased contact angle of polyamide 66 membranes, obtaining a high resistance to contamination of up to 73.5%. Moreover, the formed membranes still have high mechanical strength.

Reversible filtration redox of methylene blue in dimethylsulfoxide by manganese oxide loaded carbonaceous nanofibrous membrane through Fenton-like oxidation.

The reversible redox of methylene blue in organic solvents was highly attractive, yet was rarely reported. In this study, we realized the continuous filtration redox of methylene blue (MB) in dimethylsulfoxide (DMSO) through Fenton-like oxidization by using MnO2 loaded carbonaceous nanofibrous membrane (cPAN-MnO2). The carbonaceous nanofibrous membrane (cPAN) was fabricated through electrospun of polyacrylonitrile and subsequent carbonization. The obtained cPAN nanofibrous membrane showed excellent stability in polar DMSO. MnO2 can be readily coated on cPAN nanofibers through an in situ redox reaction between cPAN and potassium permanganate. The fabricated cPAN-MnO2 membrane exhibited instantaneous reduction property towards MB in DMSO during a gravity-driven continuous filtration process. Interestingly, MB reduction was initiated by a typical Fenton-like oxidization, where hydroxyl radicals were firstly generated from hydrogen peroxide catalyzed by MnO2 in DMSO. Then hydroxyl radicals attacked DMSO to further produce methyl radicals, which resulted in the reduction of MB. In addition, MB reduction process in DMSO was reversible. Our study provides a novel strategy for continuous redox of MB in polar organic solvent and might give new ideas for MB applications.

Amphiphilic carboxylated cellulose-g-poly(l-lactide) copolymer nanoparticles for oleanolic acid delivery.

Carboxylated cellulose nanocrystals (CCNs), as one of nanocellulose are promising hydrophilic biomass materials for drug delivery. In this work, a series of amphiphilic carboxylated cellulose-graft-Poly(L-lactide) (CC-g-PLLA) copolymers were synthesized via ring-opening polymerization (ROP) method. The copolymers were characterized by 1H-NMR, FT-IR, WXRD and TGA, and their solubility in organic solvents was improved. Then, these amphiphilic copolymers were self-assembled into nanoparticles for delivery of anticancer drug oleanolic acid (OA). The copolymer (DSPLLA 2.03) nanoparticles displayed the smallest size (196.82 ± 9.14 nm) and the highest drug loading efficiency (24.76 ± 0.58%). The nanoparticles exhibited a spherical shape, well water solubility of OA (16.9 mg/mL) and a prolonged drug release (120 h). In vitro and In vivo study indicated that the nanoparticles maintained cytotoxicity to 4T1 cells and MCF-7 cells and displayed high antitumor efficiency. The amphiphilic CC-g-PLLA copolymer nanoparticles provide a novel platform for drug delivery.