Explore the vast range of titles available.

Background Small extracellular vesicles (sEV) secreted by mesenchymal stem cells (MSC) derived from human induced pluripotent stem cells (iPSC, iMSC-sEV) are considered to have great potential in treating ischemic diseases. Angiogenesis play an important role in post-stroke recovery. However, no studies have yet been conducted to systemically examine the effect and the underlying mechanism of iMSC-sEV on angiogenesis under brain ischemia conditions. Methods Ischemic stroke model was performed in rats induced by middle cerebral artery occlusion (MCAO), and the pro-angiogenic capacity of iMSC-sEV was measured. The in vitro effects of iMSC-sEV on the migration and tube formation of endothelial cells were investigated, respectively. Autophagy and autophagy-related signaling pathway were detected in vivo and in vitro. Results We found that iMSC-sEV significantly reduced infarct volume, enhanced angiogenesis, and alleviated long-term neurological deficits in rats after stroke. We also demonstrated that iMSC-sEV increased migration and tube formation of endothelial cells in vitro. A further mechanism study revealed that the pro-angiogenic effect of iMSC-sEV was correlated with a reduction in autophagy. Furthermore, iMSC-sEV significantly activated signal transducer and activator of transcription 3 (STAT3), and suppression of STAT3 abolished iMSC-sEV-induced inhibition of autophagy and promotion of angiogenesis in vivo and in vitro. Conclusions Taken together, our data indicate that iMSC-sEV promote angiogenesis after ischemic stroke, potentially, by inhibiting autophagy, a process that is partially dependent on STAT3 activation.

Endogenous neurogenesis holds promise for brain repair and long‐term functional recovery after ischaemic stroke. However, the effects of exosomes from human urine‐derived stem cells (USC‐Exos) in neurogenesis remain unclear. This study aimed to investigate whether USC‐Exos enhanced neurogenesis and promoted functional recovery in brain ischaemia. By using an experimental stroke rat model, we found that intravenous injection of USC‐Exos enhanced neurogenesis and alleviated neurological deficits in post‐ischaemic stroke rats. We used neural stem cells (NSCs) subjected to oxygen‐glucose deprivation/reoxygenation (OGD/R) as an in vitro model of ischaemic stroke. The in vitro results suggested that USC‐Exos promoted both proliferation and neuronal differentiation of NSCs after OGD/R. Notably, a further mechanism study revealed that the pro‐neurogenesis effects of USC‐Exos may be partially attributed to histone deacetylase 6 (HDAC6) inhibition via the transfer of exosomal microRNA‐26a (miR‐26a). Taken together, this study indicates that USC‐Exos can be used as a novel promising strategy for brain ischaemia, which highlights the application of USC‐Exos.

Lead halide perovskites are promising for artificial photosynthesis but suffer from aqueous instability. Here, we stabilize CsPbI 3 quantum dots within a hydrophobic chlorine-functionalized covalent organic framework through multisite atomic-chlorine passivation, forms dual Cl-Pb coordination and Cl-I halogen bonding at the interface. This suppresses ionic migration while creating a gas-solid-liquid triphase interface for enhanced O 2 diffusion. The resulting S-scheme heterojunction spatially separates carriers to concurrently drive two-electron oxygen reduction and water oxidation for H 2 O 2 synthesis without sacrificial agents. The system achieves production rates of 20.37 mmol h −1 g −1 in seawater, with a solar-to-chemical conversion efficiency of 1.38%, and operates stably for 20 h. Importantly, natural sunlight tests yield 11.7 mmol L −1 H 2 O 2 in 10 h. Mechanistic studies confirm synergistic interfacial charge transfer and dual-reaction pathways via both oxygen reduction and water oxidation. This work demonstrates an approach for robust perovskite-based photocatalysts toward solar-driven chemical synthesis from seawater. Lead halide perovskites are promising for artificial photosynthesis but are unstable in seawater. Here, the authors report multisite atomic-chlorine passivation to stabilize CsPbI 3 quantum dots in a hydrophobic covalent organic framework, enabling efficient H 2 O 2 photosynthesis directly from seawater.

Polymer-assisted liquid exfoliation of graphite is a promising technique for the scale production of defect-free graphene. In this paper, graphene nanosheets (less than 5 layers, with lateral size about 500–1500 nm) were successfully produced by directly exfoliating graphite in low boiling point chloroform, in the presence of hydrocarbon polymers such as linear paraffin wax and hyperbranched polyethylene. The effect of polymer topological structure, molecular weight, initial graphite concentration, the ratio of polymer and graphite on the exfoliation has been investigated in detail. CH-π interaction between the hydrocarbon polymers and aromatic structure in graphite, together with the steric repulsion and solubility of absorbed polymer, facilitating the exfoliation and stabilization of graphene sheets. C–H bond involved in CH-π interaction was mainly originated from methylene (-CH2-) group, which has been revealed by nuclear magnetic resonance technique. This work is of practical importance for the understanding of mechanism in polymer-assisted liquid exfoliation of graphite.

Interfacial interaction is one of the most important factors in the construction of high-performance graphene-based elastomer composites. In this paper, graphene/poly (styrene-b-isoprene-b-styrene) (SIS) composites were prepared with solution mixing followed by an evaporation-induced self-assembly process. Various techniques such as scanning electron microscopy, UV-vis absorption spectra, tensile testing, Shore A hardness, surface resistance, thermal conductivity, and thermogravimetric analysis were conducted to characterize the microstructure and properties of the obtained composites. The results showed that the π–π stacking interfacial interaction between phenyl groups of SIS and graphene play an important role in the properties’ improvement, and the effect of interfacial interaction on the properties was revealed.

Microorganisms in insect guts have been recognized as having a great impact on their hosts' nutrition, health, and behavior. Spiders are important natural enemies of pests, and the composition of the gut microbiota of spiders remains unclear. Will the bacterial taxa in spiders be same as the bacterial taxa in insects, and what are the potential functions of the gut bacteria in spiders? To gain insight into the composition of the gut bacteria in spiders and their potential function, we collected three spider species, Pardosa laura, Pardosa astrigera, and Nurscia albofasciata, in the field, and high‐throughput sequencing of the 16S rRNA V3 and V4 regions was used to investigate the diversity of gut microbiota across the three spider species. A total of 23 phyla and 150 families were identified in these three spider species. The dominant bacterial phylum across all samples was Proteobacteria. Burkholderia, Ralstonia, Ochrobactrum, Providencia, Acinetobacter, Proteus, and Rhodoplanes were the dominant genera in the guts of the three spider species. The relative abundances of Wolbachia and Rickettsiella detected in N. albofasciata were significantly higher than those in the other two spider species. The relative abundance of Thermus, Amycolatopsis, Lactococcus, Acinetobacter Microbacterium, and Koribacter detected in spider gut was different among the three spider species. Biomolecular interaction networks indicated that the microbiota in the guts had complex interactions. The results of this study also suggested that at the genus level, some of the gut bacteria taxa in the three spider species were the same as the bacteria in insect guts. We collected three species of spiders Pardosa laura, Pardosa astrigera, and Nurscia albofasciata in the field, and high‐throughput sequencing of 16S rRNA V3 and V4 region was used to investigate the diversity of gut microbiota across three spider species. A total of 23 phyla and 150 families were identified in these three spider species. The results of this study also suggested that at the genus level, some of the gut bacteria taxa in the three spider species were the same as the bacteria in insect guts.

Vascular dementia (VD) is one of the most common types of dementia, however, the intrinsic mechanism is unclear and there is still lack of effective medications. In this study, the VD rats exhibit a progressive cognitive impairment, as well as a time‐related increasing in hippocampal neural stem cells (H‐NSCs) senescence, lost and neurogenesis decline. Then, embryonic stem cell‐derived small extracellular vesicles (ESC‐sEVs) are intravenously injected into VD rats. ESC‐sEVs treatment significantly alleviates H‐NSCs senescence, recovers compromised proliferation and neuron differentiation capacity, and reverses cognitive impairment. By microarray analysis and RT‐qPCR it is identified that several miRNAs including miR‐17‐5p, miR‐18a‐5p, miR‐21‐5p, miR‐29a‐3p, and let‐7a‐5p, that can inhibit mTORC1 activation, exist in ESC‐sEVs. ESC‐sEVs rejuvenate H‐NSCs senescence partly by transferring these miRNAs to inhibit mTORC1 activation, promote transcription factor EB (TFEB) nuclear translocation and lysosome resumption. Taken together, these data indicate that H‐NSCs senescence cause cell depletion, neurogenesis reduction, and cognitive impairment in VD. ESC‐sEVs treatment ameliorates H‐NSCs senescence by inhibiting mTORC1 activation, and promoting TFEB nuclear translocation and lysosome resumption, thereby reversing senescence‐related neurogenesis dysfunction and cognitive impairment in VD. The application of ESC‐sEVs may be a novel cell‐free therapeutic tool for patients with VD, as well as other aging‐related diseases. Hippocampal neural stem cells (H‐NSCs) senescence causes their loss and neurogenesis decline, resulting in cognitive impairment in vascular dementia (VD). Embryonic stem cells derived small extracellular vesicles (ESC‐sEVs) can rejuvenate H‐NSCs senescence by transferring miRNAs including miR‐17‐5p, miR‐18a‐5p, miR‐21‐5p, miR‐29a‐3p, and let‐7a‐5p to inhibit mTORC1 activation, and promote transcription factor EB nuclear translocation and lysosome resumption, which reverses senescence‐related neurogenesis dysfunction and cognitive impairment in VD.

Background Recent studies have highlighted the significant role of the NF-κB signaling pathway in the initiation and progression of cancer. Furthermore, long noncoding RNAs (lncRNAs) have been identified as pivotal regulators in sustaining the NF-κB signaling pathway’s functionality. Despite these findings, the underlying molecular mechanisms through which lncRNAs influence the NF-κB pathway remain largely unexplored. Methods Bioinformatic analyses were utilized to investigate the differential expression and prognostic significance of XTP6. The functional roles of XTP6 were further elucidated through both in vitro and in vivo experimental approaches. To estimate the interaction between XTP6 and NDH2, RNA pulldown and RNA Immunoprecipitation (RIP) assays were conducted. The connection between XTP6 and the IκBα promoter was examined using Chromatin Isolation by RNA Purification (ChIRP) assays. Additionally, Chromatin Immunoprecipitation (ChIP) assays were implemented to analyze the binding affinity of c-myc to the XTP6 promoter, providing insights into the regulatory mechanisms at play. Results XTP6 was remarkedly upregulated in glioblastoma multiforme (GBM) tissues and was connected with adverse prognosis in GBM patients. Our investigations revealed that XTP6 can facilitate the malignant progression of GBM both in vitro and in vivo. Additionally, XTP6 downregulated IκBα expression by recruiting NDH2 to the IκBα promoter, which resulted in elevated levels of H3K27me3, thereby reducing the transcriptional activity of IκBα. Moreover, the progression of GBM was further driven by the c-myc-mediated upregulation of XTP6, establishing a positive feedback loop with IκBα that perpetuated the activation of the NF-κB signaling pathway. Notably, the application of an inhibitor targeting the NF-κB signaling pathway effectively inhibited the continuous activation induced by XTP6, leading to a significant reduction in tumor formation in vivo. Conclusion The results reveal that XTP6 unveils an innovative epigenetic mechanism instrumental in the sustained activation of the NF-κB signaling pathway, suggesting a promising therapeutic target for the treatment of GBM.

To meet the requirement of sustainable development, bio-based adsorbents were developed for the removal of dye contaminant. To improve the adsorption capacity of pure sodium alginate (SA) adsorbent for the removal of methylene blue (MB), aromatic bio-based tannin (Tan) was incorporated through the cross-linking with calcium ion. The obtained Tan/SA composite hydrogel beads were characterized with SEM, FTIR and TG, demonstrating that millimeter-sized beads were obtained through calcium cross-linking with enhanced thermal stability. The maximum capacity (247.2 mg/g) at optimal condition (pH = 12, T = 45 °C) was obtained for the 40%Tan/SA adsorbents, with a removal efficiency of 82.4%. This can be ascribed to the electrostatic attraction between SA and MB, as well as the formation of π–π stacking between Tan and MB. The adsorption process for MB is endothermic, and chemical adsorption, the removal efficiency was exceeded 90% after five cycles.

Gliomas are primary intracranial space lesions with a high mortality rate. Current treatments for glioma are very limited. Recently, immunotargeted therapy of the glioma microenvironment has been developed. Members of the 70 kDa heat shock protein (HSP70) family are involved in the development of many tumors and immunity. HSPA6 protein belongs to the HSP70 family; However, the biological function of this protein in gliomas has yet to be evaluated. In the present study, a range of analyses, involving protein networks, survival, clinical correlation, and function, revealed that the expression of HSPA6 was negatively correlated with clinical prognosis and closely associated with immunity, invasion, and angiogenesis. Quantitative protein analysis confirmed that HSPA6 was expressed at high levels in patients with glioblastoma. Vitro experiments further verified that HSPA6 enhanced the malignant progression of glioma cells by promoting proliferation, invasion and anti-apoptosis. We also found that HSPA6 was closely correlated with genomic variations and tumor microenvironment. Collectively, we demonstrated that HSPA6 may represent a new therapeutic target to improve the prognosis of patients with gliomas.