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With advances in nanotechnology, nanoparticles have come to be regarded as carriers of therapeutic agents and have been widely studied to overcome various diseases in the biomedical field. Among these particles, mesoporous silica nanoparticles (MSNs) have been investigated as potential nanocarriers to deliver drug molecules to various target sites in the body. This review introduces the physicochemical properties of MSNs and synthesis procedures of MSN-based nanoplatforms. Moreover, we focus on updating biomedical applications of MSNs as a carrier of therapeutic or diagnostic cargo and review clinical trials using silica-nanoparticle-based systems. Herein, on the one hand, we pay attention to the pharmaceutical advantages of MSNs, including nanometer particle size, high surface area, and porous structures, thus enabling efficient delivery of high drug-loading content. On the other hand, we look through biosafety and toxicity issues associated with MSN-based platforms. Based on many reports so far, MSNs have been widely applied to construct tissue engineering platforms as well as treat various diseases, including cancer, by surface functionalization or incorporation of stimuli-responsive components. However, even with the advantageous aspects that MSNs possess, there are still considerations, such as optimizing physicochemical properties or dosage regimens, regarding use of MSNs in clinics. Progress in synthesis procedures and scale-up production as well as a thorough investigation into the biosafety of MSNs would enable design of innovative and safe MSN-based platforms in biomedical fields.

Oxidative stress is a key driver of mucosal damage in ulcerative colitis (UC). Antioxidant supplementation may restore redox balance, but its clinical efficacy remains controversial. To evaluate the effects of natural antioxidant substances supplementation on oxidation/antioxidant biomarkers and clinical outcomes in UC patients. The databases included PubMed, Embase, Web of Science, and Cochrane Library (up to July 2025) were searched, and RCTs comparing oral antioxidants with placebo in UC were included. The primary outcomes were changes in oxidative stress markers (MDA, SOD, TAC, GPX). The secondary outcomes included the short IBD questionnaire (SIBDQ) score and the simple clinical colitis activity index (SCCAI) score. 9 articles involving 624 patients were included in this study. Compared to placebo group, antioxidant substances supplementation could significantly reduce the level of MDA ( P  = 0.001, SMD=-1.09, 95% CI −1.75 to −0.43), increased the levels of SOD, TAC, GPX in patients with UC ( P  = 0.02, SMD = 0.57, 95% CI 0.10 to 1.04; P  = 0.0004, SMD = 0.74, 95% CI   0.33 to 1.16; P  = 0.004, SMD = 0.69, 95% CI  0.22 to 1.16). In addition, antioxidant substances supplementation remarkably decreased the SCCAI score of UC patients ( P  = 0.04, SMD=-0.62, 95% CI −1.21 to −0.04), thus improving the disease activity. However, there is no significant difference in the change of IBDQ score ( P  = 0.13, SMD = 0.55, 95% CI −0.17 to 1.28). Natural antioxidant substances supplementation effectively enhanced antioxidant capacity and ameliorated oxidation status, improved the disease activity of UC patients, but had no significant impact on their quality of life. This study will provide a basis for the selection of adjuvant therapy drugs for UC.

Myocardial infarction (MI) is a fatal heart disease that affects millions of lives worldwide each year. This study investigated the roles of HIF-1α/lncRNA-TUG1 in mitochondrial dysfunction and pyroptosis in MI. CCK-8, DHE, lactate dehydrogenase (LDH) assays, and JC-1 staining were performed to measure proliferation, reactive oxygen species (ROS), LDH leakage, and mitochondrial damage in hypoxia/reoxygenation (H/R)-treated cardiomyocytes. Enzyme-linked immunoassay (ELISA) and flow cytometry were used to detect LDH, creatine kinase (CK), and its isoenzyme (CK-MB) levels and caspase-1 activity. Chromatin immunoprecipitation (ChIP), luciferase assay, and RNA-immunoprecipitation (RIP) were used to assess the interaction between HIF-1α, TUG1, and FUS. Quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting, and immunohistochemistry were used to measure HIF-1α, TUG1 and pyroptosis-related molecules. Hematoxylin and eosin (HE), 2,3,5-triphenyltetrazolium chloride (TTC), and terminal deoxynucleotidyl transferase dUTP risk end labelling (TUNEL) staining were employed to examine the morphology, infarction area, and myocardial injury in the MI mouse model. Mitochondrial dysfunction and pyroptosis were induced in H/R-treated cardiomyocytes, accompanied by an increase in the expression of HIF-α and TUG1. HIF-1α promoted TUG1 expression by directly binding to the TUG1 promoter. TUG1 silencing inhibited H/R-induced ROS production, mitochondrial injury and the expression of the pyroptosis-related proteins NLRP3, caspase-1 and GSDMD. Additionally, H/R elevated FUS levels in cardiomyocytes, which were directly inhibited by TUG1 silencing. Fused in sarcoma (FUS) overexpression reversed the effect of TUG1 silencing on mitochondrial damage and caspase-1 activation. However, the ROS inhibitor N-acetylcysteine (NAC) promoted the protective effect of TUG1 knockdown on H/R-induced cardiomyocyte damage. The in vivo MI model showed increased infarction, myocardial injury, ROS levels and pyroptosis, which were inhibited by TUG1 silencing. HIF-1α targeting upregulated TUG1 promotes mitochondrial damage and cardiomyocyte pyroptosis by combining with FUS, thereby promoting the occurrence of MI. HIF-1α/TUG1/FUS may serve as a potential treatment target for MI.

N-Acetylcysteine (NAc) has been shown to play a diversity of favorable health-related roles (e.g., antioxidant, paracetamol antidote, mucolytics, neuroprotective agent). Having said that, here in this study, we evaluate the health-promoting properties of NAc, particularly its ability to modulate organismal longevity. We note that 1 mg/ml NAc prolonged the lifespan of Drosophila. Furthermore, it was observed that NAc increased the capability of these flies to resist environmental stresses measured by starvation and paraquat stress assays. In an effort to reveal cellular mechanisms behind this interesting phenomenon, qPCR was performed, uncovering that transcript levels of catalase and phospholipid hydroperoxide glutathione peroxidase—key enzymes to fend off reactive oxygen species (ROS) assaults, were up-regulated. Correspondingly, enzyme activities of catalase and glutathione peroxidase were increased as well. Combined, we hope our research helps broaden the spectrum of clinical application for NAc so that one may eventually determine if NAc is a potentially useful anti-aging agent by encouraging others to scrutinize the hidden health benefits of NAc.

TREM2 plays a critical role in the alleviation of Alzheimer’s disease by promoting Aβ phagocytosis by microglia, but the detailed molecular mechanism underlying TREM2-induced direct phagocytic activity of Aβ remains to be revealed. We found that learning and memory functions were improved in aged TREM2 TG mice, with the opposite effects in KO mice. The amount of phagocytosed Aβ was significantly reduced in the primary microglia of KO mice. CD36 expression in primary microglia was greater in TG than in WT mice but was substantially decreased in KO mice. The expression of C/EBPα, an upstream transcriptional activator of CD36, was also elevated in primary microglia of TG mice but decreased in KO mice. The transcription of CD36 was markedly increased by TREM2 overexpression, and this effect was suppressed by a mutation of the C/EBPα binding site on the CD36 promoter. The TREM2-induced expression of CD36 and C/EBPα was inhibited by treatment with PI3K/AKT signaling blockers, and phosphorylation of AKT was elevated in TREM2-overexpressing BV2 cells. The present study provides evidence that TREM2 is required for preventing loss of memory and learning in Alzheimer’s disease by regulating C/EBPα-dependent CD36 expression and the consequent Aβ phagocytosis.

Catalytic asymmetric [2 + 4] cycloadditions of 3-vinylindoles with ortho-quinone methides and their precursors were carried out in the presence of chiral phosphoric acid to afford a series of indole-containing chroman derivatives with structural diversity in overall high yields (up to 98%), good diastereoselectivities (up to 93:7 dr) and moderate to excellent enantioselectivities (up to 98% ee). This approach not only enriches the chemistry of catalytic asymmetric cycloadditions involving 3-vinylindoles but is also useful for synthesizing chiral chroman derivatives.

Plasmon hybridization theory, inspired by molecular orbital theory, has been extremely successful in describing the near-field coupling in clusters of plasmonic nanoparticles, also known as plasmonic molecules. However, the vibrational modes of plasmonic molecules have been virtually unexplored. By designing precisely configured plasmonic molecules of varying complexity and probing them at the individual plasmonic molecule level, intramolecular coupling of acoustic modes, mediated by the underlying substrate, is observed. The strength of this coupling can be manipulated through the configuration of the plasmonic molecules. Surprisingly, classical continuum elastic theory fails to account for the experimental trends, which are well described by a simple coupled oscillator picture that assumes the vibrational coupling is mediated by coherent phonons with low energies. These findings provide a route to the systematic optical control of the gigahertz response of metallic nanostructures, opening the door to new optomechanical device strategies.

The AKT signaling pathway plays critical roles in the resolution of inflammation. However, the underlying mechanisms of anti-inflammatory regulation and signal coordination remain unclear. Here, we report that anti-inflammatory AKT signaling is coordinated by glutamyl-prolyl-tRNA synthetase 1 (EPRS1). Upon inflammatory activation, AKT specifically phosphorylates Ser999 of EPRS1 in the cytoplasmic multi-tRNA synthetase complex, inducing release of EPRS1. EPRS1 compartmentalizes AKT to early endosomes via selective binding to the endosomal membrane lipid phosphatidylinositol 3-phosphate and assembles an AKT signaling complex specific for anti-inflammatory activity. These events promote AKT activation-mediated GSK3β phosphorylation, which increase anti-inflammatory cytokine production. EPRS1-deficient macrophages do not assemble the early endosomal complex and consequently exacerbate inflammation, decreasing the survival of EPRS1-deficient mice undergoing septic shock and ulcerative colitis. Collectively, our findings show that the housekeeping protein EPRS1 acts as a mediator of inflammatory homeostasis by coordinating compartment-specific AKT signaling. The PI3K/AKT signaling pathway is carefully regulated in specific cellular compartments. Lee and colleagues show that the housekeeping gene glutamyl-prolyl-tRNA synthetase 1 coordinates early endosome-specific AKT signaling necessary for inflammation resolution.

Large-scale wireless sensor networks are characterized by stringent energy and computation restrictions. It is exceedingly difficult to change a sensor network’s environment configurations, such as the number of sensor nodes, after deployment of the nodes. Although several simulators are able to variously construct simulation models for sensor networks before their deployment, the configurations should be modified with extra human effort as the simulators cannot freely generate diverse models. In this paper, we propose a novel framework, called a system entity structure and model base for large-scale wireless sensor networks (WSN-SES/MB), which is based on discrete event system specification formalism. Our proposed framework synthesizes the structure and models for sensor networks through our modeling construction process. The proposed framework achieves time and cost savings in constructing discrete event simulation-based models. In addition, the framework increases the diversity of simulation models by the process’s pruning algorithm. The simulation results validate that the proposed framework provides up to 8% time savings and up to 23% cost savings as compared to the manual extra effort.