Background: The metastasis of oral cancer is one of the main causes of death. However, the mechanisms underlying oral cancer metastasis have not been completely elucidated. Fermitin family member 1 (FERMT1) plays an -oncogene role in many cancers; however, the role of FERMT1 in oral squamous cell cancer (OSCC) remains unclear.Methods: In this study, OSCC cells were treated with 5 ng/ml recombinant human Transforming growth factor-β1 (TGF-β1) protein. FERMT1 expression was measured in OSCC cell lines by RT-qPCR and western blotting. The effect of FERMT1 knockdown on the migration and invasion of OSCC cells was evaluated by Transwell assay. The epithelial-mesenchymal transition (EMT) and PI3K/AKT signaling pathway-related mRNA expression and protein levels were assessed by RT-qPCR and western blotting.Results: We found that FERMT1 expression was elevated in TGF-β1-induced OSCC cell lines, and knockdown of FERMT1 inhibited the migration and invasion in TGF-β1-induced OSCC cells. FERMT1 silencing inhibited vimentin, N-cadherin, matrix metalloproteinase 9 (MMP-9) expression and promoted E-cadherin expression, suggesting that FERMT1 silencing inhibited EMT in TGF-β1-induced OSCC cells. Furthermore, FERMT1 silencing inactivated the PI3K/AKT signaling pathway in TGF-β1-induced OSCC cells. Activation of the PI3K/AKT signaling pathway reversed the effect of FERMT1 silencing on OSCC cell migration, invasion, and EMT.Conclusions: FERMT1 silencing inhibits the migration, invasion, and EMT of OSCC cells via inactivation of the PI3K/AKT signaling pathway, suggesting that FERMT1 is a novel and potential therapeutic target for anti-metastatic strategies for OSCC.

Microplastics are a pervasive pollutant in aquatic ecosystems, raising critical environmental and public health concerns and driving the need for advanced detection technologies. Microscopic hyperspectral imaging (micro-HSI), known for its ability to simultaneously capture spatial and spectral information, has shown promise in microplastic analysis. However, its widespread application is hindered by limitations such as low signal-to-noise ratios (SNR) and reduced sensitivity to smaller microplastic particles. To address these challenges, this study investigates the use of Ag nanoarrays as reflective substrates for micro-HSI. The localized surface plasmon resonance (LSPR) effect of Ag nanoarrays enhances spectral resolution by suppressing background reflections and isolating microplastic reflection bands from interference. This improvement results in significantly increased SNR and more distinct spectral features. When analyzed using a 3D-2D convolutional neural network (3D-2D CNN), the integration of Ag nanoarrays improved classification accuracy from 90.17% to 98.98%. These enhancements were further validated through Support Vector Machine (SVM) analyses, demonstrating the robustness and reliability of the proposed approach. This study demonstrates the potential of combining Ag nanoarrays with 3D-2D CNN models to enhance micro-HSI performance, offering a novel and effective solution for precise microplastics detection and advancing chemical analysis, environmental monitoring, and related fields.

Epilepsy (EP) is a neurological disorder characterized by abnormal, sudden neuronal discharges. Seizures increase extracellular glutamate levels, causing excitotoxic damage. Glutamate transporter type 1 (GLT-1) and its human homologue excitatory amino acid transporter-2 (EAAT2) clear 95% of extracellular glutamate. Studies on neurodegenerative diseases suggest that trichostatin A (TSA), a broad-spectrum histone deacetylase (HDAC) inhibitor, can increase GLT-1/EAAT2 transcription. However, the precise mechanism by which TSA modulates GLT-1/EAAT2 levels remains unclear. This research demonstrated that TSA increases GLT-1/EAAT2 expression through histone acetylation, exerting substantial antiepileptic effects. Our results identify a promising therapeutic strategy for EP involving the modulation of glutamate transporters to mitigate seizures. Future research should explore the specific mechanisms underlying the effects of TSA and its potential clinical applications. Acute and chronic EP models were induced using kainic acid (KA) to assess the effects of TSA on the seizure threshold and frequency. Electrophysiological recordings of the hippocampus were used to evaluate the impact of TSA on neuronal excitability. RNA-Seq was used to analyse changes in glutamate transporter-related gene expression. Western blot analysis and qRT‒PCR were used to assess the influence of TSA on HDAC expression. To validate the role of GLT-1/EAAT2 in the antiepileptic effects of TSA, the impact of the GLT-1/EAAT2 inhibitor dihydrokainic acid (DHK) on the effects of TSA was assessed. Glutamate release was measured, and microdialysis was used to determine the glutamate content in the cerebrospinal fluid. Finally, metabolomics analysis was used to explore changes in amino acid levels in the hippocampus following TSA treatment to further confirm the antiepileptic potential of TSA. TSA effectively inhibited seizures in both acute and chronic models. It reduced the amplitude of excitatory postsynaptic currents (PSCs) and the frequency of spontaneous excitatory PSCs in the hippocampus without affecting inhibitory PSCs. Transcriptome analysis was used to identify glutamate transmission-related targets and revealed significant upregulation of the GLT-1 and EAAT2 genes in the hippocampus, which was confirmed by qRT‒PCR and Western blotting. Acetylation-induced upregulation of GLT-1/EAAT2 was observed, and inhibition of these transporters by DHK reduced the seizure-mitigating effects of TSA, underscoring the role of GLT-1/EAAT2 in clearing glutamate and its contribution to the observed antiepileptic effects of TSA. Our findings highlight the crucial role of GLT-1/EAAT2 in mediating the impact of TSA on glutamatergic transmission and seizure activity. These insights pave the way for the development of novel therapeutic approaches for EP involving the modulation of glutamate transporters.

The present study aims to develop a more valuable innovative aquaculture feed for the sustainable Lates calcarifer aquaculture industry. An experiment with a completely random design was developed with five groups containing 0% immunostimulant and 0.5% ginger, 1.0% garlic, 0.15% palm carotene alone or in combination. Each diet was randomly assigned to triplicate groups of 30 fish (10.06 ± 0.09 g) per tank. The fish were fed once daily to apparent satiation. Throughout the 56‐day feeding trial, the results suggest that although no significant differences were observed among almost all experimental groups in growth performance, feed efficiency, fish composition and disease resistance, the palm carotene supplementations downregulated intestinal tumor necrosis factor alpha ( TNF-α ) and interleukin (IL)‐6 expression, decreased sum scores of liver pathological changes, increased intestinal villus surface (VS) compared with the control group. Moreover, the combined treatment shows more promising immune gene expression (intestinal IL-1 beta ( IL-1β ) was also downregulated compared to the control), liver and intestinal protection (lower sum scores of liver pathological changes and larger intestinal VS than palm carotene alone supplementation, goblet cell (GC) number per intestinal villus was also increased compared to the control) effects on L. calcarifer infected with Vibrio parahaemolyticus . Therefore, a combination of 0.5% ginger, 1.0% garlic, and 0.15% palm carotene in the diet of L. calcarifer can be used as an immune booster due to fishmeal substitution to obtain better immunocompetence.