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Background The brain–gut–microbiota axis plays a role in the pathogenesis of stress-related disorders such as depression. In this study, we examined the effects of fecal microbiota transplantation (FMT) in mice with antibiotic-treated microbiota depletion. Methods The fecal microbiota was obtained from mice subjected to chronic social defeat stress (CSDS) and control (no CSDS) mice. FMT from these two groups was performed to antibiotic-treated mice. 16S rRNA analysis was performed to examine the composition of gut microbiota. Furthermore, the effects of subdiaphragmatic vagotomy in depression-like phenotypes after ingestion of microbes were examined. Results The ingestion of fecal microbiota from CSDS-susceptible mice resulted in an anhedonia-like phenotype, higher plasma levels of interleukin-6 (IL-6), and decreased expression of synaptic proteins in the prefrontal cortex (PFC) in antibiotic-treated mice but not in water-treated mice. 16S rRNA analysis suggested that two microbes ( Lactobacillus intestinalis and Lactobacillus reuteri ) may be responsible for the anhedonia-like phenotype in antibiotic-treated mice after FMT. Ingestion of these two microbes for 14 days led to depression- and anhedonia-like phenotypes, higher plasma IL-6 levels, and decreased expression of synaptic proteins in the PFC of antibiotic-treated mice. Interestingly, subdiaphragmatic vagotomy significantly blocked the development of behavioral abnormalities, elevation of plasma IL-6 levels, and downregulation of synaptic proteins in the PFC after ingestion of these two microbes. Conclusions These findings suggest that microbiota depletion using an antibiotic cocktail is essential for the development of FMT-induced behavioral changes and that the vagus nerve plays a key role in behavioral abnormalities in antibiotic-treated mice after the ingestion of L. intestinalis and L. reuteri . Therefore, it is likely that the brain–gut–microbiota axis participates in the pathogenesis of depression via the vagus nerve.

Epidemiological studies suggest that exposure to herbicides during pregnancy might increase risk for autism spectrum disorder (ASD) in offspring. However, the precise mechanisms underlying the risk of ASD by herbicides such as glyphosate remain unclear. Soluble epoxide hydrolase (sEH) in the metabolism of polyunsaturated fatty acids is shown to play a key role in the development of ASD in offspring after maternal immune activation. Here, we found ASD-like behavioral abnormalities in juvenile offspring after maternal exposure to high levels of formulated glyphosate. Furthermore, we found higher levels of sEH in the prefrontal cortex (PFC), hippocampus, and striatum of juvenile offspring, and oxylipin analysis showed decreased levels of epoxy-fatty acids such as 8 (9)-EpETrE in the blood, PFC, hippocampus, and striatum of juvenile offspring after maternal glyphosate exposure, supporting increased activity of sEH in the offspring. Moreover, we found abnormal composition of gut microbiota and short-chain fatty acids in fecal samples of juvenile offspring after maternal glyphosate exposure. Interestingly, oral administration of TPPU (an sEH inhibitor) to pregnant mothers from E5 to P21 prevented ASD-like behaviors such as social interaction deficits and increased grooming time in the juvenile offspring after maternal glyphosate exposure. These findings suggest that maternal exposure to high levels of glyphosate causes ASD-like behavioral abnormalities and abnormal composition of gut microbiota in juvenile offspring, and that increased activity of sEH might play a role in ASD-like behaviors in offspring after maternal glyphosate exposure. Therefore, sEH may represent a target for ASD in offspring after maternal stress from occupational exposure to contaminants.

Neuroinflammation is an important cause of poor prognosis in patients with spinal cord injury. pyroptosis is a new type of inflammatory cell death. Treg cells has been shown to play an anti-inflammatory role in a variety of inflammatory diseases, including inflammatory bowel disease, amyotrophic lateral sclerosis, and arthritis. However, little is known about Treg cells' potential role in pyroptosis following spinal cord injury. The aim of this research was to look into the effect of Treg cells to motor function recovery, pyroptosis and the mechanism behind it after SCI. Here, we found that pyroptosis mainly occurred in microglia on the seventh day after spinal cord injury. Konckout Treg cells resulted in widely pyroptosis and poor motor recovery after SCI. In conversely, over-infiltration of Treg cell in mice by tail vein injection had beneficial effects following SCI.Treg cell-derived exosomes promote functional recovery by inhibiting microglia pyroptosis in vivo. Bioinformatic analysis revealed that miRNA-709 was significantly enriched in Treg cells and Treg cell-secreted exosomes. NKAP has been identified as a miRNA-709 target gene. Moreover, experiments confirmed that Treg cells targeted the NKAP via exosomal miR-709 to reduce microglia pyroptosis and promote motor function recovery after SCI. More importantly, The miR-709 overexpressed exosomes we constructed significantly reduced the inflammatory response and improved motor recovery after spinal cord injury. In brief, our findings indicate a possible mechanism for communication between Treg cells and microglia, which opens up a new perspective for alleviating neuroinflammation after SCI.

The aim of this study was to evaluate the value of copeptin in predicting mortality including both short-term and long-term mortality in patients with acute coronary syndrome (ACS). Potential studies were searched and selected through PubMed, Embase and Cochrane databases up to December 2019. The predictive performance was evaluated by the pooled sensitivity and specificity, and summary receiver operating characteristic curves. Cochran's Q test and I.sup.2 index were used to assess between-study heterogeneity, and Deek's test and funnel plots were used to assess publication bias. Total six studies comprising 2269 patients were included in this meta-analysis. The area under the receiver operating characteristic curve of copeptin in predicting mortality in patients with ACS was 0.73 (95% CI: 0.69-0.77). The pooled sensitivity and specificity of copeptin were 0.77 (95% CI: 0.59-0.89) and 0.60 (95% CI: 0.47-0.71), respectively. Significant between-study heterogeneity was identified in both sensitivity (P = 0.01; I.sup.2 = 69.76%) and specificity (P<0.001; I.sup.2 = 97.32%) among the six included studies. The meta-regression analysis indicated that the number of study centers was significantly associated with the heterogeneity of sensitivity (P = 0.03), whereas the study design (P = 0.03) and duration of follow-up (P<0.001) were significantly associated with the heterogeneity of specificity. Copeptin has acceptable prognostic value for mortality in patients with ACS. Further studies based on multimarker strategy are needed to evaluate the prognostic value of copeptin for ACS in conjunction with other well-established biomarkers.

Accumulation of amyloid-β (Aβ), which results in the formation of senile plaques that cause oxidative damage and neuronal cell death, has been accepted as the major pathological mechanism of Alzheimer’s disease (AD). Hence, inhibition of Aβ-induced oxidative damage and neuronal cell apoptosis represents the effective strategies in combating AD. Ginsenoside Re (Re) has pharmacological effects against Aβ-induced neurotoxicity. However, its molecular mechanism remains elusive. The present study evaluated the effect of Re against Aβ-induced cytotoxicity and apoptosis in SH-SY5Y cells, and investigated the underlying mechanism. We demonstrate that Re inhibits the Aβ-triggered mitochondrial apoptotic pathway, as indicated by maintenance of mitochondrial functional, elevated Bcl-2/Bax ratio, reduced cytochrome c release, and inactivation of caspase-3/9. Re attenuated Aβ-evoked reactive oxygen species (ROS) production, apoptosis signal-regulating kinase 1 (ASK1) phosphorylation, and JNK activation. ROS-scavenging abrogated the ability of Re to alter ASK-1 activation. Simultaneously, inhibition of JNK abolished Re-induced Bax downregulation in Aβ-challenged SH-SY5Y cells. In addition, Re enhanced activation of the nuclear factor-E2-related factor 2 (Nrf2) in Aβ-induced SH-SY5Y cells. Knockdown of Nrf2 by small interfering RNA targeting Nrf2 abolished the protective effect of Re. Our findings indicate that Re could be a potential therapeutic approach for the treatment of AD.

EEG signals capture information through multi-channel electrodes and hold promising prospects for human emotion recognition. However, the presence of high levels of noise and the diverse nature of EEG signals pose significant challenges, leading to potential overfitting issues that further complicate the extraction of meaningful information. To address this issue, we propose a Granger causal-based spatial–temporal contrastive learning framework, which significantly enhances the ability to capture EEG signal information by modeling rich spatial–temporal relationships. Specifically, in the spatial dimension, we employ a sampling strategy to select positive sample pairs from individuals watching the same video. Subsequently, a Granger causality test is utilized to enhance graph data and construct potential causality for each channel. Finally, a residual graph convolutional neural network is employed to extract features from EEG signals and compute spatial contrast loss. In the temporal dimension, we first apply a frequency domain noise reduction module for data enhancement on each time series. Then, we introduce the Granger–Former model to capture time domain representation and calculate the time contrast loss. We conduct extensive experiments on two publicly available sentiment recognition datasets (DEAP and SEED), achieving 1.65% improvement of the DEAP dataset and 1.55% improvement of the SEED dataset compared to state-of-the-art unsupervised models. Our method outperforms benchmark methods in terms of prediction accuracy as well as interpretability.

Background To explore the underlying causality between leukocyte telomere length (LTL) and four gastrointestinal diseases, we designed a two-sample bidirectional Mendelian randomization study. Methods Two-sample Mendelian randomization (MR) was used to explore genetic causality between LTL and four gastrointestinal diseases, including irritable bowel syndrome (IBS), gastroesophageal reflux disease (GERD), gastrointestinal ulcers disease (GUD), and nonalcoholic fatty liver disease (NAFLD). We utilized inverse-variance weighted (IVW) as the primary method for MR analysis. Supplementary analyses were conducted using methods such as MR-Egger regression, weighted-median, Maximum Likelihood (MaxLik), Robust adjusted profile score (MR-RAPS), Contamination mixture (ConMix), and MR-mix. Cochran’s Q was calculated to check for heterogeneity. The MR-Egger regression and MR pleiotropy residual sum and outlier (MR-PRESSO) were detected for pleiotropy. Results The IVW analysis suggests that there may be a potential causal relationship between LTL and two diseases (odds ratio (OR): 1.062; 95% confidence interval (CI): 1.003, 1.124; p  = 0.038 for IBS and OR: 0.889; 95% CI: 0.798, 0.990; p  = 0.032 for GERD). However, other methods do not entirely align with the results of the IVW analysis. In the reverse MR analysis, we did not find statistically significant associations between LTL and these four diseases. Conclusion The current evidence does not definitively rule out a causal relationship between LTL and these four gastrointestinal diseases but suggests a potential association between LTL and IBS, or LTL and GERD. Exploring the relationship between gastrointestinal diseases and LTL may offer new insights into the onset, progression, and treatment of these diseases.

Inspired by natural organisms, biomimetic materials with exceptional biocompatibility, degradability, and multifunctionality have emerged as promising candidates for biomedical applications. Lignin, a plant-derived organic polymer, has gained attention due to its intrinsic antioxidant activity, adhesive properties, and biocompatibility. Despite its structural advantages, challenges in stability, biodegradability, and practical implementation hinder its utilization. Structural modifications through chemical/physical treatments or microbial/enzymatic can optimize lignin’s bioactivity, mechanical strength, and adhesion, enabling applications in drug delivery, Ultraviolet (UV) shielding, sensing, and wound healing. This review outlines lignin sources, modification principles, and adhesion of biomaterials mechanisms, while showcasing innovative lignin-based materials in biomedical contexts. We highlight their roles in therapeutic delivery systems, tissue engineering & regenerative medicine, and functional biomedical devices, emphasizing lignin’s low toxicity and environmental adaptability. By addressing current limitations in processing techniques and clinical translation, we discuss lignin’s potential to bridge laboratory research and practical medical solutions. The analysis concludes with an evaluation of lignin’s untapped value in sustainable biomedicine, proposing strategies to overcome scalability and standardization barriers. This synthesis provides critical insights for advancing lignin-based technologies toward clinical implementation while maintaining ecological sustainability.

The ability of transgenic plants to respond to sudden environmental pollution accidents has become viable. Nonetheless, there is a dearth of research regarding the mechanism by which transgenic plants degrade organic pollutants. Hence, this study aimed to elucidate the process of organic pollutant degradation by plants, offering theoretical support for the application of transgenic plant emergency phytoremediation technology. In this investigation, we developed a 3D-QSAR pharmacophore model to represent the collective impact of plant resistance and phytodegradation. This was achieved by employing integrated effect values following treatment with a sine function approach. Moreover, we have undertaken an inaugural exploration of the coregulatory mechanism involved in plant resistance and pollutant degradation within plants. Additionally, we applied virtual molecular modification techniques for analysis and validation, striving for a more indepth understanding of the molecular-level enhancement mechanism related to the degradation of pollutants within plant organisms. The mechanism analysis results of the Hypo 1 pharmacophore model were verified, indicating that hydrophobic characteristics affect the resistance and degradation of PCBs in plants, significantly affecting the degradation effect of pollutants in plants.