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Mental health is becoming a major concern for students in today’s fast-changing world. Mental health challenges have impact on every aspect of life including performance which pointed to early identification of risk levels. Recent reports show a rapid rise in anxiety, depression, and stress among students. This need urge for intelligent systems that can support mental health monitoring in educational environments. Existing methods often lack accuracy, and the ability to capture complex psychological patterns. This study aims to address these gaps by developing an interpretable deep learning model that predicts student mental health risk using FT-Transformer and LSTM architectures. The model integrates a Cross-Attention Attribution Layer (CAAL), which combines feature attention with temporal attention, making the ensemble intrinsically interpretable. The approach captures both global feature relationships and time-based emotional variations. Feature engineering based on entropy and uncertainty patterns further strengthens the model’s ability to detect subtle risk signals. The proposed method is compared with several baseline models, including SVM, Logistic Regression, Random Forest, standalone LSTM, and FT-Transformer. Empirical analysis shows that the proposed model achieves the highest accuracy of 95%, outperforming all baselines. These findings are validated through explainable AI techniques, global feature-importance analysis, and multiple statistical tests for effective framework to support student mental health assessment.

Against the backdrop of the global rapid transition to an aging society, how to utilize smart home technology to achieve efficient and personalized aging-friendly transformation has become a common focus in academic and practical fields. This study proposes a space generation and optimization framework integrated with Artificial Intelligence (AI), aiming to create a dynamically adaptive living environment for elderly users in a data-driven manner. First, the study deploys a multi-type sensor system in typical elderly households to collect multi-dimensional data, including behavior trajectories, activity intensity, and spatial usage heat of space usage. Subsequently, it uses Long Short-Term Memory (LSTM) network to model time-series behaviors, extract daily activity patterns, and establish a mapping relationship between behaviors and needs based on these patterns. On this basis, a Reinforcement Learning (RL) mechanism is introduced. By constructing a reward function centered on safety, convenience, and individual preferences, the spatial layout is continuously optimized through iteration. Furthermore, Conditional Generative Adversarial Network (cGAN) is used to generate spatial sketch designs, which significantly improves the efficiency of interaction and visualization. The study conducts empirical verification in three elderly household samples. Comparative experimental results show that: The coverage rate of activity areas increases to 71.6%, the spatial idle rate decreases to 12.9%, and the user satisfaction score rises from 2.9 to 4.7 (out of 5). Meanwhile, the behavior recognition accuracy of the LSTM model reaches 91.8%. The spatial layout adaptability optimized by RL increases by 22.7%. In addition, the user feedback mechanism effectively promotes continuous optimization, significantly enhancing the system’s personalized response capability. In general, this study achieves two main objectives. Firstly, it proposes an intelligent space generation and optimization method specifically designed for elderly users. Secondly, it addresses the deficiencies in existing research regarding dynamic adaptation and personalized design. This is accomplished through the synergy of behavior modeling and generative optimization. As a result, the study provides a technically practical path for the aging-friendly transformation of smart homes.

The main pathological mechanism of intervertebral disc degeneration (IVDD) is the programmed apoptosis of nucleus pulposus (NP) cells. Oxidative stress is a significant cause of IVDD. Whether mitophagy is induced by strong oxidative stress in IVDD remains to be determined. This study aimed to investigate the relationship between oxidative stress and mitophagy and to better understand the mechanism of IVDD in vivo and in vitro. To this end, we obtained primary NP cells from the human NP and subsequently exposed them to TBHP. We observed that oxidative stress induced mitophagy to cause apoptosis in NP cells, and we suppressed mitophagy and found that NP cells were protected against apoptosis. Interestingly, TBHP resulted in mitophagy through the inhibition of the HIF-1α/NDUFA4L2 pathway. Therefore, the upregulation of mitochondrial NDUFA4L2 restricted mitophagy induced by oxidative stress. Furthermore, the expression levels of HIF-1α and NDUFA4L2 were decreased in human IVDD. In conclusion, these results demonstrated that the upregulation of NDUFA4L2 ameliorated the apoptosis of NP cells by repressing excessive mitophagy, which ultimately alleviated IVDD. These findings show for the first time that NDUFA4L2 and mitophagy may be potential therapeutic targets for IVDD. Disc degeneration: Mitochondria at the root of the problem A study in rats highlights the role of mitochondria in intervertebral disc degeneration (IVDD), one of the most important and prevalent predisposing factors for lower back pain. Previous studies have shown that in IVDD, oxidative stress results in the gradual loss of cells in the inner part of vertebral discs which cushion the space between vertebrae. Sheng-Dan Jiang and Lei-Sheng Jiang at Shanghai Jiaotong University School of Medicine found that oxidative stress in these cells causes the selective degradation of mitochondria by preventing the expression of a protein that is essential for mitochondrial function. Overexpressing this protein in the intervertebral discs of rats with IVDD alleviated degeneration, suggesting that restoring mitochondrial function could be an effective therapeutic strategy for easing the pain associated with the condition.

Intervertebral disc degeneration (IVDD) is the most common contributor to low back pain (LBP). Recent studies have found that oxidative stress and reactive oxygen species (ROS) play an important role in IVDD. As a by‐product of aerobic respiration, ROS is mainly produced in the mitochondria by the electron transport chain and other mitochondrial located proteins. With the excessive accumulation of ROS, mitochondria are also the primary target of ROS attack in disc cells. A disrupted balance between intracellular ROS production and antioxidant capacity will lead to oxidative stress, which is the key contributor to cell apoptosis, cell senescence, excessive autophagy, and mitochondrial dysfunction. As the pivotal ingredient of oxidative stress, mitochondrial dysfunction manifests as imbalanced mitochondrial dynamics and dysregulated mitophagy. Mitochondria can alter their own dynamics through the process of fusion and fission, so that disabled mitochondria can be separated from the mitochondrial pool. Moreover, mitophagy participates by clearing these dysfunctional mitochondria. Abnormality in any of these processes either increases the production or decreases the clearance of ROS, leading to a vicious cycle that results in the death of intervertebral disc cells in large quantities, combined with degradation of the extracellular matrix and overproduction of matrix metalloproteinase. In this review, we explain the changes in mitochondrial morphology and function during oxidative stress‐mediated IVDD and highlight the important role of mitochondria in this process. Eventually, we summarize the IVDD therapeutic strategies targeting mitochondrial dysfunction based on current understanding of the role of oxidative stress in IVDD. Graphic overview of the role of mitochondrial dysfunction in the pathogenesis of IVDD. An imbalance between ROS intercellular production and antioxidant defense capacity will directly give rise to the occurrence of oxidative stress, which is mainly represented by cell apoptosis, abnormal autophagy, cell senescence, and mitochondrial dysfunction. Among the oxidative stress‐related pathophysiological processes, mitochondrial dysfunction plays an essential role in the disc pathology of IVDD, which manifests as imbalanced dynamics and dysregulated mitophagy. ROS promotes the fusion of mitochondria, which decreases their fission process, so that disabled mitochondria can be separated from the mitochondrial pool. Further, mitophagy serves as the quality control mechanism, which can be dysregulated under the condition of oxidative stress by overwhelmingly clearing both dysfunctional and normal mitochondria. Overall, the effects of mitochondria dysfunction result in the massive disc cell death with overproduction of MMP and the degradation of ECM, eventually the pathogenesis of IVDD.

Ticks transmit diverse pathogens that cause human and animal diseases, leading to an increasing number of new challenges around the world. Genomic data research could help advance our learning of phylogenetic analysis and molecular evolution. Mitochondrial genome DNA has been helpful in illustrating the phylogenetic analysis of eukaryotes containing ticks. In this research, we sequenced and assembled the circular complete mitogenome information of Haemaphysalis kolonini. The 14,948-bp mitogenome consists of 37 genes which included 13 genes for protein-coding, two genes for ribosomal RNA, 22 genes for transfer RNA, and two control regions (D-loops). Overall, the composition and arrangement of genes were compared with Haemaphysalis ticks previously recorded in Genbank. The phylogenetic tree based on Maximum likelihood (ML) and Bayesian inference (BI) computational algorithms showed that H. kolonini has a close relationship with Haemaphysalis inermis. The complete mitogenome data provide a preferable perception to the phylogenetic relationship than the single-gene data analysis. To our knowledge, this is the first research exploring the complete mitogenome for the species H. kolonini. Our results provide new insights for further research on the evolution, population genetics, systematics, and molecular ecology of ticks.

The liver and intestine are susceptible to the oxidative damage which could result in several diseases. Choline deficiency induced oxidative damage in rat liver cells. Thus, this study aimed to investigate the potential molecular mechanisms responsible for choline deficiency-induced oxidative damage. Juvenile Jian carp were fed diets differing in choline content [165 (deficient group), 310, 607, 896, 1167 and 1820 mg/kg diet] respectively for 65 days. Oxidative damage, antioxidant enzyme activities and related gene expressions in the hepatopancreas and intestine were measured. Choline deficiency decreased choline and phosphatidylcholine contents, and induced oxidative damage in both organs, as evidenced by increased levels of oxidative-stress markers (malondialdehyde, protein carbonyl and 8-hydroxydeoxyguanosine), coupled with decreased activities of antioxidant enzymes [Copper-zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD), glutathione peroxidase (GPx) and glutathione-S-transferase (GST)]. However, choline deficiency increased glutathione contents in the hepatopancreas and intestine. Furthermore, dietary choline deficiency downregulated mRNA levels of MnSOD, GPx1b, GST-rho, mGST3 and Kelch-like ECH associating protein 1 (Keap1b) in the hepatopancreas, MnSOD, GPx1b, GPx4a, GPx4b, GST-rho, GST-theta, GST-mu, GST-alpha, GST-pi and GST-kappa in the intestine, as well as intestinal Nrf2 protein levels. In contrast, choline deficiency upregulated the mRNA levels of GPx4a, GPx4b, mGST1, mGST2, GST-theta, GST-mu, Keap1a and PKC in the hepatopancreas, mGST3, nuclear factor erythoid 2-related factor 2 (Nrf2) and Keap1a in the intestine, as well as hepatopancreatic Nrf2 protein levels. This study provides new evidence that choline deficiency-induced oxidative damage is associated with changes in the transcription of antioxidant enzyme and Nrf2/Keap1 signaling molecules in the hepatopancreas and intestine. Additionally, this study firstly indicated that choline deficiency induced varied change patterns of different GPx and GST isoforms. Meanwhile, the changes of some GPx and GST isoforms caused by choline deficiency in the intestine were contrary to those in the hepatopancreas.

Ectomycorrhizal fungi (EMF) are key symbiotic microbial components for the growth and health of trees in urban greenspace habitats (UGSHs). However, the current understanding of EMF diversity in UGSHs remains poor. Therefore, in this study, using morphological classification and molecular identification, we aimed to investigate EMF diversity in three EMF host plants: Cedrus deodara in the roadside green belt, and C. deodara , Pinus massoniana , and Salix babylonica in the park roadside green belt, in Guiyang, China. A total of 62 EMF Operational Taxonomic Units (OTUs) were identified, including 13 EMF OTUs in the C. deodara roadside green belt, and 23, 31, and 9 EMF OTUs in the park green belts. C. deodara , P. massoniana , and S. babylonica were respectively identified in park green belts. Ascomycota and Basidiomycota were the dominant phylum in the EMF communities in roadside and park green habitat, respectively. The Shannon and Simpson indexes of the C. deodara EMF community in the park green belt were higher than those in the roadside green belt. EMF diversity of the tree species in the park green belt was P. massoniana  >  C. deodara  >  S. babylonica . Differences in EMF community diversity was observed among the different greening tree species in the UGSHs. UGSHs with different disturbance gradients had a significant impact on the EMF diversity of the same greening tree species. These results can be used as a scientific reference for optimizing the design and scientific management of UGSHs.

β-Conglycinin has been identified as one of the major feed allergens. However, studies of β-conglycinin on fish are scarce. This study investigated the effects of β-conglycinin on the growth, digestive and absorptive ability, inflammatory response, oxidative status and gene expression of juvenile Jian carp (Cyprinus carpio var. Jian) in vivo and their enterocytes in vitro. The results indicated that the specific growth rate (SGR), feed intake, and feed efficiency were reduced by β-conglycinin. In addition, activities of trypsin, chymotrypsin, lipase, creatine kinase, Na(+),K(+)-ATPase and alkaline phosphatase in the intestine showed similar tendencies. The protein content of the hepatopancreas and intestines, and the weight and length of the intestines were all reduced by β-conglycinin. β-Conglycinin increased lipid and protein oxidation in the detected tissues and cells. However, β-conglycinin decreased superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx) and glutathione reductase (GR) activities and glutathione (GSH) content in the intestine and enterocytes. Similar antioxidant activity in the hepatopancreas was observed, except for GST. The expression of target of rapamycin (TOR) gene was reduced by β-conglycinin. Furthermore, mRNA levels of interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β) genes were increased by β-conglycinin. However, β-conglycinin increased CuZnSOD, MnSOD, CAT, and GPx1b gene expression. In conclusion, this study indicates that β-conglycinin induces inflammation and oxidation, and causes dysfunction of intestinal digestion and absorption in fish, and finally reduces fish growth. The results of this study provide some information to the mechanism of β-conglycinin-induced negative effects.

Aflatoxin B1 (AFB1) is kind of a common mycotoxin in food and feedstuff. Aquafeeds are susceptible to contamination of AFB1. In teleost fish, the spleen and head kidney are key immune organ. Moreover, the fish skin is a critical mucosal barrier system. However, there was little study on the effects of dietary AFB1 on the immune response of these immune organs in fish. This study aimed to explore the impacts of oral AFB1 on the immune competence and its mechanisms in the skin, spleen, and head kidney of grass carp. Our work indicated that dietary AFB1 reduced antibacterial compounds and immunoglobulins contents, and decreased the transcription levels of antimicrobial peptides in grass carp immune organs. In addition, dietary AFB1 increased the transcription levels of pro-inflammatory cytokines and reduced the transcription levels of anti-inflammatory cytokines in the grass carp immune organs, which might be regulated by NF-κB and TOR signaling, respectively. Meanwhile, we evaluated the content of AFB1 in the grass carp diet should not exceed 29.48 μg/kg diet according to the levels of acid phosphatase and lysozyme. In summary, dietary AFB1 impaired immune response in grass carp skin, spleen, and head kidney.

Water hammer in pipelines is a difficult problem in fluid transmission field. Especially, there exists some friction items of pipeline transient model such that the simulation model is not consistent to the experimental results. By using the friction model proposed by Kagawa and the model of impulse response function, the pressure transients are calculated with and without cavitation. The corresponding simulation results involving pressure, velocity, steady and dynamic frictions, cavitation volume are analyzed to reveal the effect of friction item on pressure transients. Moreover, the features of steady and dynamic frictions are captured in pipelines with upstream and downstream valves. The comparative simulation results of two friction models have verified that the friction model using an impulse response function has higher consistency between simulation and experimental results of pipeline transients.