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Historical inference attacks pose a critical privacy threat in mobile edge computing (MEC), where adversaries exploit long-term task and location patterns to infer users’ sensitive information. To address this challenge, we propose a privacy-preserving task scheduling framework that adaptively balances privacy protection and system performance under dynamic vehicular environments. First, we introduce a dynamic privacy-aware adaptation mechanism that adjusts privacy levels in real time according to vehicle mobility and network dynamics. Second, we design a dual-algorithm framework composed of two complementary solutions: a Markov Approximation-Based Online Algorithm (MAOA) that achieves near-optimal scheduling with provable convergence, and a Privacy-Aware Deep Q-Network (PAT-DQN) algorithm that leverages deep reinforcement learning to enhance adaptability and long-term decision-making. Extensive simulations demonstrate that our proposed methods effectively mitigate privacy leakage while maintaining high task completion rates and low energy consumption. In particular, PAT-DQN achieves up to 14.2% lower privacy loss and 19% fewer handovers than MAOA in high-mobility scenarios, showing superior adaptability and convergence performance.

The recent outbreak of betacoronavirus Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), which is responsible for the Coronavirus Disease 2019 (COVID-19) global pandemic, has created great challenges in viral diagnosis. The existing methods for nucleic acid detection are of high sensitivity and specificity, but the need for complex sample manipulation and expensive machinery slow down the disease detection. Thus, there is an urgent demand to develop a rapid, inexpensive, and sensitive diagnostic test to aid point-of-care viral detection for disease monitoring. In this study, we developed a clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR associated proteins (Cas) 12a-based diagnostic method that allows the results to be visualized by the naked eye. We also introduced a rapid sample processing method, and when combined with recombinase polymerase amplification (RPA), the sample to result can be achieved in 50 minutes with high sensitivity (1–10 copies per reaction). This accurate and portable detection method holds a great potential for COVID-19 control, especially in areas where specialized equipment is not available.

This study investigates the knowledge, attitudes, and practices (KAP) of patients diagnosed with temporomandibular joint disorder (TMD). Conducted at Shenzhen University General Hospital from October to November 2024, the cross-sectional analysis utilized questionnaires to assess demographic data, KAP scores, and mental health indicators, including the Patient Health Questionnaire-9 (PHQ-9) and Generalized Anxiety Disorder 7-item scale (GAD-7). A total of 229 valid responses were analyzed, revealing that 72.9% of participants were female. Notably, 47.2% reported no depression, while 87.8% indicated no or mild anxiety. Mean KAP scores were as follows: knowledge 8.59 ± 5.77, attitude 38.46 ± 12.28, and practice 40.37 ± 7.85, with significant positive correlations between knowledge and attitude ( r  = 0.304, P  = 0.002), knowledge and practice ( r  = 0.187, P  = 0.004), and attitude and practice ( r  = 0.374, P  < 0.001). Structural equation modeling demonstrated that both knowledge and attitude had significant direct effects on practice (β = 0.269, P  < 0.001; β = 0.271, P  < 0.001, respectively). The findings suggest that TMD patients have inadequate knowledge and negative attitudes, underscoring the need for enhanced education and positive attitude promotion to improve self-care and treatment outcomes. Clinically, tailored patient education programs and behavioral counselling should be integrated into routine TMD management to improve adherence, symptom control, and quality of life.

Large-scale COVID-19 vaccinations are currently underway in many countries in response to the COVID-19 pandemic. Here, we report, besides generation of neutralizing antibodies, consistent alterations in hemoglobin A1c, serum sodium and potassium levels, coagulation profiles, and renal functions in healthy volunteers after vaccination with an inactivated SARS-CoV-2 vaccine. Similar changes had also been reported in COVID-19 patients, suggesting that vaccination mimicked an infection. Single-cell mRNA sequencing (scRNA-seq) of peripheral blood mononuclear cells (PBMCs) before and 28 days after the first inoculation also revealed consistent alterations in gene expression of many different immune cell types. Reduction of CD8+ T cells and increase in classic monocyte contents were exemplary. Moreover, scRNA-seq revealed increased NF-κB signaling and reduced type I interferon responses, which were confirmed by biological assays and also had been reported to occur after SARS-CoV-2 infection with aggravating symptoms. Altogether, our study recommends additional caution when vaccinating people with pre-existing clinical conditions, including diabetes, electrolyte imbalances, renal dysfunction, and coagulation disorders.

Systemic lupus erythematosus (SLE) and primary Sjögren's syndrome (pSS) are common systemic autoimmune diseases that share a wide range of clinical manifestations and serological features. This study investigates genes, signaling pathways, and transcription factors (TFs) shared between SLE and pSS. Gene expression profiles of SLE and pSS were obtained from the Gene Expression Omnibus (GEO). Weighted gene co-expression network analysis (WGCNA) and differentially expressed gene (DEG) analysis were conducted to identify shared genes related to SLE and pSS. Overlapping genes were then subject to Gene Ontology (GO) and protein-protein interaction (PPI) network analyses. Cytoscape plugins cytoHubba and iRegulon were subsequently used to screen shared hub genes and predict TFs. In addition, gene set variation analysis (GSVA) and CIBERSORTx were used to calculate the correlations between hub genes and immune cells as well as related pathways. To confirm these results, hub genes and TFs were verified in microarray and single-cell RNA sequencing (scRNA-seq) datasets. Following WGCNA and limma analysis, 152 shared genes were identified. These genes were involved in interferon (IFN) response and cytokine-mediated signaling pathway. Moreover, we screened six shared genes, namely and , out of which three genes, namely and were found to be highly expressed in both microarray and scRNA-seq datasets. IFN response and ITGB2 signaling pathway were identified as potentially relevant pathways. In addition, STAT1 and IRF7 were identified as common TFs in both diseases. This study revealed and as the shared genes and identified STAT1 and IRF7 as the common TFs of SLE and pSS. Notably, the IFN response and ITGB2 signaling pathway played vital roles in both diseases. Our study revealed common pathogenetic characteristics of SLE and pSS. The particular roles of these pivotal genes and mutually overlapping pathways may provide a basis for further mechanistic research.

Osteosarcoma (OS) is a rare but aggressive malignancy. Despite previous reports, molecular characterization of this disease is not well understood, and little is known regarding OS in Chinese patients. Herein, we analyzed the genomic signatures of 73 Chinese OS cases. TP53, NCOR1, LRP1B, ATRX, RB1, and TFE3 were the most frequently mutated gene in our OS cohort. In addition, the genomic analysis of Western OS patients was performed. Notably, there were remarkable disparities in mutational landscape, base substitution pattern, and tumor mutational burden between the Chinese and Western OS cohorts. Specific molecular mechanisms, including DNA damage repair (DDR) gene mutations, copy number variation (CNV) presence, aneuploidy, and intratumoral heterogeneity, were associated with disease progression. Additionally, 30.1% of OS patients carried clinically actionable alterations, which were mainly enriched in PI3K, MAPK, DDR, and RTK signaling pathways. A specific molecular subtype incorporating DDR alterations and CNVs was significantly correlated with distant metastasis‐free survival and event‐free survival, and this correlation was observed in all subgroups with different characteristics. These findings comprehensively elucidated the genomic profile and revealed novel prognostic factors in OS, which would contribute to understanding this disease and promoting precision medicine of this population. Here, a distinctive genomic profile was revealed in Chinese patients with osteosarcoma (OS). Specific molecular mechanisms were found to be associated with disease progression. Additionally, a novel molecular subtype incorporating DNA damage repair gene mutations and copy number variations was identified, which can effectively define the risk stratification of localized OS and better predict metastasis or recurrence.

The land reclaimed from the seaside may have a long-term subsidence trend, which poses a potential geohazard in the future land use. Xiamen Xiang’an New Airport (XXNA) is built on reclaimed land since 2016. Based on the spaceborne Sentinel-1 data between January 2018 to April 2019 and the time series interferometric synthetic aperture radar (InSAR) technique, this paper analyzed the reclaimed land subsidence evolution at XXNA in this period. InSAR measurements show that XXNA is suffering from severe subsidence, mainly in three regions because of the earth and sand compacting. By analyzing the spatial subsidence characterizations of the main subsiding areas combined with historical land reclamation and future land use planning, we find the potential threat of subsidence to future land use. Correlation between subsidence and the period of reclamation was found, indicating that the consolidation and compression in dredger fill is the main cause of subsidence. By combining subsidence monitoring results with different land use types and adopting the Expectation (Ex) and Entropy (En) methods, we analyzed the key area with potential subsidence geo-hazard. This work shows that with SAR interferometry, it is possible to find the large area ground subsidence in the airport reclaimed area. The areas with potential subsidence geo-hazards are consistent with the deep reclaimed earth, which means high subsidence risk in the future.

Rewarding experiences are often well remembered, and such memory formation is known to be dependent on dopamine modulation of the neural substrates engaged in learning and memory; however, it is unknown how and where in the brain dopamine signals bias episodic memory toward preceding rather than subsequent events. Here we found that photostimulation of channelrhodopsin-2–expressing dopaminergic fibers in the dentate gyrus induced a long-term depression of cortical inputs, diminished theta oscillations, and impaired subsequent contextual learning. Computational modeling based on this dopamine modulation indicated an asymmetric association of events occurring before and after reward in memory tasks. In subsequent behavioral experiments, preexposure to a natural reward suppressed hippocampus-dependent memory formation, with an effective time window consistent with the duration of dopamine-induced changes of dentate activity. Overall, our results suggest amechanism by which dopamine enables the hippocampus to encode memory with reduced interference from subsequent experience.

Background Non-alcoholic fatty liver disease (NAFLD) is characterized by abnormal lipid accumulation in hepatocytes and defective autophagy has been implicated in its pathogenesis. Human umbilical cord-derived MSCs (hUC-MSCs) have shown therapeutic potential in treating NAFLD, while underlying molecular mechanisms remained largely unknown. Methods Male C57BL/6J mice fed a choline-deficient high fat diet (CD-HFD) and HepG2 cells exposed to palmitic acid/oleic acid were established as in vivo and in vitro models of NAFLD, respectively. Both models were subjected to treatment with human umbilical cord-derived MSCs (hUC-MSCs). Lipid content, proinflammatory cytokines, fibrosis markers and the hepatic transcriptome were assessed to determine the effect of hUC-MSCs. Results Here, hUC-MSCs decreased hepatic lipid content and alanine aminotransferase/aspartate aminotransferase levels, as well as attenuated inflammation and fibrosis in choline-deficient high-fat diet (CD-HFD)-induced NAFLD mice. Mechanistically, hUC-MSCs restored impaired autophagic flux and mitigated liver steatosis through the AMPK-mTOR-TFEB pathway in both NAFLD mice and oleic acid/palmitic acid-induced “fatty” HepG2 cells. Of note, hUC-MSCs have been found to promote nuclear translocation of TFEB in PA/OA-induced HepG2 cells. Additionally, TFEB knockdown partially attenuated the effect of hUC-MSCs on enhancing autophagy and lipid metabolism in vitro. Conclusions This study suggests that hUC-MSCs represent a potential therapeutic approach to treating NAFLD through activating TFEB-mediated autophagy.

Background Mixed connective tissue disease (MCTD) is a rare autoimmune disease, and little is known about its pathogenesis. Furthermore, MCTD, systemic lupus erythematosus (SLE), and primary Sjögren’s syndrome (pSS) share many clinical, laboratory, and immunological manifestations. This overlap complicates early diagnosis and accurate treatment. Methods The transcriptomic profiling of peripheral blood mononuclear cells (PBMCs) from MCTD patients was performed using both bulk RNA sequencing and single-cell RNA sequencing (scRNA-seq) for the first time. Additionally, we applied MCTD scRNA-seq data, along with datasets from SLE (GSE135779) and pSS (GSE157278) from the Gene Expression Omnibus database, to characterize and compare the similarities and heterogeneity among MCTD, SLE, and pSS. Results We first resolved transcriptomic changes in peripheral blood immune cells of MCTD, and then revealed the shared and unique features among MCTD, SLE, and pSS. Analyses showed that the percentage of CD8 + effector T cells was increased, while mucosal-associated invariant T cells were decreased in all three diseases. Genes related to the ‘interferon (IFN) γ response’ and ‘IFN α response’ were significantly upregulated. SCENIC analysis revealed activation of STAT1 and IRF7 in disease states, targeting IFN-related genes. The IFN-II signaling network was notably elevated in all three diseases. Unique features of MCTD, SLE, and pSS were also identified. Conclusion We dissected the immune landscape of MCTD at single-cell resolution, providing new insights into the development of novel biomarkers and immunotherapies for MCTD. Furthermore, we offer insights into the transcriptomic similarities and heterogeneity across different autoimmune diseases, while highlighting prospective therapeutic targets.