Search Results (1,278)

UAV delivery and ground transfer scheduling in emergency scenarios represent critical technological systems for enhancing disaster response capabilities and safeguarding lives and property. This study systematically reviews recent advances across eight core research domains: UAV emergency delivery systems, ground–air integrated transportation coordination, emergency logistics optimization, UAV path planning and scheduling algorithms, collaborative optimization between ground vehicles and UAVs, emergency response decision support systems, low-altitude economy and urban air traffic management, and intelligent transportation system integration. Research findings indicate that UAV delivery technologies in emergency contexts have evolved from single-aircraft applications to intelligent multi-modal collaborative systems, demonstrating significant advantages in medical supply distribution, disaster relief, and search-and-rescue operations. Current technological development exhibits four major trends: hybrid optimization algorithms, multi-UAV cooperation, artificial intelligence enhancement, and real-time adaptation capabilities. However, critical challenges persist, including regulatory framework integration, adverse weather adaptability, cybersecurity protection, human–machine interface design, cost–benefit assessment, and standardization deficiencies. Future research should prioritize distributed decision architectures, robustness optimization, cross-domain collaboration mechanisms, emerging technology integration, and practical application validation. This comprehensive review provides systematic theoretical foundations and practical guidance for emergency management agencies in formulating technology development strategies, enterprises in investment planning, and research institutions in determining research priorities. Full article

Tavapadon, a novel oral dopamine-D1R/D5R partial agonist, has been studied in recent years for the treatment of late-stage development Parkinson’s disease (PD). Levodopa, a dopamine precursor that currently remains the gold-standard first-line therapy for PD motor symptoms, serves as a benchmark against emerging dopaminergic agents. By selectively activating D1-family receptors on direct-pathway medium neurons, Tavapadon differs in that it delivers levodopa-level motor benefit while avoiding its many D2R/D3R-mediated adverse effects. In placebo-controlled trials, Tavapadon produced clear, clinically meaningful gains in motor function and day-to-day activities, as captured by the Unified Parkinson’s Disease Rating Scale (UPDRS). Recent late-stage results have revealed that Tavapadon maintains superior UPDRS outcomes in de novo patients and, when added to levodopa, extended “ON” time periods of reliable motor control free of troublesome dyskinesia, without introducing new safety concerns. In studies, nausea, headache, and somnolence were the most frequent adverse events. Hallucinations, orthostatic hypotension, and impulse-control disorders remained comparable to placebo, reflecting minimal D2R/D3R-mediated effects. Preclinical primate studies have demonstrated levodopa-like motor rescue with markedly less dyskinesia, a pattern mirrored in clinical add-on trials. Collectively, evidence indicates that Tavapadon can match levodopa-mediated symptomatic efficacy, lower dyskinesia liability compared with levodopa or earlier full D1 receptor (D1R) agonists, and offer the convenience of once-daily dosing characteristics, which may bridge the therapeutic gap between levodopa and the current D2R/D3R agonists in PD management. In the present investigation, the emerging clinical role for Tavapadon is described, along with the mechanism of action, clinical efficacy, safety, and future directions. Full article

Ferroptosis is a new mode of cell death, which is characterized by inducing the accumulation of lipid peroxides dependent on iron ions and reactive oxygen species. It has been found that ferroptosis can lead to follicle atresia by promoting granulosa cell death and increasing its reactive oxygen species content, but the specific mechanism has not been elucidated. Through transcriptome sequencing, we found that ferroptosis markers and related genes were upregulated in porcine atretic follicles. PTGS2 was found to be differentially expressed between atretic and healthy follicles. By inhibiting NF-κB nuclear translocation, inhibition of the PTGS2 gene expression reduced the degree of ferroptosis in granulosa cells and rescued granulosa cell death and oxidative stress caused by ferroptosis. Therefore, we propose that the NF-κB/PTGS2 axis plays a key role in ferroptosis-induced granulosa cell death, leading to follicular atresia. Melatonin, a neurohormone secreted by the pineal gland of the upper thalamus, is involved in the regulation of various metabolic, immune, reproductive, and other processes. In the ferroptosis treatment group, melatonin treatment alleviated the degree of ferroptosis (downregulation of ferroptosis marker genes and markers) and decreased the expression of PTGS2. In summary, we have demonstrated that melatonin inhibits ferroptosis via the NF-κB/PTGS2 axis in granulosa cells. Full article

Maritime transportation requires reliable navigational safety communications to ensure vessel safety and operational efficiency. The Maritime Single Window (MSW) enables vessels to submit all maritime data digitally without human intervention. NAVTEX (Navigational Telex) messages provide navigational warnings, meteorological warnings and forecasts, piracy, and search and rescue information that require integration into automated MSW system. However, NAVTEX transmissions experience message corruption when Forward Error Correction (FEC) mechanisms fail, marking unrecoverable characters with asterisks. Current standards require discarding messages exceeding 4% error rates, resulting in safety information loss. Traditional human interpretation of corrupted messages creates limitations that prevent automated MSW integration. This paper presents the application of Masked Language Modeling (MLM) with Transformer encoders for automated NAVTEX message restoration. Our approach treats asterisk characters as masked tokens, enabling bidirectional context processing to reconstruct corrupted characters. We evaluated MLM against dictionary-matching and n-gram models using 69,658 NAVTEX messages with corruption ranging from 1% to 33%. MLM achieved 85.4% restoration rate versus 44.4–64.0% for statistical methods. MLM maintained residual error rates below the 4% threshold for initial corruption up to 25%, while statistical methods exceeded this limit at 10%. This automated restoration capability supports MSW integration while preserving critical safety information during challenging transmission conditions. Full article

Cancer stem cells (CSCs), a subpopulation of tumor cells endowed with self-renewal capacity, drive cancer initiation and progression. While long non-coding RNAs (lncRNAs) are increasingly recognized as critical regulators of CSC stemness, their specific roles in gastric cancer stem cells (GCSCs) remain poorly understood. This study investigates the functional significance of lncRNA TSPEAR-AS2 in modulating GCSC properties and uncovers its underlying molecular mechanisms. Through integrated whole-transcriptome sequencing, bioinformatics analysis, and validation in 48 paired gastric cancer tissues and adjacent normal tissues, TSPEAR-AS2 was identified as a differentially expressed lncRNA upregulated in both GCSCs and tumor samples. Functional experiments revealed that TSPEAR-AS2 overexpression significantly enhanced GCSC sphere-forming ability, proliferation, cell cycle progression, epithelial–mesenchymal transition (EMT), and expression of stemness markers (CD54, CD44, OCT4, NANOG, and SOX2) while suppressing apoptosis. Conversely, TSPEAR-AS2 knockdown attenuated these malignant phenotypes. In vivo tumorigenicity assays in nude mice further confirmed that TSPEAR-AS2 promotes tumor growth, with overexpression accelerating and knockdown inhibiting tumor formation. Mechanistically, bioinformatics predictions and dual-luciferase reporter assays established TSPEAR-AS2 as a competing endogenous RNA (ceRNA) that sponges miR-15a-5p, thereby derepressing the miR-15a-5p target gene CCND1. Rescue experiments demonstrated that overexpression of miR-15a-5p phenocopied TSPEAR-AS2 knockdown, reducing GCSC stemness, while miR-15a-5p inhibition rescued the effects of TSPEAR-AS2 suppression. Collectively, these findings reveal a novel TSPEAR-AS2/miR-15a-5p/CCND1 regulatory axis that sustains GCSC stemness and tumorigenicity. These results highlight TSPEAR-AS2 as a potential therapeutic target for eradicating gastric cancer stem cells and improving clinical outcomes. Full article

An airship is a lighter-than-air vehicle that offers static lift without consuming much power. This property makes it a potential candidate for many commercial applications. The target applications include rescue operations, surveillance, communication, a data collection platform for research activities and payload delivery that requires hovering capabilities, etc. To successfully apply airships in these applications and many others, airship autonomous control development is of paramount importance. To accomplish this goal, the initial step is to model airship dynamics that cover the complete flight envelope accurately. The goal is to develop a flight simulator that can test the advanced autonomous control algorithms. In the proposed work, first, the nonlinear six-degree-of-freedom equations of motion are developed using Newtonian mechanics. These equations are used to develop a flight simulator for the University of Engineering and Technology Taxila (UETT) airship. Airship responses to different control inputs are investigated, and the results are validated with the available data in the literature for other airship projects. Also, the obtained longitudinal and lateral eigenmodes show good agreement with the experimental flight data of the UETT airship. The extensive simulation results favour the dynamic analysis of the airship. Full article

Fire is a disaster that seriously threatens people’s lives. Because fires occur suddenly and spread quickly, especially in densely populated places or areas where it is difficult to evacuate quickly, it often causes major property damage and seriously endangers personal safety. Therefore, it is necessary to detect the occurrence of fires accurately and promptly and issue early warnings. This study introduces YOLOv11-CHBG, a novel detection model designed to identify flames and smoke. On the basis of YOLOv11, the C3K2-HFERB module is used in the backbone part, the BiAdaGLSA module is proposed in the neck, the SEAM attention mechanism is added to the model detection head, and the proposed model is more lightweight, offering potential support for fire rescue efforts. The model developed in this study is shown by the experimental results to achieve an average precision (mAP@0.5) of 78.4% on the Dfire datasets, with a 30.8% reduction in parameters compared to YOLOv11. The model achieves a lightweight design, enhancing its significance for real-time fire and smoke detection, and it provides a research basis for detecting fires earlier, preventing the spread of fires and reducing the harm caused by fires. Full article

Background: Hepatocellular carcinoma (HCC) remains a global health challenge with limited therapeutic efficacy. Photodynamic therapy (PDT) using 5,10,15-triethoxycarbonyl P(V) corrole (1-P) shows promise, but its molecular mechanisms and regulatory factors, particularly the role of SIRT1, are poorly understood. Methods: The effects of 1-P combined with red light irradiation (625 nm) on HCC cells (HepG2, PLC/PRF5, MHCC97H) were evaluated via MTT, clonogenic assays, flow cytometry (apoptosis, mitochondrial membrane potential, ROS), and Western blotting (p53, Bax, Bcl-2, cleaved caspase-3, SIRT1). SIRT1-overexpressing cells and xenograft mouse models were used to validate its regulatory role. Results: 1-P with irradiation dose-dependently inhibited cell viability (IC50: 0.965–1.478 μM), suppressed clonogenicity, induced apoptosis (up to 68.8%), reduced mitochondrial membrane potential, and elevated ROS. Mechanistically, 1-P upregulated Bax/p53/cleaved caspase-3 and downregulated Bcl-2/SIRT1. SIRT1 overexpression rescued 1-P-induced apoptosis (30–50% reduction), restored mitochondrial function, and attenuated ROS accumulation. In vivo, 1-P significantly inhibited tumor growth in mice, but SIRT1 overexpression diminished this effect (p < 0.05). Conclusions: 1-P exerts potent photodynamic anticancer effects via mitochondrial dysfunction, oxidative stress, and apoptosis induction. SIRT1 is a critical modulator of 1-P activity, highlighting its potential as a therapeutic target to enhance PDT efficacy in HCC. Full article

Mammalian circadian rhythms, governing ~24 h oscillations in behavior, physiology, and hormone levels, are orchestrated by transcriptional–translational feedback loops centered around the core clock protein cryptochrome 1 (CRY1). While CRY1 ubiquitination is known to regulate clock function, the roles of specific ubiquitination sites remain unclear. Here, we identify lysine 151 (K151) as a critical residue modulating the circadian period through non-canonical mechanisms. Using site-directed mutagenesis, we generated CRY1-K151Q/R mutants mimicking constitutive deubiquitination. Circadian rescue assays in Cry1/2-deficient cells revealed period shortening (K151Q: −2.25 h; K151R: −1.4 h; n = 3, p < 0.01, Student’s t-test), demonstrating K151’s functional importance. Despite normal nuclear localization kinetics, K151Q/R mutants exhibited reduced transcriptional repression in luciferase assays, a weakened interaction with BMAL1 by the luciferase complementation assay, and enhanced binding to E3 ligase FBXL12 (but not FBXL3) while showing more stability than wild-type CRY1. Notably, the absence of ubiquitination-linked degradation or altered FBXL3 engagement suggests a ubiquitination-independent mechanism. We propose that CRY1-K151 serves as a structural hub fine-tuning circadian periodicity by modulating core clock protein interactions rather than through traditional ubiquitin-mediated turnover. These findings redefine the mechanistic landscape of post-translational clock regulation and offer new therapeutic avenues for circadian disorders. Full article

Adipose tissue development plays a critical role in determining carcass quality and meat production efficiency in swine; however, the regulatory mechanisms governing fat deposition remain incompletely understood. Circular RNAs (circRNAs), characterized by high stability and resistance to RNase R degradation, have emerged as important epigenetic regulators of livestock traits. This study investigated the regulatory role of circIDH2 in adipogenic differentiation of porcine preadipocytes and the underlying molecular mechanisms. Functional assays revealed that silencing circIDH2 markedly promoted preadipocyte proliferation while inhibiting differentiation and lipid accumulation; conversely, circIDH2 overexpression produced the opposite effects. Mechanistically, circIDH2 acted as a molecular sponge for miR-193a-5p through complementary base pairing, thereby relieving the repression of its target gene RASGRP4, a positive regulator of adipogenesis. Furthermore, this study demonstrated that miR-193a-5p promoted proliferation but suppressed the differentiation of porcine preadipocytes, whereas RASGRP4 inhibited proliferation while promoting adipogenic differentiation. Rescue experiments further confirmed the regulatory relationship among circIDH2, miR-193a-5p, and RASGRP4. In summary, the findings indicated that circIDH2 functioned as a key regulator of adipogenesis by modulating the miR-193a-5p/RASGRP4 axis, thereby suppressing preadipocyte proliferation and promoting adipogenic differentiation. These results provide a theoretical foundation for future investigations into the regulatory mechanisms of adipose tissue development. Full article

Language-guided multimodal fusion, which integrates information from both visible and infrared images, has shown strong performance in image fusion tasks. In low-light or complex environments, a single modality often fails to fully capture scene features, whereas fused images enable robots to obtain multidimensional scene understanding for navigation, localization, and environmental perception. This capability is particularly important in applications such as autonomous driving, intelligent surveillance, and search-and-rescue operations, where accurate recognition and efficient decision-making are critical. To enhance the effectiveness of multimodal fusion, we propose a text-guided infrared and visible image fusion network. The framework consists of two key components: an image fusion branch, which employs a cross-domain attention mechanism to merge multimodal features, and a text-guided module, which leverages the CLIP model to extract semantic cues from image descriptions containing visible content. These semantic parameters are then used to guide the feature modulation process during fusion. By integrating visual and linguistic information, our framework is capable of generating high-quality color-fused images that not only enhance visual detail but also enrich semantic understanding. On benchmark datasets, our method achieves strong quantitative performance: SF = 2.1381, Qab/f = 0.6329, MI = 14.2305, SD = 0.8527, VIF = 45.1842 on LLVIP, and SF = 1.3149, Qab/f = 0.5863, MI = 13.9676, SD = 94.7203, VIF = 0.7746 on TNO. These results highlight the robustness and scalability of our model, making it a promising solution for real-world multimodal perception applications. Full article

Geographic atrophy or late-stage dry age-related macular degeneration (AMD) is characterized by drusen deposition and progressive retinal pigment epithelium (RPE) degeneration, leading to irreversible vision loss. The formation of drusen leads to dyshomeostasis, oxidative stress, and irreversible damage to the RPE. In this study, we used an in vitro model of oxidized low-density lipoprotein (ox-LDL)-induced human RPE damage/death to investigate the mechanism through which a sterically hindered phenol antioxidant compound, PMC (2,2,5,7,8-pentamethyl-6-chromanol), protects the RPE against ox-LDL-induced damage. We show that PMC exerts its protective effect by preventing the upregulation of stress-responsive heme oxygenase-1 (HMOX1/HO-1) and NAD(P)H: quinone oxidoreductase (NQO1) at the mRNA and protein levels. This effect was due to PMC’s blockade of ROS generation, which in turn blocked nuclear translocation of the nuclear factor erythroid 2-related factor 2 (Nrf2) transcription factor, ultimately preventing the upregulation of antioxidant response elements (AREs), including HMOX1 and NQO1. The key role of HO-1 was demonstrated when the protective effect of PMC was inhibited by the knockdown of HMOX1. Additionally, PMC treatment under different experimental conditions and at different time points revealed that the continuous presence of PMC is required for the optimal protection against ox-LDL-induced cytotoxicity, defining the cellular pharmacokinetics of this molecule. Our data demonstrate the involvement of a key antioxidant pathway through which PMC mitigates the oxidative stress induced by ox-LDL and provides a potential therapeutic strategy for suppressing RPE degeneration/damage during AMD progression. Full article

Rafiq syndrome (RAFQS) is a rare autosomal recessive disorder that is classified as a type II congenital disorder of glycosylation (CDG-II), and caused by MAN1B1 gene mutation. To date, 24 pathogenic MAN1B1 mutations have been reported in association with MAN1B1-CDG. However, the underlying pathogenic mechanisms remain poorly understood. In this study, we recruited a consanguineous family from Pakistan with multiple affected individuals exhibiting mild facial dysmorphism, developmental delay, and intellectual disability. Utilizing exome sequencing and homozygosity mapping, we identified a novel MAN1B1 mutation (c.772_775del) that co-segregated with RAFQS in this family. Analysis of public single-cell transcriptomic data revealed that MAN1B1 is predominantly expressed in dorsal progenitors and intermediate excitatory neurons during human brain development. Knockdown of Man1b1 in primarily cultured mouse excitatory neurons disrupted axon growth, dendrite formation, and spine maturation, and could not be rescued by truncated variants identified in the family. Furthermore, in utero, electroporation experiments revealed that Man1b1 knockdown in the murine cortex impaired neural stem cells’ proliferation and differentiation, as well as cortical neuron migration. Collectively, these findings elucidate a critical role for MAN1B1 in the etiology of RAFQS and demonstrate that loss-of-function mutation in MAN1B1 disrupt neuro-developmental processes, providing mechanistic insights into the pathogenesis of this disorder. Full article

This study proposes a hierarchical framework with task priority perception for mission planning, to enhance multi-UAV coordination in maritime emergency search and rescue. By establishing a hierarchical decoupling optimization mechanism, the complex multi-region coverage problem is decomposed into two stages: task allocation and path planning. First, a coverage voyage estimation model is constructed based on regional geometric features to provide basic data for subsequent task allocation. Second, an improved multi-objective, multi-population grey wolf optimizer (IM2GWO) is designed to solve the task allocation problem; this integrates adaptive genetic operations and the multi-population coevolutionary mechanism. Finally, a globally optimal coverage path is generated based on the improved dynamic programming (DP). Simulation results indicate that the proposed method effectively reduces total task duration while boosting overall coverage benefits through the aggregation of high-value regions. IM2GWO demonstrates statistically superior performance with respect to the Pareto front distribution index across all test scenarios. Meanwhile, the path planning module based on DP can effectively reduce the overall coverage path cost. Full article

In disaster relief operations, integrating disaster reconnaissance, material delivery, and effect evaluation into a temporal task chain can significantly reduce emergency response cycles and improve rescue efficiency. However, since multiple types of heterogeneous UAVs need to be coordinated during the rescue temporal task chains assignment process, this places higher demands on the real-time dynamic decision-making and system fault tolerance of its task assignment algorithm. This study addresses the sequential dependencies among disaster reconnaissance, material delivery, and effect evaluation stages. A task allocation model for heterogeneous UAV swarm targeting temporal task chains is formulated, with objectives to minimize task completion time and energy consumption. A dynamic coalition formation algorithm based on temporary leader election and multi-round negotiation mechanisms is proposed to enhance continuous decision-making capabilities in complex disaster environments. A simulation scenario involving twenty heterogeneous UAVs and seven temporal rescue task chains is constructed. The results show that the proposed algorithm reduces average task completion time by 15.2–23.7% and average fuel consumption by 18.3–26.4% compared with cooperative network protocols and distributed auctions, with up to a 43% reduction in fuel consumption fluctuations. Full article