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This study introduces a novel robust finite-time adaptive sliding mode control (FTSMC) strategy, emphasizing its contributions to the synchronized deployment of hydraulically actuated multi-arm systems in confined environments, such as coal bunker cleaning. Key innovations include the integration of adaptive sliding mode control with guaranteed finite-time convergence, a distributed leader–follower framework, and a graph-theoretical communication topology for localized interactions. Specifically, we developed a dynamic model for a multi-agent system comprising one leader and multiple followers, incorporating nonlinear dynamics and unknown external disturbances. The proposed controller ensures rapid finite-time convergence of tracking errors while maintaining robustness against parameter uncertainties, frictional forces, and external perturbations. The theoretical analysis, based on Lyapunov stability, rigorously proves the boundedness and convergence of all system states. Simulation results on a three-arm robotic platform validate the method’s superiority, demonstrating higher tracking accuracy, faster convergence, and stronger disturbance rejection compared with baseline controllers, including SMC, ETASMC, PID, Fixed-Time Consensus Control (FTCC), Disturbance Observer-Based Control (DOBC), and Adaptive Sliding Mode Control (ASMC). This research provides a practical and scalable solution for multi-arm coordination in unstructured environments, significantly advancing the autonomy and reliability of industrial robotic systems.

With the development of nanotechnology, significant progress has been made in the design, and manufacture of nanoparticles (NPs) for use in clinical treatments. Recent increases in our understanding of the central role of macrophages in the context of inflammation and cancer have reinvigorated interest in macrophages as drug targets. Macrophages play an integral role in maintaining the steady state of the immune system and are involved in cancer and inflammation processes. Thus, NPs tailored to accurately target macrophages have the potential to transform disease treatment. Herein, we first present a brief background information of NPs as drug carriers, including but not limited to the types of nanomaterials, their biological properties and their advantages in clinical application. Then, macrophage effector mechanisms and recent NPs-based strategies aimed at targeting macrophages by eliminating or re-educating macrophages in inflammation and cancer are summarized. Additionally, the development of nanocarriers targeting macrophages for disease diagnosis is also discussed. Finally, the significance of macrophage-targeting nanomedicine is highlighted, with the goal of facilitating future clinical translation.

Culinary culture shock (CCS)—the discomfort and ambivalence travelers feel when encountering unfamiliar foods—remains underexplored from a short-horizon, trip-bounded perspective. While prior work notes both attractions and impediments of food in tourism, a process-oriented account of how ordinary travelers experience and navigate CCS during brief trips is still limited. This study examines CCS in Guangzhou, China and delineates how it shapes travelers’ evaluations of place. We adopt a qualitative design, combining 30 semi-structured interviews with in situ ethnographic observations across markets, street-food settings, restaurants, and guided food tours, supplemented by document analysis (e.g., visitor materials and menus). Using reflexive thematic analysis, we identify three recurrent coping trajectories—avoidance, gradual adaptation, and immersion—that unfold nonlinearly as travelers recalibrate expectations, manage sensory dissonance, and renegotiate comfort boundaries. We integrate expectancy–disconfirmation theory (EDT) with an embodied view of tasting to develop the Palate Adaptation Spiral Model (PASM), which explains CCS as recursive cycles of appraisal, strategy enactment, and re-appraisal within the span of a trip. Social influence (peers, guides, and service staff) operates as a cross-cutting mechanism that can accelerate adaptation or entrench avoidance depending on cue valence and credibility. The study clarifies the scope of CCS as general travel encounters (not restricted to culinary-motivated tourists) and specifies contextual conditions under which negative reactions are reversible. Theoretically, we connect EDT to short-term culinary adaptation through PASM; practically, we outline design levers—pre-trip expectation management, pictorial/transparent menus, and guide-mediated tasting sequences—to reduce anxiety and support constructive exploration.

There is a major limitation in the immunotherapy for solid cancer is that it only benefited a minority of cancer patients. This study aims to investigate whether the differential composition of the lung microbiome could affect the sustained clinical responses in lung cancers treated with immunotherapy. Twenty-seven non-responders and 19 responders treated with anti-PD-1 therapy were included in the discovery set. Bacterial load in bronchoalveolar lavage from lung cancer patients was examined by quantitative PCR of 16S rRNA copies. Bacterial 16S rDNA was sequenced using the Illumina HiSeq on the 16S rDNA V3-V4 variable region. Operational taxonomic unit (OTU) analysis was performed using VSEARCH v2. The α-diversity and β-diversity were calculated using QIIME software. The mean copy number of bacterial 16S DNA levels significantly decreased after anti-PD-1 treatment (after: 1.8 ± 0.6×10 copies per milliliter vs prior to treatment: 3.3 ± 1.1x10 , p = 0.0036). In addition, longitudinal analysis revealed that microbial diversity was reduced taxonomically after treatment compared to those prior to the treatment (Shannon values: before: 3.291 ± 0.067 vs after: 2.668 ± 0.168, p < 0.01). Further, we observed a reduction of , including phylum (p < 0.01), class (p < 0.01), order (p < 0.01), family (p < 0.01), genus (p = 0.025) in the responders post anti-PD-1 treatment. However, there was no significant difference of in non-responders. An independent cohort was used to validate the levels of , demonstrating that patients with higher abundance of prior to treatment were significantly more likely to have poor response to anti-PD-1 therapy (p < 0.001). Airway enriched prior to anti-PD-1 therapy is associated with poor response in lung cancer, which indicated that potential resistance to immunotherapy can be attributed to lung microbiome.

Platform leadership (PL) has been increasing in digital transformation enterprises. This study explores the effects, pathways, and boundary conditions of PL on employee deviant innovation (EDI). In this study, 444 valid questionnaires were collected from ten digital transformation enterprises. Using conservation of resources theory and digital leadership theory, we built a parallel mediation model in which PL influenced EDI through psychological safety (PS) and creative self-efficacy (CSE), and verified the moderating effect of digital leadership (DL). The empirical results are as follows: (1) PL positively impacts EDI. (2) PL positively influences PS and CSE. (3) PS and CSE positively contribute to EDI. (4) PS and CSE mediate the relationship between PL and EDI. (5) DL moderates the relationship between PL and EDI, as well as between CSE and EDI. This study departs from traditional leadership theories by examining a new leadership style, PL, to inspire deviant innovation behavior among employees in digital transformation enterprises. This reveals the influencing mechanisms and provides new theoretical support for leadership and innovation management.

Lung adenocarcinoma (LUAD) represents the most frequently diagnosed histological subtype of non-small cell lung cancer with the highest mortality worldwide. Transcriptional dysregulation is a hallmark of nearly all kinds of cancers. In the study, we identified that the POU domain, class 6, transcription factor 1 (POU6F1), a member of the POU family of transcription factors, was closely associated with tumor stage and death in LUAD. We revealed that POU6F1 was downregulated in LUAD tissues and downregulated POU6F1 was predictive of an unfavorable prognosis in LUAD patients. In vitro assays, including CCK8, soft agar, transwell, clone formation, wound-healing assay, and nude mouse xenograft model all revealed that POU6F1 inhibited the growth and invasion of LUAD cells. Mechanistically, POU6F1 bound and stabilized retinoid-related orphan receptor alpha (RORA) to exert the transcriptional inhibition of hypoxia-inducible factor 1-alpha (HIF1A) and alter the expression of HIF1A signaling pathway-associated genes, including ENO1, PDK1, and PRKCB, thereby leading to the suppression of LUAD cells. Collectively, these results demonstrated the suppressive role of POU6F1/RORA in the progression of LUAD and may potentially be used as a target for the treatment of LUAD.

Background Timely identification of epidermal growth factor receptor (EGFR) mutation and anaplastic lymphoma kinase (ALK) rearrangement status in patients with non-small cell lung cancer (NSCLC) is essential for tyrosine kinase inhibitors (TKIs) administration. We aimed to use artificial intelligence (AI) models to predict EGFR mutations and ALK rearrangement status using common demographic features, pathology and serum tumor markers (STMs). Methods In this single-center study, demographic features, pathology, EGFR mutation status, ALK rearrangement, and levels of STMs were collected from Wuhan Union Hospital. One retrospective set (N = 1089) was used to train diagnostic performance using one deep learning model and five machine learning models, as well as the stacked ensemble model for predicting EGFR mutations, uncommon EGFR mutations, and ALK rearrangement status. A consecutive testing cohort (n = 1464) was used to validate the predictive models. Results The final AI model using the stacked ensemble yielded optimal diagnostic performance with areas under the curve (AUC) of 0.897 and 0.883 for predicting EGFR mutation status and 0.995 and 0.921 for predicting ALK rearrangement in the training and testing cohorts, respectively. Furthermore, an overall accuracy of 0.93 and 0.83 in the training and testing cohorts, respectively, were achieved in distinguishing common and uncommon EGFR mutations, which were key evidence in guiding TKI selection. Conclusions In this study, driverless AI based on robust variables could help clinicians identify EGFR mutations and ALK rearrangement status and provide vital guidance in TKI selection for targeted therapy in NSCLC patients.

Abstract The purpose of this study was to set up a beagle dog model, for radiation-induced lung injury, that would be able to supply fresh lung tissues in the different injury phases for research into oxidative stress levels and mitochondrial gene expression. Blood serum and tissues were collected via CT-guided core needle biopsies from dogs in the various phases of the radiation response over a 40-week period. Levels of reactive oxygen species (ROS) and manganese superoxide dismutase 2 (MnSOD) protein expression in radiation-induced lung injury were determined by in situ immunocytochemistry; malondialdehyde (MDA) content and reductase activity in the peripheral blood were also tested; in addition, the copy number of the mitochondrial DNA and the level of function of the respiratory chain in the lung tissues were assessed. ROS showed dynamic changes and peaked at 4 weeks; MnSOD was mainly expressed in the Type II alveolar epithelium at 8 weeks; the MDA content and reductase activity in the peripheral blood presented no changes; the copy numbers of most mitochondrial genes peaked at 8 weeks, similarly to the level of function of the corresponding respiratory chain complexes; the level of function of the respiratory chain complex III did not peak until 24 weeks, similarly to the level of function of the corresponding gene Cytb. Radiation-induced lung injury was found to be a dynamically changing process, mainly related to interactions between local ROS, and it was not associated with the levels of oxidative stress in the peripheral blood. Mitochondrial genes and their corresponding respiratory chain complexes were found to be involved in the overall process.

This study evaluates integrated shipboard freshwater production and fresh air pretreatment on a 20,000 TEU-class container vessel, addressing its freshwater demand and the inefficient recovery of exhaust waste heat from the main engine. The system integrates rotary dehumidification, seawater condensation, and water purification. A theoretical model was developed to evaluate the system performance, incorporating design, thermodynamic modeling, parameter optimization, and adaptability analyses under various operating conditions. The results indicate that under optimal conditions (seawater at 25 °C, outlet temperature difference of 2 °C), the single-stage system is predicted to produce approximately 1.45 m3 of freshwater per day, meeting 20.7% of the vessel’s freshwater requirement. The auxiliary electrical energy consumption, estimated based on standard engineering correlations, is 1–1.5 kWh/m3, representing a 70–80% reduction compared to conventional reverse osmosis systems (3–6 kWh/m3). The sensitivity coefficient for seawater temperature was −0.334, whereas that for output temperature was −0.167. A two-stage series configuration has the potential to further improve the demand satisfaction rate to 41–61%. Overall, the proposed system enables the cascade utilization of ship waste heat and functional integration of air pretreatment and freshwater production, offering a promising auxiliary engineering solution for energy conservation, emission reduction, and onboard freshwater self-sufficiency in marine applications.

Retinoic acid receptor-related orphan receptors (RORs) include RORα (NR1F1), RORβ (NR1F2), and RORγ (NR1F3). These receptors are reported to activate transcription through ligand-dependent interactions with co-regulators and are involved in the development of secondary lymphoid tissues, autoimmune diseases, inflammatory diseases, the circadian rhythm, and metabolism homeostasis. Researches on RORs contributing to cancer-related processes have been growing, and they provide evidence that RORs are likely to be considered as potential therapeutic targets in many cancers. RORα has been identified as a potential therapeutic target for breast cancer and has been investigated in melanoma, colorectal colon cancer, and gastric cancer. RORβ is mainly expressed in the central nervous system, but it has also been studied in pharyngeal cancer, uterine leiomyosarcoma, and colorectal cancer, in addition to neuroblastoma, and recent studies suggest that RORγ is involved in various cancers, including lymphoma, melanoma, and lung cancer. Some studies found RORγ to be upregulated in cancer tissues compared with normal tissues, while others indicated the opposite results. With respect to the mechanisms of RORs in cancer, previous studies on the regulatory mechanisms of RORs in cancer were mostly focused on immune cells and cytokines, but lately there have been investigations concentrating on RORs themselves. Thus, this review summarizes reports on the regulation of RORs in cancer and highlights potential therapeutic targets in cancer.