Search Results (5,120)

This paper addresses the trajectory tracking control problem of underactuated ships in ocean engineering, which faces the dual challenges of tracking error time–performance regulation and robustness design due to the system’s underactuated characteristics, model uncertainties, and external disturbances. Aiming to address the issues of traditional finite-time control (convergence time dependent on initial states) and fixed-time control (control chattering and parameter conservativeness), this paper proposes a predefined-time adaptive control framework that integrates an event-triggered mechanism and neural networks. By constructing a Lyapunov function with time-varying weights and designing non-periodic dynamically updated dual triggering conditions, the convergence process of tracking errors is strictly constrained within a user-prespecified time window without relying on initial states or introducing non-smooth terms. An adaptive approximator based on radial basis function neural networks (RBF-NNs) is employed to compensate for unknown nonlinear dynamics and external disturbances in real-time. Combined with the event-triggered mechanism, it dynamically adjusts the update instances of control inputs, ensuring prespecified tracking accuracy while significantly reducing computational resource consumption. Theoretical analysis shows that all signals in the closed-loop system are uniformly ultimately bounded, tracking errors converge to a neighborhood of the origin within the predefined-time, and the update frequency of control inputs exhibits a linear relationship with the predefined-time, avoiding Zeno behavior. Simulation results verify the effectiveness of the proposed method in complex marine environments. Compared with traditional control strategies, it achieves more accurate trajectory tracking, faster response, and a substantial reduction in control input update frequency, providing an efficient solution for the engineering implementation of embedded control systems in unmanned ships. Full article

Nutrition plays a fundamental role in promoting health and preventing chronic diseases, with bioactive food components offering a therapeutic potential in biomedical applications. Among these, edible oils are recognised for their functional properties, which contribute to disease prevention and metabolic regulation. The proposed study aims to evaluate the quality of four bioactive oils (olive oil, sunflower oil, tomato seed oil, and pumpkin seed oil) by analysing their thermal behaviour through infrared (IR) imaging. The study designed a customised electronic system to acquire thermographic signals under controlled temperature and humidity conditions. The acquisition system was used to extract thermal data. Analysis of the acquired thermal signals revealed characteristic heat absorption profiles used to infer differences in oil properties related to stability and degradation potential. A hybrid deep learning model that integrates Convolutional Neural Networks (CNNs) with Long Short-Term Memory (LSTM) units was used to classify and differentiate the oils based on stability, thermal reactivity, and potential health benefits. A signal analysis showed that the AI-based method improves both the accuracy (achieving an F1-score of 93.66%) and the repeatability of quality assessments, providing a non-invasive and intelligent framework for the validation and traceability of nutritional compounds. Full article

MicroRNA-211 (miR-211) is a versatile regulatory molecule that plays critical roles in cellular homeostasis and disease progression through the post-transcriptional regulation of gene expression. This review comprehensively examines miR-211’s multifaceted functions across various biological systems, highlighting its context-dependent activity as both a tumor suppressor and oncogene. In physiological contexts, miR-211 regulates cell cycle progression, metabolism, and differentiation through the modulation of key signaling pathways, including TGF-β/SMAD and PI3K/AKT. miR-211 participates in retinal development, bone physiology, and protection against renal ischemia–reperfusion injury. In pathological conditions, miR-211 expression is altered in various diseases, particularly cancer, where it may be a useful diagnostic and prognostic biomarker. Its stability in serum and differential expression in various cancer types make it a promising candidate for non-invasive diagnostics. The review also explores miR-211’s therapeutic potential, discussing both challenges and opportunities in developing miRNA-based treatments. Understanding miR-211’s complex regulatory interactions and context-dependent functions is crucial for advancing its clinical applications for diagnosis, prognosis, and targeted therapy in multiple diseases. Full article

Background: The candidate therapeutic peptide TnP demonstrates broad, system-level regulatory capacity, revealed through integrated network analysis from transcriptomic data in zebrafish. Our study primarily identifies TnP as a multifaceted modulator of drug metabolism, wound healing, proteolytic activity, and pigmentation pathways. Results: Transcriptomic profiling of TnP-treated larvae following tail fin amputation revealed 558 differentially expressed genes (DEGs), categorized into four functional networks: (1) drug-metabolizing enzymes (cyp3a65, cyp1a) and transporters (SLC/ABC families), where TnP alters xenobiotic processing through Phase I/II modulation; (2) cellular trafficking and immune regulation, with upregulated myosin genes (myhb/mylz3) enhancing wound repair and tlr5-cdc42 signaling fine-tuning inflammation; (3) proteolytic cascades (c6ast4, prss1) coupled to autophagy (ulk1a, atg2a) and metabolic rewiring (g6pca.1-tg axis); and (4) melanogenesis-circadian networks (pmela/dct-fbxl3l) linked to ubiquitin-mediated protein turnover. Key findings highlight TnP’s unique coordination of rapid (protease activation) and sustained (metabolic adaptation) responses, enabled by short network path lengths (1.6–2.1 edges). Hub genes, such as nr1i2 (pxr), ppara, and bcl6aa/b, mediate crosstalk between these systems, while potential risks—including muscle hypercontractility (myhb overexpression) or cardiovascular effects (ace2-ppp3ccb)—underscore the need for targeted delivery. The zebrafish model validated TnP-conserved mechanisms with human relevance, particularly in drug metabolism and tissue repair. TnP’s ability to synchronize extracellular matrix remodeling, immune resolution, and metabolic homeostasis supports its development for the treatment of fibrosis, metabolic disorders, and inflammatory conditions. Conclusions: Future work should focus on optimizing tissue-specific delivery and assessing genetic variability to advance clinical translation. This system-level analysis positions TnP as a model example for next-generation multi-pathway therapeutics. Full article

Fungi, from saprophytes to pathogens, face predictable daily fluctuations in light, temperature, humidity, and nutrient availability. To cope, they have evolved an internal circadian clock that confers a major adaptive advantage. This review critically synthesizes current knowledge on the molecular architecture and physiological relevance of fungal circadian systems, moving beyond the canonical Neurospora crassa model to explore the broader phylogenetic diversity of timekeeping mechanisms. We examine the core transcription-translation feedback loop (TTFL) centered on the FREQUENCY/WHITE COLLAR (FRQ/WCC) system and contrast it with divergent and non-canonical oscillators, including the metabolic rhythms of yeasts and the universally conserved peroxiredoxin (PRX) oxidation cycles. A central theme is the clock’s role in gating cellular defenses against oxidative, osmotic, and nutritional stress, enabling fungi to anticipate and withstand environmental insults through proactive regulation. We provide a detailed analysis of chrono-pathogenesis, where the circadian control of virulence factors aligns fungal attacks with windows of host vulnerability, with a focus on experimental evidence from pathogens like Botrytis cinerea, Fusarium oxysporum, and Magnaporthe oryzae. The review explores the downstream pathways—including transcriptional cascades, post-translational modifications, and epigenetic regulation—that translate temporal signals into physiological outputs such as developmental rhythms in conidiation and hyphal branching. Finally, we highlight critical knowledge gaps, particularly in understudied phyla like Basidiomycota, and discuss future research directions. This includes the exploration of novel clock architectures and the emerging, though speculative, hypothesis of “chrono-therapeutics”—interventions designed to disrupt fungal clocks—as a forward-looking concept for managing fungal infections. Full article

Today, mechatronic systems are required to operate reliably and safely. However, actuators can fail, causing the system to malfunction or, in the worst case, resulting in an accident. A clear example of this is the motors of unmanned aerial vehicles. If any of them fail, the vehicle loses control, resulting in a catastrophe and potentially leading to the partial or total loss of the system. Therefore, there is a need to design robust control strategies that allow the system to continue operating even with the loss of one of its actuators. Based on the above, this work presents a controller capable of performing output regulation while tolerating actuator faults in actuated robotic platforms. In contrast to traditional output regulation theory, where a known exosystem provides the reference signal, the proposed approach employs a High-Gain Observer (HGO) to estimate and generate the reference signal from an unknown exosystem. Additionally, an Unknown Input (UI) observer is used to estimate actuator faults, enabling the computation of a fault-tolerant control. The methodology is tested in simulation and real-time experiments on the well-known Furuta pendulum system to illustrate the effectiveness of the proposed approach. Full article

Maize–soybean intercropping is widely practised to improve land use efficiency, but shading from maize often limits soybean growth and productivity. Melatonin, a plant signaling molecule with antioxidant and growth-regulating properties, has shown potential in mitigating various abiotic stresses, including low light. This study investigated the efficacy of applying foliar melatonin (MT) to enhance shade tolerance and yield performance of soybean under intercropping. Four melatonin concentrations (0, 50, 100, and 150 µM) were applied to soybean grown under mono- and intercropping systems. The results showed that intercropping significantly reduced growth, photosynthetic activity, and yield-related traits. However, the MT application, particularly at 100 µM (MT₁₀₀), effectively mitigated these declines. MT₁₀₀ improved plant height (by up to 32%), leaf area (8%), internode length (up to 41%), grain yield (32%), and biomass dry matter (30%) compared to untreated intercropped plants. It also enhanced SPAD chlorophyll values, photosynthetic rate, stomatal conductance, chlorophyll fluorescence parameters such as Photosystem II efficiency (ɸPSII), maximum PSII quantum yield (Fv/Fm), photochemical quenching (qp), electron transport rate (ETR), Rubisco activity, and soluble protein content. These findings suggest that foliar application of melatonin, especially at 100 µM, can improve shade resilience in soybean by enhancing physiological and biochemical performance, offering a practical strategy for optimizing productivity in intercropping systems. Full article

Red blood cell (RBC) production from bone marrow hematopoietic stem cells (BMHSCs) in vitro overlooks the mechanical signals of the bone marrow niche and overly relies on growth factors. Considering that the fate of hematopoietic stem cells (HSCs) is determined by the natural bone marrow microenvironment, differences in mechanical microenvironments provide a reference for the regulation of HSC differentiation. This study seek to reveal the role of mechanobiology cues in erythropoiesis and provide a new perspective for the design of in vitro erythropoiesis platforms. The hydrogel platforms we designed simulate the stiffness gradient of the bone marrow niche to culture HSCs and induce their differentiation into the erythroid system. Cells on the low-stiffness scaffold have higher potential for erythrocyte differentiation and faster differentiation efficiency and promote erythrocyte differentiation after erythropoietin (EPO) restriction. In vivo transplantation experiments demonstrated that these cells have the ability for continuous proliferation and differentiation into mature erythrocytes. By combining mechanical cues with in vitro erythrocyte production, this method is expected to provide insights for in vitro hematopoietic design and offer a scalable cell manufacturing platform for transfusion medicine. Full article

The focal “hot spot” neuropathologies in COVID-19 infection are revealing footprints of a hidden underlying collapse of a novel ultrafast ultradian Piezo2 signaling system within the nervous system. Paradoxically, the same initiating pathophysiology may underpin the systemic findings in COVID-19 infection, namely the multiorgan SARS-CoV-2 infection-induced vascular pathologies and brain–body-wide systemic pro-inflammatory signaling, depending on the concentration and exposure to infecting SARS-CoV-2 viruses. This common initiating microdamage is suggested to be the primary damage or the acquired channelopathy of the Piezo2 ion channel, leading to a principal gateway to pathophysiology. This Piezo2 channelopathy-induced neural switch could not only explain the initiation of disrupted cell–cell interactions, metabolic failure, microglial dysfunction, mitochondrial injury, glutamatergic synapse loss, inflammation and neurological states with the central involvement of the hippocampus and the medulla, but also the initiating pathophysiology without SARS-CoV-2 viral intracellular entry into neurons as well. Therefore, the impairment of the proposed Piezo2-induced quantum mechanical free-energy-stimulated ultrafast proton-coupled tunneling seems to be the principal and critical underlying COVID-19 infection-induced primary damage along the brain axes, depending on the loci of SARS-CoV-2 viral infection and intracellular entry. Moreover, this initiating Piezo2 channelopathy may also explain resultant autonomic dysregulation involving the medulla, hippocampus and heart rate regulation, not to mention sleep disturbance with altered rapid eye movement sleep and cognitive deficit in the short term, and even as a consequence of long COVID. The current opinion piece aims to promote future angles of science and research in order to further elucidate the not entirely known initiating pathophysiology of SARS-CoV-2 infection. Full article

This paper presents a simulation-based investigation into control strategies for mitigating the consequences of cyber-assault on the steering systems of the Maritime Autonomous Surface Ships (MASS). The study focuses on two simulation experiments conducted within the Simulink/MATLAB environment, utilizing the catamaran “Nymo” MASS mathematical model to represent vessel dynamics. Cyber-attacks are modeled as external disturbances affecting the rudder control signal, emulating realistic interference scenarios. To assess control resilience, two configurations are compared during a representative turning maneuver to a specified heading: (1) a Proportional–Integral–Derivative (PID) regulator augmented with a Least Mean Squares (LMS) adaptive filter, and (2) a Nonlinear Autoregressive Moving Average with Exogenous Input (NARMA-L2) neural network regulator. The PID and LMS configurations aim to enhance the disturbance rejection capabilities of the classical controller through adaptive filtering, while the NARMA-L2 approach represents a data-driven, nonlinear control alternative. Simulation results indicate that although the PID and LMS setups demonstrate improved performance over standalone PID in the presence of cyber-induced disturbances, the NARMA-L2 controller exhibits superior adaptability, accuracy, and robustness under adversarial conditions. These findings suggest that neural network-based control offers a promising pathway for developing cyber-resilient steering systems in autonomous maritime vessels. Full article

Murine microglia exhibit rapid self-renewal upon removal from the postnatal brain. However, the signaling pathways that regulate microglial repopulation remain largely unclear. To address this knowledge gap, we depleted microglia from mixed glial cultures using anti-CD11b magnetic particles and cultured them for 4 weeks to monitor their repopulation ability in vitro. Flow cytometry and immunocytochemistry revealed that anti-CD11b bead treatment effectively eliminated >95% of microglia in mixed glial cultures. Following removal, the number of CX3CR1-positive microglia gradually increased; when a specific threshold was reached, repopulation ceased without any discernable rise in cell death. Cell cycle and 5-ethynyl-2′-deoxyuridine incorporation assays suggested the active proliferation of repopulating microglia at d7. Time-lapse imaging demonstrated post-removal division of microglia. Colony-stimulating factor 1 receptor-phosphoinositide 3-kinase-protein kinase B signaling was identified as crucial for microglial repopulation, as pharmacological inhibition or neutralization of the pathway significantly abrogated repopulation. Transwell cocultures revealed that resident microglia competitively inhibited microglial proliferation probably through contact inhibition. This in vitro microglial removal system provides valuable insights into the mechanisms underlying microglial proliferation. Full article

Aging is a well-known, complex physiological process characterized by progressive functional decline and increased susceptibility to disease, particularly in the cardiovascular and nervous systems. While genetic and environmental factors can shape its advancement, molecular regulators such as vascular endothelial growth factor (VEGF) and dopamine signaling have emerged as critical factors in maintaining vascular and neural health. VEGF promotes angiogenesis and tissue repair, while dopamine, primarily recognized for its neuromodulatory roles, regulates vascular tone and appears to modulate VEGF activity. Despite substantial research on their roles in cardiovascular and neurodegenerative diseases, little is known about how VEGF and dopamine interact in the aging process, particularly in healthy versus unhealthy aging contexts. This review describes existing evidence on the independent and potentially complementary roles of VEGF and dopamine in aging, emphasizing their influence on maintaining or improving neurovascular health. It also explores how lifestyle interventions may be beneficial in modulating VEGF and dopamine signaling pathways in the aging population. By addressing the current knowledge gap surrounding VEGF–dopamine crosstalk, this review highlights the need for further investigation into their combined effects and targeting molecular interaction to unlock new research avenues for innovative strategies for healthy aging and the potential treatment of age-related diseases. Full article

Acetate may act as a signaling molecule, regulating Paracin 1.7 production via quorum sensing (QS) in Lacticaseibacillus paracasei HD1.7. The “acetate switch” phenomenon requires mechanistic exploration to optimize Paracin 1.7 production. The “acetate switch” phenomenon delays with higher glucose levels (30 h, 36 h, and 96 h). Before the occurrence of the “acetate switch”, the ATP content increases and peaks at the “acetate switch” point and the NAD⁺/NADH ratio decreases, indicating energy changes. Moreover, the QS genes used for the pre-regulation of bacteriocin, such as prcKR, comCDE, were highly expressed. After the “acetate switch”, the ATP content decreased and the QS genes for the post-regulation of bacteriocin were highly expressed, such as rggs234 and sigma70-1/70-2. The “acetate switch” could act as an energy switch, regulating bacterial growth and QS genes. Before and after the “acetate switch”, some metabolic pathways were significantly altered according to the transcriptomic analysis by HD1.7 and HD1.7-Δpta. In this study, acetate was used as an input signal to regulate the two-component system, significantly influencing the bacteriocin expression system. And this study clarifies the roles of acetate, energy, and quorum sensing in promoting Paracin 1.7 production, providing a theoretical basis for optimizing the bacteriocin fermentation process of HD1.7. Full article

β-hydroxybutyrate (BHB) is the most abundant ketone body produced during ketosis, a process initiated by glucose depletion and the β-oxidation of fatty acids in hepatocytes. Traditionally recognized as an alternative energy substrate during fasting, caloric restriction, and starvation, BHB has gained attention for its diverse signaling roles in various physiological processes. This review explores the emerging therapeutic potential of BHB in the context of sarcopenia, metabolic disorders, and neurodegenerative diseases. BHB influences gene expression, lipid metabolism, and inflammation through its inhibition of Class I Histone deacetylases (HDACs) and activation of G-protein-coupled receptors (GPCRs), specifically HCAR2 and FFAR3. These actions lead to enhanced mitochondrial function, reduced oxidative stress, and regulation of inflammatory pathways, with implication for muscle maintenance, neuroprotection, and metabolic regulation. Moreover, BHB’s ability to modulate adipose tissue lipolysis and immune responses highlight its broader potential in managing chronic metabolic conditions and aging. While these findings show BHB as a promising therapeutic agent, further research is required to determine optimal dosing strategies, long-term effects, and its translational potential in clinical settings. Understanding BHB’s mechanisms will facilitate its development as a novel therapeutic strategy for multiple organ systems affected by aging and disease. Full article

Prolactin (PRL) is a hormone primarily associated with lactation, but it plays various roles in both men and women. PRL belongs to the family of peptide hormones, including placental lactogen and growth hormone. Interestingly, PRL is a pleiotropic hormone affecting several physiological and pathological conditions, including fertility. Moreover, several pathophysiological roles have been associated with this hormone, including those of the immune system, autoimmune disorders, asthma, and ageing. Additionally, PRL receptors are ubiquitously expressed in tissues, including the mammary gland, gonads, liver, kidney, adrenal gland, brain, heart, lungs, pituitary gland, uterus, skeletal muscle, skin blood cells, and immune system. Therefore, in the present paper, we cover the potential role that PRL may play in asthma by promoting inflammation and modulating immune responses. The detection of its receptor in lung tissue suggests a direct role in airway smooth muscle contractility through activation of signaling pathways such as JAK2-STAT5, MAPK/ERK1/2, and PI3K/Akt, as well as influencing ionic currents that regulate cell contraction, proliferation, and survival. In this sense, this review aims to explore the potential involvement of PRL in asthma pathophysiology by examining its interactions with intracellular signaling pathways and its possible impact on airway smooth muscle contractility and immune modulation. Full article