Polyoxymethylene dimethyl ethers (PODE) and biodiesel, as low-carbon oxygenated fuels, can effectively improve engine combustion performance and reduce pollutant emissions. This study systematically investigates the effects of direct-injection fuel types (D100, B100 and P10D90) and PODE blending ratios (10%, 30% and 50%) on in-cylinder combustion, emission components and energy distribution of a turbocharged common-rail engine based on the single-fuel (SF) and dual-fuel (DF) modes. The results show that in both combustion modes, biodiesel (B100) exhibits the earliest ignition phase and the highest combustion pressure peak due to the high cetane number and high oxygen content. The introduction of methanol enhances the premixed combustion intensity in DF mode, and the peak values of premixed heat release rate of pure diesel (D100) and diesel-PODE (10% volume PODE, P10D90) increase by 68.40% and 64.10%, respectively. As the methanol torque substitution ratio (MTSR) increases, the combustion rate in DF mode increases, the combustion heat release process becomes more concentrated, cyclic variability intensifies, the ignition delay (ID) lengthens, and the combustion duration (CD) shortens. P10D90 has the relatively low emission levels of incomplete combustion products, especially CH3OH and HCHO emissions. When the PODE blending ratio (PBR) rises from 10% to 50%, the ID and CD in DF mode decrease by 9.19% and 4.94%, respectively, and Soot emissions in SF and DF modes decrease by 16.67% and 23.80%, respectively. With the increase of MTSR and PBR, NO2 emissions in DF mode significantly increase, the proportion of engine effective work is improved, while the exhaust losses decrease.
Postharvest losses in citrus fruit are significantly driven by Penicillium digitatum, the causal agent of green mold. Elucidating the mechanisms by which P. digitatum infects citrus can provide a theoretical basis for developing safe and effective postharvest disease control strategies. However, the key virulence factors mediating its pathogenicity remain poorly understood. Here, we identified a cerato-platanin effector, PdCP1, via a bioinformatics pipeline and confirmed its essential role in infection through overexpression assays. The secreted PdCP1 promotes pathogen virulence by inducing host reactive oxygen species accumulation and reducing defense enzyme activities, leading to oxidative damage in fruit tissues. Mechanistically, PdCP1 interacts with PdSkp1, a core component of the ubiquitin-proteasome system. This interaction is associated with the suppression of the alpha-linolenic acid metabolism pathway and the disruption of ROS homeostasis, thereby compromising citrus disease resistance. The present study provides new thoughts on the role and mechanism of effector protein involved P. digitatum pathogenesis.
Merkel cells, functioning as critical tactile receptors in human skin, exhibit remarkable sensitivity to light-touch stimuli, and the three-dimensional morphology of these receptors demonstrates a high adaptation to their forcefield sensing functions. We propose a fluid-structure interaction (FSI) hypothesis: the characteristic short fingerlike protrusions on the Merkel cell surface act as biomechanical micro-amplifiers, significantly enhancing their perception efficacy for light touch. To validate this hypothesis, we developed a micropillar array chip with biomimetic protrusion morphologies to replicate the stratified micro mechanical environment of native skin in vitro. Integrating micro-particle image velocimetry (mu PIV) and finite element analysis (FEA), the research reveals that under ultra-gentle mechanical stimulation (< 1 mN), these protrusions alter local hydrodynamic characteristics by enhancing localized vorticity and shear strain, thereby functioning as micro-amplifiers for tactile signals. The results indicate that, compared to the smooth control structures without protrusions, the biomimetic microstructures with protrusions increase the local vorticity and the wall friction coefficient. This localized physical field amplification directly facilitates the effective transmission of stress to the cell membrane and its subsequent deformation. Utilizing microfluidic trapping and ultrasonic phased array stimulation, we verified at the cellular level that these amplified mechanical signals can significantly enhance the activation of Piezo channels, manifested as prominent calcium influx. This study not only elucidates the mechanism by which Merkel cell protrusions exert mechanical signal amplification through microenvironmental modulation from a micromechanical perspective, but also provides a biomimetic framework and theoretical guidance for the design of highly sensitive artificial electronic skin.
Coal-fired thermal power plants have been an important way to produce heat and power, but they account for a great proportion of anthropogenic carbon dioxide emissions, responsible for climate change. Partially replacing it with ammonia is a potential way to reduce carbon footprint while enhancing combustion characteristics. Extensive experimental and numerical investigations have been carried out on the pollutant formation, flame stability, thermodynamic, and techno-economic aspects of ammonia/coal co-firing thermal power plants, which are important to the development and application. This work aims to provide a comprehensive review of the recent progress of such a combustion strategy, advancing its practical application. First, pollutant formation, including NOx, soot, and carbon-related emissions, and control strategies, as well as mitigation mechanisms, are presented. Then, flame morphology and combustion stability, which are rarely reviewed in previous works, are analyzed in detail, along with the enhancement mechanisms. The thermodynamic performances of such combustion systems are also provided. This is followed by technical-economic analysis, including the levelized cost of energy and life cycle assessment. The main achievements of ammonia/coal co-firing are described in terms of carbon reduction, technical and economic feasibility. Future research directions, such as chemical mechanism modeling and pollutant formation interaction, are finally concluded.
Pain severity in osteoarthritis (OA) often dissociates from the extent of cartilage structural damage, indicating that non-structural mechanisms contribute to symptom persistence. Here, we identify articular chondrocytes as active orchestrators of pathological neurovascular invasion through a pathogenic secretome, rather than merely passive victims of degeneration. Integrated human single-cell transcriptomic analysis reveals that OA chondrocytes undergo phenotypic reprogramming characterized by coordinated activation of angiogenic and neurotrophic programs. Functionally, inflammatory chondrocytes directly promote endothelial angiogenesis and sensory axon outgrowth, linking chondrocyte-derived signals to neurovascular invasion and sustained pain. To therapeutically target this upstream mechanism, we engineered MMP-13-responsive celecoxib-loaded hyaluronic acid methacrylate microspheres (HMPC) for disease-adaptive delivery to degenerative cartilage. HMPC suppresses chondrocyte COX-2 activity and remodels the pathological chondrocyte secretome through restoration of miR-339-5p_R-5 and miR-103-3p_R-2, thereby inhibiting angiopoietin-2 (Angpt2)-mediated angiogenesis and brain-derived neurotrophic factor (Bdnf)-driven sensory neurogenesis. In murine OA models, HMPC markedly alleviates pain-related behaviors, reduces neurovascular infiltration, and preserves joint structure. Collectively, this study supports a chondrocyte-centric framework in which reprogrammed chondrocytes govern neurovascular invasion through microRNA-dependent secretome regulation and introduces a smart biomaterial-enabled strategy with disease-modifying potential for OA pain intervention.
