This study investigates thermal plasma-assisted pyro-gasification as an intensified allothermal route for converting biomass-derived bio-oil and representative oxygenated compounds into H2- and CO-rich syngas. An integrated experimental–numerical framework combined bio-oil fractionation, model-oil formulation, gasification tests, optical shadowgraphy, and supporting plasma-droplet calculations. Gas-phase tests using methane, acetic acid, and ethanol showed that H2 and CO dominated the permanent gas and that conversion increased with plasma specific enthalpy and the dimensionless specific-enthalpy ratio. Shadowgraphy identified rapid comb-type primary jet breakup followed by stripping or tear-off secondary fragmentation. The numerical framework is defined as a steady, two-dimensional axisymmetric Eulerian-Lagrangian model employing temperature-dependent properties, RNG k-ε turbulence, an optically thin LTE plasma representation, and Kelvin-Helmholtz WAVE breakup. Quantitative comparisons gave experimental/simulated Sauter mean diameters of 110/121 μm after optical-cutoff correction and thermocouple temperature-rise deviations of 7.4–18.5%. The combined evidence indicates that intrinsic kinetics were not the sole limitation under the tested gas-phase conditions; plasma-reactant contact, energy transfer, effective exposure time, injection geometry, and liquid heat/mass transfer were also decisive.
A series of Mn(I)-based photoinduced carbon monoxide releasing molecules (1–4) with the general formula of fac-[MnX(CO)3(NN)]0/+ (X = Br and diphenyl(2-pyridyl)phosphine; N-N = 2,2’-Bipyridine and 1,10-phenanthroline) was synthesized and evaluated for their potential CO-releasing properties and anticancer potential against four malignant and normal cell lines. Cytotoxicity screening showed selective activity toward human acute monocytic leukaemia cells (THP-1) cells, with higher activity observed under the dark conditions indicating that the complexes rather than CO release are primarily responsible for the observed in vitro anticancer activity. Lipophilicity has been shown to alter biological activity, with higher membrane permeability increasing cytotoxic effects. Among the tested complexes, the bromide complexes exhibited stronger cytotoxicity, while the corresponding phosphine compounds showed improved selectivity and reduced toxicity toward normal cells. Mechanistic studies demonstrated that these compounds target mitochondria, inducing dose-dependent modulation of mitochondrial membrane potential and reactive oxygen species production. Additionally, the bromide complexes induced a significant G2/M cell-cycle arrest.
Biophilic design is acknowledged as a crucial strategy for improving student engagement, enhancing their well-being, cognitive performance, and engagement in contemporary learning environments. However, existing biophilic evaluation methods are largely static and require cross-cultural validation, especially across East Asian and Middle Eastern environments. Egypt and China were chosen for this study because they offer a strong comparative framework and have different climates, educational philosophies, and degrees of technology integration. Simultaneously, the development of architectural techniques capable of assessing the biophilic impact of mixed reality (MR) technologies has lagged behind the fast incorporation of MR technology in schools. By creating and evaluating the Biophilic Measurement Assessment Equation (BMAE), a quantitative model that incorporates Traditional Biophilic Elements (TBE), Immersive Biophilic Elements (IBE), and Behavioral and Emotional Indicators (BEI), this work fills in these gaps. Cross-cultural empirical research with a sample of 200 students was carried out at four international schools, two in Egypt and two in China. Data were analyzed using Partial Least Squares Structural Equation Modeling (PLS-SEM). The results demonstrate strong measurement reliability and model fit (SRMR = 0.058), with biophilic factors explaining 72% of the variance in learning cognitive engagement (R² = 0.72). Among the constructs, BEI emerged as the strongest predictor (β = 0.392), followed by TBE (β = 0.312) and IBE (β = 0.278), all statistically significant (p < 0.001). The findings establish BMAE as a robust, transferable assessment framework, offering a methodological contribution to evidence-based architectural design of immersive biophilic learning environments across diverse cultural settings.
This study examines the seismic fragility of cable‑stayed bridges using an integrated probabilistic framework that explicitly incorporates spatial variability of ground motion, soil liquefaction, and nonlinear cable behavior. A detailed numerical model of the seven‑span, 730 m Suez Canal Bridge is developed in OpenSees and analyzed through nonlinear incremental dynamic analysis using twenty recorded bedrock ground motions from the PEER database. Spatial variability is represented through apparent seismic wave velocities of 100, 430, and 1000 m/s and benchmarked against uniform excitation to quantify wave‑passage effects. Soil profiles corresponding to dense sand, dry loose sand, and saturated loose sand are considered, with liquefaction simulated through a thin soft interlayer. A slackening‑based fragility methodology is introduced, evaluating cable vulnerability through loss of pretension rather than conventional yield‑strain criteria. Fragility functions are developed for elastomeric bearings, expansion joints, tower drift, section curvature, and cable yielding and slackening across four damage states using peak ground velocity as the intensity measure. Results indicate that spatial variability induces mixed, mechanism‑dependent effects: wave passage reduces displacement‑controlled fragility in bearings and expansion joints by desynchronizing support motions, whereas higher apparent wave velocities create more coherent support movement that increases curvature demands in towers and piers. For stay cables, spatial variability induces phase‑lag motions that trigger earlier and stronger slackening. Liquefaction further amplifies fragility for bearings, joints, and piers through soil softening and increases slackening susceptibility without significantly affecting cable yield strain. These findings highlight the importance of considering wave propagation, soil softening, and pretension loss in fragility assessments.
Ischemic acute kidney injury (AKI) remains a major clinical challenge, characterized by high morbidity, mortality, and a substantial risk of progression to chronic kidney disease. Accumulating evidence indicates that ischemic AKI is not merely a transient hemodynamic disorder but a complex, biologically orchestrated process driven by microvascular dysfunction, innate immune activation, inflammatory signaling, and maladaptive tissue repair. Despite advances in supportive care, effective disease-modifying therapies are still lacking. Recent studies have highlighted that key signaling pathways, including Toll-like receptor/nuclear factor-κB (TLR/NF-κB), Janus kinase/signal transducer and activator of transcription (JAK/STAT), purinergic P2X7 receptor–inflammasome signaling, heat-shock protein–mediated stress responses, and phosphoinositide 3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) cascades, govern the initiation, amplification, and resolution of ischemic renal injury. These pathways converge on downstream cellular effectors such as cell adhesion molecules (CAMs), which orchestrate leukocyte recruitment, endothelial-epithelial interactions, and spatial propagation of inflammation within the renal microvasculature. Natural compounds have emerged as promising therapeutic candidates for ischemic AKI due to their pleiotropic pharmacological properties and ability to modulate multiple pathogenic signaling networks simultaneously. A growing body of experimental evidence demonstrates that polyphenols, glycosides, saponins, and related phytochemicals attenuate ischemic renal injury by suppressing inflammatory signaling, reducing CAM expression, preserving microcirculatory integrity, and promoting adaptive repair. Furthermore, advances in nanocarrier-based delivery systems have substantially enhanced the translational potential of these compounds by improving bioavailability, renal targeting, and pathway-specific modulation. In this review, we provide a comprehensive, signaling-centered analysis of ischemic AKI pathogenesis and systematically map natural compounds to their molecular targets and downstream inflammatory effectors. By integrating mechanistic insights with emerging nanotherapeutic strategies, this work offers a structured framework for the rational development of multi-target, mechanism-based interventions for ischemic AKI. It highlights key challenges and future directions for clinical translation.
