Search Results (597)

Ultraviolet radiation (UVR) exposure accelerates skin aging by disrupting cellular homeostasis and inducing epigenetic changes, such as promoter hypermethylation of key regulatory genes. However, the molecular mechanisms underlying UVR-driven epigenetic silencing remain poorly understood. By integrating high-throughput DNA methylation profiling with co-regulatory network analysis, we identified KIT as a hub gene in a photoaging-associated methylation module. Pathway enrichment further revealed coordinated hypermethylation of the canonical Wnt/β-catenin signaling pathway, establishing the Wnt/KIT axis as a critical epigenetic-signaling nexus in UVR-induced skin fibroblast aging. In immortalized human skin fibroblasts (HSFs), UVR suppressed Wnt signaling, leading to KIT promoter hypermethylation, transcriptional silencing, and premature photoaging. Gain-of-function studies revealed that reversing KIT hypermethylation either via Wnt pathway activation or KIT overexpression effectively mitigated photoaging-associated phenotypes. Crucially, we found that puerarin (PUE), a natural isoflavone, reversed UVR-induced epigenetic silencing by directly interacting with β-catenin, reactivating Wnt signaling, and restoring KIT expression. PUE treatment preserved cellular function in UVR-damaged fibroblasts. These findings establish the Wnt/β-catenin-KIT axis as a critical epigenetic driver of skin aging and highlight puerarin as a promising therapeutic candidate for targeted anti-aging intervention. Full article

Radiation-induced trismus (RIT) is a common and function-limiting late complication of radiotherapy for head and neck cancers, particularly when the masticatory muscles and temporomandibular joint receive high doses. Despite advances in intensity-modulated radiotherapy, RIT remains a significant survivorship problem, and robust biological biomarkers capable of predicting individual susceptibility are lacking. Heat shock protein 27 (HSP27; HSPB1) is a small heat shock protein that regulates multiple cellular stress responses, including proteostasis, cytoskeletal dynamics, redox homeostasis, apoptosis, and inflammatory signaling. In head and neck malignancies, HSP27 overexpression has been associated with treatment resistance and fibrosis-prone tissue remodeling. Experimental studies further demonstrate that HSP27 promotes transforming growth factor-β-mediated myofibroblast differentiation and extracellular matrix deposition, whereas pharmacologic or genetic inhibition attenuates radiation- or bleomycin-induced pulmonary fibrosis in vivo. Evidence from skeletal muscle biology also indicates that HSP27 modulates muscle integrity, denervation-associated atrophy, inflammatory signaling, and cytoskeletal stability. Although HSP27 has been widely investigated in radiation responses, fibrosis, and skeletal muscle stress adaptation, its potential involvement in the pathogenesis of RIT has not been systematically examined. This review proposes a conceptual framework in which HSP27 functions as an integrative molecular mediator linking radiation-induced oxidative stress, endothelial injury, and fibro-atrophic remodeling within the masticatory apparatus. By integrating current evidence on the epidemiology, dosimetric determinants, imaging correlates, and pathophysiology of RIT with the structural and functional biology of HSP27, this review provides the first tissue-specific synthesis of molecular stress signaling and clinical mechanisms relevant to RIT susceptibility. We further suggest that HSP27 signaling may influence susceptibility to fibro-neuromuscular injury in irradiated masticatory tissues. Given the absence of direct experimental or clinical evidence in this setting, these considerations are derived from mechanistic convergence across related biological systems and should be interpreted as biologically plausible but unproven, with potential implications for future biomarker development and biologically informed prevention strategies. Full article

In energy conversion semiconductor devices, radiation damage is directly related to the long-term stability of β-voltaic batteries. In this study, single-crystalline silicon P⁺NN⁺ devices and P⁺-silicon materials with SiO₂ surface passivation were irradiated using a ~70 keV accelerator electron beam in a nitrogen atmosphere for 2 min, 10 min, 1 h, 6 h, and 12 h. The tritium-voltaic output decreased rapidly within the first 2 min of electron beam irradiation and then decayed slowly. After 1 h of irradiation, both the output short-circuit current (Isc) and open-circuit voltage (Voc) remained stable. The effects of the damage were analyzed using typical samples irradiated for 1 h. Neutron reflectometry (NR) was employed as the primary characterization method, while X-ray photoelectron spectroscopy (XPS)—combined with Ar⁺ etching—and secondary ion mass spectrometry (SIMS) were used to verify radiation-induced structural changes at the SiO₂ surface and SiO₂/Si interface. It was found that nitrogen atoms from the atmosphere penetrated the SiO₂ layer to a depth of approximately 5–10 nm, forming a non-stoichiometric SiON structure, without further diffusion into deeper layers. Irradiation significantly increased the thickness of the SiO₂/Si interface transition layer to about 14–18.5 nm, and the SiO₂ structure within this layer became relatively loose. It can be inferred that tritium-voltaic batteries using SiO₂-surface-passivated single-crystalline silicon P⁺NN⁺ devices as energy-conversion units and packaged in a nitrogen atmosphere can stably provide power for 10 years, with an Isc reduction of no more than 12% and a Voc reduction of no more than 6%, excluding the spontaneous decay of tritium. Full article

Millimeter-wave radar imaging plays an increasingly important role in autonomous driving road perception due to its robustness under adverse weather conditions. However, radar images are inherently contaminated by multiplicative speckle noise, which severely degrades structural continuity, weakens target boundaries, and limits the perception of road scenes and surrounding objects. To address this problem, this paper proposes a structural-prior deep learning network for millimeter-wave radar image enhancement. The proposed framework first introduces an adaptive Otsu-based masking strategy to extract salient scattering structures and generate a coarse image structural prior for subsequent restoration. Guided by this prior, the network performs progressive feature enhancement through a continuous attention mechanism that integrates residual channel attention, context-aware feature extraction, and convolutional block attention, thereby enabling effective multi-scale representation learning while suppressing signal-dependent speckle interference. In addition, a composite loss function is designed by combining logarithmic denoising gain, total variation regularization, and a $\beta$-index edge-preservation term to jointly improve noise suppression, spatial smoothness, and structural fidelity. The proposed method is evaluated on the synthetic UC Merced dataset under different noise intensities and via cross-domain inference on the real-world RADIATE millimeter-wave radar dataset for autonomous driving scenarios. Experimental results demonstrate that the proposed network consistently outperforms conventional filtering methods and representative deep learning baselines in terms of PSNR, SSIM, $\beta$-index, and ENL while providing a superior preservation of road structures, target contours, and scene geometry. Ablation studies further confirm the effectiveness of the structural-prior guidance and continuous attention design. Furthermore, the network achieves a rapid inference latency of 12.35 milliseconds. These results indicate that the proposed method provides an effective and robust solution for millimeter-wave radar image enhancement and offers practical value for downstream road-scene perception in autonomous driving environments. Full article

Background/Objectives: Radon is a naturally occurring radioactive gas and the leading source of natural radiation exposure worldwide; however, its systemic biological effects in children remain poorly understood. This study examined the association between cumulative indoor radon exposure and inflammatory biomarkers among children residing in rural communities of the Aqmola region in Kazakhstan. Methods: The study included 87 children and adolescents (42 exposed and 45 controls). Radon exposure was measured in residential and school environments, and a composite Radon Exposure Index (REI) was constructed to estimate cumulative exposure over time. Serum concentrations of inflammatory biomarkers, including C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-8 (IL-8), were measured using validated immunoassay methods. Multivariable linear regression models adjusted for age, sex, body mass index, pubertal development stage, and heating type were used to evaluate associations between REI and biomarker levels. Results: Children and adolescents living in the radon-exposed community had significantly higher REI values than controls (7.75 ± 0.85 vs.4.83 ± 0.41, respectively). Among the biomarkers examined, CRP, TNF-α, IL-1β, IL-8 and IL-6 were not significantly associated with radon exposure. Conclusions: These findings do not support the use of the evaluated inflammatory biomarkers as indicators of early biological effects of environmental radon exposure in this population. However, the clear exposure contrast observed between study settings underscores the ongoing public health relevance of radon as an environmental hazard. Continued efforts to monitor and mitigate radon exposure in high-risk regions remain essential, particularly in environments where children spend substantial amounts of time. Full article

Keloids and hypertrophic scars are fibroproliferative disorders of wound healing characterized by excessive extracellular matrix deposition, constant inflammation, and high recurrence rates despite appropriate management. Conventional therapies, including surgical excision, corticosteroid injections, laser therapy, and radiation, can provide temporary relief. However, treatment failure remains common, specifically in refractory keloids. Recent findings suggest these outcomes cannot be fully explained by technical or mechanical factors alone, and pathological scarring may reflect underlying immune and neuroimmune dysfunction. Current evidence shows prolonged activation of pro-inflammatory and pro-fibrotic cytokine pathways like IL-6, TNF-α, TGF-β, and IL-17 drives sustain fibroblast activation and disrupts normal wound healing and remodeling. Additionally, the skin functions as an integrated neuro-endocrine-immune organ, allowing bidirectional communication between cutaneous nerves, immune cells, and stromal tissue. Neurogenic inflammation is mediated by neuropeptides, mast cell activation, and stress-induced hypothalamic–pituitary–adrenal axis dysregulation, which further amplifies inflammation within scar tissue. Psychiatric comorbidities like depression, anxiety, and chronic psychological stress serve as a positive feedback mechanism and are increasingly recognized as biologically active contributors to immune dysregulation. This review highlights critical gaps in current management strategies and emphasizes the need for biologically informed, multidisciplinary approaches to improve long-term outcomes for keloid and hypertrophic scar management. Full article

The rotational evolution of pulsars is governed by torque mechanisms whose mathematical structure encodes fundamental symmetries of the underlying physics. We demonstrate that the standard spin-down equation $\dot{f}=-sf-r{f}^3-g{f}^5$ derives from a discrete antisymmetry requirement, namely invariance of the torque under reversal of rotation sense, which restricts the frequency dependence to odd integer powers. We show that physically motivated plasma processes systematically break this symmetry, introducing fractional frequency exponents: viscous Ekman pumping at the crust–superfluid boundary layer ($f^{3/2}$), magnetohydrodynamic turbulent dissipation via Kolmogorov and Sweet–Parker cascades ($f^{10/3}$, $f^{11/3}$), non-linear superfluid vortex dynamics ($f^{5/2}$), and saturated r-mode oscillations ($f^{7-2\beta }$). The central result is an exact analytical resolution of the long-standing Crab pulsar braking index puzzle: the observed $n=2.51\pm 0.01$, which has defied explanation for nearly four decades, emerges naturally from the superposition of magnetic dipole radiation ($\dot{f}\propto f^3$) and boundary layer Ekman pumping ($\dot{f}\propto f^{3/2}$), with analytically derived coefficients yielding a dipole-component surface field $B_p=6.2\times {10}^{12}$ G—higher than the standard $\sqrt{P\dot{P}}$ estimate of $3.8\times {10}^{12}$ G, because that formula conflates dipole and non-dipole torques, but lower than applying the Larmor formula to the full spin-down rate ($7.6\times {10}^{12}$ G), since $32.7\%$ of the total torque is non-radiative boundary-layer dissipation. We develop the Riemann–Liouville fractional calculus formalism for these equations, showing that fractional derivatives break time-translation symmetry through intrinsic memory effects, with solutions expressed in terms of Mittag-Leffler and Fox H-functions that interpolate continuously between exponential (fully symmetric) and power-law (scale-free symmetric) relaxation. Lambert–Tsallis $W_q$ functions with non-extensive parameter q encoding broken statistical symmetry enable equation-of-state-independent inference of neutron star compactness and tidal deformability. Our framework establishes a unified symmetry-based classification of pulsar spin-down mechanisms and predicts frequency-dependent braking indices evolving at rate $\mathrm{d}n/\mathrm{d}t\sim 2\times {10}^{-4}$ yr⁻¹, yielding $\mathrm{\Delta }n\approx 0.01$ over 50 years—testable with current pulsar timing programmes. The formalism provides a coherent theoretical foundation connecting plasma microphysics at the neutron star interior to macroscopic observables in electromagnetic and gravitational wave channels. Full article

Background/Objectives: Stereotactic body radiation therapy (SBRT) provides improved pain response and local control for spinal metastases. However, management of local failure after initial SBRT is challenging. We report institutional outcomes, dosimetry, and toxicity for reSBRT following SBRT. Methods: We retrospectively reviewed 61 lesions (55 patients) treated with reSBRT after prior SBRT. Both SBRT courses delivered a median dose of 27 Gy. Patients underwent clinical and radiological evaluation every three months. Toxicity was graded using CTCAE v5.0. Dosimetric parameters for the spinal cord (SC), cauda equina (CE), planning organ-at-risk volumes (PRV), and thecal sac were converted to equivalent dose in 2 Gy fractions (EQD₂) using the linear–quadratic model (α/β = 2). Results: Median follow-up was 10.3 months. Forty lesions (65%) were cervicothoracic and 21 (35%) were lumbosacral. One- and two-year overall survival (OS) were 45% and 29%, respectively, and one- and two-year local control (LC) were 89% and 88%, respectively. Gastrointestinal primary tumors were associated with inferior LC (HR 2.41, 95% CI 1.11–5.23, p = 0.026). Fifteen patients (27%) reported myelitis/neuropathic symptoms during follow-up; four (7%) developed new post-radiation myelitis or neuropathy (RMN) without radiologic progression. Five patients (9%) developed vertebral compression fractures (VCF). Cumulative EQD₂ was not significantly associated with RMN (p = 0.344); all affected patients had thecal sac EQD₂ > 95.5 Gy and relevant nerve roots EQD₂ > 108 Gy. Conclusions: ReSBRT provided a favorable LC with acceptable toxicity. High cumulative dose to the thecal sac and nerve roots may contribute to neurologic toxicity as peripheral nerve injury. Full article

The inefficient utilization of industrial by-product phosphogypsum, coupled with the increasing global demand for cooling, has spurred the development of sustainable radiative cooling materials. Compared with conventional cooling coatings that primarily rely on expensive synthetic materials or complex fabrication processes, this study provides a promising cost-effective and sustainable route for integrating industrial solid waste valorization with zero-energy cooling technologies. In this study, we fabricated a composite coating (β-HPG@CA/SiO₂@OTS) consisting of β-hemihydrate phosphogypsum (β-HPG), a derivative product of phosphogypsum, cellulose acetate (CA), SiO₂ particles and octadecyltrichlorosilane (OTS) by a facile combination of blade coating and spraying, which exhibited strong solar reflectivity (90.9%), high mid-infrared emissivity (98.7%) and satisfactory superhydrophobicity (157°). The as-prepared composite achieved an ambient temperature drop of 18.7 °C under direct sunlight during sunny weather, achieving a net cooling power of 92.23 W/m². Meanwhile, the composite coating exhibits excellent durability after prolonged immersion in strongly acidic and alkaline solutions, ultraviolet radiation and outdoor testing. Owing to its simple fabrication process and robust cooling performance, this coating shows promise for scalable production and practical outdoor applications, such as building envelopes and equipment enclosures. Full article

Accounting for over 1.2 million new diagnoses worldwide in 2022, non-melanoma skin cancer (NMSC) represents the most common human cancer, predominantly manifesting as basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). NMSC serves as a powerful natural model for studying how environmental exposure, the exposome, reprograms the epigenome to drive carcinogenesis. Chronic ultraviolet radiation (UVR), the dominant risk factor, induces DNA damage and inflammation that dysregulate epigenetic enzymes (e.g., DNMTs, HDACs). These effects are layered with perturbations from β-HPV infection and cutaneous dysbiosis, altering DNA methylation, histone modifications, and non-coding RNA and miRNA expression in a multistep carcinogenic process. This review synthesizes the central role of epigenetic regulation as the critical interface between genetic susceptibility and cumulative exposome factors in NMSC pathogenesis. We integrate how UVR, HPV, and inflammation converge to remodel the keratinocyte epigenome. Finally, we evaluate the translational potential of this knowledge for refined risk stratification through epigenetic biomarkers and discuss emerging therapeutic strategies, including epidrugs, that target these dysregulated pathways for advanced NMSC management. Full article

Contamination of water resources by organic pollutants is a major environmental issue. Utilizing photocatalytic materials for the degradation of these pollutants presents a viable strategy for environmental clean-up. This study introduces the synthesis of an organic/inorganic hybrid photocatalyst of β-cyclodextrin (β-CD)/reduced graphene oxide (rGO) and titanium oxide (TiO₂) nanoparticles. The nanocomposite was characterized by using FT-IR, XRD, SEM, and EDAX, and the photocatalytic activity was studied by measuring the photodegradation of methylene blue (MB) under simulated solar radiation. The synthesized nanocomposite showed excellent stability and performance, with up to 92% photodegradation of MB. To further enhance the photocatalytic activity, the synthesized nanocomposite underwent modification with Ag and Pt nanoparticles. Within 90 min, photodegradation rates of 100% and 97% for MB were attained with Pt and Ag nanoparticles that were loaded at 5 wt.%, respectively. The photocatalyst’s reusability was evaluated through multiple usage cycles. Additionally, the impact of functionalization on the band gap alteration of TiO₂ is reported. Full article

Ionizing radiation affects enzymes, which are essential for most cellular functions, by inducing chemical alterations in their molecular structures, often resulting in the inhibition of their activities. Unraveling the molecular and kinetic mechanisms driving these effects requires irradiation protocols that ensure accurate dose delivery, spatial homogeneity, and reproducibility. In this study, we established a systematic experimental framework that adapts a medical linear accelerator (LINAC) as a precision source for biochemical irradiation experiments. A rigorous protocol was developed that allows enzyme solutions to be irradiated under strictly defined and verifiable dosimetric conditions. Using this approach, we quantified the radiation-induced modulation of enzyme activity in two representative enzymes: invertase (β-fructofuranosidase) and collagenase. For invertase, a pronounced nonlinear decrease in enzyme activity was observed, with the enzyme retaining approximately only 2.2% of its initial activity at 50 Gy. Conversely, collagenase activity exhibited an exponential dose–response behavior over the dose range 0.1–200 Gy, yielding a global inactivation constant of $K = 0.015 {\mathrm{G}\mathrm{y}}^{-1}$. Complementary SDS–PAGE analysis revealed no detectable radiation-induced protein fragmentation or aggregation under the investigated conditions. These results confirm enzyme-specific radiation sensitivity and demonstrate the efficacy of this LINAC-based methodology for quantitative dose–effect studies. Overall, this work provides a versatile experimental tool for applied radiation research, bridging the gap between clinical medical physics and fundamental biochemistry. Full article

This study presents a TCAD model of a SiGe HBT designed for high-speed data transfer, with a cutoff frequency of 246.5 GHz and a β-value up to 416.7. Comprehensive single-event transient (SET) irradiation simulations were performed by injecting charges at different junctions with various angles. The influence of SET on data transfer was further evaluated at circuit level by loading the SET model from TCAD simulation into a high-speed laser diode driver circuit. Hence, this work employed a collector dummy structure in the designed HBT to build radiation-hardened devices. Simulation results indicate significant mitigation of the single-event transient current, which could be reduced to 10%, compared with non-hardened devices. Full article

Spatially resolved absolute intensities of the atomic lines $H_{\alpha }$, $H_{\beta }$, $H_{\gamma }$, and $H_{\delta }$ have been measured and analyzed in pure hydrogen plasma in the linear plasma device PSI-2. Two regimes have been investigated, with nominal (0.04 Pa) and elevated (0.5 Pa) gas pressure in the sample chamber. The measurements have been compared with local 0D calculations taking into account radiation from $H(n=1)$, $H_2$, and $H_2^{+}$ channels. A baseline plasma chemical mechanism developed in magnetic fusion research was applied to calculate the $H_2^{+}$ density. Both the plasma chemical mechanism and the population factors applied are based on Sawada–Fujimoto collision-radiative model of atomic and molecular hydrogen. The calculations were found to reproduce both the absolute radiation and the line radiation intensity ratios measured in the 0.04 Pa experiment with electron temperature $T_e$ = 2–10 eV and electron density ∼5 × 10¹⁷ m⁻³. An exception is the $H_{\alpha }/H_{\gamma }$ intensity ratio, which tends to be overestimated by the model. The calculations suggest that the majority of the observed Balmer radiation in this regime is due to the $H_2^{+}$ channel. At the same time, both the applied simplified approach without detailed transport modeling and the baseline mechanism were found to be inappropriate for the 0.5 Pa experiment with reduced $T_e$ = 1–5 eV. This experimental regime can serve as a benchmark of more sophisticated hydrogen plasma models. Full article

Radiotherapy is essential for treating head and neck cancer but frequently leads to radiation-induced fibrosis (RIF) in salivary glands (SGs). RIF develops through a cascade of radiation-triggered events, including DNA damage, excessive oxidative stress, and epithelial cell death. Persistent injury can cause cells to become senescent and release inflammatory signals, fueling chronic inflammation. These processes activate pathways, particularly TGF-β/SMAD, resulting in fibroblast activation, myofibroblast differentiation, and extracellular matrix accumulation. Potential treatments include drugs, mesenchymal stem/stromal cell (MSC) therapy, and gene-transfer approaches. In which, MSC therapy is particularly promising as MSCs can migrate to injured tissue and support epithelial regeneration. Yet progress is limited by the difficulty of expanding human acinar cells (ACs) in vitro. To address this gap, tunable alginate–gelatin–hyaluronic acid (AGHA) bioink hydrogels have emerged as a suitable system as gelatin provides adhesion sites for AC attachment and 3D organoid formation, alginate offers tunable mechanical support through ionic crosslinking, and hyaluronic acid contributes essential cues for cell adhesion, migration, and morphogenesis. The aim of this review is to synthesize current understanding of the mechanisms driving RIF, evaluate available therapeutic strategies, and highlight the role of AGHA in generating engineered SG constructs to test MSC therapies for RIF. Full article