Physchem

Radiation-induced hardening (RIH) severely degrades the mechanical performance and service stability of metallic nuclear structural materials. High-entropy alloys (HEAs) have emerged as promising radiation-tolerant candidates owing to their unique lattice distortion effect and excellent mechanical properties, yet they are still susceptible to RIH under irradiation environments. In this work, molecular dynamics simulations were performed to reveal the atomic-scale RIH mechanism of the equiatomic FeNiCrCoCu HEA. The threshold displacement energy was calculated, and weaker anisotropy was observed compared with medium-entropy alloys and pure Ni, due to severe lattice distortion of the HEA. Overlapping radiation cascade simulations further demonstrated continuous defect generation and aggregation with increasing irradiation dose up to 0.09 dpa. Comparative nanoindentation simulations were conducted on pristine and irradiated HEAs to clarify the coupled evolution of defects and dislocations during plastic deformation. Different from the conventional hardening mechanism, irradiation-induced defects serve as stress concentrators to facilitate initial dislocation nucleation, leading to earlier pop-in behavior at lower indentation loads in irradiated samples. During loading, radiation-induced defects interact with geometrically necessary dislocations and form dense, stable entangled dislocation networks. Upon unloading, residual defects exert strong pinning forces that prevent dislocation network contraction and preserve permanent dislocation substructures. The synergistic effects of defect-induced dislocation pinning and constrained dislocation propagation dominate the RIH behavior of FeNiCrCoCu HEA. This work clarifies the intrinsic atomic-scale mechanism of irradiation hardening in HEAs, providing theoretical guidance for the design and optimization of advanced radiation-resistant nuclear structural materials.

The development of reusable and efficient photocatalysts through sustainable synthesis strategies is of growing interest aimed at the treatment of dye-contaminated water. In this study, graphene oxide (GO) was synthesized and subsequently functionalized with silver nanoparticles using Sidr (Ziziphus spina-christi) and marine macroalgae (Ulva lactuca) extracts as biogenic agents to obtain an Ag-GO/UL-S nanocomposite. A distinctive feature of this approach is the integration of marine Ulva lactuca and terrestrial Sidr extracts as renewable biogenic resources during the fabrication of the Ag-GO nanocomposite. The structural, morphological, and optical characteristics of synthesized materials were verified using XRD, SEM, FTIR, and UV-Vis spectrophotometry. XRD analysis confirmed the characteristic layered structure of GO and the presence of crystalline Ag phases in Ag-GO/UL-S, while FTIR and SEM provided evidence of surface functionalization and morphological modification. The photocatalytic performance of GO and Ag-GO/UL-S was evaluated toward Bromophenol Blue (BPB) under UV irradiation. After 60 min of irradiation, GO achieved 63.95% BPB degradation, whereas Ag-GO/UL-S exhibited an enhanced degradation efficiency of 73.82%. The corresponding apparent first-order rate constants increased from 0.01534 min⁻¹ for GO to 0.01846 min⁻¹ for Ag-GO/UL-S, indicating an improved photocatalytic degradation rate following Ag incorporation and biogenic functionalization. Furthermore, the Ag-GO/UL-S photocatalyst retained 87.37% of its initial activity after five consecutive cycles, compared with 80.22% for GO. These results demonstrate that the incorporation of Ag together with Sidr and Ulva lactuca biogenic constituents enhances the photocatalytic performance and reusability of GO, highlighting Ag-GO/UL-S as a promising green-synthesized photocatalyst for the treatment of BPB-contaminated water.

Breast cancer (BC) is a serious global health problem with increasing incidence and mortality, while current treatments are often associated with severe side effects and drug resistance. Therefore, new therapeutic agents with enhanced efficacy and minimal adverse effects are needed. Our previous study reported the anti-angiogenic effect of Monacolin X, a secondary metabolite of a marine-sponge-associated fungus, using combined in vitro, ex vivo, in vivo (including a DMBA-induced mammary carcinoma rat model) and in silico approaches, identifying VEGFR2 as its principal target. In this study, molecular docking and molecular dynamics (MD) simulations were performed to investigate the interactions between Monacolin X and key anti-angiogenic targets, including IGFR, EGFR, neuropilin 1 (NRP1), Tie-2, VEGFR1/2, and PDGFRα, using Schrödinger Glide XP. Selective inhibitors were used for comparison. Docking analysis showed significant binding affinities of Monacolin X toward IGFR (G-score = −9.05), PDGFRα (−7.57), VEGFR1 (−7.42), Tie-2 (−7.40), VEGFR2 (−7.515), EGFR (−6.80), and NRP1 (−5.15), with hydrogen bonding, hydrophobic contacts, and electrostatic interactions contributing to stable complexes. Notably, IGFR and Tie-2 exhibited strong interactions, suggesting potential inhibition of angiogenic signaling. MD simulations were performed for 50 ns at 300 K and 1 bar; complex stability was assessed using RMSD and RMSF analyses, and the persistence of key active site hydrogen bonds was quantified as a percentage of simulation frames. MM-PBSA binding free-energy calculations further supported the thermodynamic feasibility of these interactions. Overall, these findings highlight Monacolin X’s potential as an anti-angiogenic agent for BC. However, further in vitro and in vivo studies are required to validate its efficacy and clinical relevance.